COVID-19 and Heart Failure: From Epidemiology During the Pandemic to Myocardial Injury, Myocarditis, and Heart Failure Sequelae

Abstract

A close and intriguing relationship has been suggested between heart failure (HF) and coronavirus disease 2019 (COVID-19). First, COVID-19 pandemic represented a global public health emergency in the last year and had a catastrophic impact on health systems worldwide. Several studies showed a reduction in HF hospitalizations, ranging from 30 to 66% in different countries and leading to a subsequent increase in HF mortality. Second, pre-existing HF is a risk factor for a more severe clinical course of COVID-19 and an independent predictor of in-hospital mortality. Third, patients hospitalized for COVID-19 may develop both an acute decompensation of chronic HF and de-novo HF as a consequence of myocardial injury and cardiovascular (CV) complications. Myocardial injury occurred in at least 10% of unselected COVID-19 cases and up to 41% in critically ill patients or in those with concomitant CV comorbidities. Few cases of COVID-19-related acute myocarditis, presenting with severe reduction in the left ventricular (LV) ejection fraction and peculiar histopathological findings, were described. However, recent data suggested that COVID-19 may be associated with both systolic and diastolic LV dysfunction, with LV diastolic impairment, pulmonary hypertension, and right ventricular dysfunction representing the most frequent findings in echocardiographic studies. An overview of available data and the potential mechanisms behind myocardial injury, possibly leading to HF, will be presented in this review. Beyond the acute phase, HF as a possible long-term consequence of cardiac involvement in COVID-19 patients has been supposed and need to be investigated yet.

Human Cardiac Organoids to Model COVID-19 Cytokine Storm Induced Cardiac Injuries

“…2H , hCOs and COVID-19 hearts also shared common downregulated genes, which were aligned with key GO terms such as “muscle organ development” (GO:0007517), and “cardiac muscle tissue morphogenesis” (GO:0055008). The downregulated cardiomyocyte structure pathways are consistent with acute reductions in cardiac output (acute heart failure, cardiogenic shock in COVID-19 patients with acute cardiac injuries 40 . A significant portion of differences in the downregulated pathways between the IL-1β treated hCOs and COVID-19 hearts is associated with metabolism (e.g., tricarboxylic acid cycle, mitochondrion organization), which was attributed to underdeveloped mitochondria of immature hPSC-CMs compared to adult human cardiomyocytes 41 .…”

Renin–angiotensin system modulation and outcomes in patients hospitalized for interstitial SARS-CoV2 pneumonia: a cohort study

“…In our study population, in line with the experimental studies in which restoring the ACE1/ACE2 balance limited the lung injury in SARS-CoV respiratory infection [ 8 , 11 , 35 ], a slightly less severe respiratory involvement emerged in the RASi group, as reflected by the differences found between groups in terms of P/F and RR at the nadir of the respiratory involvement. On the contrary, in recent studies on COVID-19 patients with HF, in which poorer outcomes are expected and in which the pre-existing lung fluid handling and gas diffusion process impairment can be worsened by the superimposed infection, chronic treatment with RASi agents was not associated with less respiratory involvement, increased risk of death or better outcomes [ 36 , 37 ]. In this context, there is a lack of data exploring the relation between ongoing treatment with ACEis/ARBs and the severity of the clinical course of the SARS-CoV2 infection.…”

The Influence of Socioeconomic Status on the Prognosis and Profile of Patients Admitted for Acute Heart Failure during COVID-19 Pandemic: Overestimated Aspects or a Multifaceted Hydra of Cardiovascular Risk Factors?

“…Even if current literature data emphasize the high costs associated with COVID-19 hospitalization, this aspect refers mainly to cases with severe infection, with COVID-19 as the primary pathology leading to emergency admission [ 45 ]. Specifically for HF, there are intriguing data: on the one hand, the number of HF-related hospitalizations has decreased by 30–66% during pandemic period, compared to 2017–2019 [ 46 , 47 , 48 ], on the other hand, the costs per patient have increased due to severe presentations, requiring advanced supportive care and costly equipment and medication [ 47 ]. Even in patients with mild forms of the viral infection, there are additional laboratory tests or explorations, not routinely performed in HF, but highly recommended in COVID-19, such as D-dimers or computed tomography [ 49 ], which additionally augment the healthcare financial burden.…”