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(searched for: Cardiovascular Manifestations of COVID-19)
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Mohamad Kanso, Thomas Cardi, Halim Marzak, Alexandre Schatz, Loïc Faucher, Lélia Grunebaum, Olivier Morel, Laurence Jesel
European Heart Journal - Case Reports; doi:10.1093/ehjcr/ytaa449

Abstract:
Background Since the onset of the COVID-19 pandemic, several cardiovascular manifestations have been described. Among them, venous thromboembolism (VTE) seems to be one of the most frequent, particularly in intensive care unit patients. We report two cases of COVID-19 patients developing acute pulmonary embolism (PE) after discharge from a first hospitalization for pneumonia of moderate severity. Case summary Two patients with positive RT-PCR test were initially hospitalized for non-severe COVID-19. Both received standard thromboprophylaxis during the index hospitalization and had no strong predisposing risk factors for VTE. Few days after discharge, they were both readmitted for worsening dyspnoea due to PE. One patient was positive for lupus anticoagulant. Discussion Worsening respiratory status in COVID-19 patients must encourage physicians to search for PE since SARS-CoV-2 infection may act as a precipitant risk factor for VTE. Patients may thus require more aggressive and longer thromboprophylaxis after COVID-19 related hospitalization.
Luis Ortega‐Paz, Davide Capodanno, Gilles Montalescot, Dominick J Angiolillo
Journal of the American Heart Association; doi:10.1161/jaha.120.019650

Abstract:
Coronavirus disease 2019 (COVID‐19) is an infectious disease caused by severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) which has posed a significant threat to global health. Although the infection is frequently asymptomatic or associated with mild symptoms, in a small proportion of patients it can produce an intense inflammatory and prothrombotic state that can lead to acute respiratory distress syndrome, multiple organ failure, and death. Angiotensin‐converting enzyme 2 (ACE2), highly expressed in the respiratory system, has been identified as a functional receptor for SARS‐CoV‐2. Notably, ACE2 is also expressed in the cardiovascular system and there are multiple cardiovascular implications of COVID‐19. Cardiovascular risk factors and cardiovascular disease have been associated with severe manifestations and poor prognosis in patients with COVID‐19. Importantly, patients with COVID‐19 may have thrombotic and coagulation abnormalities promoting a hypercoagulable state, resulting in an increased rate of thrombotic and thromboembolic events. This review will describe the pathophysiology of the cardiovascular involvement following infection by SARS‐CoV‐2, with a focus on thrombotic and thromboembolic manifestations and implications for antithrombotic management.
FahimehAlsadat Shojaei, Zahra Habibi, Sogand Goudarzi, Fatemeh Dehghani Firouzabadi, Sahar Memar Montazerin, Homa Najafi, Farima Kahe, Kaveh Momenzadeh, Mahshid Mir, Faris Khan, et al.
Published: 22 November 2020
Medical Hypotheses; doi:10.1016/j.mehy.2020.110410

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Jayakanthan Kabeerdoss, Rakesh Kumar Pilania, Reena Karkhele, T. Sathish Kumar, Debashish Danda, Surjit Singh
Rheumatology International pp 1-14; doi:10.1007/s00296-020-04749-4

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Published: 19 November 2020
by MDPI
Cells, Volume 9; doi:10.3390/cells9112508

Abstract:
SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus’s pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.
Cecilia Schweblin, Anne Lise Hachulla, Marco Roffi, Frédéric Glauser
European Heart Journal - Case Reports; doi:10.1093/ehjcr/ytaa371

