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Yu. G. Gorb, V. I. Strona, O. V. Tkachenko, S. A. Serik, V. V. Ryabukha
Ukraïnsʹkij žurnal medicini, bìologìï ta sportu, Volume 6, pp 22-36; doi:10.26693/jmbs06.03.022

Abstract:
The features of the pathogenesis and course of type 2 diabetes mellitus and diseases of the cardiovascular system comorbid with it are considered in patients of elderly and old age – coronary artery disease, arterial hypertension, chronic heart failure. The leading role of insulin resistance, hyperglycemia and dyslipidemia in the development of metabolic, homeostatic disorders, the formation of oxidative stress and endothelial dysfunction, which, together with age-related changes in the body, contribute to the progression of type 2 diabetes mellitus and microvascular complications, primarily diabetic cardiomyopathy. Particular attention is paid to the relationship between cognitive impairment, type 2 diabetes mellitus and chronic heart failure. The main factors that worsen the course and prognosis of type 2 diabetes mellitus in elderly patients, in particular, hypertension, atrial fibrillation, diabetic polyneuropathy, nephropathy, and other concomitant diseases, have been identified. Lack of compensation for type 2 diabetes due to metabolic disorders leads to the development of diabetic cardiovascular autonomic neuropathy, diabetic cardiomyopathy along with the progression of atherosclerotic lesions of different localization. The course of type 2 diabetes in these patients is often complicated by geriatric syndrome, which contains a set of cognitive impairment, senile weakness, depression, functional disorders, polymorbidity. Cognitive disorders negatively affect the course of type 2 diabetes and its complications, significantly disrupting the process of teaching patients the methods of self-control, following the advice of a doctor. It is noted that the management of this category of patients should be individual and include adequate correction of hyperglycemia to prevent microvascular complications and hypoglycemic conditions, as well as reduce cardiovascular mortality and maintain quality of life. Rational selection of drugs, taking into account the factors that determine their impact on the body of elderly patients with type 2 diabetes mellitus and possible adverse drug reactions, will increase the effectiveness and safety of drug therapy in such patients. Optimizing therapeutic approaches for elderly patients with type 2 diabetes requires effective changes in the health care system to provide them with comprehensive medical and social care according to their special needs
Bastian Brune, Johannes Korth, Sebastian Dolff, Benjamin Wilde, Winfried Siffert, Andreas Kribben, Oliver Witzke
Nephrology Dialysis Transplantation, Volume 36; doi:10.1093/ndt/gfab106.005

Abstract:
Background and Aims Arterial hypertension is one of the most common diseases of the cardiovascular system worldwide and is still the cause of most deaths in Germany. Data on interactions of the endothelin-system with the renin-angiotensin- and the sympathoadrenergic system in the regulation of systemic hemodynamics in humans are lacking. In our present investigation we study the effects of Endothelin A-, Alpha1- and Angiotensin II-type-1-receptor antagonization on the systemic pressor effects of intravenous Endothelin-1-application in young, healthy men. In addition, we analyzed the effects of the genetic variations of the GNB3 C825T-polymorphism on hemodynamic changes. GNB3 825CT/TT-allele-carriers are considered to have a higher risk for multiple diseases with structural, vascular degeneration, such as arterial hypertension, diabetes mellitus and obesity. Method 21 healthy male volunteers were included in this double- blind, randomized, placebo-controlled cross-over study and were studied on four days. Endothelin-1 (ET-1) (0.5, 1, 2.5, 5 ng/kg/min for 20 min each) was given intravenous 2.0 hours after oral application of either placebo or Doxazosin, 3.5 hours after oral application of Candesartan (Candesartan 8 mg) or in the presence of a continuous infusion of the ET-A-selective antagonist BQ123 (60 μg/min). Blood pressure (BP) and heart rate (HR) were recorded and total peripheral resistance (TPR) was measured using impedance cardiography. ET-1-dose-response curves were analyzed with ANOVA. Data are presented as mean ± SD. Since we suspected an effect of the GNB3 C825T-polymorphism we divided the overall collective into 2 sub-collectives according to the GNB3 C825T-genotypes (n = 21, GNB3 825CC: n = 10, GNB3 825CT/TT: n = 11). Our analyses considered the overall collective and compared the sub-collectives intraday and interday. Results ET-1 increased systolic blood pressure (SBD) (p ≤ 0,01), diastolic blood pressure (DBD) and mean arterial pressure (MBP) as well as total peripheral resistance (TPR) (each p ≤ 0,001) with decreasing heart rate (HR5) (p ≤ 0,05). Elevation of blood pressure existed in both sub-collectives (GNB3 825CC: SBD & MBD: p ≤ 0,01, DBP & TPR: p ≤ 0,05, GNB3 825CT/TT: DBD, MBD & TPR: p ≤ 0,01, SBP p ≤ 0,05). Antagonization of ETA-receptors reversed the effect in the overall collective as well as in the sub-collectives. Both, Doxazosin, as well as Candesartan led to a decrease in blood pressure, however, dose-response relationship was influenced more by doxazosin (DBD: p ≤ 0,001, MBD: p ≤ 0,01) than by candesartan (all values: p > 0,05). For both drugs, blood pressure and TPR remained elevated under maximum ET-1-application compared to baseline measurement. Blood pressure dependent heart rate changes were observed in the overall collective and in GNB3 825CC-allele-carriers under sole ET-1-therapy (p ≤ 0.05) (Fig. 1). Candesartan reversed the effect of ET-1 on the sub-collectives (p > 0.05). GNB3 825CT/TT-allele-carriers showed no reduction in heart rate under ET-1-application, but with accompanying candesartan therapy (p ≤ 0.01) (Fig. 2). The genotype collectives thus behaved oppositely to the drugs in this respect. Conclusion In summary, ET-1 increased systolic, diastolic and mean arterial blood pressure as well as systemic vascular resistance. Doxazosin, Candesartan and BQ123 led to a decrease in blood pressure. Blood pressure and TPR remained elevated under maximum ET-1 application plus Candesartan or Doxazosin. The heart rate changes of the genotype-separated sub-collectives were opposite when ET-1 was administered compared to ET-1 and Candesartan.
INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), Volume 17, pp 175-188; doi:10.22141/2224-0721.17.2.2021.230573

Abstract:
This review article summarizes the existing literature on the current state of the problem of diabetes mellitus and arterial hypertension. According to the World Health Organization, hypertension and type 2 diabetes mellitus, after obesity, are among the leading cardiovascular risk factors that are most common among the world’s population. Over the past 30 years, the prevalence of hypertension has decreased to a quarter of the world’s population, but the incidence of diabetes mellitus has increased from 4.7 to 8.5 %, and the forecast for the future indicates a further dramatic increase. Improving awareness, treatment and control of these diseases is a major goal of the global health system. The prevalence of hypertension in patients with type 2 diabetes mellitus is up to three times higher than in patients without diabetes mellitus, and the combination of hypertension and diabetes mellitus significantly increases the likelihood of developing cardiovascular disease. The unfavorable relationship between these two conditions, accelerating the processes of atherosclerosis, can cause negative pathophysiological changes in the cardiovascular system. Also, it is known that cardiovascular autonomic neuropathy, resulting from damage to the autonomic nerve fibers that innervate the heart and blood vessels, is a significant complication of type 2 diabetes mellitus, especially in the presence of systemic hypertension. In particular, the issues related to common pathophysiological mechanisms, main systemic and metabolic factors that may contribute to the development of diabetes mellitus and hypertension comorbidity are analyzed. Classification, features of diagnosis of arterial hypertension, assessment of the disorders of the organs mediated by arterial hypertension are presented. Issues related to the main approaches of arterial hypertension treatment in diabetes mellitus are analyzed, namely prescription of the inhibitors of the renin-angiotensin system, calcium channel blockers, thiazide, and thiazide-like diuretics, beta-adrenergic receptor antagonists, alpha-blockers, mineralocorticoid-receptor antagonists as well as the features of combined therapy and treatment of resistant arterial hypertension.
Published: 1 April 2021
Indian Heart Journal; doi:10.1016/j.ihj.2021.04.002

Abstract:
The cause-effect of conduction disturbance in chronic lesion of coronary arteries is complicated. This study was designed to evaluate coexistent CAD in patients with symptomatic bradyarrhythmia to find common anatomic basis for conduction disturbances and its relationship to conventional coronary risk factors. In this prospective observational study, 929 patients who admitted for symptomatic bradyarrhythmia requiring permanent pacemaker implantation were included. All included patients underwent coronary angiography and were divided into groups based on angiographic findings. Association between conduction disturbances and these groups were analyzed. A total of 929 patients with mean age of 63.1 years were included in our study. We found age ≥50 years, male sex, presence of diabetes and hypertension as statistically significant predictors of abnormal coronary angiography. Obstructive CAD (≥50% stenosis) was found in 34.4% patients. Prevalence of single vessel disease, double vessel disease and triple vessel disease was 15.3%, 10.2% and 8.9% respectively. Severe coronary obstruction (≥90% obstruction) was found in 16.25% patients. Revascularization was advised in three fourth of cases of obstructive CAD. Approximately two third of patients didn’t have significant obstruction in coronaries supplying the conduction system. Type 4 was the commonest anatomy in obstructive CAD. SA Nodal artery was found more diseased in patients of SSS with p value of 0.01. Obstructive CAD was found in one third of patients undergoing PPI. Age ≥50 years, male sex, diabetes and hypertension were found significantly correlated with presence of CAD and may act as important markers for the judgment of further coronary evaluation.
I. O. Buzdugan, O. I. Fediv, S. V. Roborchuk, L. О. Voloshyna
Ukrainian Therapeutical Journal pp 14—19-14—19; doi:10.30978/utj2021-1-14

Abstract:
Objective — to investigate the functional state of endothelium and methods of correction of endothelial dysfunction in patients with gastric and duodenal peptic ulcers (GPU and DPU) in combination with hypertension (AH) and type 2 diabetes mellitus (DM2). Materials and methods. The investigation involved 100 patients, who were divided into the groups: group 1 consisted of 20 apparently healthy individuals (AHI), group 2 included 40 patients with GPU (n = 23) and DPU (n = 17) without signs of AH and DM2, group 3 involved 40 patients with GPU (n = 15) and DPU (n = 25) in combination with hypertension and DM2. The groups were sub‑divided into subgroups A and B depending on the H. pylori strains’ toxigenicity: group A included patients with CagA+ VacA+ strains’ combination, groups B — infected with H. pylori with a combination of strains of CagA+ or VacA+. All patients were administered the traditional antihelicobacter therapy (AHBT) (esomeprazole 20 mg twice daily + amoxicillin 1.0 g twice daily + clarithromycin 500 mg twice daily for 10 days). To increase the effectiveness of eradication therapy, 40 patients in addition to AHBT, received a combined probiotic (Bifidobacterium bifidum, B. lactis, Enterococcusus acidophilus, L. paracasei, L. plantarum, L. rhamnosus, L. salivarius) 1 sachet twice a day for 1 month. Eradication control was monitored 4 weeks after completion of treatment. Results. The increased expression of the vascular cell adhesion molecule‑1 (VCAM‑1) and the number of desquamated endothelial cells (DEK) and improvement of the oxidant‑antioxidant system have been established. Before the treatment, in comparison with the levels in AHI, levels of sVCAM exceeded in 5.88 times (р < 0.05), of erythrocytic malondialdehyde in 1.92 times (р < 0.05), and levels of the reduced glutathione was lower by 46.39 % (р < 0.05). The use of triple therapy improved the endothelial condition and the state of the oxidative‑antioxidant system, and additional application of probiotic promoted more effective correction of the indices of endothelial state and oxidative‑antioxidant system by means of maximal decrease of the levels of sVCAM and erythrocytic malondialdehyde and increase of the reduced glutathione levels. Conclusions. The presence of H. pylori, in particular its toxigenic strains, results in the development of endothelial disfunction in patients with GPU and DPU, combined with arterial hypertension and DM 2. When combined with hypertension and DM2, the course of GPU and DPU is accompanied with «mutual burden» syndrome resulting in the exhaustion of the antioxidant defense system and increased indexes of the glutathione system.
Published: 25 March 2021
by MDPI
Nutrients, Volume 13; doi:10.3390/nu13041076

Abstract:
In the past few decades, research has focused on the importance of addressing modifiable risk factors as a means of lowering the risk of cardiovascular disease (CVD), which represents the worldwide leading cause of death. For quite a long time, it has been considered that ethanol intake has a biphasic impact on the cardiovascular system, mainly depending on the drinking pattern, amount of consumption, and type of alcoholic beverage. Multiple case-control studies and meta-analyses reported the existence of a “U-type” or “J-shaped” relationship between alcohol and CVD, as well as mortality, indicating that low to moderate alcohol consumption decreases the number of adverse cardiovascular events and deaths compared to abstinence, while excessive alcohol use has unquestionably deleterious effects on the circulatory system. However, beginning in the early 2000s, the cardioprotective effects of low doses of alcohol were abnegated by the results of large epidemiological studies. Therefore, this narrative review aims to reiterate the association of alcohol use with cardiac arrhythmias, dilated cardiomyopathy, arterial hypertension, atherosclerotic vascular disease, and type 2 diabetes mellitus, highlighting literature disagreements over the risk and benefits of low to moderate drinking on the cardiovascular system.
Jernej Letonja, Matej Završnik, Jana Makuc, Maja Šeruga, Ana Peterlin, Ines Cilenšek,
Bosnian Journal of Basic Medical Sciences; doi:10.17305/bjbms.2020.5368

