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.

Patients with preexisting cardiovascular disease (CVD) who develop coronavirus disease 2019 (COVID-19) have worse outcomes than patients without CVD.
Infection with severe acute respiratory syndrome coronavirus 2
(SARS-CoV-2) can directly or indirectly lead to myocardial injury.

Although fulminant viral myocarditis due to COVID-19 appears to be uncommon, recent data suggest that direct myocardial injury may
occur in some individuals.

This paper on JAMA contextualizes the emerging data on the risk of heart failure, particularly heart failure with preserved ejection fraction (HFpEF), in patients during both the acute phase of COVID-19 illness and the chronic
phase of recovery in COVID-19 survivors.

This is important to elucidate, because infection with COVID-19 may be associated with HFpEF through several pathways:
1) COVID-19 may cause HFpEF via direct viral infiltration, inflammation, or cardiac fibrosis; it may unmask subclinical HFpEF in individuals with underlying risk factors;

2) or it may exacerbate preexisting HFpEF.

Key issues are discussed involving the link between COVID-19 and risk of HFpEF due to their shared inflammatory pathophysiology and cardiometabolic risk profiles and the potential for an increase in the individual- and population-level effects of HFpEF in the aftermath of the pandemic.

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