- A new study finds that about 50 percent of people hospitalized with severe COVID-19 have evidence of heart damage.
- Researchers investigated patients with COVID-19 who were discharged from care until June 2020 from six U.K.-based hospitals. The study examined 148 patients.
publishedlast July found people who experienced a mild form of COVID-19 might develop heart issues.
All data and statistics are based on publicly available data at the time of publication. Some information may be out of date.
Millions of people in the United States have contracted SARS-CoV-2, the virus that causes COVID 19, with many returning to full health within weeks of falling ill. But for some patients, the after-effects of the disease can cause long-term health issues.
A new study finds that about 50 percent of people hospitalized with severe COVID-19 will show evidence of heart damage — even months after recovering from the disease.
Patients with abnormal troponin levels were offered an MRI scan of their heart after discharge. The results were compared to those from a control group of patients who did not have COVID-19 and from an additional 40 healthy volunteers.
Researchers investigated patients with COVID-19 who were discharged from care until June 2020 from six U.K.-based hospitals.
The study examined 148 people and is the largest one to investigate recuperating patients with COVID-19 who have elevated troponin levels. Elevated troponin indicates possible heart problems.
“Troponin is basically a measure of heart muscle damage,” Dr. Andrew M. Freeman, a cardiologist at National Jewish Health in Colorado, told Healthline. “So when heart muscle dies, like during a heart attack or marked inflammation, and for whatever reason, the heart muscle cells actually burst, they release an enzyme called troponin.”
Freeman explained that when someone comes to the emergency room with chest pains, the hospital staff will often test their blood for troponin to see if there was a heart attack or heart muscle damage.
“Raised troponin levels are associated with worse outcomes in COVID-19 patients,” Dr. Marianna Fontana, co-lead researcher of the study and professor of cardiology at University College London, said in a statement.
During severe COVID-19 disease, the heart may be directly affected, Fontana said.
“Unpicking how the heart can become damaged is difficult,” she continued. “But MRI scans of the heart can identify different patterns of injury, which may enable us to make more accurate diagnoses and to target treatments more effectively.”
Researchers in the study used cardiac MRI to examine the hearts of 100 German nationals who recovered from COVID-19.
Of those participants, 78 showed heart issues, and 60 had ongoing heart muscle inflammation.
According to the study, the findings were independent of the length of time after an original diagnosis, pre-existing conditions, or the disease’s severity and overall course.
Making the findings difficult to associate specifically with COVID-19 is that people most at risk for severe COVID are those with chronic medical illness that are often specifically heart-related. Fontana said these conditions include diabetes, raised blood pressure, and obesity.
Dr. Rachel-Maria Brown Talaska, director of inpatient cardiac services at Lenox Hill Hospital in New York, said that in addition to the pre-existing conditions specified by Fontana, people with severe COVID-19 also tend to have coronary artery disease and congestive heart failure.
“A majority of hospitalized patients with COVID-19 have a chronic medical illness,” she said.
The heart’s left ventricle, the chamber responsible for pumping oxygenated blood to all parts of the body, was normal in nearly 90 percent of the 148 study participants, according to the study.
However, scarring or injury to the heart muscle itself was present in about half the participants.
The pattern of scarring or injury originated from inflammation in 39 patients and from ischemic heart disease, including infarction (death of heart tissue), in 32 patients, or both in 9 patients. Twelve participants showed evidence of ongoing heart inflammation.
“Injury relating to inflammation and scarring of the heart is common in COVID-19 patients with troponin elevation discharged from hospital,” said Fontana in a statement. “But (it) is of limited extent and has little consequence for the heart’s function.”
She concluded that “more work is needed to investigate this further.”
According to Dr. Michael Goyfman, director of clinical cardiology at Long Island Jewish Forest Hills in New York, evidence that COVID-19 causes more heart damage than other infections isn’t there.
“The predominance of evidence thus far shows that COVID does not really cause excess heart damage compared to other infections,” he said. “Viral infections, in general, can cause inflammation of the heart, and since COVID is a viral infection, it can as well. The rate is probably similar as for other infections.”
The numbers are increased because “COVID is so prevalent,” Goyfman continued. “There is no evidence that COVID triggers excess heart attacks than other viral illnesses.”
Freeman thinks the number of people in the study was too small to provide a clear picture of how COVID-19 could affect the heart.
“It’s always nice to see what others are seeing and publish that data so to share knowledge with the world,” said Freeman. “But I would agree that it’s a relatively small sample size.”
He noted that if you look at the hundreds of thousands of people who had COVID-19, even in the United States, “you know a sample of 148 doesn’t give you a tremendous amount of trend information.”
New research from the United Kingdom finds that half of the study participants hospitalized with severe COVID-19 show heart damage.
Of 148 participants, researchers found heart damage caused by inflammation in 39 of those patients but emphasized that most of the participants had chronic illness before COVID-19.
Experts say the small study size and lack of evidence that COVID-19 was directly responsible for heart damage are significant limitations for the study’s findings.