Coronavirus Affects Cardiovascular Disease
COVID-19 can have a direct impact on the cardiovascular system. Pre-existing cardiovascular disease may predispose or worsen COVID-19 infection. Therefore, the impact of infection appears to be more intense if the host has cardiovascular comorbidities, especially since they are frail older people with reduced immunity.
Therapies for COVID-19 can cause potentially serious cardiovascular adverse reactions in the acute phase that require close monitoring. People with cardiovascular disease infected with the virus have an increased risk of side effects and are considered to have a poor prognosis. Chronic cardiovascular effects through impaired lipid metabolism are also known consequences of Coronaviruses.
Cardiovascular damage during COVID-19 is proven in many recently published articles, it is caused by several direct and indirect mechanisms. Here’s How Covid-19 Coronavirus Affects Cardiovascular Disease Patients Study
Direct myocardial injury
Direct myocardial damage through the angiotensin-converting enzyme receptor 2 (ACE2), which cardiomyocytes significantly express. This could be the cause of true myocarditis; According to the Audit study, SARS-CoV viral RNA was detected in 35% of human hearts autopsied during the SARS epidemic in Toronto.
The same authors confirmed that SARS-CoV can cause ACE2-dependent myocardial injury (ACE2-dependent myocardial infection), identified as a functional receptor for coronavirus (molecular modeling has strong structural similarity between SARS-CoV and SARS receptor domains). VOC 2).
Indirect myocardial damage due to heart attack
Indirect myocardial damage due to type 1 infarction (rupture of the plaque favored by infection such as influenza) or type 2 (secondary to inadequate demand and myocardial oxygen supply secondary to respiratory failure, cytokine storm).
Acute myocardial injury
Acute myocardial injury (myocardial injury): A certain number of patients admitted for hypoxemic pneumonitis and / or acute respiratory distress syndrome under COVID-19 will develop acute myocardial lesions defined by an increase and / or decrease in troponin associated myocardial involvement.
Significant differences in troponin levels were observed between cured and deceased patients. In a meta-analysis with 341 patients, troponin elevation was higher in severe forms of COVID-19 and was associated with a poorer prognosis.
However, troponin may be elevated in patients with chronic kidney failure or in those who develop acute kidney failure as part of sepsis.
Given the frequency and nonspecific nature of troponin elevation in patients infected with COVID-19, physicians are advised to measure troponin only if the diagnosis of acute myocardial infarction or myocarditis is suspected. The elevation of troponin and BNP should be interpreted in the general context of the infection (compared to clinical data and other imaging techniques).
In a series of 150 cases of COVID-19, 68 deaths have been recorded with 27 cases of myocarditis, including 5 known as fulminants. Other authors have described deaths from fulminant forms with autopsy results that show a mononuclear infiltrate in myocardial tissue.
An observation published in the EHJ showed the efficacy of the combination of corticosteroid immunoglobulins in the treatment of a case of fulminant myocarditis due to Coronavirus.
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