In about 7% of people with confirmed novel coronavirus disease 2019 (COVID-19), and 22% of the critically ill, the virus injures the heart, probably by either attacking it directly or causing a cytokine storm that leads to myocyte apoptosis, according to afrom the Columbia University Division of Cardiology in New York.
Reports from China document patients presenting with palpitations and chest pain without the typical fever and cough.
The exact mechanism of injury is uncertain, but for now, “it appears that the incidence of fulminant myocarditis and profound cardiogenic shock is low; however, the rate of recovery and mode of treatment are yet to be determined,” wrote authors led by, a cardiologist and assistant professor of medicine at Columbia.
High-sensitivity cardiac troponin I (hs-cTnI) might be prognostic. In one Chineseof hospitalized patients, median hs-cTnI levels were 2.5 pg/mL in survivors on day 4 of symptoms and did not change significantly during follow-up. Among people who died, day 4 hs-cTnI was 8.8 pg/mL and climbed to 290.6 pg/mL by day 22.
“The rise in hs-cTnI tracks with other inflammatory biomarkers … raising the possibility that this reflects cytokine storm or secondary hemophagocytic lymphohistiocytosis more than isolated myocardial injury,” Dr. Clerkin and colleagues wrote.
But there are also acute heart injury reports out of China, including one man who presented with chest pain and ST-segment elevation, but no coronary obstruction, and another who presented with fulminant myocarditis in addition to severe respiratory manifestations, but with no cardiac history.
Both had depressed left ventricular ejection fractions, enlarged left ventricles, and elevated cardiac biomarkers, and both responded to intravenous immunoglobulin and steroids, among other treatments.
Amid a surge of COVID-19 cases at Columbia, “we have seen both forms of cardiac presentations: those presenting with cardiac predominant symptoms (none have had true [ST-segment elevation myocardial infarctions] yet, but most fall in the myopericarditis group), some of which have required mechanical circulatory support, and those who seem to have secondary myocardial injury with globally elevated inflammatory biomarkers (e.g., ferritin, interleukin-6, lactate dehydrogenase, hs-cTnI, and D-dimer),” Dr. Clerkin said in an interview.
“We are discussing each of these cases in a multidisciplinary fashion with our infectious disease, pulmonary, interventional cardiology, and cardiac surgery colleagues to try to make the best decision based on what we know and as our knowledge evolves,” he said.
The exact cardiac effect of COVID-19 is unknown for now, but it is known already that it rides along with cardiovascular issues. There’s a high prevalence of hypertension, diabetes, and diagnosed cardiovascular disease among patients, but it’s unclear at this point if it’s because the virus favors older people who happen to be more likely to have those problems or if it attacks people with those conditions preferentially.
It might be the latter. The virus that causes COVID-19, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), invades cells through angiotensin converting enzyme (ACE) 2 receptors, which are highly expressed in the heart.
That raises the question of whether ACE inhibitors or angiotensin receptor blockers might help. However, “at this time, nearly all major societies have recommended against adding or stopping … antagonists in this setting, unless done on clinical grounds independently of COVID-19, given the lack of evidence,” Dr. Clerkin and his colleagues wrote.
As for heart transplants, the current thinking is to continue them without changes in immunosuppression so long as recipients test negative and haven’t been around anyone who has tested positive for a month. If a donor had COVID-19, they should have been free of the virus by polymerase chain reaction for at least 14 days. The concern is that it might be in the donor heart.
If transplant patients come down with COVID-19, the “data to date [indicate that management] is supportive care and continuation of immunosuppression for mild COVID-19 with reduction of the antimetabolite (mycophenolate or azathioprine), and further treatment based on disease severity and drug availability. Notably, one potential treatment option for COVID-19 is protease inhibitors,” the authors said, but it’s important to remember that they will increase the levels of cyclosporine, tacrolimus, and other calcineurin inhibitor transplant drugs.
At Columbia, “our processes have been adjusted” for heart transplants. “For instance, non-urgent testing (pre- and post-transplant) has been tabled, we have predominantly shifted to noninvasive screening for rejection, and each potential transplant requires more scrutiny for urgency, donor screening/risk for COVID-19, and perioperative management,” Dr. Clerkin said in the interview.
A study out of Wuhan, China, the outbreak epicenter, was reassuring. It found that routine prevention efforts were enough to protect heart transplant patients.
There was no funding, and the authors had no disclosures.
SOURCE: Clerkin KJ et al. Circulation. 2020 Mar 21.