Heart failure and COVID-19: A dynamic and changing interaction

by:
Eduardo Chuquiure-Valenzuela

In several COVID-19 cases, acute myocarditis results in focal or global myocardial inflammation, necrosis¹. Clinically presents ventricular dysfunction and tachyarrhythmias^2-3. Also, may influence in cardiac contractile worsening with a severe impact on Heart Failure (HF).

It is postulated that Heart Failure risk is mediated by a decrease in myocardial oxygen supply caused by hypoxia and severe respiratory distress. Worsening in myocardial oxygen is exaggerated by sympathetic stimulation. Myocarditis, myocardial depression, and myocyte necrosis is mediated by an increase in proinflammatory cytokines^3-4.

Acute myocardial injury during COVID-19 may be asymptomatic and can be detected only by laboratory markers. The clinical presentation of COVID-19 is extremely variable. It may be asymptomatic or cause mild symptoms such as fever, dry cough, and fatigue¹^,2,4,5. On the other side of the spectrum, a severe pneumonic distress with clinical deterioration and cardiogenic shock may be present.

A frequent cause of hospital admission among cardiac patients is COVID-19 pneumonia⁶, but the most common cause of hospitalization due to cardiovascular decompensation is HF. Prevalence of HF in COVID-19 patients^7,9-12 was dynamic and changing, according to the time of presentation and region (Figure 1). Bromage et al¹³reported a significantly lower hospitalization rate for acute HF during the COVID‐19 pandemic, but hospitalized patients had higher rates of NYHA III or IV symptoms and severe peripheral edema at admission. Heart Failure patients may be at increased risk for severe disease and complications associated to COVID-19 and can worsen HF ⁸. Mortality was reported, Shi⁹et al and Inciardi¹⁴ et al described an increment in HF mortality rates (51.2%, 63.2% respectively). Confirming the high risk of HF mortality.

With a higher risk for severe infection, worsening and complications, general recommendation for HF outpatients are social isolation, telemedicine, guideline-directed medical therapy, and self-daily care also protective measures to prevent infection⁸. Limiting hospital care and admissions based on health systems have been reorganized or reconverted. Reza et al¹⁵ and DeFilippis⁸ et al hypothesizedsevere consequences in socioeconomically disadvantaged populations especially in HF outpatients, who live in low-middle income countries in which health systems are challenged with limited access to remote care, therapeutics, and may endure disproportionate cardiovascular morbidity and mortality¹⁵.

Limitations

Variability in current reports may indicate a different clinical pattern of HF associated with COVID-19 that shows limitations of observational data, inclusion criteria heterogeneity, temporality and geographic biases, residual confounding factors that potentially affect external validity and results may not be generalizable.

Summary

Heart failure in COVID-19 pandemic has a dynamic and changing process