Abstract:
The global prevalence for diabetes mellitus nearly doubled from 4.7% in 1980 to 8.5% in 2014. Sirtuin 1 (SIRT1) is an NAD+-dependent deacetylase that is expressed in a variety of tissues. It modifies proteins that participate in DNA repair, stress, and inflammatory response. The aim of the study was to investigate the relationship between SIRT1 rs7069102 polymorphism and diabetic nephropathy (DN) in patients with T2DM. In our retrospective association study, we included 724 Slovene (Caucasian) patients who have had T2DM for at least 10 years. We classified the participants into two groups, the first group was comprised of 301 patients with DN, and the second (control) group was comprised of 423 patients without DN. We analyzed the rs7069102 polymorphism using StepOne Real-Time PCR System and TaqMan SNP Genotyping Assay. We found a statistically significant difference in the distribution of rs7069102 genotypes and alleles between the two groups. We used logistic regression analysis and adjusted for systolic pressure, arterial hypertension (AH), duration of AH, triglycerides, the value of HbA1c, carotid disease, diabetic foot, and DR. Furthermore, we discovered that patients with the CC genotype are significantly more likely to develop DN according to both the codominant (OR = 1.94; 95% CI = 1.09 – 3.45; p = 0.02) and recessive (OR = 2.39; 95% CI = 1.12 – 5.08; p = 0.02) models of inheritance. We found a significant association between the SIRT1 rs7069102 polymorphism and DN in T2DM. We speculate that SIRT1 rs7069102 might be an interesting marker of DN.
Alexandre Moura dos Santos, Rafael Giovani Misse, Isabela Bruna Pires Borges, Bruno Gualano, Alexandre Wagner Silva de Souza, Liliam Takayama, Rosa Maria R. Pereira,
Published: 8 January 2021
Advances in Rheumatology, Volume 61, pp 1-9; doi:10.1186/s42358-020-00157-1

Abstract:
Background Modifiable cardiovascular risk factors (MCRFs), such as those related to aerobic capacity, muscle strength, physical activity, and body composition, have been poorly studied in Takayasu arteritis (TAK). Therefore, the aim of the study was to investigate MCRFs and their relationships with disease status and comorbidities among patients with TAK. Methods A multicenter cross-sectional study was conducted between 2019 and 2020, in which 20 adult women with TAK were compared with 16 healthy controls matched by gender, age, and body mass index. The following parameters were analyzed: aerobic capacity by cardiopulmonary test; muscle function by timed-stands test, timed up-and-go test, and handgrip test; muscle strength by one-repetition maximum test and handgrip test; body composition by densitometry; physical activity and metabolic equivalent by IPAQ, quality of life by HAQ and SF-36; disease activity by ITAS2010 and NIH score; and presence of comorbidities. Results Patients with TAK had a mean age of 41.5 (38.0–46.3) years, disease duration of 16.0 (9.5–20.0) years, and a mean BMI of 27.7±4.5 kg/m2. Three out of the 20 patients with TAK had active disease. Regarding comorbidities, 16 patients had systemic arterial hypertension, 11 had dyslipidemia, and two had type 2 diabetes mellitus, while the control group had no comorbidities. TAK had a significant reduction in aerobic capacity (absolute and relative VO2 peak), muscle strength in the lower limbs, increased visceral adipose tissue, waist-to-hip ratio, reduced walking capacity, decreased weekly metabolic equivalent, and quality of life (P< 0.05) as compared to controls. However, there were no correlations between these MCRFs parameters and disease activity. Conclusions TAK show impairment in MCRFs; therefore, strategies able to improve MCRF should be considered in this disease.
Hanadi Marouf, Ubaid Khan, Behdad Dehbandi
Archives of Internal Medicine Research, Volume 04, pp 114-125; doi:10.26502/aimr.0062

Abstract:
Systemic arterial hypertension is considered a significant cardiovascular risk factor and is found in up to 2/3rd of patients with T2DM. Multiple clinical trials and research studies have been done to check the benefits of controlled BP in the patients with T2DM. Studies showed that people with higher BP targets in diabetic patients have general recommendations of systolic blood pressure <140 mmHg and diastolic blood pressure <90 mmHg. The multiple interlinked pathways are participated in the pathophysiological mechanisms that contributing to the increased risks of cardiovascular complications, including hypertension in diabetic patients. The therapeutic implications include pharma-cological and non-pharmacological interventions to control systemic arterial hypertension. Non-pharmacological approaches consist of lifestyle modifications, DASH diet, and sodium restriction. The pharmacological interventions include angiotensin inhibitors, calcium channel blockers, and thiazide-type diuretics, and these drugs have proven effective against hypertension in diabetic patients. In addition, the management of blood pressure is another significant factor in controlling hypertension, and this helps in monitoring the effectiveness of the treatment. Furthermore, Telehealth and Renal Denervation are two practical approaches that have been used in RCTs for BP control in hypertensive patients and have shown effective results.
T. S. Ospanova, Zh. D. Semydotska, I. O. Cherniakova, O. M. Pionova, N. S. Tryfonova, O. V. Avdieieva
Ukraïnsʹkij žurnal medicini, bìologìï ta sportu, Volume 5, pp 170-179; doi:10.26693/jmbs05.05.170

Abstract:
The problems of diagnosis, treatment, prevention of chronic obstructive pulmonary disease remain relevant due to the increase in morbidity, disability and mortality of patients. Recently, the level of renal dysfunction in the progression of chronic obstructive pulmonary disease has increased. The purpose of research was to study the indicators of renal dysfunction in chronic obstructive pulmonary disease, depending on the severity and frequency of chronic obstructive pulmonary disease exacerbations, comorbidity, respiratory function, morphological and functional state of the myocardium to optimize the diagnosis and prognosis of chronic obstructive pulmonary disease. Material and methods. The article presents the results of examination of 81 patients in different groups of chronic obstructive pulmonary disease (BCD) with comorbidity (arterial hypertension in 49 patients, diabetes mellitus type 2 – in 16, postinfarction cardiosclerosis – in 6, diffuse cardiosclerosis – in 53, angina pectoris – in 5 patients). The external respiration function was made by using a computer spirograph. The morphological and functional state of the myocardium was studied by the standard ultrasound examination. Glomerular filtration rate was estimated by using the Cockcroft-Gault formula. The A/C ratio, microalbuminuria in the morning urine portion, and the level of C-reactive protein were also studied. The results of the studies were analyzed by methods of nonparametric statistics with an assessment of differences between groups of patients using the Mann-Whitney U-test; to assess the parameters of the relationship between indicators, the method of pair rank correlation by Spearman was used. Results and discussion. Signs of renal dysfunction, hypoxia (SpO2), systemic inflammation of low intensity C-reactive protein were found only in group D of patients with chronic obstructive pulmonary disease. In the same group, the greatest number of correlations of indicators of renal dysfunction and SpO2 with various indicators of the morphofunctional state of the myocardium according to echocardiography, the frequency of exacerbations, and comorbidity with hypertension, diffuse and postinfarction cardiosclerosis was revealed. In group B and C, no correlations of indicators of renal dysfunction with other indicators were found. In the group of patients with GFR less than 90 ml/min/1.73m2, there were correlations of the A/C ratio with the frequency of exacerbations, C-reactive protein, correlations between microalbuminuria and dyspnea, daily proteinuria, and SPPA. Conclusion. In the future, it is necessary to continue the search for early specific available biomarkers of renal dysfunction that can be used for early prescription of pleiotropic therapy, and timely initiation of nephroprotection from the standpoint of network medicine
M Montenbruck, S Kelle, S Esch, A.K Schwarz, S Giusca, G Korosoglou, H Steen
European Heart Journal, Volume 41; doi:10.1093/ehjci/ehaa946.2748

Abstract:
Background Left ventricular ejection fraction (LVEF) is commonly used to assess cardiac function for patients with chronic cardiac diseases. LVEF, like most systemic function assessments, detects dysfunction once enough damage has occurred to prevent common compensatory mechanisms from maintaining cardiac output. More sensitive metrics are being evaluated to more accurately identify subclinical regional dysfunction before cardiac remodeling results in changes in LVEF and global longitudinal strain (GLS). Fast-SENC intramyocardial strain (fSENC) is a unique cardiac magnetic resonance imaging (CMR) modality that measures intramyocardial contraction in 1 heartbeat per image plane. This prospective registry compares segmental fSENC to standard CMR calculations (e.g. LVEF, volumes, mass, etc.) for patients with arterial hypertension in the absence of non-ischemic cardiomyopathy. Methods A single center, prospective registry of CMR scans acquired with a 1.5T scanner were evaluated for standard CMR calculations as well as fSENC scans. Intramyocardial LV & RV strain was quantified with MyoStrain software. Three short axis scans (basal, midventricular, & apical) were used to calculate peak strain in 16 LV & 6 RV longitudinal segments while three long axis scans (2-, 3-, & 4-chamber) were used to calculate 21 LV & 5 RV circumferential segments. Results A total of 773 scans in 650 patients with arterial hypertension but without non-ischemic cardiomyopathies were included in the study. Patients had an average (± stdev) age of 64 (13) yrs and BMI of 28 (5) kg/m2; 24% diabetes mellitus, 10% atrial fibrillation, 15% pulmonary disease, and 39% coronary artery disease. Figure 1 shows a Box & Whisker's plot demonstrating the non-linear relationship between segmental fSENC strain (% of normal LV segments ≤−17%) versus LVEF. The progression of hypertensive heart disease was associated with reduction in septal circumferential contraction despite normal LVEF. Conclusion Segmental fSENC detects subclinical LV dysfunction in patients with early hypertensive heart disease before changes in LVEF. Evaluating segmental longitudinal and circumferential fSENC peak strain provides an alternative metric that shows consistent changes in cardiac function in patients with arterial hypertension. Figure 1 Funding Acknowledgement Type of funding source: None
Amrit Pal Singh, Tajpreet Kaur, Harpal Singh Buttar
Biochemistry of Cardiovascular Dysfunction in Obesity pp 111-124; doi:10.1007/978-3-030-47336-5_6

Abstract:
Obesity is escalating all over the world and prevails among 13% of adult population. World Health Organization (WHO) has estimated that excessive body weight and obesity related incidences of type 2 diabetes mellitus (T2D) and cardiovascular diseases (CVDs) has increased nearly fourfold over the last 25 years. Excessive deposition of peripheral and visceral fat also causes metabolic syndrome and renal complications. In obese subjects, the risk of non-communicable diseases (NCDs) such as musculoskeletal and neurodegenerative disorders, infertility, and breast cancer is relatively higher than lean persons. The white adipocytes secrete a wide variety of bioactive chemicals such as adipokines, resistin, leptin, interleukins (IL-1β, IL-6), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), monocyte chemoattractant protein-1 (MCP-1), free fatty acid, macrophages infiltration, mast cell degranulation, plasminogen activator inhibitor-1 (PAI-1), endothelial adherence molecules and oxidative stress. These bioactive chemicals play crucial role in the pathogenesis of obesity-induced disorders like insulin resistance, dyslipidemia, metabolic syndrome, atherosclerosis, thrombosis, vasculopathy, high blood pressure, glomerulopathy and glomerulosclerosis. Well planned health care strategies are needed to reduce the risk of nongenetic factors associated with obesity, and their links with T2D, CVDs and renal diseases. The health-care burden related to NCDs such as obesity, T2D, and CVDs and neurodegenerative disorders, renal diseases and cancer is escalating worldwide. People need to think about the cost-effective measures such as lifestyle modifications, unhealthy dietary habits, physical activity, and consumption of healthful foods containing green vegetables, fruits, and Mediterranean-type diet consisting of olive oil, poultry and fish, dairy products, fiber rich foods, and low amount of red meat. The focus of this review is to highlight the relationships of obesity-induced production of inflammatory cytokines, adipokines, distortion of carbohydrate and lipid metabolism, kidney malfunction, activation of the renin-angiotensin-aldosterone system, arterial hypertension, and heart attack and stroke.
Favour Deborah Adaugo Onyelowe, Ebonyi State University, Kennedy Onyelowe, Kampala International University
Published: 31 July 2020
Path of Science, Volume 6, pp 4001-4007; doi:10.22178/pos.60-3

Abstract:
Cardiovascular Disease (CVD), which is also known as Heart Disease has been the most common cause of death among diabetic and sickle cell anemia (SCA) patients around the world. CVD includes coronary artery disease, stroke, and peripheral artery disease while SCA includes hemolysis. These are the main types of CVD, which is similar to hypertension because of the common risk factors they have, such as obesity, arterial remodeling, abnormal cholesterol levels, etc. Diabetes and SCA belong to the largest health emergencies of the 21st century. With the high rate of people with diabetes and SCA, the rate of Cardiovascular Disease increases rapidly. The rates of CVD in high-income countries generally have low CVD because of the monitoring systems for non-communicable diseases like CVD. However, the appearance of the novel COVID-19/SARS-CoV-2 has changed the narrative. With COVID-19/SARS-CoV-2 attacking more on people with previous health conditions associated to cardiovascular conditions, the backbone of high-income nations is broken and those leaving with high immune conditions are at less risk whether in the high income or low-income environments. The objective of this research is to review the Cardiovascular Disease conditions to the novel COVID-19/SARS-CoV-2 in Diabetic and SCA patients. This is due to the prevalence of this medical situation in the developing world or low income and densely populated countries. Cardiovascular Disease (CVD), which is also known as Heart Disease has been the most common cause of death among diabetic and sickle cell anemia (SCA) patients around the world. CVD includes coronary artery disease, stroke, and peripheral artery disease while SCA includes hemolysis. These are the main types of CVD, which is similar to hypertension because of the common risk factors they have, such as obesity, arterial remodeling, abnormal cholesterol levels, etc. Diabetes and SCA belong to the largest health emergencies of the 21st century. With the high rate of people with diabetes and SCA, the rate of Cardiovascular Disease increases rapidly. The rates of CVD in high-income countries generally have low CVD because of the monitoring systems for non-communicable diseases like CVD. However, the appearance of the novel COVID-19/SARS-CoV-2 has changed the narrative. With COVID-19/SARS-CoV-2 attacking more on people with previous health conditions associated to cardiovascular conditions, the backbone of high-income nations is broken and those leaving with high immune conditions are at less risk whether in the high income or low-income environments. The objective of this research is to review the Cardiovascular Disease conditions to the novel COVID-19/SARS-CoV-2 in Diabetic and SCA patients. This is due to the prevalence of this medical situation in the developing world or low income and densely populated countries.
Md Izolde Bouloukaki, Md Ludger Grote, MD Walter T McNicholas, Md Jan Hedner, Md Johan Verbraecken, Md Gianfranco Parati, Md Carolina Lombardi, Md Ozen K Basoglu, Md Athanasia Pataka, Oreste Marrone, et al.
Journal of Clinical Sleep Medicine, Volume 16, pp 889-898; doi:10.5664/jcsm.8354

