Post-Acute COVID-19 Syndrome and the cardiovascular system: What is known?

Post-Acute COVID-19 Syndrome (PACS) is defined by persistent symptoms >3-4 weeks after onset of COVID-19. The mechanism of these persistent symptoms is distinct from acute COVID-19 although not completely understood despite the high incidence of PACS. Cardiovascular symptoms such as chest pain and palpitations commonly occur in PACS, but the underlying cause of symptoms is infrequently known. While autopsy studies have shown that the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) rarely causes direct myocardial injury, several syndromes such as myocarditis, pericarditis, and Postural Orthostatic Tachycardia Syndrome have been implicated in PACS. Additionally, patients hospitalized with acute COVID-19 who display biomarker evidence of myocardial injury may have underlying coronary artery disease revealed by the physiological stress of SARS-CoV-2 infection and may benefit from medical optimization. We review what is known about PACS and the cardiovascular system and propose a framework for evaluation and management of related symptoms.

Clinical significance of coronavirus disease 2019 in hospitalized patients with myocardial injury.

BACKGROUND: The clinical significance of Coronavirus disease 2019 (COVID-19) as an associate of myocardial injury is controversial. HYPOTHESIS: Type 2 MI/Myocardial Injury are associated with worse outcomes if complicated by COVID-19. METHODS: This longitudinal cohort study involved consecutive patients admitted to a large urban hospital. Myocardial injury was determined using laboratory records as ≥1 hs-TnI result >99th percentile (male: >34 ng/L; female: >16 ng/L). Endotypes were defined according to the Fourth Universal Definition of Myocardial Infarction (MI) and COVID-19 determined using PCR. Outcomes of patients with myocardial injury with and without COVID-19 were assessed. RESULTS: Of 346 hospitalized patients with elevated hs-TnI, 35 (10.1%) had laboratory-confirmed COVID-19 (median age [IQR]; 65 [59-74]; 64.8% male vs. COVID-19 negative: 74 [63-83] years; 43.7% male). Cardiac endotypes by COVID-19 status (yes vs. no) were: Type 1 MI (0 [0%] vs. 115 [100%]; p < .0005), Type 2 MI (13 [16.5%] vs. 66 [83.5%]; p = .045), and non-ischemic myocardial injury (cardiac: 4 [5.8%] vs. 65 [94.2%]; p = .191, non-cardiac:19 [22.9%] vs. 64 [77.%]; p < .0005). COVID-19 patients had less comorbidity (median [IQR] Charlson Comorbidity Index: 3.0 [3.0] vs. 5.0 [4.0]; p = .001), similar hs-TnI concentrations (median [IQR] initial: 46 [113] vs. 62 [138]; p = .199, peak: 122 [474] vs. 79 [220] ng/L; p = .564), longer admission (days) (median [IQR]: 14[19] vs. 6[12]; p = .001) and higher in-hospital mortality (63.9% vs. 11.3%; OR = 13.2; 95%CI: 5.90, 29.7). CONCLUSIONS: Cardiac sequelae of COVID-19 typically manifest as Non-cardiac myocardial injury/Type 2MI in younger patients with less co-morbidity. Paradoxically, the admission duration and in-hospital mortality are increased.

Cardiovascular Manifestations and Mechanisms in Patients with COVID-19.

Coronavirus disease 2019 (COVID-19) patients with pre-existing cardiovascular disease (CVD) or with cardiovascular complications have a higher risk of mortality. The main cardiovascular complications of COVID-19 include acute cardiac injury, acute myocardial infarction (AMI), myocarditis, arrhythmia, heart failure, shock, and venous thromboembolism (VTE)/pulmonary embolism (PE). COVID-19 can cause cardiovascular complications or deterioration of coexisting CVD through direct or indirect mechanisms, including viral toxicity, dysregulation of the renin-angiotensin-aldosterone system (RAAS), endothelial cell damage and thromboinflammation, cytokine storm, and oxygen supply-demand mismatch. We systematically review cardiovascular manifestations, histopathology, and mechanisms of COVID-19, to help to formulate future research goals and facilitate the development of therapeutic management strategies.

Cardiac Troponin for Assessment of Myocardial Injury in COVID-19: JACC Review Topic of the Week.

Increases in cardiac troponin indicative of myocardial injury are common in patients with coronavirus disease-2019 (COVID-19) and are associated with adverse outcomes such as arrhythmias and death. These increases are more likely to occur in those with chronic cardiovascular conditions and in those with severe COVID-19 presentations. The increased inflammatory, prothrombotic, and procoagulant responses following severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial infarction, because of respiratory failure with hypoxia and hemodynamic instability in critically ill patients. Myocarditis, stress cardiomyopathy, acute heart failure, and direct injury from SARS-CoV-2 are important etiologies, but primary noncardiac conditions, such as pulmonary embolism, critical illness, and sepsis, probably cause more of the myocardial injury. The structured use of serial cardiac troponin has the potential to facilitate risk stratification, help make decisions about when to use imaging, and inform stage categorization and disease phenotyping among hospitalized COVID-19 patients.