Search

Background: Coronavirus Disease-2019 (COVID-19) may impair outcomes of patients with ST-segment elevation myocardial infarction (STEMI). The extent of this phenomenon and its mechanisms are unclear., Methods and results: This study prospectively included 50 consecutive STEMI patients admitted to our center for primary percutaneous coronary intervention (PCI) at the peak of the Italian COVID-19 outbreak. At admission, a COVID-19 test was positive in 24 patients (48%), negative in 26 (52%). The primary endpoint was in-hospital all-cause mortality. Upon admission, COVID-19 subjects had lower PO2/FiO2 (169 [100-425] vs. 390 [302-477], P<0.01), more need for oxygen support (62.5% vs. 26.9%, P=0.02) and a higher rate of myocardial dysfunction (ejection fraction <30% in 45.8% vs. 19.2%, P=0.04). All patients underwent emergency angiography. In 12.5% of COVID-19 patients, no culprit lesions were detected, thus PCI was performed in 87.5% and 100% of COVID-19 positive and negative patients, respectively (P=0.10). Despite a higher rate of obstinate thrombosis in the COVID-19 group (47.6% vs. 11.5%, P<0.01), the PCI result was similar (TIMI 2-3 in 90.5% vs. 100%, P=0.19). In-hospital mortality was 41.7% and 3.8% in COVID-19 positive and negative patients, respectively (P<0.01). Respiratory failure was the leading cause of death (80%) in the COVID-19 group, frequently associated with severe myocardial dysfunction., Conclusions: In-hospital mortality of COVID-19 patients with STEMI remains high despite successful PCI, mainly due to coexisting severe respiratory failure. This may be a critical factor in patient management and treatment selection.

Background: Cardiac injury is common in patients who are hospitalized with coronavirus disease 2019 (COVID-19) and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain uncertain., Methods: We conducted a systematic pathological analysis of 40 hearts from hospitalized patients dying of COVID-19 in Bergamo, Italy, to determine the pathological mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underlying mechanisms of cardiac injury., Results: Of the 40 hearts examined, 14 (35%) had evidence of myocyte necrosis, predominantly of the left ventricle. Compared with subjects without necrosis, subjects with necrosis tended to be female, have chronic kidney disease, and have shorter symptom onset to admission. The incidence of severe coronary artery disease (ie, >75% cross-sectional narrowing) was not significantly different between those with and without necrosis. Three of 14 (21.4%) subjects with myocyte necrosis showed evidence of acute myocardial infarction, defined as ≥1 cm 2 area of necrosis, whereas 11 of 14 (78.6%) showed evidence of focal (>20 necrotic myocytes with an area of ≥0.05 mm 2 but <1 cm 2 ) myocyte necrosis. Cardiac thrombi were present in 11 of 14 (78.6%) cases with necrosis, with 2 of 14 (14.2%) having epicardial coronary artery thrombi, whereas 9 of 14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and small muscular arteries. We compared cardiac microthrombi from COVID-19-positive autopsy cases to intramyocardial thromboemboli from COVID-19 cases as well as to aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19-infected patients presenting with ST-segment-elevation myocardial infarction. Microthrombi had significantly greater fibrin and terminal complement C5b-9 immunostaining compared with intramyocardial thromboemboli from COVID-19-negative subjects and with aspirated thrombi. There were no significant differences between the constituents of thrombi aspirated from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction., Conclusions: The most common pathological cause of myocyte necrosis was microthrombi. Microthrombi were different in composition from intramyocardial thromboemboli from COVID-19-negative subjects and from coronary thrombi retrieved from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction. Tailored antithrombotic strategies may be useful to counteract the cardiac effects of COVID-19 infection.