Abstract:
The association of mild obstructive sleep apnoea (OSA) with important clinical outcomes remains unclear. We aimed to investigate the association between mild OSA and systemic arterial hypertension (SAH) in the European Sleep Apnoea Database (ESADA) cohort. In a multicentre sample of 4732 patients we analyzed the risk of mild OSA (sub-classified into two groups: mildAHI 5-<11/h (apnoea-hypopnoea frequency/hour [AHI] 5 to <11/h) and mildAHI 11-<15/hOSA (AHI ≥11 to <15/h ) compared to non-apnoeic snorers for prevalent SAH after adjustment for relevant confounding factors including gender, age, smoking, obesity, daytime sleepiness, dyslipidaemia, chronic obstructive pulmonary disease, type 2 diabetes and sleep test methodology [polygraphy (PG) or polysomnography (PSG)]. SAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and non-apnoeic snorers (52 vs 45 vs 30%, p<0.001). Corresponding adjusted Odds Ratios (OR) for SAH were 1.789 (mildAHI 11-<15/h, 95% confidence interval [CI] 1.49-2.15) and 1.558 (mildAHI 5-<11/h, 95%, CI 1.34-1.82), respectively; p<0.001. In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in PG (OR = 1.779, 95% CI 1.403-2.256; p<0.001) and PSG group (OR = 1.424, 95% CI 1.047-1.939; p=0.025). Our data suggest a dose response relationship between mild OSA and SAH risk, starting from 5 events/hour in PG-recordings and continuing with a further risk increase in the 11 to <15 range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify OSA patients according to cardiovascular risk.
Guangran Yang
Published: 9 June 2020
Diabetes, Volume 69; doi:10.2337/db20-576-p

Abstract:
Objective: Carbohydrate antigen 125 was reported to be related with incident type 2 diabetes risk and coronary artery calcification. However, little was known about its role in diabetic retinopathy. This study was to analyze the relationship between carbohydrate antigen 125 and diabetic retinopathy in type 2 diabetes. Method: Type 2 diabetes people hospitalized in the department of Endocrinology without a history of tumor from March 2018 to February 2019 were enrolled. Diabetic retinopathy was diagnosed on the results of fundus photography. Serum carbohydrate antigen 125 was measured. People with cataract, other retina diseases, neoplastic diseases, cancers, hepatic failure and renal failure were excluded. Results: All the people were divided into two groups based on the results of fundus photography. There were 177 people with diabetic retinopathy and 291 people without diabetic retinopathy. There was no significant difference in age, body mass index, fasting glucose, and lipid profiles between the diabetic retinopathy group and nondiabetic retinopathy group (p>0.05). There was significantly different in gender, duration of diabetes, hypertension, HbA1c, and urinary albumin excretion rate (p<0.05). Diabetic retinopathy people had higher carbohydrate antigen 125 compared to people without diabetic retinopathy (9.75±6.14U/ml, 8.11±4.04U/ml, respectively, p<0.05). Logistic analysis showed that carbohydrate antigen 125 was associated with diabetic retinopathy after adjusting gender, duration of diabetes, HbA1c, hypertension, triglyceride, urinary albumin excretion rate and other confounding variables (adjusted OR=1.059, p<0.05). Conclusions: In this study, diabetic retinopathy had higher carbohydrate antigen 125 compared with people without diabetic retinopathy. Carbohydrate antigen 125 might be associated with diabetic retinopathy in type 2 diabetes. Further large-scale studies are needed to confirm this association. Disclosure G. Yang: None. Funding National Natural Science Foundation of China (81471009); Beijing Health System, Health and Technical Personnel of High Level Plan (2014-3-013); Capital’s Funds for Health Improvement and Research (2016-2-2054, 2020-026285-000005)
Ирина Алексеевна Туйзарова, Татьяна Сергеевна Свеклина, , Руслан Тальгатович Сардинов
ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», Volume 64, pp 117-123; doi:10.25557/0031-2991.2020.02.117-123

Abstract:
В ряде последних эпидемиологических и ретроспективных исследований представлены доказательства роли кальция и витамина D в развитие артериальной гипертензии и связанной с ней сердечной недостаточностью. Дефицит витамина D, который может встречаться у 82,5% населения, и связанное с ним нарушение обмена кальция, эпидемиологи расценивают как пандемию. Цель обзора - систематизация современных сведений о роли кальциевого гомеостаза и дефицита витамина D в формировании артериальной гипертензии. В обзоре литературы рассмотрены вопросы связи артериальной гипертензии с плазменными концентрациями кальция и холекальциферолов. Анализ данных литературы свидетельствует, что у молодых людей стойкое повышение артериального давления ассоциировано с высокими плазменными концентрациями Ca2+, а у пожилых, особенно лиц с остеопорозом - с низкими. Циркадианные колебания плазменных концентраций кальция совпадают с изменением величины артериального давления. Данные ряда проспективных исследований и метаанализов о связи артериальной гипертензии и низких концентраций холекальциферолов в крови подтверждены экспериментами на мышах с нокаутированным геном рецептора витамина D. Низкие концентрации витамина D в плазме крови сопровождаются уменьшением высвобождения оксида азота, поэтому предполагают, что витамин D является эндокринным регулятором ренин-ангиотензиновой системы. Дефицит витамина D осложняет течение заболеваний, ассоциированных с артериальной гипертензией (хроническая сердечная недостаточность, сахарный диабет второго типа, ожирение). Вне зависимости от географического места проживания у значительной части населения наблюдается дефицит холекальциферолов в крови. Уменьшение плазменных концентраций холекальциферолов у пожилых людей, особенно сочетанное с остеопорозом, ассоциируется с инсулинорезистентностью и АГ. Дефицит витамина D во время беременности и концентрации ниже 11 нг/мл при рождении и 25 нг/мл в раннем детстве увеличивают риск высокого систолического давления более чем в 1,5 раза. Заключение: результаты нескольких независимых метаанализов убедили авторов в необходимости включения активных форм витамина D в плановую терапию артериальной гипертензии. Several recent epidemiological and retrospective studies have provided evidence for the role of calcium and vitamin D in development of hypertension and related heart failure. Epidemiologists regard as a pandemic the vitamin D deficiency, which may occur in 82.5% of the population and be associated with calcium metabolism disorders. The aim of the review was to systematize current information about the role of calcium homeostasis and vitamin D deficiency in the development of hypertension. The review addresses the relationship of blood pressure (BP) with plasma concentrations of calcium and cholecalciferols. In young people, a persistent BP elevation correlates with high plasma concentrations of Ca2+ whereas in the elderly, particularly those with osteoporosis, high BP correlates with low Ca2+. Circadian fluctuations of plasma calcium parallel changes in BP. A number of prospective studies and meta-analyses has reported a relationship of hypertension and low blood cholecalciferols. These results were confirmed by experiments on knockout mice lacking the vitamin D receptor gene. Low plasma concentrations of vitamin D are associated with decreased release of nitric oxide, which suggests that vitamin D is an endocrine regulator of the renin-angiotensin system. Vitamin D deficiency complicates the course of diseases associated with hypertension (chronic heart failure, type 2 diabetes, obesity). Regardless of the geographical location of the residence, a significant part of the population has a shortage of cholecalciferols in the blood. Decreased plasma concentrations of cholecalciferols in the elderly, particularly in combination with osteoporosis, is associated with insulin resistance and hypertension. Vitamin D shortage during pregnancy and its concentrations
Valeria Cernaro, Saverio Loddo, Vincenzo Macaione, Valentina Teresa Ferlazzo, Rosalia Maria Cigala, Francesco Crea, Concetta De Stefano, Antonina Rita Rosalia Genovese, , Davide Bolignano, et al.
Nephrology Dialysis Transplantation, Volume 35; doi:10.1093/ndt/gfaa142.p0716

Abstract:
Background and Aims Kynurenine pathway of tryptophan metabolism is involved in the pathophysiology of chronic kidney disease (CKD) and diabetes mellitus (DM), mainly through the inflammation-induced activity of indoleamine 2,3-dioxygenase (IDO). Renin-angiotensin-aldosterone system inhibitors (RAASis) [angiotensin converting enzyme inhibitors (ACEis) and angiotensin II receptor antagonists (ARBs)] are recommended in these conditions to decrease proteinuria, slow CKD progression and reduce cardiovascular risk. The interactions between RAAS and the kynurenine pathway and the potential effects of RAASis have been reported in few experimental models but whether these drugs influence kynurenine levels in humans is unknown. We performed a single-centre cross-sectional observational study to evaluate tryptophan and kynurenine serum levels and IDO activity in CKD patients with and without type 2 DM, their correlations with markers of renal dysfunction, and their relationship with RAAS-inhibiting therapy. Method We enrolled 72 consecutive adult patients with CKD, of which 38 had DM, who were admitted to the Unit of Nephrology and Dialysis of our Hospital. Of them, 55 were receiving RAASis whereas 17 were not. Tryptophan was assessed by HPLC (high-performance liquid chromatography) analysis with an UltiMateTM 3000 chromatograph (Thermo Fisher Scientific, 168 Third Avenue Waltham, MA, USA); kynurenine was measured using an enzyme-linked immunosorbent assay (ELISA) kit (Catalogue n. K 7728; Immundiagnostik AG, Bensheim, Germany); IDO activity was calculated with the formula (kynurenine/tryptophan) x 100. Results Patients receiving RAASis and patients not under therapy only differed for frequency of arterial hypertension (100% vs 76.47%; P=0.002) and kynurenine levels, the latter being significantly lower in the treated group compared to the untreated one (1.56 ± 0.79 vs 2.16 ± 1.51 µmol/l; P=0.0378). Kynurenine did not correlate with estimated glomerular filtration rate (eGFR), proteinuria or albuminuria in the whole study cohort. Conversely, in patients not receiving RAASis it was inversely related to eGFR (r=-0.4862; P=0.0478) and directly related to proteinuria (ρ=0.493; P=0.0444) and albuminuria (ρ=0.542; P=0.0247); moreover, it varied across classes of albuminuria, being lower in patients with normoalbuminuria (0.98 ± 0.55 µmol/l) and higher in those with micro- (2.63 ± 1.53 µmol/l) and macroalbuminuria (3.09 ± 1.61 µmol/l) at the ANOVA test (F=4.008; P=0.042). In the same group, the relationship between IDO activity and eGFR was significant (ρ=-0.554; P=0.0210) and IDO activity differed across classes of albuminuria (F=3.702; P=0.05). Moreover, IDO activity was higher in patients with history of cardiovascular disease compared to those with no such history [10.22 (8.39 to 22.92) vs 7.57 (4.76 to 8.09) %; P=0.0343] whereas tryptophan had an opposite behaviour (17.00 ± 2.06 vs 22.00 ± 3.78 µmol/l; P=0.0036). Conclusion We observed lower kynurenine levels in CKD patients treated with RAASis compared to untreated patients, independently of the presence of DM, and a significant association between kynurenine and markers of renal damage only in the group not receiving RAASis. We could hypothesize that kynurenine may play a role in the pathophysiology of renal damage, as already suggested, and that drugs interfering with RAAS activation may act also by reducing kynurenine levels, in addition to their already known effects at the renal level. Indeed, kynurenine synthesis results to be higher in states of inflammation and RAAS has pro-inflammatory and pro-fibrotic actions; accordingly, RAASis could reduce the enzymatic activity responsible for kynurenine increase and this could be one of the mechanisms mediating the beneficial effects of RAAS inhibition on CKD progression. This may be relevant because kynurenine has shown pro-thrombotic effects and is emerging as a potential new biomarker of CKD.
Benton Maglinger, Jacqueline A. Frank, Justin F. Fraser, Jill Roberts, Amanda Trout, Ann Stowe, Jadwiga Turchan-Cholewo, Stephen Grupke, Keith Pennypacker
Published: 17 April 2020
The FASEB Journal, Volume 34, pp 1-1; doi:10.1096/fasebj.2020.34.s1.03973

Abstract:
Introduction Since 2015, mechanical thrombectomy is the standard treatment for emergent large vessel occlusion stroke. The previously published Blood and Clot Thrombectomy Registry and Collaboration (BACTRAC) protocol (clinicaltrials.gov NCT03153683) utilizes thrombectomy to isolate distal blood within the artery immediately downstream from the clot, peripheral blood proximal to the clot, and the thrombus. Methods Tissue samples were obtained in accordance with the established BACTRAC protocol and immediately frozen at −80°C. For this study, we compared the intracranial intraluminal blood distal to the thrombus, using each subject’s systemic arterial blood as an internal comparative control. 40μl aliquots of plasma were thawed and randomized to 96‐well plates and shipped on dry ice to Olink Proteomics (Olink Proteomics, Boston, MA). Cardiometabolic and inflammatory panels were run on 1μl aliquots using a proximity extension assay (PEA) with proximal blood plasma as an internal control for each subject and distal blood plasma as the injury site sample. Protein data were analyzed as average protein expression levels in distal plasma as compared to average protein expression levels in proximal plasma. Results 25 adult subjects (>18yrs) were included in the study, of which 15 (60%) were female. Median age was 64 (24–91). 16 subjects (64%) had hypertension, 15 (60%) had BMI > 25, 10 (40%) were active smokers, 6 (24%) had previous stroke, 4 (16%) had type II diabetes, and 4 (16%) had hyperlipidemia. Mean infarct time was 513 ± 246 minutes and mean infarct volume was 58,172 ± 82,284 mm3. Proteins with the greatest change in expression in the cardiometabolic panel were superoxide dismutase 1 (SOD1), CD59, lipocalin‐2 (LCN2), and defensin alpha 1 (DEFA1). Proteins with greatest change in expression in the inflammatory panel were interleukin 4 (IL‐4), AXIN1, interleukin 1 alpha (IL‐1a), sirtuin 2 (SIRT2), interleukin 5 (IL‐5) and leukemia inhibitory factor (LIF). There was a significant sex difference in expression levels of interleukin 20 receptor subunit alpha (IL‐20RA) (p=0.04) and IL‐4 (p=0.03). Conclusions These protein data show a complex set of intraluminal responses occurring distal to the thrombus in acute ischemic stroke. Changes in SOD1, LIF, and SIRT2 demonstrate neuroprotective and anti‐inflammatory activity, LCN2 and DEFA1 suggest a response similar to antimicrobial activity, and proteins such as IL‐4 and IL‐5 suggest eosinophil activation and a Th2 phenotype. Future studies will focus on the relationships of proteins with infarct time, infarct volume, and functional outcomes. Such analyses will provide insight into the initial molecular and cell signaling in response to ischemic stroke in the human condition. Support or Funding Information The project described was supported by the National Center for Advancing Translational Sciences, through Grant UL1TR001998 and UKHealthCare. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. Grant through Center for Clinical and Translational Science
Pablo Amair M, Ildefonzo Arocha Rodulfo
Revista Colombiana de Nefrología, Volume 7, pp 60-69; doi:10.22265/acnef.7.1.356

