Obesity an important cause of high output heart failure

Obesity an important cause of high output heart failure

Conventionally we have been taught that causes of high output failure are anemia, thyrotoxicosis, beriberi and arteriovenous fistula. But modern day data is changing. A retrospective analysis of patients with high output heart failure from the cath lab of Mayo Clinic [1] showed that obesity was the commonest cause contributing to almost one third of cases. This was followed by liver disease and arteriovenous shunts contributing about one fourth of cases each, lung disease and (16%) and myeloproliferative disorders (8%). Of course some bias in these percentages is possible because patients with anemia, thyrotoxicosis and beriberi are unlikely to be referred for cardiac catheterization as part of evaluation of high output failure! In fact they excluded a case of thyrotoxicosis and cases with severe anemia were excluded as it is a well described reversible condition.

The need for perfusing large amount of tissue in obesity is possibly the cause of vasodilation and high output failure. There is excessive reduction of afterload, plasma volume expansion and higher ventricular filling pressures, which contribute to the pathophysiology of high output heart failure. Left ventricular efficiency is halved when it utilises fatty acids instead of glucose as primary substrate. Obesity related sodium retention and plasma volume expansion causes significant cardiac dilatation.

A new concept is the leptin-aldosterone-neprilysin axis which comes into play in heart failure due to obesity [2]. It contributes to all the three types of heart failure which can be seen in obesity – heart failure with reduced ejection fraction (HFrEF), heart failure with preserved ejection fraction (HFpEF) and high output heart failure. Signalling through leptin receptor in obesity increases activity of the sympathetic nervous system and renin-angiotensin system. Renal sympathetic nerves cause overactivity of neprilysin, which in turn reduces the counterbalancing effect of natriuretic peptides.

References

1. Reddy YN, Melenovsky V, Redfield MM, Nishimura RA, Borlaug BA. High-Output Heart Failure: A 15-Year Experience. J Am Coll Cardiol. 2016 Aug 2;68(5):473-82. (Open Access)

2. Packer M. Leptin-Aldosterone-Neprilysin Axis: Identification of Its Distinctive Role in the Pathogenesis of the Three Phenotypes of Heart Failure in People With Obesity. Circulation. 2018 Apr 10;137(15):1614-1631.