High-output cardiac failure: a forgotten phenotype in clinical practice.

Abstract

INTRODUCTION\nThe knowledge on high-output cardiac failure (HOCF) has greatly improved in the last two decades. One of the advances was the identification of a new phenotype of HOCF, characterized by absence of ventricular dilation, already associated with liver disease, arteriovenous fistulas (AVF), lung disease, myelodysplastic syndromes, and obesity. However, it has been noted that any aetiology can present with one of the two phenotypes, depending on the evolution.\n\n\nOBJECTIVE\nTo describe, through an integrative review, the physiopathology and aetiologies of HOCF and to discuss phenotypes associated with this condition.\n\n\nMETHODS\nRevisions, guidelines, case-controls, cohort studies and clinical studies were searched in MEDLINE and LILACS, using the connectives in the cardiac output, high database [MeSH Terms] OR high cardiac output [All Fields].\n\n\nDISCUSSION\nTwo distinct phenotypes are currently described in the HOCF, regardless of the aetiology: 1) one with enlarged cardiac chambers; and 2) with normal heart chambers. The mechanisms related to HOCF are vasodilation, arteriovenous shunts that cause increased microvascular density, reduced systemic vascular resistance (RSVR), and high metabolism. These mechanisms lead to activation of the renin-angiotensin-aldosterone system, sodium and water retention, activation of neprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodeling and a consequent increase in cardiac output >8L/min.\n\n\nCONCLUSION\nMany aetiologies of HOCF have been described and some of them are potentially curable. Prompt recognition of this condition and proper treatment may lead to better outcomes.