Cardiac injuries in coronavirus disease 2019 (COVID-19)

Abstract

As the coronavirus disease 2019 (COVID-19) epidemic worsens, this global pandemic is impacting more than 200 countries/regions and more than 4,500,000 confirmed cases worldwide. COVID-19 is caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), which might attack not only the respiratory system, but also the other important organs, including the heart. It was reported that COVID-19 patients with a past history of cardiovascular diseases would have a higher mortality. Meanwhile, elevated troponin levels were frequently observed in COVID-19 cases. Besides the comprehensive treatments for COVID-19, as a cardiologist, we should also remain vigilant about the cardiac injuries, especially those with severe emergent cardiovascular symptoms.

Keywords: COVID-19; Cardiovascular system; Injury; SARS-CoV-2.

Fig. 1

(A) Different immunological mechanisms between acute myocarditis and FM. Myocarditis exhibits a broad spectrum of symptoms from mild chest pain to acute heart failure. The most significant clinical presentation of FM is the sudden onset of cardiac dysfunction. In acute myocarditis, the controllable immune response followed by virus replication could eliminate virus with minimal tissue damage and relatively mild cardiac symptoms. However, over-activated immune response could induce extremely magnified inflammation and rapid deterioration of cardiac function in FM. (B) The relationship between common etiologies of FM and over-activated inflammation. Over-activated inflammation plays a central role in the pathogenesis of FM: 1) cardiotropic virus directly invade cardiomyocytes, which induces heart tissue injury and inflammation. Over-activated inflammation could further promote heart damage and lead to multiple organs dysfunction. 2) In drugs induced FM, the combination of drugs and tumor could trigger inflammation. Increased circulating cytokines promote inflammatory infiltration in off-target organs, especially the heart. Besides, some of the drugs could directly attack cardiomyocytes, which further exacerbates cardiac function. 3) Non-cardiotropic virus attack its target organ (lung in the most cases) and trigger inflammation. Increased circulating cytokines then induce heart and the other organs damage through different ways. (C) Balance between pro-inflammatory and anti-inflammatory mechanisms during virus infection. Generally, the immune system could maintain a perfect balance through exquisite self-regulation between pro- and anti-inflammatory mechanisms. After infection, pro-inflammatory mechanisms are prevailed to facilitate pathogens clearance. Once the pathogens are eliminated, the anti-inflammatory mechanisms would calm down immune response and prevent over-activated immune response mediated damage. But under extreme conditions, the immune response is excessively activated, and the overwhelming pro-inflammatory response will induce cytokine storm.