Sleep · 2004
Provocation of ventricular ectopy by cheyne-stokes respiration in patients with heart failure.
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Leung Richard S T, Diep Tung M, Bowman Michael E, Lorenzi-Filho Geraldo, Bradley T Douglas
Аннотация
STUDY OBJECTIVES: Previous reports have suggested an association between Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) and ventricular ectopy, but there has been relatively little evidence of a cause-effect relationship. The objective of this study was to determine whether CSR-CSA directly provokes ventricular ectopy and, if so, whether it is associated with any particular phase of the CSR-CSA breathing cycle.
DESIGN: We compared the frequency of ventricular premature beats (1) between the apneic and hyperpneic phases of CSR-CSA, (2) between periods of CSR-CSA and periods of regular breathing during sleep, and (3) in response to the elimination of CSR-CSA by administration of a low concentration of inhaled CO2.
SETTING: Hospital-based cardiopulmonary sleep laboratory.
PATIENTS: Twenty-three patients with heart failure and CSR-CSA.
MEASUREMENTS AND RESULTS: Ventricular premature beats were found to occur 40% more frequently during the hyperpneic phase than the apneic phase of CSR-CSA (mean+/-SD, 7.0+/-7.4 versus 4.9+/-5.7 ventricular premature beats per minute, P = .003). Ventricular premature beat frequency was also found to be higher during periods of CSR-CSA than during periods of regular breathing occurring either spontaneously (median [25th, 75th percentile], 2.2 [1.2, 6.5] versus 1.1 [0.8, 2.0] ventricular premature beats per minute, P = .027), or induced through inhalation of CO2 (from 4.7+/-3.8 to 3.3+/-4.0 ventricular premature beats per minute, P = .048).
CONCLUSIONS: CSR-CSA provokes ventricular ectopy that is most pronounced during the hyperpneic phase. Such an increase in ventricular premature beats might contribute to the higher mortality rates reported in heart failure patients with CSR-CSA.
DESIGN: We compared the frequency of ventricular premature beats (1) between the apneic and hyperpneic phases of CSR-CSA, (2) between periods of CSR-CSA and periods of regular breathing during sleep, and (3) in response to the elimination of CSR-CSA by administration of a low concentration of inhaled CO2.
SETTING: Hospital-based cardiopulmonary sleep laboratory.
PATIENTS: Twenty-three patients with heart failure and CSR-CSA.
MEASUREMENTS AND RESULTS: Ventricular premature beats were found to occur 40% more frequently during the hyperpneic phase than the apneic phase of CSR-CSA (mean+/-SD, 7.0+/-7.4 versus 4.9+/-5.7 ventricular premature beats per minute, P = .003). Ventricular premature beat frequency was also found to be higher during periods of CSR-CSA than during periods of regular breathing occurring either spontaneously (median [25th, 75th percentile], 2.2 [1.2, 6.5] versus 1.1 [0.8, 2.0] ventricular premature beats per minute, P = .027), or induced through inhalation of CO2 (from 4.7+/-3.8 to 3.3+/-4.0 ventricular premature beats per minute, P = .048).
CONCLUSIONS: CSR-CSA provokes ventricular ectopy that is most pronounced during the hyperpneic phase. Such an increase in ventricular premature beats might contribute to the higher mortality rates reported in heart failure patients with CSR-CSA.