No Worsening Cardiac Dysfunction in Long COVIDAugust 5, 2022
In Norway, COVID survivors did not show progressive changes in cardiac structure and function that would explain persistent symptoms months later, a cohort study showed.
From 3 to 12 months after hospitalization, echocardiography in 182 patients revealed no significant overall changes in any measures of left ventricular (LV) or right ventricular structure and function. This was despite over half of patients reporting dyspnea at 3 months, which largely persisted through 12 months.
The most frequent pathologies on echocardiography were:
- Low LV global longitudinal strain (19% at 3 months and 15% at 12 months, P=0.44)
- Low LV ejection fraction (16% and 14%, P=0.44)
- Diastolic dysfunction (13% and 17%, P=0.17)
Cardiac structure and function ultimately bore no relationship with shortness of breath. Furthermore, there was no significant change in arrhythmia burden between 3 and 12 months, reported Charlotte Ingul, MD, PhD, of Norwegian University of Science and Technology in Trondheim, and colleagues of the PROLUN group. Their manuscript was published in Clinical Cardiology.
“Although we did not have pre‐COVID echocardiographic data on the participants, these findings suggest that there is limited long‐term cardiac remodeling and progressive dysfunction after hospitalization for COVID‐19, and that cardiac recovery from the acute disease predominantly occurs within the first 3 months,” the authors wrote.
Prior studies have reported cardiac dysfunction in the acute phase of COVID illness. However, the long-term significance of a finding like diffuse fibrosis, myocardial edema, or myocardial scar is unclear.
Even so, cardiac involvement long after SARS-CoV-2 infection is supported by the National COVID Cohort Collaborative’s finding that incident heart failure (HF) increased by 45% after COVID hospitalization.
An author of that study, HF specialist Marat Fudim, MD, MHS, of Duke Clinical Research Institute in Durham, North Carolina, said he suspected this is driven by HF that is likely induced via a general deterioration of the cardiovascular and pulmonary state and makes itself apparent months to years later.
“How to square a relatively benign cardiac echocardiogram trend in the Norwegian study and repeat studies showing high HF incidence is that COVID is a multisystem disease and I suspect most of the harm is done outside the heart,” Fudim told MedPage Today.
“Insults to the autonomic, pulmonary, and vascular system likely drive what we consider as long COVID. The heart might be more or less unharmed in those cases, yet patients suffer dyspnea, fatigue, dizziness, palpitations, and tachycardia,” he said. “Whether those cases can be all classified as HF or not I don’t know.”
PROLUN was a prospective observational study conducted at six major hospitals in Norway. Participants were people who had been hospitalized with COVID‐19 from February to June 2020.
Included in the present analysis were those who underwent echocardiography 3 and 12 months after leaving the hospital. Due to limited capacity, 24-hour ECG monitoring at 12 months was limited to people who had an arrhythmia at 3 months.
The study cohort averaged 58 years old, and 59% were men. Mean BMI was 28.2. One in five had been hospitalized with severe COVID-19 illness.
Ingul’s group acknowledged that the observational study was subject to various biases. Moreover, data had been collected in the early days of the pandemic, when today’s SARS-CoV-2 variants were not yet in circulation.
Ingul has received lecture fees from Bayer AG.
Fudim had no disclosures.