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Cardiovascular risk factors such as arterial hypertension, type 2 diabetes mellitus (DM2) and dyslipidemia are commonly involved with chronic kidney disease (CKD) and its contribution to long-term cardiovascular morbidity. Diffuse endothelial dysfunction and atherosclerosis are believed to be part of the common pathophysiology in diabetic and non-diabetic CKD, particularly in the elderly. Age is the main determinant of glomerular filtration rate (GFR) and effective renal plasma flow and has been reported that the presence of hypertension at baseline enhances the yearly decline in creatinine clearance. Dyslipidemia may directly affect the kidney by causing deleterious renal lipid disturbances (renal lipotoxicity), as well as indirectly through systemic inflammation and oxidative stress, vascular injury, hormones change and other signaling molecules with renal action. Several cross-sectional studies found that impaired glucose tolerance, as well as the presence of left ventricular hypertrophy, was associated with an increase in the slope of the inverse relationship between age and GFR in subjects with never-treated essential hypertension. Most of the drugs used to reduce the burden of risk factor on cardiovascular disease also benefit the renal function. So, we propose the cardiorenal continuum as a preventive strategy to protect both organ and reduce the deleterious impact of the cardiovascular risk factor on the renal function considering both organs as a functional and physiopathological binomial. Los factores de riesgo cardiovascular (FRCV) como hipertensión arterial (HTA), diabetes mellitus tipo 2 (DM2) y dislipidemia suelen estar involucrados con la enfermedad renal crónica (ERC) y su contribución a la morbilidad cardiovascular. La disfunción endotelial difusa y la aterosclerosis están conceptualizadas como parte de la fisiopatología de la ERC en diabéticos y no diabéticos, particularmente en ancianos. La edad es el principal determinante de la tasa de filtración glomerular (TFG) y flujo plasmático renal efectivo y se ha reportado que la presencia de HTA favorece la declinación en la depuración de creatinina. La dislipidemia puede afectar directamente el riñón causando trastorno renal lipídico (lipotoxicidad renal) e indirectamente a través de la inflamación sistémica y estrés oxidativo, agresión vascular y cambios humorales y de otras moléculas de señalización con acción renal. Varios estudios transversales han encontrado que el deterioro a la tolerancia glucosada y la presencia de hipertrofia ventricular izquierda están asociados con un aumento en la pendiente de la relación inversa entre edad y TFG en sujetos con HTA no tratada. La mayoría de las drogas empleadas para reducir la carga de los FRCV también son beneficiosas para la función renal. De tal forma que se propone al continuo cardiorrenal como una estrategia preventiva para proteger ambos órganos y reducir el impacto deletéreo de los FRCV sobre la función renal partiendo del punto de vista de un binomio funcional y fisiopatológico.
, Abdullah M. AlShehri
Journal of International Medical Research, Volume 48; doi:10.1177/0300060520903623

Abstract:
To investigate the inter-relationships between left ventricular mass (LVM), left ventricular (LV) geometry and arterial stiffness parameters (aortic pulse wave velocity [Ao-PWV] and heart rate-corrected augmentation index [c-AIx]) in patients with chronic heart failure (CHF). This study was a secondary analysis of existing data that were collected from patients with CHF New York Heart Association class I–III with reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF). Transthoracic echocardiography was performed on all patients, along with measurement of arterial stiffness parameters (Ao-PWV and c-AIx) using sphygmocardiography. A total of 73 patients (58 males) with a mean ± SD age of 55.9 ± 11.6 years were enrolled in this study. Of these, 20 patients (27.4%) had systemic hypertension, 46 (63.0%) had type 2 diabetes mellitus. Ischaemic heart disease was the main aetiology of CHF (63 of 73 patients; 86.3%). In multiple linear regression, the left ventricular mass index (LVMI) was significantly associated with c-AIx (β = –1.59) and EF (β = –1.51). Comparison of Ao-PWV among the four LV geometric patterns revealed significant differences. In this cohort of CHF patients, LVMI was predicted by c-AIx and EF. The corresponding values of Ao-PWV were parallel in different LV geometric patterns and confirmed their adverse prognostic values.
, Alperen Tekin
Published: 16 March 2020
The publisher has not yet granted permission to display this abstract.
Juan Ariel Jara Guerrero
Journal of Diabetes Research Review & Reports pp 1-27; doi:10.47363/jdrr/2020(2)103

Abstract:
Dysregulated glucose metabolism promote inflammation in monocytes and macrophages from patients with atherosclerotic coronary artery disease. Men with metabolic syndrome are at increased risk for sudden cardiac death, and the incident sudden death is not explained by obesity or traditional cardiovascular risk factors (Kurl, 2016), but the ingested nutritional iron. Individuals with increased abdominal adiposity exhibit an increased risk of heart failure, in spite of there are oweweigtht or not (Cavalera, 2014), because the insulin resistance contribute to increased myocardial fibrosis in the absence of hypertension (Quilliot, 2005). Iron overload, and plasma viscosity contributes to cardiovascular risk in the general population, particularly in men (Van der A, 2005; Junker, 1998). Iron influences glucose metabolism, even in the absence of significant iron overload, and its reduction may alleviate coronary heart disease and reduced or prevent their complications: High stored or free iron levels (measured by serum ferritin or catalytic iron concentrations) elevate risk for development of coronary atherosclerosis, because labile iron accelerates endothelial dysfunction and originates oxidative injury that promotes systemic and vascular inflammation, phrothrombotic conditions and insulin resistance (Williams, 2002). High serum ferritin is strongly and independently associated with acute myocardial infarction and constitutes a novel risk factor in acute sudden event (Holay, 2012). Iron plays a direct and causal role in diabetes pathogenesis mediated both by β-cell failure and insulin resistance (Simcox, 2013). In the general population, body iron stores are positively associated with the development of glucose intolerance, type 2 diabetes and gestational diabetes. In this way, blood donation significant drops in the incidence of cardiovascular events, as well as in procedures such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting (Holsworth, 2013): frequent blood donations decreased iron stores in healthy volunteers, improving insulin sensitivity and hemodynamic parameters. Iron and oxygen-derived free radicals are important in the pathogenesis of postischemic reperfusion injury and contributes substantially to endothelial dysfunction in acute coronary syndromes (Chekanov, 2002; Duffy, 2001) , and a high iron diet potentially increase ischemic damage induced by transient ischemia and early reperfusion (García-Yébenes, 2012) in animals and humans. Iron, hyperinsulinemia, and hyperglycemia act in concert to up regulate free-radical reactions (Facchini, 2000) and this metal excess accelerated the development of atherosclerosis and its accumulation may promotes illness, particularly, ischemic cardiovascular diseases. Insulin resistance in macrophages promotes formation of a necrotic core in atherosclerotic plaques by enhancing macrophage apoptosis, and exposure it to circulating blood in the event of plaque rupture can precipitate thrombosis, leading to unstable angina pectoris, myocardial infarction and sudden death (Rask.Madsen, 2012, rev). In humans phlebotomy slows progression of peripheral vascular disease and blood donation lowers significantly the risk of myocardial infarction (Salonen, 1998), particularly in insulin-resistant subjects. On the contrary, exogenous iron into healthy individuals provoked endothelial dysfunction accompanied by increased generation of superoxide radical in whole blood (Vinchi, 2014, rev). A causal relationship between pre-diabetes and cardiovascular disease exist (Ford, 2010, rev). Humans lack effective mechanisms to excrete excess iron, and excessive dietary iron uptake cause iron deposition in heart, and pancreas (Kulaksis, 2008) leading to sudden death and occult diabetes mellitus. Iron play an underappreciated role in the development of insulin resistance and insulin resistance-induced heart failure. In a chronic and acute way, Insulin resistance is an early and major factor in the development of heart failure and acute iron induced insulin resistance in cardiomyocytes (Sung, 2019). 1- Introduction 2- Catalytic Iron; Irreversible Oxidizer 3- Excess Hemoglobin and Cardiocerebrovascular Pathology 4- Free Iron as a promoter of Ischemic Heart Disease 5- Excess Ferritin and pathogenesis of Endothelial Dysfunction 6- Hyperinsulinemia as a Sudden Death Promoter. The determining role of Iron 7- Iron accumulated in excess and pathogenesis of Diabetes: High hemoglobin versus High Ferritin 8- Iron and atherosclerosis. The evidence 9- Blood Donation. Cardiovascular Pathology Protector
Yanli Yang, Xiaolei Yang, Jiayue Ren,
Published: 1 March 2020
The publisher has not yet granted permission to display this abstract.
, Eira Cerda-Reyes, , Ana K. Salas-García, Samantha Cabrera-Palma, Guillermo Cabrera-Álvarez, Carlos Cortez-Hernández, Luis A Pérez-Arredondo, Emma Purón-González, Edgar Coronado-Alejandro, et al.
Published: 28 January 2020
F1000Research, Volume 9; doi:10.12688/f1000research.21918.1

Abstract:
Background: Nonalcoholic fatty liver disease (NAFLD) is a serious worldwide health problem, with an estimated global prevalence of 24%; it has a notable relationship with other metabolic disorders, like obesity and type 2 diabetes mellitus (T2DM). Nonalcoholic steatohepatitis (NASH) is one of the most important clinical entities of NAFLD, which is associated with an increased risk of progression to liver cirrhosis and hepatocellular carcinoma (HCC). Mexico is one of the countries with the highest prevalence of metabolic diseases; therefore, we sought to investigate the impact that these clinical entities have in the progression to advanced fibrosis in Mexican patients with NASH. Methods: We performed a multicenter retrospective cross-sectional study, from January 2012 to December 2017. A total of 215 patients with biopsy-proven NASH and fibrosis were enrolled. NASH was diagnosed according NAS score and liver fibrosis was staged by the Kleiner scoring system. For comparing the risk of liver fibrosis progression, we divided our sample into two groups. Those patients with stage F0-F2 liver fibrosis were included in the group with non-significant liver fibrosis (n=178) and those individuals with F3-F4 fibrosis were included in the significant fibrosis group (n=37). We carried out a multivariate analysis to find risk factors associated with liver fibrosis progression. Results: From the 215 patients included, 37 had significant liver fibrosis (F3-4). After logistic regression analysis T2DM (p=0.044), systemic arterial hypertension (p=0.014), cholesterol (p=0.041) and triglycerides (p=0.015) were the main predictor of advanced liver fibrosis. Conclusions: In a Mexican population, dyslipidemia was the most important risk factor associated with advanced liver fibrosis and cirrhosis.
, Małgorzata Poręba, Marta Jurdziak, Ewa Trzmielewska, Katarzyna Gocławska, Arkadiusz Derkacz, Grzegorz Mazur, ,
Advances in Clinical and Experimental Medicine, Volume 29, pp 63-70; doi:10.17219/acem/111808

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The most commonly recognized cardiovascular risk factors (CVRF) include smoking cigarettes, manifestation of arterial hypertension (AH), hypercholesterolemia, hypertriglyceridemia, manifestation of type 2 diabetes mellitus (DM), and the presence of overweight or obesity. In recent years, investigations have documented the significance of asymmetric dimethylarginine concentration (ADMA) in the pathogenesis of diseases affecting the cardiovascular system. To evaluate the relationship between the number of CVRF and blood ADMA concentration. The study was conducted on a sample of 138 individuals (mean age 54.90 ±10.38 years). Among the participants, we distniguished subgroups with no CVRF (group A, n = 21), with 1-2 CVRF (group B, n = 53), with 3-4 CVRF (group C, n = 55), and with 5-6 CVRF (group D, n = 9). Plasma concentrations of arginine and of endogenous methylarginines were estimated. Plasma ADMA concentrations proved to be significantly higher in groups B, C and D than those in group A. Regression analysis allowed us to demonstrate that in the studied population of patients, manifestation of type 2 DM, followed by AH and hypercholesterolemia, were linked to the highest probability of elevated plasma ADMA concentration. Higher concentration of ADMA in the blood may be a marker for higher cardiovascular risk, especially associated with hypertension, type 2 DM and hypercholesterolemia.
, N. Sokolnikova
Archives of Cardiovascular Diseases Supplements, Volume 12; doi:10.1016/j.acvdsp.2019.09.395

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To determine the relationship between blood pressure (BP), lipid metabolism and levels of IL-1β and IL-6 in patients with type 2 diabetes mellitus (T2DM). Ninety six patients with T2DM (mean age 52.74 ± 9.56, 38 women) were examined, and 20 healthy volunteers. A systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were measured; levels of total cholesterol (TC), high density lipoprotein cholesterol (HDL), triglycerides (TG), low density lipoprotein cholesterol (LDL)were determined. The levels of IL-1-β and IL-6 were determined by the immune-enzymatic method. SBP (mm Hg) in main group −141.76 ± 1.31, in control group - 120.75 ± 1.51; DAT (mm Hg)–88.43 ± 0.68 and 77.75 ± 0.85, respectively; MAP −106.23 ± 0.87 and 92.08 ± 0.98, respectively (P < 0.05). TC (mmol/L) in the main group was 5.29 ± 0.15, in the control group− 4,06 ± 0.05; TG (mmol/L) 1.20 ± 0.02 and 1.3 ± 0.03, respectively; LDL (mmol/L) 3.28 ± 0.14 and 2.01 ± 0.04, respectively (P < 0.05). IL-1β (ng/mL) in main group was 13.58 ± 0.29, control group − 8.12 ± 0.24; IL-6 (ng/mL) 12.37 ± 0.3 and 8.83 ± 0.22, respectively (P < 0.05). Significant correlations were revealed between the studied indices in the main group: SBP and TC (r = 0.29), SBP and TG (r = 0.28), SBP and LDL (r = 0.28), SBP and IL-1β (r = 0.41), SBP and IL-6 (r = 0.25); DBT and IL-1β (r = 0.25); MAP and TC (r = 0.26), MAP and TG (r = 0.29), MAP and LDL (r = 0.27), MAP and IL-1β (r = 0.39), MAP and IL-6 (r = 0.28). There were no significant correlations in the control group. The revealed interrelations indicate that the risk of arterial hypertension is increased even with a slight elevation of BP in patients with T2DM. The reasons for this include not only the increase of vascular resistance and the decrease of the elasticity of the vascular wall, but also the progression of dyslipidemia and deployment of systemic inflammatory response due to the increased levels of proinflammatory cytokines IL-1β and IL-6.
Published: 28 December 2019
Diabetes mellitus, Volume 22, pp 405-416; doi:10.14341/dm10312

