دورية أكاديمية
Cell-Specific Mechanisms in the Heart of COVID-19 Patients.
| العنوان: | Cell-Specific Mechanisms in the Heart of COVID-19 Patients. |
|---|---|
| المؤلفون: | Tsai EJ; Division of Cardiology, Columbia University Vagelos College of Physicians & Surgeons, New York, NY (E.J.T.)., Cˇiháková D; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD (D.C.)., Tucker NR; Masonic Medical Research Institute, Utica, NY (N.R.T.). |
| المصدر: | Circulation research [Circ Res] 2023 May 12; Vol. 132 (10), pp. 1290-1301. Date of Electronic Publication: 2023 May 11. |
| نوع المنشور: | Journal Article; Review; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural |
| اللغة: | English |
| بيانات الدورية: | Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0047103 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1524-4571 (Electronic) Linking ISSN: 00097330 NLM ISO Abbreviation: Circ Res Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Baltimore, MD : Lippincott Williams & Wilkins Original Publication: Baltimore, Md. Grune & Stratton. |
| مواضيع طبية MeSH: | COVID-19*/complications , Myocarditis* , Heart Diseases*, Humans ; SARS-CoV-2 ; Endothelial Cells ; Hospital Mortality ; Post-Acute COVID-19 Syndrome ; Heart ; Troponin ; Myocytes, Cardiac |
| مستخلص: | From the onset of the pandemic, evidence of cardiac involvement in acute COVID-19 abounded. Cardiac presentations ranged from arrhythmias to ischemia, myopericarditis/myocarditis, ventricular dysfunction to acute heart failure, and even cardiogenic shock. Elevated serum cardiac troponin levels were prevalent among hospitalized patients with COVID-19; the higher the magnitude of troponin elevation, the greater the COVID-19 illness severity and in-hospital death risk. Whether these consequences were due to direct SARS-CoV-2 infection of cardiac cells or secondary to inflammatory responses steered early cardiac autopsy studies. SARS-CoV-2 was reportedly detected in endothelial cells, cardiac myocytes, and within the extracellular space. However, findings were inconsistent and different methodologies had their limitations. Initial autopsy reports suggested that SARS-CoV-2 myocarditis was common, setting off studies to find and phenotype inflammatory infiltrates in the heart. Nonetheless, subsequent studies rarely detected myocarditis. Microthrombi, cardiomyocyte necrosis, and inflammatory infiltrates without cardiomyocyte damage were much more common. In vitro and ex vivo experimental platforms have assessed the cellular tropism of SARS-CoV-2 and elucidated mechanisms of viral entry into and replication within cardiac cells. Data point to pericytes as the primary target of SARS-CoV-2 in the heart. Infection of pericytes can account for the observed pericyte and endothelial cell death, innate immune response, and immunothrombosis commonly observed in COVID-19 hearts. These processes are bidirectional and synergistic, rendering a definitive order of events elusive. Single-cell/nucleus analyses of COVID-19 myocardial tissue and isolated cardiac cells have provided granular data about the cellular composition and cell type-specific transcriptomic signatures of COVID-19 and microthrombi-positive COVID-19 hearts. Still, much remains unknown and more in vivo studies are needed. This review seeks to provide an overview of the current understanding of COVID-19 cardiac pathophysiology. Cell type-specific mechanisms and the studies that provided such insights will be highlighted. Given the unprecedented pace of COVID-19 research, more mechanistic details are sure to emerge since the writing of this review. Importantly, our current knowledge offers significant clues about the cardiac pathophysiology of long COVID-19, the increased postrecovery risk of cardiac events, and thus, the future landscape of cardiovascular disease. Competing Interests: Disclosures None. |
| التعليقات: | Erratum in: Circ Res. 2023 Jun 23;133(1):e18. (PMID: 37347837) |
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| معلومات مُعتمدة: | R01 HL138528 United States HL NHLBI NIH HHS; R01 HL118183 United States HL NHLBI NIH HHS; R01 HL136586 United States HL NHLBI NIH HHS; K01 HL140187 United States HL NHLBI NIH HHS |
| فهرسة مساهمة: | Keywords: COVID-19; endothelial cells; myocardium; pericytes; single-cell analysis; thromboinflammation; viral tropism |
| المشرفين على المادة: | 0 (Troponin) |
| تواريخ الأحداث: | Date Created: 20230511 Date Completed: 20230515 Latest Revision: 20230622 |
| رمز التحديث: | 20240829 |
| مُعرف محوري في PubMed: | PMC10171292 |
| DOI: | 10.1161/CIRCRESAHA.123.321876 |
| PMID: | 37167361 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1524-4571 |
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| DOI: | 10.1161/CIRCRESAHA.123.321876 |