Understanding Obesity-Related High Output Heart Failure and Its Implications

Abstract

Morbid obesity remains most common cause of high output failure. The prevalence of the obesity is growing when two-thirds of American adults already are overweight or obese. Obesity is the risk factor for heart disease and eventually leads to heart failure. High output heart failure is common in obese patients and is characterized by high cardiac output, decreased systemic vascular resistance, and increased oxygen consumption. It often occurs in patients with chronic severe anemia, hyperthyroidism, pregnancy, arterial-venous fistulas, and liver disease. However, the pathogenesis of obesity-related high output heart failure is not fully understood. The clinical management of obesity-related high output heart failure follows conventional heart failure regimens due to lack of specific clinical recommendations. This article reviews the possible pathophysiological mechanisms and causes that contribute to obesity-related high output heart failure. This review also focuses on the implications for clinical practice and future research involved with omics technologies to explore possible molecular pathways associated with obesity-related high output heart failure.

Obesity-Related High-Output Heart Failure

“…Two different phenotypes have been identified in obesity-related high-output HF: one with enlarged cardiac chambers and another with normal cardiac chambers 23 . If the myocardium must adapt to the increased demand, the left ventricle dilates and eccentric hypertrophy remodeling occurs 17,24 . Some obese patients develop obesity-related high-output HF when the myocardium is unable to meet the demands of the body despite these adaptations 24 .…”

“…Obesity-related high-output HF has also been compared with diseases with a similar presentation. Patients with obesity-related high-output HF have a high likelihood of being misdiagnosed with HF with preserved ejection fraction as they both have a preserved left ventricular ejection fraction greater than 45% to 50% 4,17 . In addition, obesity-related high-output HF may not be identified appropriately due to being secondary to obesity 5 .…”

“…The pathogenesis of obesity-related high-output HF is not well defined and the pathophysiology of high-output HF is unique to each etiology 5,17 . Although the precipitating factors of high-output HF may be different, some mechanisms are seen across all types of high-output HF.…”

“…Evidence for treatment and management of obesity-related high-output HF is limited and there are no clinical practice guidelines 17,24 . Few patients with obesity-related high-output HF received medical treatment other than diuretics 4,24 .…”

Test

“…Initially, testing directed vascular constriction, utilizing nitrates as well as hydralazine, but also pathologically stimulated neuro-hormonal system design, utilizing angiotensin-converting enzymatic (ACE) inhibition, angiotensin ii receptor blockers (ARBS), beta-blockers but also mineralocorticoid antagonists (MRAS). Such tests presented proof a speci ic regarding cardiac arrest as for lowered level (free), the diagnosis might enhance ventricles role, signs, and symptoms, along with mortality and morbidity [8]. as much recent times, other goals but also narrative therapies have now been recognized such as HFrEF.…”