The Effects of the SARS-CoV-2 Virus on the Cardiovascular System and Coagulation State Leading to Cardiovascular Diseases: A Narrative Review

Abstract

The novel coronavirus pandemic has led to morbidity and mortality throughout the world. Until now, it is a highly virulent contagion attacking the respiratory system in humans, especially people with chronic diseases and the elderly who are most vulnerable. A majority of afflicted are those suffering from cardiovascular and coronary diseases. In this review article, an attempt has been made to discuss and thoroughly review the mode of therapies that alleviate cardiac complications and complications due to hypercoagulation in patients infected with the SARS-CoV-2 virus. Presently a host of thrombolytic drugs are in use like Prourokinase, Retelapse, RhTNK-tPA and Urokinase. However, thrombolytic therapy, especially if given intravenously, is associated with a serious risk of intracranial haemorrhage, systemic haemorrhage, immunologic complications, hypotension and myocardial rupture. The effects of the SARS-CoV-2 virus upon the cardiovascular system and coagulation state of the body are being closely studied. In connection to the same, clinical prognosis and complications of thrombolytic therapy are being scrutinized. It is noteworthy to mention that myocardial oxygen supply/demand mismatch, direct myocardial cells injury and acute plaque rupture are the multiple mechanisms responsible for acute coronary syndrome and cardiac complications in Covid-19 infection. However, this review has limitations as data available in this context is limited, scattered and heterogenous that questions the reliability of the same. So, more multi-centric studies involving representative populations, carried out meticulously, could further assist in responding better to cardiac complications among Covid-19 patients.

Pathogenesis and histological changes of nephropathy associated with COVID‐19

“…Hypotension is an important mechanism of prerenal kidney injury in COVID‐19 patients, and may be caused by fever, sepsis, dehydration caused by diarrhea and vomiting, myocarditis, right heart failure leading to hemodynamic instability, and renal venous congestion 43–46 . Furthermore, prerenal kidney injury may also be caused by the high positive end‐expiratory pressure levels required for mechanical ventilation 47 .…”

Fibrinogen level in coronary artery disease people with COVID-19 patients in Iraq

“…The wide distribution of COVID-19 nucleic acid in respiratory tract, saliva, feces, and breastmilk indicates that direct viral attack to the target cells may be an alternative reason (Lymperopoulos et al, 2021). Angiotensin-converting enzyme 2 (ACE2) is a receptor providing the main entry site for SARS-CoV to invade human cells, and this in turn facilitates direct damage of virus through the course of infection (Bhat et al, 2022.). recently reported that ACE2 was highly expressed in the heart (Vineis et al, 2019), ACE2 is more than a critical gateway for SARS-COV2 entry, it's also the functional disruption of it and can cause the loss of cardiopulmonary homeostasis during COVID-19 (Al-Kindi & Zidar, 2022).…”

2023 Chinese expert consensus on the impact of COVID-19 on the management of cardiovascular diseases

“…Postmortem studies in patients with COVID-19 revealed cardiac hypertrophy, right ventricular dilatation and evidence of right ventricular involvement (19%), lymphocytic myocarditis (14%-40%), focal pericarditis (19%), endocardial thrombosis (14%) or endothelitis, and small vessel thrombosis (19%) [7][8][9] . The high expression of ACE2 in cardiomyocytes renders them susceptible to injury by SARS-Cov-2 [10][11][12] . SARS-Cov-2 infection produces cytotoxic effects, activates the innate immunity (eg, interferon signal transduction, apoptosis, reactive oxygen stress [ROS] and antiviral pathways) [13] , inhibits metabolic pathways and suppresses ACE2 expression.…”