New research suggests COVID-19 can interfere with the complex electrical system that keeps the heart beating at regular intervals, furthering our understanding of how the virus can affect some patients’ heart and cardiovascular function.
The study, led by Dr. Khalid Changal, a cardiology fellow in The University of Toledo College of Medicine and Life Sciences, was recently published in the journal BMC Cardiovascular Disorders.
“We know that COVID-19 causes inflammation of the heart and we know patients who have heart disease experience worse outcomes with COVID,” Changal said. “Our study suggests COVID affects not only the heart muscle but the electrical system of the heart as well. This is something new.”
An intricate system of electrical impulses controls both the rhythm and rate of the heart. Disruptions to those signals can lead to irregular heartbeat conditions such as atrial fibrillation and, rarely, more dangerous and potentially life-threatening heart rhythm disturbances like ventricular fibrillation.
To determine whether COVID-19 was interfering with the heart’s electrical signals, Changal and a team of researchers that included scientists and physicians at UToledo, ProMedica, Detroit Medical Center and Owens Community College looked for what’s called QTc prolongation — essentially a condition in which the heart takes longer to recharge between beats.
Researchers analyzed electrocardiogram data collected from a group of nearly 300 patients with no history of the condition who were hospitalized with COVID-19 early last year.
Of those patients, one in four showed evidence of the prolonged time between heartbeats during their hospitalization.
While some patients who developed a change in their heartbeat had no known preexisting conditions, the condition was more likely to occur in older patients and those with underlying cardiovascular disease, liver disease or kidney disease.
“QTc prolongation can be a marker that the heart is unhealthy. Those patients could have the potential to develop serious or even life-threatening heart rhythm problems,” Changal said. “Our findings suggest it’s important to closely monitor hospitalized COVID-19 patients for this, particularly those with underlying heart, liver or kidney conditions.”
The study did not find that patients with QTc prolongation were more likely to die from COVID-19; however, researchers did note patients who developed the condition were more likely to be discharged to a skilled nursing facility rather than immediately returning home.
Notably, the study also found patients who were taking ACE inhibitors — medications commonly used to treat high blood pressure and heart failure — were less likely to develop QTc prolongation.
Whether to continue hospitalized COVID-19 patients on ACE inhibitors has been a topic of debate among the medical community, Changal said, as there were concerns the medication might increase some patients’ susceptibility to the virus.
Additional research has indicated those fears appear to be unfounded, but Changal’s study is the first to suggest ACE inhibitors may play a protective role against COVID-19 interfering with heart signals.
QTc prolongation caused by a viral infection or medication is generally a reversible phenomenon, and Changal said heart function should return to normal once patients have cleared the virus, but more research is needed.
“We weren’t able to evaluate patients after they were discharged, and we don’t know whether those with COVID-19 could be more likely to have heart rhythm problems down the road,” Changal said. “We’re still learning how this virus affects us, both during the acute phase and later down the road. This is an important area for future study.”