cardiovascular system

In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.

Third, Huang’s study noted that high concentration of IL-1β, IFN-γ, IP-10 and MCP-1 could be detected in patients infected with 2019-nCoV, which might lead to activated T-helper-1 (Th1) cell responses [4]. Furthermore, they also found that ICU patients had much higher concentrations of inflammatory factors than those non-ICU patients, suggesting that the cytokine storm was associated with disease severity

Second, hypoxaemia may be also an important reason of cardiac injury. In Huang’s study, 32% COVID-19 patients had various degree of hypoxaemia and need required high-flow nasal cannula or higher-level oxygen support. In Chen’s study, up to 76% of patients require oxygen therapy. Due to severe 2019-nCoV infection, the pneumonia may cause significant gas exchange obstruction, leading to hypoxaemia, which significantly reduces the energy supply by cell metabolism, and increases anaerobic fermentation, causing intracellular acidosis and oxygen free radicals to destroy the phospholipid layer of cell membrane. Meanwhile, hypoxia-induced influx of calcium ions also leads to injury and apoptosis of cardiomyocytes.

The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury.

Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells

Among the people who died from COVID-19 reported by the NHC, 11.8% of patients without underlying CVD had substantial heart damage, with elevated levels of cTnI or cardiac arrest during hospitalization.

and respiratory dysfunction and hypoxaemia caused by COVID-19, resulting in damage to myocardial cells.

some of the patients first went to see a doctor because of cardiovascular symptoms. The patients presented with heart palpitations and chest tightness rather than with respiratory symptoms, such as fever and cough, but were later diagnosed with COVID-19.

Common complications among the 138 patients included shock (12 [8.7%]), ARDS (27 [19.6%]), arrhythmia (23 [16.7%]), and acute cardiac injury (10 [7.2%]). Patients who received care in the ICU were more likely to have one of these complications than non-ICU patients.