Flávia B Nerbass1, Vera M C Salemi2, Rodrigo P Pedrosa3, Natanael de P Portilho1, Julio C A Ferreira-Filho2, Henrique T Moriya4, Murillo O Antunes2, Edmundo Arteaga-Fernández2, Luciano F Drager5, Geraldo Lorenzi-Filho6. 1. Sleep Laboratory, Pulmonary Division, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil. 2. Cardiomyopathy Unit, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil. 3. Sleep Laboratory, Pulmonary Division, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil; Hospital Dom Hélder Câmara - IMIP Hospitalar, Recife, Brazil. 4. Biomedical Engineering Laboratory, University of São Paulo, São Paulo, Brazil. 5. Hypertension Unit, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil. 6. Sleep Laboratory, Pulmonary Division, Heart Institute (InCor) University of São Paulo Medical School, São Paulo, Brazil. Electronic address: geraldo.lorenzi@gmail.com.
Abstract
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.
RCT Entities:
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.