Abstract:
BACKGROUND: Normoglycaemia in patients with diabetes mellitus type 1 (T1DM) after simultaneous pancreas-kidney transplantation (SPKT) is very interesting in regards to chronic kidney disease (CKD) complications dynamics depending of posttransplantation period and possible targets of potential treatment from the point of view metabolic memory AIM: To evaluate the relationship between oxidative stress indicators and advanced glycation end products and complications of end-stage renal disease (ESRD) in patients with T1DM аnd a long-term history of diabetes decompensation, who reached stable euglycemia after SPKT. MATERIALS AND METHODS: The study included 20 patients with compensation of carbohydrate metabolism after SPKT performed from November 2011 to September 2018. Assessment included examination of complications of ESRD (arterial hypertension, dyslipidemia, anemia, mineral and bone disorder) and analysis of "metabolic memory" markers: 3-nitrothyrosine (3-NT), superoxide dismutase (SOD), advanced glycation end products (AGE) and AGE receptor (RAGE). We performed follow-up examination of patients included in the early postoperative period (1st day/week) in 6-12 months after SPKT. RESULTS: All patients with DM1 duration for 22 [19; 28] years, diabetic nephropathy (DN) 8 [6; 14] years and duration of renal replacement therapy (dialysis) for 3 [1.5; 4] years reached euglycemia (HbA1c 5,5 [5,1; 5,8] %; С-peptide 3,2 [2,45; 3,63] ng/ml) after 6 month of surgical treatment. Despite of stable graft function (estimated glomerular filtration rate (eGFR) CKD-EPI 84 [69; 95] ml/min/1.73m2) 35% of patients still needed antihypertensive therapy, 40% needed treatment with recombinant human erythropoietin (RHuEPO) and 15% ferrotherapy. With vitamin D deficiency, observed in 80% of cases (13.3 [9.3; 18.5] ng/ml), 55% of patients had secondary hyperparathyroidism, 45% osteoporosis. The results of the correlation analysis revealed the association of the state of ESRD target organs with the studied "metabolic memory" markers: oxidative stress and AGE-RAGE system. CONCLUSIONS: SPKT as the way to achieve compensation of carbohydrate metabolism and uremia does not provide regress of diabetes and complications of ESRD. Analysis of "metabolic memory" markers indicate their direct contribution to the persistence of metabolic consequences of diabetic nephropathy (DN). Found trends need more long-lasting observation and enlargement of study groups.
Phue Khaing, Pooja Pandit, Bharat Awsare,
Published: 18 December 2019
Comprehensive Physiology, Volume 10, pp 297-316; doi:10.1002/cphy.c190018

Abstract:
Obesity, diabetes mellitus, and the metabolic syndrome are important risk factors for the development of cardiovascular disease, with significant impact on human morbidity and mortality. Several decades of research have accumulated considerable knowledge about the mechanisms by which metabolic conditions precipitate systemic cardiovascular diseases. In short, these mechanisms are thought to involve changes in the external environment of vascular cells, which are mediated by the pro‐inflammatory effects of adipokines, free fatty acids, and hyperglycemia. Thus, it has been hypothesized that the pulmonary circulation, witnessing similar insults as the systemic circulation, may be equally vulnerable to the development of vascular disease. Accordingly, recent attention has focused on exploring the mechanistic and epidemiological relationships among obesity, type 2 diabetes mellitus, metabolic syndrome, and pulmonary vascular diseases. In this article, we discuss in detail the preclinical evidence showing a modest but perceivable impact of metabolic disorders on the pulmonary circulation. In addition, we review the existing epidemiological studies examining the relationship among cardiovascular risk factors and pulmonary vascular diseases, using the acute respiratory distress syndrome and pulmonary arterial hypertension as examples. We conclude by discussing areas of limitations in the field and by suggesting future directions for investigation, including the notion that the pulmonary circulation may, in fact, be a resilient entity in the setting of some metabolic perturbations. © 2020 American Physiological Society. Compr Physiol 10:297‐316, 2020.
, , , Magdalena Mizia-Szubryt, Agnieszka Sikora-Puz, Klaudia Gieszczyk-Strózik
Published: 6 November 2019
Cardiology Journal, Volume 26, pp 483-492; doi:10.5603/cj.a2017.0135

Abstract:
Background: The role of the adipokines in the pathogenesis of aortic stenosis (AS) is not well established. The aim was to evaluate the relationship between adipokines and clinical characteristics as well as echocardiographic indices and noninvasive markers of vascular remodeling in patients with severe AS with preserved ejection fraction (EF). Methods: Sixty-five patients (F/M: 38/27; age: 68.3 ± 9.0 years; body mass index [BMI]: 29.6 ± 4.3 kg/m 2 ) with severe AS with preserved EF: 33 patients with paradoxical low-flow low-gradient AS (PLFLG AS) and 32 patients with normal flow high-gradient AS (NFHG AS) were prospectively enrolled into the study. Twenty-four subjects (F/M: 14/10; age: 65.4 ± 8.7 years; BMI: 29.6 ± 4.3 kg/m 2 ) who matched as to age, sex, BMI and coronary artery disease (CAD) constituted the control group (CG). Clinical data and markers of vascular remodeling were related to the serum adipokines. Results: There were no differences in the adipokines concentrations in the AS/CG. Patients with AS and coexisting CAD were characterized by decreased serum adiponectin (9.9 ± 5.5 vs. 12.7 ± 5.8 μg/mL, p = 0.040) and leptin (8.3 ± 7.8 vs. 21.6 ± 17.1 ng/mL, p < 0.001) levels compared to subjects without CAD. There were no differences in the serum adipokines concentrations between patients with PLFLG AS and NFHG AS. Systemic hypertension, diabetes, hyperlipidemia or markers of vascular remodeling did not discriminate adipokines concentrations. Multivariate regression analysis indicated that age (F = 3.02; p = 0.015) and E/E’ index (F = 0.87, p = 0.032) were independent predictors of the adiponectin level in the AS group. Conclusions: The presence of AS with preserved EF did not change the adipokine serum profile. Adipokines levels were modified by coexisting atherosclerosis but not the typical cardiovascular risk factors or the hemodynamic type of AS.
Published: 29 October 2019
by MDPI
Marine Drugs, Volume 17; doi:10.3390/md17110613

Abstract:
The term metabolic/cardiometabolic/insulin resistance syndrome could generally be defined as the co-occurrence of several risk factors inclusive of systemic arterial hypertension. Not only that organizations, such as the world health organization (WHO) have identified high blood pressure as one of the main risk factors of the cardiometabolic syndrome, but there is also a link between the occurrence of insulin resistance/impaired glucose tolerance and hypertension that would consequently lead to type-2 diabetes (T2D). Hypertension is medicated by various classes of synthetic drugs; however, severe or mild adverse effects have been repeatedly reported. To avoid and reduce these adverse effects, natural alternatives, such as bioactive peptides derived from different sources have drawn the attention of researchers. Among all types of biologically active peptides inclusive of marine-derived ones, this paper’s focus would solely be on fish and fishery by-processes’ extracted peptides and products. Isolation and fractionation processes of these products alongside their structural, compositional and digestion stability characteristics have likewise been briefly discussed to better address the structure-activity relationship, expanding the reader’s knowledge on research and discovery trend of fish antihypertensive biopeptides. Furthermore, drug-likeness of selected biopeptides was predicted by Lipinski’s rules to differentiate a drug-like biopeptide from nondrug-like one.
T Hamaoka, H Murai, H Sugimoto, Y Mukai, Y Okabe, H Tokuhisa, O Inoue, S Takashima, T Kato, S Usui, et al.
European Heart Journal, Volume 40; doi:10.1093/eurheartj/ehz748.0064

Abstract:
Background Diabetes mellitus (DM) is a well-known risk factor for cardiovascular diseases. Augmented sympathetic nerve activity plays an important role in the progressive worsening disease severity. Most of anti-diabetic drugs were demonstrated to not only decrease blood glucose, but also increase sympathetic nerve activity. Recently, it has been reported that sodium glucose cotransporter 2 (SGLT2) inhibitor has beneficial effects on cardiovascular events in spite of the decrease in blood glucose in type 2 DM patients. The underlying mechanisms remain speculative; however, it is assumed that SGLT2 inhibitor would improve sympathetic nerve activity in type 2 DM patients. Purpose The purpose of this study was to evaluate the effect of SGLT2 inhibitor on sympathetic nerve activity in type 2 DM patients. Methods This study was designed as the prospective single-arm study. Type2 DM patients whose HbA1c >7.0% with at least one atherosclerotic risk factors (Hypertension, obesity, smoking history, aging ...) were included. Patients who had renal failure (eGFR80 years old) were excluded. We measured blood glucose, HbA1c and blood insulin concentration at baseline and 12 weeks after treatment of dapagliflozin (5mg/day). Muscle sympathetic nerve activity (MSNA) was applied to scrutinize accurate sympathetic nerve activity in type 2 DM patients. Also, baroreflex sensitivity was calculated by examining the relationship between MSNA and beat to beat diastolic blood pressure. Results Eleven type2 DM patients were included in this study. Body mass index, blood pressure, HbA1c and blood insulin concentration tended to decrease at 12weeks after dapagliflozin (body mass index: 27.2±6.3 vs. 24.9±3.2 kg/m2. systolic blood pressure: 121±12.3 vs. 118±13.6 mmHg. diastolic blood pressure: 74.3±6.3 vs. 72.5±7.6 mmHg. HbA1c: 7.6±0.3 vs. 7.2±0.7%. insulin: 9.7±7.2 vs. 8.8±5.1 μU/ml). Dapagliflozin significantly decrease MSNA and heart rate compared to baseline (46.7±7.5 vs. 38.6±6.9 bursts/minute, P 12 weeks administration decreased MSNA Conclusion Our data demonstrated that dapagliflozin significantly decreased MSNA and HR beyond the lowering effect of blood glucose in type2 DM patients. These results indicate the favorable effect of SGLT2 inhibitor might be, in part, attributed to the improvement in sympathetic nerve activity.
, Daria A. Kashtanova, Ekaterina N. Dudinskaya, Olga N. Tkacheva
Published: 14 September 2019
Healthy Ageing and Longevity pp 329-348; doi:10.1007/978-3-030-24970-0_20

Abstract:
Age-associated arterial wall changes create an enzymatically and metabolically favorable environment for cardiovascular diseases development. Understanding the essence of the processes underlying the development of CVD can open up new opportunities for more effective preventive actions. Age, gender, blood pressure, lipid levels, type 2 diabetes mellitus are traditional cardiovascular risk factors used in the most popular models, such as Framingham and SCORE. However, these risk stratification systems have a number of limitations and explain no more than 50% reduction in mortality from cardiovascular diseases. There is not enough information on the association between signs of arterial wall aging and factors that determine the aging processes in general and in their interaction with cardiovascular risk factors. The aim of the work was to study the relationship between parameters of arterial wall aging, traditional risk factors, hormonal status, leukocyte telomere length. A total of 303 ambulatory participants (104 males and 199 females) were recruited. The subjects ranged between 23 and 91 years of age, with a mean age of 51.8 ± 13.3 years. Based on the results obtained, the following conclusions can be drawn: the value of traditional cardiovascular risk factors for the vascular wall changes is reduced in older age; carbohydrate metabolism disorders and hypertension are “universal” risk factors most closely associated with the arterial wall condition in both younger and older group. To predict changes in the vascular wall, it is advisable to study insulin resistance, growth hormone, insulin-like growth factor-1 activity and leukocyte telomere length along with conventional cardiovascular risk factors.
K. Bhaskar,
Indian Journal of Cardiovascular Disease in Women WINCARS, Volume 4, pp 121-121; doi:10.1055/s-0039-3400198

Abstract:
Vitamin D is one of the fat-soluble vitamins that has been a focus of increasing attention in recent times due to its presence in all tissues. Although traditionally described in bone and calcium metabolism, research has shown its active role in various other physiological processes of cardiovascular, respiratory, immune systems, and metabolism of lipids and sugars. Vitamin D receptors are known to be present in all parts of vascular sheath like endothelium, smooth muscle cells suggesting its active role in maintaining homeostasis. Vitamin D deficiency has been shown in association with various disorders like hypertension, diabetes, asthma, cardiovascular, peripheral vascular, cancer, and autoimmunity. Vitamin D deficiency is known to be associated with vasoconstriction leading to increased stiffness and peripheral vascular disease. Vascular stiffness comprises various physical parameters like compliance, distensibility, and elasticity. Clinically these are measured with pulse wave velocity (PWV) and augmentation pressure (AG)/augmentation Index (AI). Vitamin D levels were inversely associated with PWV and AI but supplementation has not yielded consistent positive results. In a study by Murat Sunbul supplementation of vitamin D has improved PWV and AI in patients with deficiency.[1] In another study done by Chitalia et al, vitamin D showed positive effect on endothelial function but no such effect on arterial stiffness in chronic kidney disease patients.[2] Tsuru et al studied the effect of age and gender on AI and AG with findings of continued increase in AG with age, whereas AI varied with gender, height, and type of vessel leading to final conclusion of AG as a suitable parameter of arterial stiffness than AI.[3] Chua et al, in a review, opined that vitamin D deficiency is an independent risk factor for peripheral vascular disease that can be corrected easily.[4] Vitamin D deficiency acts as an epigenetic factor tilting the balance toward vasoconstriction, thereby predisposing the development of essential hypertension.[5] In this issue of Indian Journal of Cardiovascular Diseases in Women, authors tried to analyze the relationship between vitamin D insufficiency and deficiency with peripheral vascular resistance (PVR).[6] They have assessed PVR, cardiac output, cardiac index, systolic blood pressure, PWV, AG, and AI. High PVR and systolic blood pressure were observed in majority of these patients without any gender difference. There was no statistical significance in AG and AI in both genders. This study could not find any gender variations with respect to above parameters. Small size is the main drawback and further prospective studies with large sample are needed to substantiate these findings. This study can be considered for publication as there is lot of growing interest in this topic.
Вадим Викторович Генкель, ,
Тромбоз, гемостаз и реология pp 45-51; doi:10.25555/thr.2019.2.0879

