Cardiac injury in patients infected with the novel Coronavirus (COVID-19) seems to be associated with higher morbimortality. We provide a broad review of the clinical evolution of COVID-19, emphasizing its impact and implications on the cardiovascular system. The pathophysiology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by overproduction of inflammatory cytokines (IL-6 and TNF-α) leading to systemic inflammation and multiple organ dysfunction syndrome, acutely affecting the cardiovascular system. Hypertension (56.6%) and diabetes (33.8%) are the most prevalent comorbidities among individuals with COVID-19, who require hospitalization. Furthermore, cardiac injury, defined as elevated us-troponin I, significantly relates to inflammation biomarkers (IL-6 and C-reactive protein (CRP), hyperferritinemia, and leukocytosis), portraying an important correlation between myocardial injury and inflammatory hyperactivity triggered by viral infection. Increased risk for myocardial infarction, fulminant myocarditis rapidly evolving with depressed systolic left ventricle function, arrhythmias, venous thromboembolism, and cardiomyopathies mimicking STEMI presentations are the most prevalent cardiovascular complications described in patients with COVID-19. Moreover, SARS-CoV-2 tropism and interaction with the RAAS system, through ACE2 receptor, possibly enhances inflammation response and cardiac aggression, leading to imperative concerns about the use of ACEi and ARBs in infected patients. Cardiovascular implications result in a worse prognosis in patients with COVID-19, emphasizing the importance of precocious detection and implementation of optimal therapeutic strategies.
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| http://dx.doi.org/10.1038/s41371-020-0387-4 | DOI Listing |
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