European Heart Journal

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ISSN / EISSN : 0195-668X / 1522-9645
Published by: Oxford University Press (OUP) (10.1093)
Total articles ≅ 46,184
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European Heart Journal, Volume 42, pp 3581-3585;

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Coronary artery disease (CAD) is one of the major global health care and economic burdens. Since percutaneous coronary intervention (PCI) began with balloon angioplasty in 1977, it has more recently been considered that PCI with drug-eluting stents (DES) implantation is the most commonly employed treatment option for patients with CAD.1 As time has progressed, there have been exciting technological advancements in the field, including several new-generation DES with thinner stent struts, new anti-proliferative agents, biodegradable polymer (BP) coating, and even bioabsorbable stents for better clinical outcomes.2,3 However, complications, such as in-stent restenosis, late thrombosis, local chronic inflammation, and re-occlusion, are still problems of DES implantations, meaning that deep analysis of their...
, , David Celermajer, Wei Li, Tal Geva, , Massimo Griselli, , Michael A Gatzoulis
Atrial septal defects (ASDs) represent the most common congenital heart defect diagnosed in adulthood. Although considered a simple defect, challenges in optimal diagnostic and treatment options still exist due to great heterogeneity in terms of anatomy and time-related complications primarily arrhythmias, thromboembolism, right heart failure and, in a subset of patients, pulmonary arterial hypertension (PAH). Atrial septal defects call for tertiary expertise where all options may be considered, namely catheter vs. surgical closure, consideration of pre-closure ablation for patients with atrial tachycardia and suitability for closure or/and targeted therapy for patients with PAH. This review serves to update the clinician on the latest evidence, the nuances of optimal diagnostics, treatment options, and long-term follow-up care for patients with an ASD.
Jack Ansell, Sasha Bakhru, Bryan E Laulicht, Gregory Tracey, Stephen Villano, Daniel Freedman
Aims Ciraparantag is a reversal agent for anticoagulants including direct oral anticoagulants. The aim was to evaluate the efficacy and safety of ciraparantag to reverse anticoagulation induced by apixaban or rivaroxaban in healthy elderly adults. Methods and results Two randomized, placebo-controlled, dose-ranging trials conducted in healthy subjects aged 50–75 years. Subjects received apixaban (Study 1) 10 mg orally twice daily for 3.5 days or rivaroxaban (Study 2) 20 mg orally once daily for 3 days. At steady-state anticoagulation subjects were randomized 3:1 to a single intravenous dose of ciraparantag (Study 1: 30, 60, or 120 mg; Study 2: 30, 60, 120, or 180 mg) or placebo. Efficacy was based on correction of the whole blood clotting time (WBCT) at multiple timepoints over 24 h. Subjects and technicians performing WBCT testing were blinded to treatment. Complete reversal of WBCT within 1 h post-dose and sustained through 5 h (apixaban) or 6 h (rivaroxaban) was dose related and observed with apixaban in 67%, 100%, 100%, and 17% of subjects receiving ciraparantag 30 mg, 60 mg, 120 mg, or placebo, respectively; and with rivaroxaban in 58%, 75%, 67%, 100%, and 13% of subjects receiving ciraparantag 30 mg, 60 mg, 120 mg, 180 mg, or placebo, respectively. Adverse events related to ciraparantag were mild, transient hot flashes or flushing. Conclusions Ciraparantag provides a dose-related reversal of anticoagulation induced by steady-state dosing of apixaban or rivaroxaban. Sustained reversal was achieved with 60 mg ciraparantag for apixaban and 180 mg ciraparantag for rivaroxaban. All doses of ciraparantag were well tolerated.
Artificial intelligence (AI) has given the electrocardiogram (ECG) and clinicians reading them super-human diagnostic abilities. Trained without hard-coded rules by finding often subclinical patterns in huge datasets, AI transforms the ECG, a ubiquitous, non-invasive cardiac test that is integrated into practice workflows, into a screening tool and predictor of cardiac and non-cardiac diseases, often in asymptomatic individuals. This review describes the mathematical background behind supervised AI algorithms, and discusses selected AI ECG cardiac screening algorithms including those for the detection of left ventricular dysfunction, episodic atrial fibrillation from a tracing recorded during normal sinus rhythm, and other structural and valvular diseases. The ability to learn from big data sets, without the need to understand the biological mechanism, has created opportunities for detecting non-cardiac diseases as COVID-19 and introduced challenges with regards to data privacy. Like all medical tests, the AI ECG must be carefully vetted and validated in real-world clinical environments. Finally, with mobile form factors that allow acquisition of medical-grade ECGs from smartphones and wearables, the use of AI may enable massive scalability to democratize healthcare.
Hongtu Cui, Yanghui Chen, Ke Li, Rui Zhan, Mingming Zhao, Yangkai Xu, Zhiyong Lin, Yi Fu, Qihua He, , et al.
Aims Aortic aneurysm and dissection (AAD) are high-risk cardiovascular diseases with no effective cure. Macrophages play an important role in the development of AAD. As succinate triggers inflammatory changes in macrophages, we investigated the significance of succinate in the pathogenesis of AAD and its clinical relevance. Methods and results We used untargeted metabolomics and mass spectrometry to determine plasma succinate concentrations in 40 and 1665 individuals of the discovery and validation cohorts, respectively. Three different murine AAD models were used to determine the role of succinate in AAD development. We further examined the role of oxoglutarate dehydrogenase (OGDH) and its transcription factor cyclic adenosine monophosphate-responsive element-binding protein 1 (CREB) in the context of macrophage-mediated inflammation and established p38αMKOApoe–/– mice. Succinate was the most upregulated metabolite in the discovery cohort; this was confirmed in the validation cohort. Plasma succinate concentrations were higher in patients with AAD compared with those in healthy controls, patients with acute myocardial infarction (AMI), and patients with pulmonary embolism (PE). Moreover, succinate administration aggravated angiotensin II-induced AAD and vascular inflammation in mice. In contrast, knockdown of OGDH reduced the expression of inflammatory factors in macrophages. The conditional deletion of p38α decreased CREB phosphorylation, OGDH expression, and succinate concentrations. Conditional deletion of p38α in macrophages reduced angiotensin II-induced AAD. Conclusion Plasma succinate concentrations allow to distinguish patients with AAD from both healthy controls and patients with AMI or PE. Succinate concentrations are regulated by the p38α–CREB–OGDH axis in macrophages.
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