Abstract Body (Do not enter title and authors here): Introduction:
High output heart failure (HOHF) can be attributed to a wide array of diseases such as severe anemia, hyperthyroidism, arteriovenous fistulas, cirrhosis, chronic lung disease, and morbid obesity. Amongst the causes, obesity is the most common, accounting for 31% of those diagnosed with HOHF; however, there is limited data regarding this topic despite the increasing prevalence of obesity worldwide. We recount a unique case of HOHF in a young woman.
Case Description:
A 22-year-old woman with a history of class 3 obesity (body mass index 60.1 kg/m2) presented with shortness of breath for 3 weeks and new bilateral lower extremity edema. She was found to have newly reduced left ventricular function of 10-15% with severe dilation of the left ventricle and global hypokinesis. Her cardiac catheterization showed insignificant coronary artery disease. However, hemodynamics showed elevated filling pressures, a cardiac index of 4.6 L/min/m2 and output of 11.9 L/min, both measured by thermodilution; establishing a diagnosis of high output heart failure. The patient’s right ventricular biopsy returned and showed chronic cardiomyopathy, demonstrated by hypertrophied myocytes. Other etiologies of HOHF were ruled out with further workup, including arteriovenous shunting, thyroid disease, liver disease, and pulmonary pathologies. The etiology of her HOHF was ultimately attributed to severe obesity. After diuresis, the patient was discharged on guideline directed medical therapy, which included sacubitril-valsartan, metoprolol succinate, spironolactone, and empagliflozin. She was set to follow up with advanced heart failure and bariatric surgery.
Conclusion:
HOHF is due to unmet demands by the body, by increased oxygen consumption or by decrease systemic vascular resistance. The pathophysiology for HOHF due to obesity is not entirely understood, however there are several working hypotheses. The pathophysiology stems from obesity causing increased leptin, neprilysin, and decreased adiponectin; increased vasoactive adipokines increasing increased vasodilation; insulin resistance causing cardiac remodeling seen as impaired diastology with low ejection fractions. Treatment of HOHF due to morbid obesity is with bariatric surgery and lifestyle changes. However, given the role of active adipokines in this disease, future studies can aim to investigate intervening at this level to prevent severe consequences, as seen in our patient.