IJCS | Volume 33, Nº4, July and August 2020

413 COVID-19 and Heart Failure HF is associated with high morbidity and mortality with high costs for the health system and represents the final phenotype of many cardiovascular disorders. In recent decades, the incidence of HF has remained stable, however the prevalence has increased over time, mainly in relation to HFpEF, probably due to the longer survival of patients secondary to the available therapeutic resources. A study conducted in the population served by the Family Medical Program in Niterói, state of Rio de Janeiro, showed a prevalence of HF of 9.3%, of which 59% had the HFpEF phenotype, assessed in individuals aged 45 years or over. 15 In general, patients with HFpEF are older, women, and diagnosed with hypertension. The prevalence of other risk factors varies according to the criteria used in the methodology to define and select patients with HFpEF 16,17 (figure 2). Biomarkers with a prognostic impact on CVD can be valuable in this high risk subgroup. Hospitalized patients should have their levels of natriuretic peptides, D-dimer, and troponin monitored. Troponin, in particular, can be an ally in the early detection of cardiac complications. 18 Small elevations (2 to 3 times above the cutoff), may be due to pre-existing diseases. However, high elevations (> 5 times above the cutoff) may be the result of severe respiratory failure, tachycardia, hypoxia, or shock, due to COVID-19, or indicate direct myocardial injury as seen in myocarditis, Takotsubo syndrome, or even type 1 acute myocardial infarction, triggered by COVID-19. 19 The measurement of these biomarkers in an outpatient setting has not been studied, but it could be useful for monitoring signs of severity in this high risk group, along with O2 saturation. Metabolic diseases, COVID-19, and HFpEF In the metabolic context, obesity and dysglycemia are common comorbidities in HFpEF. Obesity determines hemodynamic overload, left ventricular and atrial remodeling, in addition to activation of the renin‑angiotensin-aldosterone system, a mechanism directly involved in the pathophysiology of COVID-19. Furthermore, obesity stimulates the sympathetic nervous system, natriuretic peptides, Adiponectine- induced inflammatory diseases and oxidative stress. This altered milieu results in different degrees of myocardial and vascular functional impairment, usually without significant systolic ventricular dysfunction, but with a typical phenotypic manifestation of HFpEF. 20 Recent data show that people with obesity may also experience more symptoms of COVID-19 and are more Figure 1 – Pathophysiological mechanisms of myocardial injury in COVID-19 and its relationship with HFpEF and comorbidities. Mesquita et al. HFpEF and COVID-19 Int J Cardiovasc Sci. 2020; 33(4):412-418 Viewpoint