COVID-19 Severity: Lung-Heart Interplay

Abstract

In December 2019, a novel COVID-19 infection caused by SARS-CoV-2 has emerged as a global emergency. In a few months, the pathogen has infected millions of people in the world. Primarily SARS-CoV-2 infects the pulmonary system which ultimately leads to ARDS and lung failure. The majority of patients develop milder symptoms but the infection turns severe in a huge number of people, which ultimately results in enhanced mortality in COVID-19 patients. Co-morbid conditions, primarily cardiovascular complications and diabetes, have been reported to show a strong correlation with COVID-19 severity. Further, the onset of myocardial injury secondary to pulmonary damage has been observed in critically ill patients who have never reported heart-related ailments before. Due to drastic health risks associated with virus infection, the unprecedented disruption in normal business throughout the world has caused economic misery. Apparently, newer treatments are urgently needed to combat the virus particularly to reduce the severity burden. Therefore, understanding the crosstalk between lung and heart during COVID-19 might give us better clarity for early diagnosis followed by appropriate treatment in patients with the likelihood of developing severe symptoms. Accordingly, the present review highlights the potential mechanisms that may explain the crosstalk between lung and heart so that effective treatment/management strategies can be evolved swiftly in this direction.

Keywords: ARDS; COVID-19; SARS-CoV-2; cardiovascular disease; lung-heart interplay.; respiratory failure.

Fig. (1)

Role of ACE2/ACEi/ ARB in COVID-19: In the RAAS system, angiotension 1 is hydrolysed by ACE to form Ang II, which further leads to the release of aldosterone and consequently causes vasoconstriction and electrolyte imbalance. On the other hand, ACE2 converts Ang II to Ang (1-7) peptide, thus supporting hypertensive effects. SARS-CoV-2 binds to ACE2 to get entry into the cell and downregulates/degrades ACE2 afterward, which ultimately enhances the activity of ACE and its inflammatory effects. ARB/ACEi are ACE inhibitors and promote vasodilation and anti-hypertensive effects.

Fig. (2)

Impact of Immune dysregulation and hypoxia on lung- heart interplay during COVID-19: Abrupt inflammatory response in combination with hypoxia results in an imbalance of pro-coagulants/coagulant factors, endothelial damage and vasoconstriction. In addition, it causes activation of immune cells, deposition of fibrin, thrombin and release of ULVWF. These multiple factors cause physiological destruction in the form of thromboembolism/micro thrombosis and ensuing ARDS and cardiac damage.