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Original Research: Sleep Disorders |

Acute Effects of Nasal CPAP in Patients With Hypertrophic Cardiomyopathy

Flávia B. Nerbass, PT, PhD; Vera M.C. Salemi, MD, PhD; Rodrigo P. Pedrosa, MD, PhD; Natanael de P. Portilho, MD; Julio C.A. Ferreira-Filho, MD, PhD; Henrique T. Moriya, PhD; Murillo O. Antunes, MD; Edmundo Arteaga-Fernández, MD, PhD; Luciano F. Drager, MD, PhD; Geraldo Lorenzi-Filho, MD, PhD
Author and Funding Information

FUNDING/SUPPORT: The authors have reported to CHEST that no funding was received for this study.

aSleep Laboratory, Pulmonary Division, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil

bCardiomyopathy Unit, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil

cHypertension Unit, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil

dHospital Dom Hélder Câmara – IMIP Hospitalar, Recife, Brazil

eBiomedical Engineering Laboratory, University of São Paulo, São Paulo, Brazil

CORRESPONDENCE TO: Geraldo Lorenzi-Filho, MD, PhD, Sleep Laboratory, Pulmonary Division, Heart Institute (InCor), Av Enéas Carvalho de Aguiar, 44, São Paulo, Brazil 05403-900


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(5):1050-1058. doi:10.1016/j.chest.2016.05.004
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Background  Hypertrophic cardiomyopathy (HCM) is a common genetic disease that may cause left ventricular outflow tract (LVOT) obstruction, heart failure, and sudden death. Recent studies have shown a high prevalence of OSA among patients with HCM. Because the hemodynamics in patients with LVOT obstruction are unstable and depend on the loading conditions of the heart, we evaluated the acute effects of CPAP on hemodynamics and cardiac performance in patients with HCM.

Methods  We studied 26 stable patients with HCM divided into nonobstructive HCM (n = 12) and obstructive HCM (n = 14) groups (LVOT gradient pressure lower or higher than 30 mm Hg, respectively). Patients in the supine position while awake were continuously monitored with beat-to-beat BP measurements and electrocardiography. Two-dimensional echocardiography was performed at rest (baseline) and after 20 min of nasal CPAP at 1.5 cm H2O and 10 cm H2O, which was applied in a random order interposed by 10 min without CPAP.

Results  BP, cardiac output, stroke volume, heart rate, left ventricular ejection fraction, and LVOT gradient did not change during the study period in either group. CPAP at 10 cm H2O decreased right atrial size and right ventricular relaxation in all patients. It also decreased left atrial volume significantly and decreased right ventricular outflow acceleration time, suggesting an increase in pulmonary artery pressure in patients with obstructive HCM.

Conclusions  The acute application of CPAP is apparently safe in patients with HCM, because CPAP does not lead to hemodynamic compromise. Long-term studies in patients with HCM and sleep apnea and nocturnal CPAP are warranted.

Trial Registry  ClinicalTrials.gov; No. NCT01631006; URL: www.clinicaltrials.gov

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