There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function.Twenty-nine OSA patients and 12 control subjects were studied using technetium99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP.

Background: Previous studies have yielded disparate results regarding the effect of obstructive sleep apnoea (OSA) syndrome on left ventricular (LV) function. Objectives: In order to clarify this, we performed a prospective study investigating OSA patients with no history of systemic hypertension, coronary artery disease, myocardial, pericardial or valvular problems, asthma or chronic obstructive pulmonary disease before and after treatment with nasal continuous positive airway pressure (nCPAP). Methods: Fifteen patients (3 women, 12 men) with an apnoea/hypopnoea index >15 (mean ± SD = 52 ± 21) were studied with complete polysomnography, ambulatory blood pressure monitoring, M-mode two-dimensional echocardiography and pulsed Doppler echocardiography in two phases, i.e. before and after 12–14 weeks of nCPAP therapy. We measured systolic and diastolic blood pressure (BP) separately in the daytime and night-time, isovolumic relaxation time (IVRT), the ratio of peak early filling velocity (E) to peak late velocity (A) diastolic transmitral flow (E/A), posterior wall thickness (PWT) and septal thickness (IVST). The shortening fraction (SF) was also calculated. Eleven overweight non-apnoeic normal subjects matched for age were used as the control group. Results: Our results showed that the patient group exhibited, before treatment, LV diastolic, but not systolic, dysfunction compared with the normal group (IVRT = 94.3 ± 11.6 ms, p < 0.05; E/A = 0.94 ± 0.26, p < 0.02; SF = 39.9 ± 4.1%, not significant (NS); IVST = 9.9 ± 1.2 mm, NS; PWT = 8.3 ± 1.2 mm, NS). Moreover, the patient group developed diastolic hypertension both in the daytime and night-time (BP/diastolic/daytime = 93.3 ± 9.2 mm Hg, BP/diastolic/night-time = 90.3 ± 10.7 mm Hg). After 12–14 weeks of nCPAP treatment (no change in body mass index), significant improvement in LV diastolic function and a drop in blood pressure were noticed (IVRT = 85.6 ± 8.8 ms, p < 0.05; E/A = 1.07 ± 0.3, p < 0.05; BP/diastolic/daytime = 86.3 ± 5.5 mm Hg, p < 0.02; BP/diastolic/night-time = 83.9 ± 8.6 mm Hg, p < 0.05) in our patient group. Conclusions: We conclude that repetitive apnoeas/hypopnoeas are very important factors in the development of both LV diastolic dysfunction and diastolic systemic hypertension in patients with OSA syndrome. Treatment with nCPAP leads to significant improvement in both ventricular function and systemic hypertension.

Background: Limited information exists regarding the development of pulmonary hypertension in patients with obstructive sleep apnea (OSA) in the absence of lung and heart comorbidity. Objectives: The aims of this study were to investigate whether OSA patients without any other cardiac or lung disease develop pulmonary hypertension, and to assess the effect of continuous positive airway pressure (CPAP) treatment on pulmonary artery pressure (P_PA). Methods: Twenty-nine patients aged 51 ± 10 years with OSA and 12 control subjects were studied with pulsed-wave Doppler echocardiography for estimation of P_PA before and after 6-month effective treatment with CPAP. Results: A significantly higher mean P_PA was found in OSA patients as compared to control subjects (17.2 ± 5.2 vs. 12.1 ± 1.9 mm Hg, p < 0.001). Six out of the 29 OSA patients had mild pulmonary hypertension (P_PA ≧ 20 mm Hg). Significant differences were observed between pulmonary hypertensive and normotensive OSA patients with respect to age (62 ± 4 vs. 48 ± 15 years, respectively, p < 0.05), body mass index (41 ± 7 vs. 32 ± 4 kg/m², p < 0.02) and daytime P_aO₂ (81 ± 9 vs. 92 ± 9 mm Hg, p < 0.05). CPAP treatment was effective in reducing mean P_PA in both groups of pulmonary hypertensive and normotensive OSA patients (decreases in P_PA from 25.6 ± 4.0 to 19.5 ± 1.5 mm Hg, p < 0.001; from 14.9 ± 2.2 to 11.5 ± 2.0 mm Hg, respectively, p < 0.001). Conclusions: A proportion (20.7%) of OSA patients without any other lung or heart disease and characterized by older age, greater obesity and lower daytime oxygenation develop mild pulmonary hypertension which has been partially or completely reversed after 6-month CPAP treatment. In conclusion, OSA alone constitutes an independent risk factor for the development of pulmonary hypertension.