Mechanisms of Covid-induced Heart failure

Abstract

Sars-Cov-2 binds to ACE-2 receptor, resulting in excess amount of ACE-1 dependent angiotensin production. Sars-Cov-2 has four stages of symptoms, 80% if symptomatic patients have been shown to only suffer a “mild” disease course, meanwhile 20% endure stage 3, which is characterized by conditions such as ARDS, shock, and multiorgan failure. The binding of Covid to ACE receptors promotes the conversion of angiotensin 1 to angiotensin 2, constricting blood vessels, leading to thrombosis, lack of oxygen, and Ischemia. In Cardiac injury, the Covid receptor becomes represented in the heart, inducing in a pro-inflammatory increase, high cytokine concentrations, myocyte cardiac apoptosis, cardiac arrythmia, cardiac fibrotic tissue, myocarditis, and Heart failure. Cytokine storms associated with production of S1P, TNF activation of MMPs prompts myocardial depression, dilation of LV, and Heart failure. Covid-induced Sepsis corresponds with dysregulated host immune responses, increased pro-inflammatory mediators, fluid leakage, increase in cGMP, LV dysfunction, and arrythmia. Blood clots in the capillaries surrounding the kidneys generate renal impairment. Progression of renal impairment generates a state of systemic inflammation. Increased sodium content in the body results in elevated plasma blood and uncontrolled hypervolemia. Emotional and physical stresses during Sars-Cov-2 induce blood gas changes, angiotensin converting enzyme imbalance, and immune/inflammatory factors. Overactivation of the SNS induces Takotsubo syndrome. In ARDS, fluid leak in the membrane gas exchange region of the lung results in vascular remodeling. Inducing further vascular remodeling as part of the body’s response to hypoxia. The constant vascular remodeling triggers RHF.