Title:High-output Cardiac Failure: A Forgotten Phenotype in Clinical Practice
Volume: 18
Issue: 1
Author(s): Diane Xavier de Ávila*, Humberto Villacorta, Wolney de Andrade Martins and Evandro Tinoco Mesquita
Affiliation:
- Postgraduate Program in Cardiovascular Sciences, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil
- Amyloidosis Center, Complexo Hospitalar de Niterói - DASA, Rio de Janeiro, Brazil
Keywords:
High output cardiac failure, reduced systemic vascular resistance, heart failure, ventricular dilation, arteriovenous fistulas, metabolism.
Abstract:
Introduction: The 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 the 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.
Objective: The study aims to describe, through an integrative review, the physiopathology and aetiologies
of HOCF and to discuss phenotypes associated with this condition.
Methods: Revisions, 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).
Discussion: Two 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.
Conclusion: Many 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.
