Cleveland, OH, Toronto, ON, and Antwerp, Belgium -With obesity and heart failure both common in a growing elderly population, clinicians are more often likely to encounter heart disorders that are at least partially secondary to sleep-disordered breathing (SDB). Two reports suggest, for example, that cardiac effects of the most common SDB, obstructive sleep apnea (OSA), may include a range of complex arrhythmias [1] as well as independent ventricular remodeling effects in patients with symptomatic nonischemic dilated cardiomyopathy (NIDCM) [2].

In a separate study of patients with OSA but no clinical heart disease, six months of continuous positive airway pressure (CPAP) therapy appeared to reverse what may have been cardiac structural changes caused by the sleep disorder [3].

In a subanalysis from the longitudinal Sleep Heart Health Study, which encompassed 6441 persons in the community who were at least 40 years old, 228 subjects identified with severe SDB in an overnight study were compared with 338 who were matched for age, sex, race, and body-mass index (BMI) and were free of SDB.

Those with SDB showed a significantly and independently increased prevalence of atrial fibrillation, nonsustained VT, and complex ventricular ectopy during sleep, report Dr Reena Mehra (Case Western Reserve University, Cleveland, OH) and associates in the April 15, 2006 issue of the American Journal of Respiratory and Critical Care Medicine. There was no observed increase in conduction-delay arrhythmia rates.

The first epidemiologic study of its kind, according to Mehra and associates, it "provides one potential explanation for the observed increase in sudden death with sleep apnea." The findings may also account for some of the observed rise in atrial-fibrillation rates, they write, given the susceptibility to the arrhythmia among the growing ranks of obese persons.

Patients with OSA have an increased likelihood of NIDCM and, among those with associated HF, show distinct cardiac hypertrophic changes that don't increase LV mass but add to remodeling effects typically associated with nonischemic HF in the absence of OSA, according to a small study published online March 2, 2006 in the American Journal of Respiratory and Critical Care Medicine.

In such cases, the superimposed myocardial effects consist primarily of septal-wall thickening that produces a less eccentric echocardiographic appearance than what is generally seen with NIDCM alone, write Dr Kengo Usui (Toronto Rehabilitation Institute, ON) and associates.

In their observational analysis of 21 and 26 patients with and without OSA, respectively, all of whom had symptomatic NIDCM, the degree of septal remodeling was independently proportional to the observed frequency of apnea-hypopnea events. The sleep studies were performed by personnel who were blinded to echocardiographic findings.

This greater degree of LV thickening may put HF patients with OSA at greater risk for adverse cardiovascular events than those without OSA.

Left ventricular hypertrophy was present in 48% of the OSA patients and 15% of the others (p=0.016). The OSA group also showed significantly greater interventricular septal-wall (ISW) thickness (p<0.001). But the groups didn't differ significantly in posterior-wall thickness, LV mass, or LV dimensions at systole or diastole.

The findings point to the manifestation of OSA-related LV remodeling in NIDCM as a "superimposition LV wall thickening, particularly affecting the septum, upon a dilated LV chamber," the group writes. However, "they do not establish whether the relationship between OSA and LV thickening was causal. Nevertheless, this greater degree of LV thickening may put HF patients with OSA at greater risk for adverse cardiovascular events than those without OSA." Given that CPAP can improve LV function in patients with HF, according to Usui and associates, such therapy might potentially promote reverse remodeling in those with OSA and NIDCM.

Severe OSA in the absence of clinical heart disease was associated with cardiac structural and functional changes that appeared to reverse after six months of CPAP therapy in a study from the April 4, 2006 issue of the Journal of the American College of Cardiology [3].

Echocardiographic evaluation of noncardiac OSA patients could potentially disclose such changes "that may, without treatment, have profound cardiovascular consequences," write the investigators, Dr Bharati Shivalkar (University Hospital Antwerp, Belgium) and colleagues,

The therapeutic effects of CPAP mirror those of chronic beta-blockade in heart failure but "are achieved nonpharmacologically.

The group compared echo findings before and after CPAP in 43 patients with severe, symptomatic OSA and 40 age- and sex-matched "overweight" but otherwise "healthy" control subjects. Compared with the controls, patients had significantly greater baseline mean blood pressure (p<0.01), pulmonary artery pressure (p=0.004), right ventricular dimensions (p<0.001), and ISW thickness (p<0.001) and lower LVEF (p=0.012), The patients also showed significantly decreased stroke volume (p=0.008) and systolic velocities by tissue-Doppler imaging (p<0.004).

In multivariate analysis, apnea-hypopnea-event frequency rose with greater right-ventricular dimensions and ISW thickness and with decreasing tissue-Doppler velocities measured at the mitral-valve annulus (p<0.001 for all correlations).

The 25 OSA patients who had undergone six months of CPAP not only slept more soundly, they also showed significant improvements in cardiac structure and performance, including heart rate, stroke volumes, RV dimensions and wall motion, ISW thickness, pulmonary artery pressure, systolic and diastolic blood pressures, and annular tissue-Doppler velocities at the mitral and tricuspid valves (p=0.02-0.001). There was no change in BMI to account for the improvements, the group writes.

The therapeutic effects of CPAP mirror those of chronic beta-blockade in heart failure, observe Shivalkar and colleagues, but "are achieved nonpharmacologically by reducing the oxygen demand, increasing the oxygen supply, and altering the central sympathetic outflow."