Abstract:
Цель исследования: изучить частоту встречаемости нарушений в системе протеина С у пациентов высокого и очень высокого риска сердечнососудистых осложнений (ССО), а также выявить взаимосвязи данных нарушений и тяжести атеросклеротического поражения периферических артерий. Материалы и методы. В исследование были включены 165 пациентов высокого и очень высокого риска ССО. Скрининг нарушений в системе протеина С проводили с использованием набора реагентов Парустест (ООО ТехнологияСтандарт, Россия). Резистентность фактора Va к активированному протеину С определяли с использованием набора реагентов Фактор VPCтест (ООО ТехнологияСтандарт, Россия). По полученным данным рассчитывали нормализованное отношение (НО). Всем пациентам проводили ультразвуковое дуплексное сканирование артерий каротидного бассейна и артерий нижних конечностей (АНК). Результаты. Медиана НО протеина С составляла 1,20 0,801,60. Снижение НО менее 0,7 было выявлено у 16 (9,69 ) пациентов. Резистентность к АПС была установлена у 1 (0,61 ) больного. По результатам корреляционного анализа снижение НО протеина С ассоциировалось с увеличением степени стенозирования сонных артерий и АНК. По результатам полиномиального логистического регрессионного анализа снижение НО протеина С менее 0,7 с поправкой на такие факторы как пол, возраст, курение, артериальная гипертензия, сахарный диабет 2го типа, скорость клубочковой фильтрации и содержание липопротеинов низкой плотности ассоциировалось с увеличением относительного риска выявления тяжелого сочетанного поражения периферических артерий с их стенозированием более 50 в 10,8 раз (95 ДИ 1,8363,8 p 0,009). Заключение. У пациентов высокого и очень высокого риска ССО нарушения в системе протеина С выявлялись в 9,69 случаев. Снижение НО протеина С ассоциировалось с увеличением тяжести атеросклеротического поражения периферических артерий. Наличие у пациента нарушений в системе протеина С ассоциировалось с увеличением относительного риска выявления тяжелого сочетанного поражения периферических артерий в 10,8 раза. Aim: to study frequency of protein C system abnormalities in patients with a high and very high cardiovascular risk and to reveal the relationship of these disorders and the severity of atherosclerosis of peripheral arteries. Materials and methods. The study included 165 patients at high and very high cardiovascular risk. Screening of abnormalities in the protein C system was carried out using Parustest (OOO TechnologyStandard, Russia). Resistance factor Va to APS was determined using Factor VPCtest (OOO TechnologyStandard, Russia). The obtained data were used to calculate the normalized ratio (NO). All patients underwent ultrasound duplex scanning of carotid arteries and lower limb arteries. Results. The median NO of protein C was 1.20 0.801.60. A decrease in NO less than 0.7 was diagnosed in 16 (9.69 ) patients. Resistance to APC was established in 1 (0.61 ) patient. A decrease in the NO of protein C was associated with an increase in the degree of stenosis of carotid arteries and lower limb arteries. According to the results of the polynomial logistic regression analysis, the decrease in the NO protein C less than 0.7, adjusted for factors such as sex, age, smoking, hypertension, type 2 diabetes mellitus, glomerular filtration rate and low density lipoprotein content was associated with an increase in the relative risk of identifying severe combined atherosclerosis of peripheral arteries in 10.8 times (95 CI 1.8363.8 p 0.009). Conclusion. In patients with a high and very high cardiovascular risk abnormalities of the protein C system were detected in 9.69 of cases. Reduction of the normalized ratio of protein C was associated with an increase in the severity of peripheral arteries atherosclerosis. The presence of abnormalities in the protein C system was associated with a 10.8fold increase in the relative risk of detecting a severe combined atherosclerosis of peripheral arteries.
, N. Sokolnikova, M. Filonenko
Journal of Hypertension, Volume 37; doi:10.1097/01.hjh.0000572788.03086.af

Abstract:
To determine the relationship between blood pressure (BP), lipid metabolism and levels of IL-1beta and IL-6 in patients with type 2 diabetes mellitus (T2DM). A total of 96 patients with T2DM (mean age 52.74 ± 9.56, 38 women) and 20 healthy volunteers were examined. A systolic blood pressure (SBP, mmHg), diastolic blood pressure (DBP, mmHg), and mean arterial pressure (MAP) were measured; levels of total cholesterol (TC), high density lipoprotein cholesterol (HDL), triglycerides (TG) were determined by biochemical method (mmol/L), the level of low density lipoprotein cholesterol (LDL) was calculated by Friedwald's formula. The levels of IL-1-beta and IL-6 were determined by ELISA (ng/ml). SBP in main group - 141.76 ± 1.31, in control group - 120.75 ± 1.51; DAT - 88.43 ± 0.68 and 77.75 ± 0.85, respectively; MAP - 106.23 ± 0.87 and 92.08 ± 0.98, respectively. All the results in the studied groups were statistically significant. The study of cholesterol metabolism also revealed significant differences: TC in the main group was 5.29 ± 0.15, in the control group - 4,06 ± 0.05; TG 1.20 ± 0.02 and 1.3 ± 0.03, respectively; LDL 3.28 ± 0.14 and 2.01 ± 0.04, respectively. The levels of proinflammatory cytokines significantly differed in studied groups: IL-1beta in main group was 13,58 ± 0,29, control group - 8,12 ± 0,24; IL-6 12.37 ± 0.3 and 8.83 ± 0.22, respectively. Significant (p The revealed interrelations indicate that the risk of arterial hypertension is increased even with a slight elevation of BP in patients with T2DM. The reasons for this include not only the increase of vascular resistance and the decrease of the elasticity of the vascular wall, but also the progression of dyslipidemia and deployment of systemic inflammatory response due to the increased levels of proinflammatory cytokines IL-1beta and IL-6.
K. Konstantinou, C. Tsioufis, E. Mantzouranis, N. Vogiatzakis, A. Koumelli, A. Kasiakogias, I. Leontsinis, P. Iliakis, I. Liatakis, E. Koutra, et al.
Journal of Hypertension, Volume 37; doi:10.1097/01.hjh.0000572508.53360.6d

Abstract:
Blood pressure variability (BPV) has been mainly studied through the prism of congestive heart failure (CHF) and hypertension, but not in the setting of an acute coronary syndrome (ACS). The aim of the present study was to assess blood pressure variability (BPV) in patients hospitalized for myocardial infarction (MI). We studied 211 patients (79.8% male; mean age 62.33 years) who were hospitalized because of ST-elevation myocardial infarction (STEMI) and Non ST–elevation myocardial infarction (NSTEMI). All patients underwent baseline estimation of clinical and laboratory parameters during their hospitalization. Additionally, BPV was estimated based on daily measurements of BP during hospitalization and with 24-hour ambulatory BP monitoring during the third day of hospital stay. The parameters of BPV analyzed were: a) standard deviation (SD) of systolic BP, b) SD of diastolic BP, c) the coefficient of variation (CV) of systolic BP and d) the average real variability (ARV) of systolic and diastolic BP. From the total population, 28.9% had family history of cardiovascular disease, 67.3% were hypertensives, 27% had diabetes mellitus (DM), 58.8% were smokers and 23.7% had previous history of coronary artery disease. Regarding the type of myocardial infarction, 49.3% were admitted for STEMI and 78.5% had coronary revascularization. From the ambulatory BP, ARV SBP was 9.32 ± 2mmHg while NSTEMI patients demonstrated significantly higher values of ARV SBP compared to STEMI (9.72 ± 2 mmHg vs 8.9 ± 1.7 mmHg; p = 0.002). Using univariate analysis, the type of MI (STEMI and NSTEMI) was significantly related to ARV SBP (r = 0.215, p In patients admitted for MI there is a relationship between the ARV and the type of myocardial infarction. These findings suggest differential impact of hemodynamic load on the cardiovascular system in patients with STEMI and NSTEMI.
, Tannia Viveros-Ruiz
Published: 3 April 2019
F1000Research, Volume 8; doi:10.12688/f1000research.17122.1

Abstract:
The metabolic syndrome (MetS) concept gathers in a single entity a set of metabolic abnormalities that have in common a close relationship with ectopic deposit of lipids, insulin resistance, and chronic low-grade inflammation. It is a valuable teaching tool to help health professionals to understand and integrate the consequences of lipotoxicity and the adverse metabolic consequences of insulin resistance. Also, it is useful to identify subjects with a high risk for having incident type 2 diabetes. Systems biology studies have gained a prominent role in understanding the interaction between adipose tissue dysfunction, insulin action, and the MetS traits and co-morbidities (that is, non-alcoholic steatohepatitis, or NASH). This approach may allow the identification of new therapeutic targets (that is, de novo lipogenesis inhibitors for NASH). Treatment targets on MetS are the adoption of a healthy lifestyle, weight loss, and the control of the co-morbidities (hyperglycemia, dyslipidemia, arterial hypertension, among others). The long-term goals are the prevention of type 2 diabetes, cardiovascular events, and other MetS-related outcomes. In the last few decades, new drugs derived from the identification of innovative treatment targets have come on the market. These drugs have positive effects on more than one MetS component (that is, hyperglycemia and weight control). New potential treatment targets are under study.
John M. Bauza, Morgan W. Carson‐Marino, Kelly M. DeMars, Kubra M. Tuna, Darrice S. Montgomery, Brian D. Sanz, Eduardo Candelario‐Jalil, Abdel A. Alli
Published: 1 April 2019
The FASEB Journal, Volume 33, pp 551.5-551.5; doi:10.1096/fasebj.2019.33.1_supplement.551.5

Abstract:
Background According to 2018 AHA/ASA guidelines, stroke remains a leading cause of death and long-term disability in the U.S. and worldwide. Despite prevention efforts, risk factors such as hypertension attributes to worse clinical outcomes. The therapeutic window for stroke is limited to fibrinolytic therapy. Protein Kinase C-epsilon activity provides resistance against oxidative stress. Objective The objective of this study was to test the hypothesis that the cell-specific Protein Kinase C-epsilon /Ca2+/calmodulin-dependent protein kinase II-alpha (CaMKII-alpha) system contributes to homeostatic dysfunction, glial hypersensitivity, and cell death mechanisms. Here, we aimed to investigate key protein expression changes in tissue after middle cerebral artery (MCA) onset in animals. Our primary and secondary endpoints assess significant expression differences for astrocyte-specific glial fibrillary acidic protein and microglia/macrophage-specific ionized calcium adaptor molecule 1. Methods We used a transient MCA occlusion model to quantify cell and tissue-type-specific expression changes by Western blot after oxygen deprivation of N2:O2 (99:1) and ischemic-reperfusion intervals of 4, 14, 24, 48, 72-hrs after a 90-min occlusion. Neuroprotective potential is determined by Protein Kinase C-epsilon expression after reperfusion onset. IHC and TTC staining is used to evaluate lesion volume and metabolic activity. All experiments were randomized and double-blinded. Results Oxygen-deprived cell lines and tissue were confirmed by HIF1-alpha expression and distribution. Global expression changes reveal an inverse correlation between Protein Kinase C-epsilon and glial immunoreactivity. Calcium-independent Protein Kinase C-epsilon expression levels are most significant at 24-hrs after MCA reperfusion onset in cortical and subcortical tissue. Conclusion Our data provides new evidence of a tissue- and cell-type-specific mechanism of protein regulation in the Protein Kinase C-epsilon /Ca2+/CaMKII-alpha pathway after stroke. The findings suggest an inverse relationship between glial activation and Protein Kinase C-epsilon expression. Reduced Protein Kinase C-epsilon expression in cells and tissue may exacerbate gliosis. Significant changes to Protein Kinase C-epsilon and CaMKII-alpha activities in tissue often results in abnormal Ca2+ homeostasis, dysfunctional calcium-dependent potassium conductance, and cytoskeletal deformation. Additional studies are needed to further elucidate the complex role of Ca2+ and its regulation in the context of acute and chronic neurodegenerative conditions. Support or Funding Information This project was funded by the U.S. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases (Grant K01 DK099617; to A.A.A.) and the University of Florida College of Medicine. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Ashfaq Ahmad, Sara K. Dempsey, Zdravka Daneva, Ningjun Li, Pin‐Lan Li, Joseph K. Ritter
Published: 1 April 2019
The FASEB Journal, Volume 33, pp 678.7-678.7; doi:10.1096/fasebj.2019.33.1_supplement.678.7