Abstract:
Background Venous thrombo-embolic events have been described in hospitalized patients with coronavirus disease 2019 (COVID-19), suggesting the presence of coagulopathy induced by the viral infection. To date, only rare cases of arterial thrombosis related to COVID-19 have been reported. Case summary A 54-year-old patient with an influenza-like illness 15 days earlier, which resolved, and no known cardiovascular risk factor presented with acute right lower limb ischaemia. A computed tomography angiogram of the abdominal aorta and lower extremities showed, in the absence of vascular disease, a subocclusive thrombosis of the right common iliac artery and an occlusion of the right internal iliac, profunda femoral, and popliteal arteries. On the left side, the computed tomography angiogram demonstrated a non-occlusive thrombosis of the common femoral artery. The patient underwent emergency surgical thrombectomy as well as endovascular revascularization on the right side followed by therapeutic anticoagulation, with normalization of the limb perfusion. A nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by real-time reverse transcription–PCR (rRT–PCR) was negative three times. Haemostasis analysis showed a mild hyperfibrinogenaemia and a shortening of the activated partial thromboplastin time. An extensive screening for cardio-embolism was negative. As the thrombotic event was unexplained, antibody testing for SARS-CoV-2 was performed and the result was positive. Discussion Venous thrombosis and pulmonary embolisms have been observed in COVID-19. As in our case, the first reports on COVID-19-associated arterial thrombotic events have emerged. A better understanding of the coagulopathy in COVID-19 is essential to guide prevention and treatment of venous as well as arterial thrombo-embolic events.
Jun Yasuhara, Kae Watanabe, Hisato Takagi, Naokata Sumitomo, Toshiki Kuno
Published: 18 November 2020
Abstract:
Background: Multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19 has been increasingly recognized. However, the clinical features of MIS-C and the differences from Kawasaki disease remain unknown. The study aims to investigate the epidemiology and clinical course of MIS-C. Methods: PubMed and EMBASE were searched through August 30, 2020. Observational studies describing MIS-C were included. Data regarding demographic features, clinical symptoms, laboratory, echocardiography and radiology findings, treatments, and outcomes were extracted. Study-specific estimates were combined using one-group meta-analysis in a random-effects model. Results: A total of 27 studies were identified including 917 MIS-C patients. The mean age was 9.3 (95% confidence interval [CI], 8.4-10.1). The pooled proportions of Hispanic and Black cases were 34.6% (95% CI, 28.3-40.9) and 31.5% (95% CI, 24.8-38.1), respectively. The common manifestations were gastrointestinal symptoms (87.3%; 95% CI, 82.9-91.6) and cardiovascular involvement such as myocardial dysfunction (55.3%; 95% CI, 42.4-68.2), coronary artery aneurysms (21.7%; 95% CI, 12.8-30.1) and shock (65.8%; 95% CI, 51.1-80.4), with marked elevated inflammatory and cardiac markers. The majority of patients received intravenous immunoglobulin (81.0%; 95% CI, 75.0-86.9), aspirin (67.3%; 95% CI, 48.8-85.7), and corticosteroids (63.6%; 95% CI, 53.4-73.8) with a variety of anti-inflammatory agents. Although myocardial dysfunction improved in 55.1% (95% CI, 33.4-76.8) at discharge, the rate of extracorporeal membrane oxygenation use was 6.3% (95% CI, 2.8-9.8) and the mortality was 1.9% (95% CI, 1.0-2.8). Conclusion: Our findings suggest that MIS-C leads to multiple organ failure, including gastrointestinal manifestations, myocardial dysfunction and coronary abnormalities, and has distinct features from Kawasaki disease.
Zain Ahmed, Avinainder Singh, Lina Vadlamani, Maxwell Eder, Zaniar Ghazizadeh, Jakob Park, Manan Pareek, Justin Pacor, Chad Gier, Carlos Mena-Hurtado, et al.
Circulation, Volume 142; doi:10.1161/circ.142.suppl_3.16397

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Joey Junarta, Joshua M Riley, Behzad B Pavri
Circulation, Volume 142; doi:10.1161/circ.142.suppl_3.14980

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Ruifang Yang, Sokol Kalaveshi, David Goldgrab, Jearim Craig, Stephen Mester, Christian Perzanowski
Circulation, Volume 142; doi:10.1161/circ.142.suppl_3.15403

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