Left ventricular hypertrophy independent of hypertension in patients with obstructive sleep apnoea

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To evaluate cardiac structure and function as well as blood pressure in the obstructive sleep apnoea syndrome (OSAS), we investigated 61 male patients and 61 male controls with M-mode and two-dimensional echocardiography. All patients had a history of habitual snoring and a diagnosed light to severe OSAS by previous investigations of nocturnal oxygen saturation status. No subject in the control group had a history of OSAS or hypertension. Body weight was higher in the OSAS patients than in the controls (P<0.001). Fifty per cent (31 out of 61) of the OSAS patients had systemic hypertension; 17 of these 31 were on pharmacological antihypertensive treatment. Neither the systolic nor the diastolic blood pressures were found to correlate to the severity of the OSAS (desaturation index). The heart rate was higher at rest in the OSAS patients with or without systemic hypertension compared to the controls with or without a blood pressure level above 165/95 mmHg (P<0.05 and P<0.01, respectively). Left ventricular (LV) internal dimensions as assessed by echocardiography did not differ between the two groups, while the interventricular septum and the LV posterior wall were thicker in the OSAS group. Thus, the LV mass and the LV mass index were significantly higher among the OSAS patients (P<0.001 and P<0.001). The LV mass index was approximately 15% higher among the 30 normotensive OSAS patients with no history of cardiac disease compared with the normotensive controls (P<0.05). Patients and controls without antihypertensive treatment, matched by weight (n=20), had different LV mass (259 ± 12 versus 221 ± 8g, P=0.01), despite there being no difference in the daytime blood pressure. The ejection fraction and the left atrial dimension did not differ between patients and controls. Measures of LV structure or function were not correlated to the severity of the OSAS as depicted by desaturation index or minimal nocturnal oxygen saturation during nocturnal investigations. Thus, both systemic hypertension and LV hypertrophy seem to be common phenomena in OSAS. We did not find the severity of OSAS to be predictive of systemic hypertension or LV structural changes. Also, OSAS patients without hypertension had LV hypertrophy, the development of which may be partly due to other pathophysiological mechanisms.

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