Abstract:
Kidney is the major organ responsible for long term regulation of blood pressure. Impaired renal sodium excretion and perfusion pressure is main driver of hypertension. This perfusion pressure and renal sodium excretion is called as acute pressure natriuresis (PN). It was surprising to know that none of the study explained the role of endocannabinoids (ECs) in PN and importance of EC hydrolyzing enzymes in the modulation of PN mechanism. This study set out with the primary objective that after acute increase in mean arterial pressure (MAP) either anandamide (AEA) or 2-arachidonoyl glycerol (2-AG) is released in the kidney which modulate PN by lowering MAP, natriuretic and diuretic activities. Secondly, effect of genetic and pharmacological ablation of fatty acid amide hydrolase (FAAH) genes in mice modulate the PN relationship. Mice were anesthetized and cannulation was done in trachea, jugular vein, carotid artery and bladder. PN model was established in animals by ligations of celiac and superior mesenteric arteries (CML) and abdominal aorta (AL) while MAP and UV were observed at 10 minutes intervals in FAAH wild type and its knock out littermate. Ligation of celiac and mesenteric arteries resulted in increase in MAP (from baseline to CML-1 phase) 91 to 121 (mmHg) with corresponding increase in UV from 9 to 17 (ul/min/g kwt) and urinary sodium (UNa) from 1.3 to 3.0 (umol/min/g kwt). MAP and UV reported at CML-2 ligation was 113 mmHg and 17 ul/min/g kwt. MAP at AL-1 and AL-2 was noted as 119 and 104 (mmHg) with corresponding increase in UV 21 and 26 (ul/min/g kwt) while UNa was noted as 3.4 umol/min/g kwt. Pretreatment with selective FAAH inhibitor in the medulla of the kidney resulted in increase in MAP from baseline 88 to 131 and 109 mmHg at CML-1, CML-2 respectively while MAP was also observed 119 and 123 mmHg at AL-1 and AL-2 phase. There was significant increase (p<0.05) in UV after pretreatment with FAAH inhibitor which was noted 26 and 28 (ul/min/g kwt) at CML-1 and CML-2 while 49 and 48 (ul/min/g kwt) at AL-1 and AL-2 respectively. FAAH KO animals shifted MAP and UV curves of PN study towards right when compared to FAAH WT group. Analytical data showed significant increase (P<0.05) in 2-AG levels in the kidney and plasma samples of FAAH WT animals underwent through PN when compared to control FAAH WT while AEA levels was significantly higher (p<0.05) in the kidney of FAAH KO animals with PN as compared to respective control group. It can be concluded that endocannabinoids are released in response to acute increase in MAP and results in diuretic and natriuretic activities which lowers the MAP and keep PN relationship intact. Lastly, regional blocking of FAAH in the kidney shift the MAP and UV curves of the PN models towards left and positively modulate the PN relationship. Support or Funding Information This work was supported by National Institute of Diabetes and Digestive and Kidney Disorders grant, DK102539 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Lei Wei, Chuan Chen, Yong-Qiang Dai, Li Ding, Hai-Yan Li, Yan-Jun Lin, Hao-Tian Wu, Zhen Wu, Zheng-Qi Lu
Chinese Medical Journal, Volume 132, pp 491-494; doi:10.1097/cm9.0000000000000084

Abstract:
To the Editor: Ischemic stroke remains a major cause of death and disability worldwide and contributes to the rising costs of health care. Thrombolytic therapy with tissue plasminogen activator (tPA, alteplase) is beneficial for the treatment of acute ischemic stroke. However, only 40% to 50% of stroke patients show a significant improvement after treatment. In addition, the use of alteplase is restricted because symptomatic intracranial hemorrhage (sICH) occurs in 1.7% to 6.4% of treated patients.[1] 25-hydroxyvitamin D (25(OH)D), which is the major circulating metabolite of vitamin D, has been confirmed to be closely related to cerebrovascular disease (CVD). A series of studies indicated that vitamin D deficiency was associated with an increased risk of ischemic stroke, high stroke severity and poor functional outcomes.[2] The aim of this study was to examine the relationship between serum 25(OH)D levels and functional outcomes in patients treated with intravenous thrombolysis for acute ischemic stroke in a Chinese population. We retrospectively analyzed patients with acute ischemic stroke who were treated with intravenous alteplase in our stroke unit from February 2014 to January 2017. All patients with a clinical diagnosis of ischemic stroke and a National Institutes of Health Stroke Scale (NIHSS) score of less than 24 received IV alteplase (0.9 mg/kg) within 4.5 hours of stroke onset after obtaining informed consent. The inclusion and exclusion criteria for receiving alteplase, as well as the thrombolytic protocol, strictly followed the European Cooperative Acute Stroke Study (ECASS) II and ECASS III criteria. None of the patients had a history of 25(OH)D deficiency or received oral replenishment. Patients with incomplete baseline data (43 cases, 41 lacking 25(OH)D level data) or those that were lost to follow-up (13 cases) were excluded. As such, a total 208 patients were enrolled in this study. Data were collected by physicians with experience in acute stroke care using predefined criteria. The NIHSS and modified Rankin Scale (mRS) scores were evaluated by certified raters. This study was approved by the ethics committee of the Third Affiliated Hospital of Sun Yat-sen University. All subjects involved in the study provided written informed consent. Blood samples were collected within 24 hours of hospital admission and after at least 8 hours of fasting. Serum 25(OH)D levels were measured with a commercially available enzyme-linked immunosorbent assay kit (Immunodiagnostic Systems Limited, Bolton, UK) according to the manufacturer's instructions. A 25(OH)D level Baseline characteristics, including age, sex, body mass index (BMI) and medical history (atrial fibrillation, coronary artery disease, current smoking, diabetes mellitus, hypertension, and previous stroke/transient ischemic attack [TIA]), were collected. Onset-to-treatment time and blood pressure (BP) on admission were recorded. Laboratory data examined included blood cell count, C-reactive protein (CRP) level and glucose level on admission; and total cholesterol (TC), high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), and homocysteine (HCY) levels within 24 hours after admission. Information on previous use of antiplatelet, anticoagulant, antidiabetic, and statin drugs (including type and dose) was collected. Outcomes, which were defined as any intracerebral hemorrhage (ICH), symptomatic ICH (sICH), good functional outcome, all-cause death, and major disability, were assessed in the 3-month follow-up period after stroke onset. A sICH was defined as clinical neurological deterioration (an increment of the NIHSS scores of 4 or greater) in addition to any hemorrhage identified on CT/MRI. Outcomes were assessed by the mRS score at 3-month follow-up visit.
, Maria Callejo, Bianca Barreira, , , , , Angel Cogolludo, Laura Moreno,
Published: 28 January 2019
PLOS ONE, Volume 14; doi:10.1371/journal.pone.0211281

Abstract:
Diabetes is a very strong predictor of chronic systemic vascular diseases and acute cardiovascular events. Recently, associations between metabolic disorders and pulmonary hypertension have also been reported in both humans and animal models. In order to get some further insight into the relationship of pulmonary hypertension with obesity, insulin resistance and hyperglycemia, herein we have used the Zucker diabetic fatty rats (ZDF/clr-lepr fa) at 20 weeks fed a standard diet and compared to their lean Zucker littermates (ZL). ZDF rats were obese, had elevated plasma glucose levels and insulin resistance, i.e. a clinically relevant model of type 2 diabetes. They presented elevated systolic, diastolic and mean pulmonary arterial pressures and a parallel increase in the Fulton index. Systemic arterial pressures were also increased but the left ventricle plus septum weight was similar in both groups and the heart rate was reduced. Wall media thickening was observed in the small pulmonary arteries from the ZDF rats. Isolated pulmonary arteries mounted in a wire myograph showed similar vasoconstrictor responses to phenylephrine and 5-HT and similar responses to the endothelium-dependent vasodilator acetylcholine. However, the iNOS inhibitor 1400W enhanced the vasoconstrictor responses in ZDF but not in ZL rats. The protein expression of eNOS and iNOS was not significantly different in the lungs of the two groups. The lung expression of Bmpr2 mRNA was downregulated. However, the mRNA expression of Kcna5, Kcnk3, Kcnq1, Kcnq4 or Kcnq5, which encode for the potassium channels Kv1.5, TASK-1, Kv7.1, Kv7.4 and Kv7.5, respectively, was similar in ZL and ZDF rats. In conclusion, ZDF rats show increased pulmonary arterial pressure, right ventricular hypertrophy, pulmonary arterial medial thickening and downregulated lung Bmpr2 despite leptin resistance. These changes were mild but are consistent with the view that diabetes is a risk factor for pulmonary hypertension.
Fernando Nestor Facio Junior, Luis Cesar Fava Spessoto, Marina Gaglianone Teodoro Da Silva
International Journal of Sciences, Volume 8, pp 24-27; doi:10.18483/ijsci.2083

Abstract:
Introduction: Erectile dysfunction (ED) is the most common cause of sexual dysfunction in men and shares several risk factors with systemic conditions, such as cardiovascular disease and metabolic syndrome (MetS). Objective: Investigate the relationship between ED and MetS among patients at a university hospital. Patients and Methods: Patients with ED were retrospectively investigated in a cross-sectional study conducted at a university hospital. The following variables were analyzed: systemic arterial hypertension, type 2 diabetes mellitus (DM2), dyslipidemia, obesity, smoking, alcohol use, low adherence to treatment or ineffective treatment, medications, glycated hemoglobin and lipids (total cholesterol, HDL and triglycerides). Results: Among the 96 patients studied, 23 (24%) met the criteria for MetS. Analyzing only one comorbidity, 10.4% of patients had hypertension, 5.2% had DM2 and 5.2% had dyslipidemia. Age ranged from 21 to 78 years (mean: 56.9 ± 12.2 years) and 52% of patients were older than 60 years of age. Abnormal glycated hemoglobin was found in 40.6%) of patients; 41.6% had dyslipidemia; 47.9% had hypertension; and 39.6% used anti-hypertensive medications. Smoking was found in 39.5% and alcohol use was found in 30.2%. The results of the chi-squared test revealed that smoking was significantly associated with hypertension, DM2 and dyslipidemia (P < 0.01). Nearly half (46.9%) of the patients had low adherence or underwent ineffective treatment. Conclusion: No association was found between erectile dysfunction and metabolic syndrome. Significant associations were found between smoking and hypertension, DM2 and dyslipidemia.
Rubia Caldas Umburanas, Priscila Costa Estabile, Rogério Pincela Mateus, Mara Cristina de Almeida, Roberto Ferreira Artoni
Published: 1 January 2019
MOJ Biology and Medicine, Volume 4, pp 22-28; doi:10.15406/mojbm.2019.04.00108

Abstract:
Systemic arterial hypertension (SAH) is a multifactorial clinical condition characterized by high and sustained levels of blood pressure (BP). Some studies have reported that variants of the angiotensin-converting enzyme (ace) gene increase the risk of hypertension. The aim of this study was to verify the existence of the relationship between the insertion/deletion (I/D) polymorphism in the ACE gene and its genotypic variants with BP in four distinct groups of hypertensive individuals and also to genetically and epidemiologically characterize the investigated samples. The study was formed of 112 individuals arranged into the following groups: normotensive (control); hypertensive and non-obese; hypertensive and obese; and, hypertensive and with type 2 diabetes mellitus (T2DM). Epidemiological data and peripheral blood were collected from participants for DNA extraction and amplification by PCR (polymerase chain reaction). The allele (D=0.5446; I=0.4554) and genotype (DD =0.2411, ID =0.6071; II =0.1518) frequencies showed low genetic differentiation (Fst<0.05) and were outside the Hardy-Weinberg equilibrium (p<0.05). There was no significant difference between the groups (chi-square=4.4335; p=0.6174). There was no association of the D allele with SAH, reinforcing the hypothesis that environmental interferences are prevalent in the evolution of SAH.
Lozano-Hernández R
Integrative Journal of Conference Proceedings, Volume 1, pp 1-3; doi:10.31031/icp.2018.01.000504

Abstract:
Lozano-Hernández R* Center of Infertility and Gynecological Diseases, University of Los Andes, Venezuela *Corresponding author:Ricardo Lozano-Hernández, Center of Infertility and Gynecological Diseases (CEDIEG) “Dr. Giovanny Vivas-Acevedo”, University of Los Andes, Mérida, Venezuela Submission: August 02, 2018;Published: September 18, 2018 Volume1 Issue1 September 2018 Dyslipidemia, hypertension and other symptoms are part of the well-known metabolic syndrome (MS). MS is extended well beyond the cardiovascular system. In infertile men the androgen deficiency is associated with increased triglycerides (TGs), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C). Increase T levels are associated with lower risk in men and with higher risk in women. It is necessary to keep in mind that cardiovascular diseases can be influenced by sex hormones and other types of hormones. Testosterone is a pleiotropic hormone that plays an important role in the human body. Through its conversion to E2, T affects bone health, including bone density. BMI has been correlated with the value of systolic blood pressure, ratio LH/FSH and T, and it was inversely correlated with the hormones FSH and PRL in infertile woman with polycystic ovary. The influence of many hormones on the cardiovascular function also depends on act directly through specific receptors in heart or vessel wall cells, whereas some act indirectly - stimulating other neuroendocrine factors. The majority of those hormones play an important role in the pathogenesis of cardiovascular diseases, which can result in the development of new medicines. In conclusion, cardiovascular diseases may be the main or associated cause of reproductive failure in infertile couples: however, the interactions that exist between the cardiovascular system and the endocrine reproductive system must be focused on each patient individually. Keywords: Dyslipidemia; Hypertension; Metabolic syndrome; Infertility Abbreviations: BMI: Body Mass Index; DHEA-S: Dehydroepiandrosterone-Sulphate; E2: Estradiol; FT: Free Testosterone; HDL-C: High-Density Lipoprotein Cholesterol; HOMA-IR: Homeostasis Model Assessment of Insulin Resistance; LDL-C: Low-Density Lipoprotein Cholesterol; PCO: Polycystic Ovary; PRL: Prolactine; T: Testosterone; TC: Total Cholesterol; TGs: Triglycerides Dyslipidemia and hypertension are frequent symptoms in infertile couples. These symptoms in compilation with other as central obesity and insulin resistance are part of the well-known metabolic syndrome (MS). Initially MS was used to predict cardiovascular disease, it is now clear that the molecular and physiologic abnormalities seen in metabolic syndrome extend well beyond the cardiovascular system. Growing evidence has linked MS and its individual symptoms to the increasing prevalence of infertility [1]. Hypertension and dyslipidemia increase the risk of long-term cardiovascular disease in type 2 diabetes [2], which are disproportionally more harmful in low- and middle-income countries than in high-income countries [3]. The relationship between androgen deficiency and atherosclerosis is controversial. Studies suggest that androgen deficiency is associated with increased triglycerides (TGs), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) in infertile men. The androgen therapy has been associated with increased levels of high-density lipoprotein cholesterol HDL-C and may improve reverse cholesterol transport [4]. The incidence of obesity (18%), overweight (30.2%), diabetes mellitus (4.7%), glucose intolerance (15%), hypertension (26%) and dysplipidemia (65%) was observed en infertile men. The dyslipidemia was isolated hypercholesterolemia, isolated triglyceridemia or both. In them a positive correlation between estradiol (E2) and follicle-stimulating hormone (FSH) was observed when estradiol levels exceed 50pg/mL [5]. In men with coronary artery disease Gensini score (to reflect the extent and severity of coronary atherosclerosis) didn´t show correlation neither with the number of involved segments nor with the androgen levels. TGs, TC and LDL-C levels also had no correlation with testosterone (T), free-testosterone (FT) nor dehydroepiandrosterone- sulphate (DHEA-S). However, FT showed negative correlation with lipoprotein (a) and C-reactive protein [6]. Another heart disease recently associated with hormonal changes is atrial fibrillation, which is the most common serious abnormal heart rhythm, and a frequent cause of ischaemic stroke. Increase T serum levels were associated with lower risk in men and with higher risk in women. So that low testosterone levels are associated with increased risk of future atrial fibrillation and/or ischaemic stroke in men, while they are protective in women [7]. Low T serum levels are observed among men with Type 2 Diabetes Mellitus and are inversely related to insulin resistance. T in diabetic men has been inversely related to body mass index (BMI), waist circumference, and glucose tolerance, pre and post insulinemia and homeostasis model assessment of insulin resistance (HOMA-IR) [8]. BMI has positive relation with the value of systolic blood pressure, ratio LH/FSH and T, and negative correlation with FSH and PRL in infertile woman with polycystic ovary (PCO). Last patients with BMI >24kg/m2 showed higher systolic pressure and DHEA- S and post insulinemia levels in comparison with a It is necessary to keep in mind that cardiovascular diseases can be influenced by sex hormones, such as other types of hormones. T is a pleiotropic hormone that plays an important role in the human body. Through its conversion to E2, T affects bone health, including bone density. There has been a renewed interest in the systemic role of T in pain, well-being, and cardiovascular function in women and men alike. It´s necessary to revisit the clinical role of T given its potential for applications to treat...
Przemysław Jaźwiec, , Monika Chaszczewska-Markowska, , ,
Respiratory Physiology & Neurobiology, Volume 254, pp 10-15; doi:10.1016/j.resp.2018.04.001

