Patients testing positive for severe acute respiratory syndrome (SARS-CoV-2), the virus that causes coronavirus disease 2019, are presenting more often with signs of heart failure with preserved ejection fraction (HFpEF).
Patients testing positive for severe acute respiratory syndrome (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19), are presenting more often with signs of heart failure with preserved ejection fraction (HFpEF), according to data published in JAMA.
HFpEF, or diastolic heart failure, is a disease state in which the left ventricle of the heart remains stiff after pumping. Because the ventricle cannot relax, even though the ability to pump is present, it fills with less blood, resulting in suboptimal delivery of blood to the body—sometimes just 40% to 49% of what is needed.
Data are continually emerging on the connection between COVID-19 and cardiac injury, with the authors of the present viewpoint concentrating on HFpEF. “This is important to elucidate,” they noted, “because infection with COVID-19 may be associated with HFpEF through several pathways.”
Their examination of shared inflammatory pathophysiology and cardiometabolic risk profiles between the 2 disease states, as well as the myocardial complications, highlight how even early studies noted elevated levels of 2 biomarkers, troponin and natriuretic peptides, indicating direct myocardial injury.
Two studies included in their review, from Israel and New York City, evaluated patients hospitalized with COVID-19 who underwent echocardiographic assessment. A majority of the patients were shown to have both right ventricular dilation and left ventricular diastolic dysfunction, both indications of HFpEF. Additional studies from Germany showed both abnormal results from cardiac MRIs in patients recovered from COVID-19 and detectable levels of SARS-CoV-2 in cardiac tissue from deceased patients.
Inflammation is a common factor linking COVID-19 and HFpEF. Interleukin (IL)-1 and IL-16, which are both released following infection with SARS-CoV-2 have also been shown to affect the myocardium, the authors noted. In addition, plasminogen activator inhibitor (PAI-1), which is released following other respiratory viruses, has been linked to a greater risk of HFpEF. Overall, viral injury can seemingly contribute to HFpEF.
The cardiometabolic risk profile is another commonality between COVID-19 and HFpEF. This profile includes older age, obesity, and metabolic syndrome. Before the pandemic, HFpEF already accounted for more than 50% of all heart failure cases, with previous study results showing annual increases of 5% to 10% from 2005 to 2014. Obesity and diabetes, meanwhile, have been increasing in prevalence, too, especially among older patient populations, the study authors stated. This subset of patients who are older, are obese, and have diabetes has been disproportionately affected by COVID-19, a disease which in turn could increase their likelihood of HFpEF because of the acute viral stressor on the myocardium.
“SARS-CoV-2 may cause HFpEF, may unmask subclinical HFpEF, or may exacerbate existing HFpEF,” the authors concluded. “Although case reports have described profound COVID-19 myocarditis leading to HFpEF, the more common manifestation in the COVID-19 era may be HFpEF related primarily to the unmasking of subclinical HFpEF and secondarily to the development of new HFpEF following infection with SARS-CoV-2.”
They point out that multiethnic population-based cohort studies and long-term data are needed to conclusively determine if there is a relationship between HFpEF and COVID-19, especially longitudinal studies that compare myocardial impairment in patients who presented with cardiac structural and functional changes before the pandemic with those presenting with the same following recovery from COVID-19.
Freaney PM, Shah SJ, Khan SS. COVID-19 and heart failure with preserved ejection fraction. JAMA. Published online September 30, 2020. doi:10.1001/jama.2020.17445