Cardiac injury was a relatively common finding in patients sick enough to require hospitalization in Wuhan, China. Significant elevations in high-sensitivity cardiac troponin I were seen in up to 20% of hospitalized COVID-19 patients. Those elevations were associated with a several-fold increase in mortality. Patients with troponin I elevations (suggesting cardiac injury) were much more likely to require mechanical ventilation than those with normal troponin I levels. Patients found to have troponin elevations were also more likely to develop ARDS (acute respiratory distress syndrome), acute renal failure, electrolyte imbalances, coagulation disorders and hypoproteinemia. Patients with elevated troponin I levels (cardiac injury) tended to be older and have multiple comorbidities such as hypertension and diabetes. Other inflammatory markers were frequently elevated in infected patients including C-reactive protein, procalcitonin, CK-MB (creatinine kinase myocardial band), myohemoglobin, BNP (beta natriuretic peptide), and D-dimer. This suggests that an intense inflammatory response (when superimposed on preexisting cardiovascular disease) may trigger myocardial injury in COVID-19 patients. There is significant controversy as to whether ACEIs (angiotensin converting enzyme inhibitors) and ARBs (angiotensin receptor blockers) mediate or contribute to myocardial injury in COVID-19 infections. Both classes of drugs are widely employed in the treatment of hypertension and heart failure. The possibility that they could be contributing to or intensifying coronavirus infections is leading both patients and doctors to question their continued therapeutic use. The COVID-19 virus utilizes the (ACE2) receptor to gain entry into human cells. According to a published report in the “Lancet Respiratory Medicine” ACE2 expression was increased in diabetics treated with either ACEIs or ARBs. An upregulation of ACE2 has also been seen with the use of thiazolidinediones and ibuprofen.
The logical conclusion to be drawn from these findings is that increased expression of ACE2 (the gateway by which the virus infects cells) would also increase susceptibility to COVID-19 infection. These drugs are more often used in patients at greatest risk for infection due to such co-morbidities such as diabetes, hypertension, and heart or kidney disease. Infection from the COVID-19 virus is likely a multi-step process and not solely dependent on the number of ACE2 receptors. Some evidence could suggest that ACEIs and ARBs may play a protective role in the lungs since they either interfere with the production of angiotensin II or “block” angiotensin receptors. Angiotensin II increases pulmonary vascular permeability, leading to a greater potential for ARDS. At this point there is no DIRECT evidence that any of the aforementioned classes of drugs increase the risk of infection from COVID-19. Patients wishing to change their medication should discuss this with their provider. It is not wise to stop taking your medicine out of fear that you could catch the coronavirus. There are other classes of drugs that can be substituted for these medications but those substitutions should be made jointly with your provider. We need more evidence to either confirm or disprove the assertions that have been made thus far. Protecting high-risk individuals from exposure to the virus is the ideal solution until we have a tested vaccine ready for use.