Sleep Apnea Treatment Improves Cardiac Condition

Treating obstructive sleep apnea (OSA) may help prevent heart failure by reversing structural and functional impairment seen with the sleep condition, according to a new study.

Researchers at the University of Birmingham (United Kingdom) and City Hospital (Birmingham, United Kingdom) conducted a study involving a total of 120 subjects (40 each of matched OSA, hypertension, and healthy cohorts) whom underwent echocardiographic examination for the assessment of septal and posterior wall thickness, left ventricular (LV) mass index, and other indices. The OSA subjects were then treated with continuous positive airway pressure (CPAP), following which the echocardiographic parameters were reassessed.

The preliminary results showed that initial moderate-to-severe OSA was associated with significantly larger left ventricles and poorer filling and emptying parameters compared with controls, similar to what was seen in hypertensive adults. However, in the OSA patients, and following six months of treatment with CPAP, most of those measures normalized or improved. CPAP therapy resulted in reduction of the posterior wall thickness and improvement in LV ejection fraction, systolic velocity, and diastolic LV impairment parameters. The study was published early online on March 13, 2012, in Circulation.

“Moderate to severe OSA causes structural and functional changes in LV function and are comparable to that seen in hypertension; these abnormalities significantly improve following CPAP therapy,” concluded lead author Gregory Lip, MD, of the University of Birmingham Center for Cardiovascular Sciences, and colleagues. “This may imply that obstructive sleep apnea could be crucial in development of left ventricular diastolic dysfunction, which may lead to heart failure and increased mortality if left untreated.”

How exactly CPAP improves systolic function is not clear, according to the researchers, but may involve reducing blood pressure, hypoxia, rapid intrathoracic pressure changes, and secondary hemodynamic disturbances. The mechanism for diastolic improvements also needs further study, but may be by correction of surges in blood pressure, hypoxia, and hypercapnia with over-activation of the sympathetic system, according to the researchers.

Related Links:
University of Birmingham
City Hospital Birmingham