Left Ventricular Morphology and Systolic Function in Sleep-Disordered Breathing

Abstract

Background-Whether sleep-disordered breathing (SDB) is a risk factor for left ventricular (LV) hypertrophy and dysfunction is controversial. We assessed the relation of SDB to LV morphology and systolic function in a community-based sample of middle-aged and older adults. Methods and Results-The present study was a cross-sectional observational study of 2058 Sleep Heart Health Study participants (mean age 65Ϯ12 years; 58% women; 44% ethnic minorities) who had technically adequate echocardiograms. A polysomnographically derived apnea-hypopnea index (AHI) and hypoxemia index (percent of sleep time with oxyhemoglobin saturation Ͻ90%) were used to quantify SDB severity. LV mass index was significantly associated with both AHI and hypoxemia index after adjustment for age, sex, ethnicity, study site, body mass index, current and prior smoking, alcohol consumption, systolic blood pressure, antihypertensive medication use, diabetes mellitus, and prevalent myocardial infarction. Adjusted LV mass index was 41.3 (SD 9.90) g/m 2.7 in participants with AHI Ͻ5 (nϭ957) and 44.1 (SD 9.90) g/m 2.7 in participants with AHI Ն30 (nϭ84) events per hour. Compared with participants with AHI Ͻ5, those with AHI Ն30 had an adjusted odds ratio of 1.78 (95% confidence interval 1.14 to 2.79) for LV hypertrophy. A higher AHI and higher hypoxemia index were also associated with larger LV diastolic dimension and lower LV ejection fraction, with a trend toward lower LV fractional shortening. LV wall thickness was significantly associated with the hypoxemia index but not with AHI. Left atrial diameter was not associated with either SDB measure. Conclusions-In

American‐Style Football and Cardiovascular Health

“…In a recent analysis of 40 collegiate ASF athletes from 2 National Collegiate Athletic Association (NCAA) programs, ASF participants with SDB (22/40, 55%), as defined by an apnea–hypopnea index ≥5, demonstrated relative impairments in LV diastolic and vascular function, as reflected by lower lateral E′ (14±3 versus 17±3 cm/s; P =0.007) and septal E′ (11±2 versus 13±2 cm/s; P =0.009) in tissue and higher pulse wave velocity (5.4±0.9 versus 4.8±0.5 m/s, P =0.02) compared with those athletes without SDB 18. Although similar pathologic cardiovascular phenotypic relationships have been demonstrated in older, more comorbid members of the general population with SDB,74, 75, 76 these data are the first to document an association between SDB and abnormal ventriculoarterial coupling patterns in youthful and relatively healthy athletic participants. At present, data defining the prevalence, physiologic correlates, and corollary clinical outcomes among active and former professional ASF athletes with SDB are unavailable.…”

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

“…[117][118][119] Obstructive sleep apnoea prolongs atrial conduction times, slows atrial conduction, reduces atrial-electrogram voltages and increases electrogram complexity. 117,118 Signal-averaged P-wave duration is increased by OSA, and decreases significantly with continuous positive airway pressure treatment.…”

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

“…Independently from hypertension and obesity, OSA impairs LV diastolic function, begets LVH, and thus may hasten HFpEF progression 126, 127, 252, 253, 254, 255, 256, 257, 258. Repetitive sleep arousals and hypoxic episodes heighten sympathetic activity and promote endothelial dysfunction, systemic inflammation, and arterial stiffness that may further increase blood pressure and accelerate atherosclerosis progression 128, 259, 260, 261, 262, 263, 264, 265…”