SARS-CoV-2 (CoV-2) myocardial injury in patients with acute on chronic heart failure (CHF) at index hospitalization has been well-characterized. Though post-acute COVID-19 (PAC) hospitalization(s) is less investigated despite evidence that CoV-2 induced inflammatory response persists for up to 3 months after initial infection.

Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation.

Patients with acute SARS-CoV-2 infection are reportedly at increased risk for future cardiovascular events; the mechanism underlying this risk remains unclear.

Management of acute and long-term COVID-19 cardiovascular syndrome is challenging and should involve a multidisciplinary team including cardiologists, intensive care specialists, infectious disease specialists, and cardiothoracic surgery specialists. A number of promising therapies were investigated during the pandemic. This chapter aims to review the best available data on acute and long-term treatment options of COVID-19 cardiovascular syndrome.

We explain what Covid-19 does to your heart and circulatory system and how it can lead to conditions such as blood clots, heart damage, palpitations and high heart rate.

A new study reveals that COVID-19 fuels dangerous plaque buildup in the arteries, making heart attacks and strokes more likely. Even after recovery, the risk remains high, stressing the importance of ongoing heart health monitoring.