Reduced Cardiac Index Is Not the Dominant Driver of Renal Dysfunction in Heart Failure.

Pubmed ID: 27173030

Pubmed Central ID: PMC4867078

Journal: Journal of the American College of Cardiology

Publication Date: May 17, 2016

Affiliation: Program of Applied Translational Research, Yale University School of Medicine, New Haven, Connecticut; Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut. Electronic address: jeffrey.testani@yale.edu.

MeSH Terms: Humans, Male, Female, Middle Aged, Heart Failure, Creatinine, Renal Insufficiency, Glomerular Filtration Rate, Catheterization, Swan-Ganz, Cardiac Output, Low, Blood Urea Nitrogen, Registries, Atrial Pressure

Grants: K23 HL114868, K24 DK090203, L30 HL115790, K23 HL128933, K23 DK097201

Authors: Testani JM, Brisco MA, Parikh CR, Hanberg JS, Ter Maaten JM, Wilson FP, Sury K, Ahmad T, Broughton JS, Assefa M, Tang WHW

Cite As: Hanberg JS, Sury K, Wilson FP, Brisco MA, Ahmad T, Ter Maaten JM, Broughton JS, Assefa M, Tang WHW, Parikh CR, Testani JM. Reduced Cardiac Index Is Not the Dominant Driver of Renal Dysfunction in Heart Failure. J Am Coll Cardiol 2016 May 17;67(19):2199-2208.

Studies:

Abstract

BACKGROUND: It is widely believed that a reduced cardiac index (CI) is a significant contributor to renal dysfunction in patients with heart failure (HF). However, recent data have challenged this paradigm. OBJECTIVES: This study sought to determine the relationship between CI and renal function in a multicenter population of HF patients undergoing pulmonary artery catheterization (PAC). METHODS: Patients undergoing PAC in either the randomized or registry portions of the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) trial were included (n = 575). We evaluated associations between CI and renal function across multiple subgroups and assessed for nonlinear, threshold, and longitudinal relationships. RESULTS: There was a weak but significant inverse correlation between CI and estimated glomerular filtration rate (eGFR), such that higher CI was paradoxically associated with worse eGFR (r = -0.12; p = 0.02). CI was not associated with blood urea nitrogen (BUN) or the BUN to creatinine ratio. Similarly, no associations were observed between CI and better renal function across multiple subgroups defined by indications for PAC or hemodynamic, laboratory, or demographic parameters. A nonlinear or threshold effect could not be identified. In patients with serial assessments of renal function and CI, we were unable to find within-subject associations between change in CI and eGFR using linear mixed modeling. Neither CI nor change in CI was lower in patients developing worsening renal function (p ≥ 0.28). CONCLUSIONS: These results reinforce evidence that reduced CI is not the primary driver for renal dysfunction in patients hospitalized for HF, irrespective of the degree of CI impairment or patient subgroup analyzed.