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Cardiopulmonary responses and prognosis in hypertrophic cardiomyopathy: a potential role for comprehensive noninvasive hemodynamic assessment.

Finocchiaro, G; Haddad, F; Knowles, JW; Caleshu, C; Pavlovic, A; Homburger, J; Shmargad, Y; Sinagra, G; Magavern, E; Wong, M; et al. Finocchiaro, G; Haddad, F; Knowles, JW; Caleshu, C; Pavlovic, A; Homburger, J; Shmargad, Y; Sinagra, G; Magavern, E; Wong, M; Perez, M; Schnittger, I; Myers, J; Froelicher, V; Ashley, EA (2015) Cardiopulmonary responses and prognosis in hypertrophic cardiomyopathy: a potential role for comprehensive noninvasive hemodynamic assessment. JACC Heart Failure, 3 (5). pp. 408-418. ISSN 2213-1787 https://doi.org/10.1016/j.jchf.2014.11.011
SGUL Authors: Finocchiaro, Gherardo

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Abstract

OBJECTIVES: This study sought to discover the key determinants of exercise capacity, maximal oxygen consumption (oxygen uptake [Vo2]), and ventilatory efficiency (ventilation/carbon dioxide output [VE/Vco2] slope) and assess the prognostic potential of metabolic exercise testing in hypertrophic cardiomyopathy (HCM). BACKGROUND: The intrinsic mechanisms leading to reduced functional tolerance in HCM are unclear. METHODS: The study sample included 156 HCM patients consecutively enrolled from January 1, 2007 to January 1, 2012 with a complete clinical assessment, including rest and stress echocardiography and cardiopulmonary exercise test (CPET) with impedance cardiography. Patients were also followed for the composite outcome of cardiac-related death, heart transplant, and functional deterioration leading to septal reduction therapy (myectomy or septal alcohol ablation). RESULTS: Abnormalities in CPET responses were frequent, with 39% (n = 61) of the sample showing a reduced exercise tolerance (Vo2 max <80% of predicted) and 19% (n = 30) characterized by impaired ventilatory efficiency (VE/Vco2 slope >34). The variables most strongly associated with exercise capacity (expressed in metabolic equivalents), were peak cardiac index (r = 0.51, p < 0.001), age (r = -0.25, p < 0.01), male sex (r = 0.24, p = 0.02), and indexed right ventricular end-diastolic area (r = 0.31, p = 0.002), resulting in an R(2) of 0.51, p < 0.001. Peak cardiac index was the main predictor of peak Vo2 (r = 0.61, p < 0.001). The variables most strongly related to VE/VCO2 slope were E/E' (r = 0.23, p = 0.021) and indexed left atrial volume index (LAVI) (r = 0.34, p = 0.005) (model R(2) = 0.15). The composite endpoint occurred in 21 (13%) patients. In an exploratory analysis, 3 variables were independently associated with the composite outcome (mean follow-up 27 ± 11 months): peak Vo2 <80% of predicted (hazard ratio: 4.11; 95% confidence interval [CI]: 1.46 to 11.59; p = 0.008), VE/Vco2 slope >34 (hazard ratio: 3.14; 95% CI: 1.26 to 7.87; p = 0.014), and LAVI >40 ml/m(2) (hazard ratio: 3.32; 95% CI: 1.08 to 10.16; p = 0.036). CONCLUSIONS: In HCM, peak cardiac index is the main determinant of exercise capacity, but it is not significantly related to ventilatory efficiency. Peak Vo2, ventilatory inefficiency, and LAVI are associated with an increased risk of major events in the short-term follow-up.

Item Type: Article
Additional Information: © 2015. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
Keywords: cardiopulmonary test, echocardiography, heart failure, hypertrophic cardiomyopathy, Cardiomyopathy, Hypertrophic, Disease Progression, Echocardiography, Doppler, Exercise Tolerance, Female, Hemodynamics, Humans, Male, Middle Aged, Oxygen Consumption, Prognosis, Humans, Cardiomyopathy, Hypertrophic, Disease Progression, Echocardiography, Doppler, Prognosis, Oxygen Consumption, Exercise Tolerance, Middle Aged, Female, Male, Hemodynamics, cardiopulmonary test, echocardiography, heart failure, hypertrophic cardiomyopathy
SGUL Research Institute / Research Centre: Academic Structure > Molecular and Clinical Sciences Research Institute (MCS)
Academic Structure > Molecular and Clinical Sciences Research Institute (MCS) > Cardiac (INCCCA)
Journal or Publication Title: JACC Heart Failure
ISSN: 2213-1787
Language: eng
Dates:
DateEvent
1 May 2015Published
3 November 2014Accepted
Publisher License: Creative Commons: Attribution-Noncommercial-No Derivative Works 4.0
PubMed ID: 25863972
Web of Science ID: WOS:000365651400011
Go to PubMed abstract
URI: https://openaccess.sgul.ac.uk/id/eprint/108228
Publisher's version: https://doi.org/10.1016/j.jchf.2014.11.011

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