Abstract:
It has recently been established that carotid bodies play a significant role in the regulation of activities of the cardiovascular system as well as in the pathogenesis of arterial hypertension, heart failure and diabetes. Aim of study was to determinate the influence of polymorphisms within genes of the renin-angiotensin-aldosterone system (RAAS) on the volume of the carotid bodies (CB) in patients with hypertension (HTA). The study group consisted of 77 patients with HTA. All patients were genotyped for single-nucleotide polymorphisms of genes coding for: angiotensinogen: rs4762, rs5049, rs5051 and rs699; angiotensin-converting enzyme: rs4343; angiotensin receptor type 1 gene (AGTR1): rs5182 and rs5186; and the aldosterone synthase: rs1799998. The estimation of volumes of CB (VrCB+lCB) was based on computed tomography angiography. Among individuals with essential hypertension certain relationships were documented between rs5182 and rs5186 polymorphisms of AGTR1 gene and rs1799998 polymorphism of CYP11B2 gene on one hand and the volume of carotid bodies on one other. Patients carrying the C alleles within the rs5182 and rs5186 of AGTR1 gene was associated with higher values of VrCB+lCB. The carriage of the T allele in the rs5182 locus of the AGTR1 gene determine lower values of VrCB+lCB. In summary, in patients with HTA a higher volume of CB may be resulted from the presence of specific genotypes in RAAS.
Mariana Cornelia Tilinca, Sandor Pal, Zoltan Preg, Eniko Barabas Hajdu, Raluca Tilinca, Marta German Sallo, Eniko Nemes Nagy
Published: 15 June 2018
Revista de Chimie, Volume 69, pp 1288-1291; doi:10.37358/rc.18.5.6311

Abstract:
The most common comorbidities in patients with diabetes mellitus are cardiovascular diseases, obesity, dyslipidemia, thyroid disorders but other associated diseases may frequently occur. Laboratory tests are useful investigation methods that may reveal the subclinical manifestations of the disease but they are also essential for patient monitoring. The aim of the study was to assess laboratory parameters and associated diseases in diabetic subjects and to implement a scoring system with a predictive role in the evolution of the cases. Material and methods: The study group consisted of 195 subjects with documented type 1 or type 2 diabetes. About half of the cases were collected from the Procardia outpatient unit, and the rest were patients admitted to the Diabetology Clinic in T�rgu Mure�. The study was performed between January - June 2017. The results of the laboratory tests, as well as the information regarding comorbidities and treatment, was collected and patients� body mass index was calculated. Based on the clinical data, a scoring system, called Diabetes Complication Severity Index (DCSI) with a predictive role, was implemented. The diabetic outpatients presented significantly better carbohydrate metabolic balance compared to the hospitalized subjects. No significant differences could be observed regarding kidney function, hepatic status and lipid profile of the two subgroups of diabetic subjects. The most important comorbidity observed in both patient groups was arterial hypertension. The hospitalized diabetic subjects had significantly higher incidence of ischemic heart disease and significantly lower incidence of thyroid disorders compared to the outpatients. The DCSI scoring system revealed that comorbidities are more frequently present in the hospitalized patients compared to the ambulant diabetic subjects. Evaluation of clinical status and laboratory results in diabetic patients followed by implementation of a scoring system based on the data obtained regarding comorbidities could help clinicians to set up an individual treatment plan for these patients, focusing on preventing other complications.
K. Konstantinou, K. Tsioufis, M. Mantzouranis, A. Koumeli, C. Fragoulis, N. Vogiatzakis, K. Dimitriadis, A. Kasiakogias, D. Tousoulis
Journal of Hypertension, Volume 36; doi:10.1097/01.hjh.0000539872.81798.02

Abstract:
The aim of the present study was to assess blood pressure variability (BPV) in patients hospitalized for acute myocardial infarction. We studied 75 patients (76% males, age 65 ± 13 years) who were hospitalized because of ST-elevation myocardial infarction (STEMI) and Non ST–elevation myocardial infarction (NSTEMI). All patients underwent baseline estimation of clinical and laboratory parameters during their hospitalization. Additionally, BPV was estimated based on double daily measurements of BP during hospitalization and with 24-hour ambulatory BP monitoring during the third day of hospital stay. The parameters of BPV analyzed were: a) standard deviation (SD) of systolic BP (24-h, daytime and nighttime), b) SD of diastolic BP (24-h, daytime and nighttime) and c) the coefficient of variation (CV) of systolic BP (24-h, daytime) and d) the average real variability (ARV) of systolic and diastolic BP across 24-h. From the total population, 20% had family history of cardiovascular events, 72% were hypertensives, 32% had diabetes, 51% were smokers and 32% had previous history of coronary artery disease. Regarding the type of myocardial infarction, 37% were admitted for STEMI and 55% had coronary revascularization. Focusing on the mean systolic and diastolic BP and their SD the values were 72 ± 6.1mmHg, 127 ± 11.4mmHg and 74.5 ± 6.5mmHg, respectively. From the ambulatory BP the daytime, nighttime and total SD of systolic BP was 11.3 ± 2.8mmHg, 9.8 ± 3.1mmHg and 11.7 ± 2.9mmHg, respectively. Moreover, ARV was 9.31 ± 2.1mmHg while CV was 10.21 ± 26 %. The type of MI (STEMI and NSTEMI) was significantly related to systolic and diastolic ARV (r = 0.29, p = 0.012 and r = 0.28, p = 0.014, respectively). In patients admitted for acute myocardial infarction there is a relationship between the ARV and the type of myocardial infarction. These findings suggest differential impact of hemodynamic load on the cardiovascular system in patients with STEMI and NSTEMI.
Comment
Gjin Ndrepepa
Coronary Artery Disease, Volume 29, pp 183-185; doi:10.1097/mca.0000000000000600

Abstract:
Uric acid (UA) is an end product of purine metabolism in humans and great apes. Historical records show that UA crystals were first described by Leeuwenhoek in 1679 in gouty tophus and, 50 years later, by Stukeley in a tophaceous joint, although the chemical composition of the crystals at that time was unknown 1. The Swedish chemist Scheele 2 is credited as being the first to identify UA in renal calculi, whereas Garrod 3 was the first to describe a method for UA measurement in serum or urine, which probably represents the first chemical test ever undertaken 1. Two developments are important for understanding why contemporary humans have particularly high UA levels: first, a stepwise loss of uricase activity – an enzyme that degrades UA to allantoin – caused by mutations in promoter regions of the uricase gene, occurring ∼15 million years ago (mid-Miocene) in hominid ancestors 4, and, second, diet and lifestyle changes that took place over the last century that contributed to an increase in serum UA level from 3.5 mg/dl in the 1920s to more than 6.0 mg/dl in the 1970s 5. The first event is considered to have been advantageous because of UA antioxidant properties and because it might have been key to the survival of our ancestors during the unfavorable climate changes that occurred during the mid-Miocene and later 6, whereas the diet (or lifestyle)-related UA elevation may have transformed UA from a beneficial physiological factor to a risk factor for various diseases including atherosclerosis and cardiovascular diseases. As elegantly articulated by Johnson et al.6, UA may represent a physiological alarm signal gone awry in western society. UA has been implicated in the genesis of cardiovascular disease since 1879 7, and it was one of the first metabolites included in the protocols of the Framingham study to be investigated as a potential risk factor for cardiovascular disease 8. However, despite the long history of and interest in UA, the UA role in the pathophysiology of cardiovascular disease, particularly coronary heart disease (CHD), remains disputable. Difficulties in determining whether UA acts as a risk marker or a risk factor for CHD may be explained by its frequent association and intricate relationship with other cardiovascular risk factors, the possibility of reverse causation and conflicting findings from epidemiological or clinical studies undertaken to investigate the association of UA with atherosclerosis or CHD. Notably, the association of UA with acute coronary events or clinical syndromes characterized by varying degrees of myocardial ischemia remains largely unexplored. In this issue of Coronary Artery Disease, the study by Larsen et al.9 assessed the association of serum UA level with coronary artery calcium (CAC; assessed by noncontrast cardiac computed tomographic scan) in healthy asymptomatic middle-aged individuals or ischemic myocardial injury in patients presenting with suspected or definite myocardial infarction (MI). The first objective was assessed in 1039 participants who were free of CHD, diabetes, atrial fibrillation, or valvular heart disease. The second objective was assessed in 772 patients with suspected MI who had preserved renal function and serial cardiac troponin I (cTnI) measurements. UA values were compared across subgroups of patients classified into the following entities: type 1 MI, type 2 MI, ischemic myocardial injury (not fulfilling MI criteria), nonischemic myocardial injury, systemic myocardial injury and the subgroup without elevated cTnI. In brief, in healthy asymptomatic individuals there was a correlation between UA level and CAC (quantified by the Agatston score), which was abolished after adjustment for age, sex, smoking, arterial hypertension and hypercholesterolemia.
, Tomasz J. Guzik,
Canadian Journal of Cardiology, Volume 34, pp 575-584; doi:10.1016/j.cjca.2017.12.005

Abstract:
Hypertension and type 2 diabetes are common comorbidities. Hypertension is twice as frequent in patients with diabetes compared with those who do not have diabetes. Moreover, patients with hypertension often exhibit insulin resistance and are at greater risk of diabetes developing than are normotensive individuals. The major cause of morbidity and mortality in diabetes is cardiovascular disease, which is exacerbated by hypertension. Accordingly, diabetes and hypertension are closely interlinked because of similar risk factors, such as endothelial dysfunction, vascular inflammation, arterial remodelling, atherosclerosis, dyslipidemia, and obesity. There is also substantial overlap in the cardiovascular complications of diabetes and hypertension related primarily to microvascular and macrovascular disease. Common mechanisms, such as upregulation of the renin-angiotensin-aldosterone system, oxidative stress, inflammation, and activation of the immune system likely contribute to the close relationship between diabetes and hypertension. In this article we discuss diabetes and hypertension as comorbidities and discuss the pathophysiological features of vascular complications associated with these conditions. We also highlight some vascular mechanisms that predispose to both conditions, focusing on advanced glycation end products, oxidative stress, inflammation, the immune system, and microRNAs. Finally, we provide some insights into current therapies targeting diabetes and cardiovascular complications and introduce some new agents that may have vasoprotective therapeutic potential in diabetes. Résumé L'hypertension et le diabète de type 2 sont des affections concomitantes fréquentes. L'hypertension est deux fois plus fréquente chez les patients atteints de diabète que chez ceux qui n'en sont pas atteints. De plus, les patients atteints d'hypertension sont souvent résistants à l'insuline et sont plus susceptibles de souffrir de diabète que les personnes normotendues. Chez les diabétiques, la principale cause de morbidité et de mortalité est la maladie cardiovasculaire, qui est exacerbée par l'hypertension. En conséquence, le diabète et l'hypertension sont étroitement interreliés en raison de facteurs de risques similaires, comme la dysfonction endothéliale, l'inflammation vasculaire, le remodelage artériel, l'athérosclérose, la dyslipidémie et l'obésité. On observe un chevauchement important entre les complications cardiovasculaires du diabète et celles de l'hypertension liées principalement à des maladies microvasculaires et macrovasculaires. Des mécanismes communs, comme une stimulation du système rénine-angiotensine-aldostérone, un stress oxydatif, une inflammation et une activation du système immunitaire, sont susceptibles de contribuer à la relation étroite entre le diabète et l'hypertension. Dans cet article, nous abordons le diabète et l'hypertension comme des affections concomitantes et nous parlons des caractéristiques physiopathologiques des complications vasculaires associées à ces affections. Nous soulignons également certains mécanismes vasculaires qui prédisposent à ces deux affections, en mettant l'accent sur les produits finaux de glycation avancée, le stress oxydatif, l'inflammation, le système immunitaire et les micro-ARN. Finalement, nous présentons certaines connaissances sur les traitements actuels ciblant le diabète et les complications cardiovasculaires et nous présentons de nouveaux agents qui pourraient avoir un pouvoir vasoprotecteur chez les patients diabétiques.
Adam Vašura, Martin Blaho, Petr Dítě, Tomáš Kupka, Pavel Svoboda, Arnošt Martínek
Published: 18 January 2018
Vnitřní lékařství, Volume 63, pp 945-948

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