To investigate whether severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2)-induced myocarditis constitutes an important mechanism of cardiac injury, a review was conducted of the published data and the authors' experience was added from autopsy examination of 16 patients dying of SARS-CoV-2 infection. Myocarditis is an uncommon pathologic diagnosis occurring in 4.5% of highly selected cases undergoing autopsy or endomyocardial biopsy. Although polymerase chain reaction-detectable virus could be found in the lungs of most coronavirus disease-2019 (COVID-19)-infected subjects in our own autopsy registry, in only 2 cases was the virus detected in the heart. It should be appreciated that myocardial inflammation alone by macrophages and T cells can be seen in noninfectious deaths and COVID-19 cases, but the extent of each is different, and in neither case do such findings represent clinically relevant myocarditis. Given its extremely low frequency and unclear therapeutic implications, the authors do not advocate use of endomyocardial biopsy to diagnose myocarditis in the setting of COVID-19., Competing Interests: Author Disclosures This study was supported by the CVPath Institute, a 501(c)(3) foundation. CVPath Institute has received institutional research support from R01 HL141425 Leducq Foundation Grant, 480 Biomedical, 4C Medical, 4Tech, Abbott, Accumedical, Amgen, Biosensors, Boston Scientific, Cardiac Implants, Celonova, Claret Medical, Concept Medical, Cook, CSI, DuNing, Inc, Edwards LifeSciences, Emboline, Endotronix, Envision Scientific, Lutonix/Bard, Gateway, Lifetech, Limflo, MedAlliance, Medtronic, Mercator, Merill, Microport Medical, Microvention, Mitralign, MitrAssist, NAMSA, Nanova, Neovasc, NIPRO, Novogate, Occulotech, OrbusNeich Medical, Phenox, Profusa, Protembis, Qool, Recor, Senseonics, Shockwave, Sinomed, Spectranetics, Surmodics, Symic, Vesper, W.L. Gore, and Xeltis. Dr. Cornelissen has received research grants from University Hospital RWTH Aachen. Dr. Guagliumi has received institutional research grants from Abbott Vascular, Boston Scientific, and Infraredx; and has served as a consultant for Abbott Vascular and Boston Scientific. Dr. Virmani has received honoraria from Abbott Vascular, Biosensors, Boston Scientific, Celonova, Cook Medical, Cordis, CSI, Lutonix Bard, Medtronic, OrbusNeich Medical, CeloNova, SINO Medical Technology, Recor Medical, Terumo Corporation, W. L. Gore, and Spectranetics; and has served as a consultant for Abbott Vascular, Boston Scientific, Celonova, Cook Medical, Cordis, CSI, Edwards Lifesciences, Lutonix Bard, Medtronic, OrbusNeich Medical, ReCore, Sinomedical Technology, Spectranetics, Surmodics, Terumo Corporation, W. L. Gore, and Xeltis. Dr. Finn has received honoraria from Abbott Vascular, Biosensors, Boston Scientific, Celonova, Cook Medical, CSI, Lutonix Bard, Sinomed, and Terumo Corporation; and has served as a consultant to Amgen, Abbott Vascular, Boston Scientific, Celonova, Cook Medical, Lutonix Bard, and Sinomed. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

The adipose tissue (AT) is an endocrine organ that produces adipocytokines (adipokines), able to influence metabolic homeostasis. In the conventional classification, there are two large AT depots, characterized by different paracrine activities: the subcutaneous AT, which would mostly produce cytokines with protective properties against cardiovascular disease; and the visceral AT, responsible for the secretion of cytokines with proinflammatory, prothrombotic, and proatherogenic effects. A third component, the epicardial AT (EAT) is now receiving increasing attention due to its unique anatomical and functional proximity to the myocardium and the coronary arteries. In rodents, the EAT protects the heart from exposure to high levels of free fatty acids, and provides energy to the myocardium under high metabolic demands. The observation that atherosclerotic plaques are more prevalent in regions of coronary arteries surrounded by the EAT, while they tend to be less present in segments penetrating the myocardium (the septal branches and segments under myocardial bridges), has led to the hypothesis of a possible role of the EAT in promoting the development of atherosclerosis through endocrine and paracrine effects, in addition to the role of biomechanical forces affecting transendothelial lipid permeability into the intima. In this article, we review the clinical and molecular evidence linking the EAT and coronary artery disease through a systematic review of the literature. We, here, discuss current diagnostic techniques in evaluating the interaction between EAT and the onset of coronary artery disease and ischaemic heart disease. Finally, we review current knowledge on the underlying mechanisms by which the EAT may affect coronary atherosclerosis, and potential clinical implications of this interaction, making the EAT an attractive target for new therapeutics in cardiovascular disease., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)