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PURPOSE: Severe obstructive sleep apnea (OSA) directly impairs left ventricular (LV) diastolic function. Left atrial volume index (LAVI), an independent predictor of future cardiovascular events, is also related to OSA severity. This study aimed to assess whether OSA is associated with an increase in LAVI independently of LV diastolic function. METHODS: Two hundred six OSA patients (apnea hypopnea index, AHI ≥ 5/h) without cardiac disease, hypertension, and diabetes were enrolled. They underwent overnight fully attended polysomnography and 2-dimensional echocardiography in order to estimate LA volumes and LV diastolic function which was assessed by the ratio of transmitral early diastolic flow velocity to late diastolic flow velocity (E/A), deceleration time, and mitral annular velocity (e') which was derived from tissue Doppler imaging. Patients were divided into two groups based on AHI, namely, group M (5 ≤ AHI < 30/h) and group S (AHI ≥ 30/h). RESULTS: The LAVI value in group S was significantly larger than that in group M (20 ± 5 vs. 23 ± 5 mL/m(2), P < 0.001). E/A in group S was significantly lower than that in group M (P < 0.001), whereas the ratio of E to e' (E/e') in group S was significantly higher than that in group M (P < 0.001). AHI showed a statistically significant correlation with LAVI (P < 0.001). On multivariate linear regression analysis, severe OSA was independently related with LAVI even after adjusting for age, sex, systolic blood pressure, body mass index, and measurements of LV diastolic function (P = 0.04). CONCLUSIONS: Severe OSA itself might directly increase LAVI, independently of LV diastolic function.

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OBJECTIVE: To evaluate whether obstructive sleep apnea (OSA) contributes directly to left ventricular (LV) diastolic dysfunction. METHODS: Seventy-four non-obese male OSA (apnea hypopnea index (AHI)⩾5/h) patients without cardiac disease, hypertension or diabetes were enrolled. Echocardiography, pulse wave velocity (PWV) measurements and laboratory testing were performed in all patients. LV diastolic function was assessed by the transmitral flow velocity (E/A ratio), and mitral annular velocity (Ea) was derived from tissue Doppler imaging (TDI). RESULTS: The E/A ratio and Ea in the severe OSA group (AHI⩾30/h) was significantly lower than those in the mild to moderate OSA group (5⩽AHI<30/h) (P<0.0001), whereas the S/D ratio, an indicator of pulmonary vein flow velocity, in the severe OSA group was significantly higher than that in the mild to moderate OSA group (P=0.04). AHI exhibited a statistically significant inverse correlation with the E/A ratio (r=-0.47, P=0.0001), but not with relative wall thickness (RWT), LV mass index (LVMI) or PWV. RWT, LVMI and PWV exhibited an inverse correlation with the E/A ratio. Multivariate linear regression analysis revealed that severe OSA was independently associated with the E/A ratio even after adjusting for age, insulin resistance, blood pressure, LV geometry, and PWV (ß=-0.23, P=0.001). CONCLUSIONS: These results indicate that severe OSA itself may contribute directly to LV diastolic dysfunction irrespective of LV geometry, arterial stiffness, obesity and its associated cardiovascular risk factors.

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Clinical significance of coronary flow velocity measurement by transthoracic Doppler echocardiography in 2 patients with unstable angina (UA) was reported. No significant abnormality was observed on electrocardiography. Coronary flow sequence of the left anterior descending coronary artery (LAD) was detected in diastole. Peak diastolic flow velocity was 11.1 cm/s in case 1 and 10.1 cm/s in case 2. On the basis of these data, emergency coronary angiography was performed in both cases. Severe stenosis was observed at the proximal portion of LAD; consequently, emergency coronary angioplasty was performed. Coronary flow velocity measurement is useful as a diagnostic strategy in UA.

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OBJECTIVES: To examine whether increased plasma levels of B-type natriuretic peptide (BNP) are associated with cardiac structural and functional abnormalities in obstructive sleep apnoea (OSA) patients, taking into consideration the confounding effect of obesity. MEASUREMENTS: In a cross-sectional study, polysomnography, echocardiography and the measurement of the serum levels of BNP were performed in 235 consecutive subjects (age 52 +/- 14 years) visiting our sleep clinic. Left ventricular hypertrophy (LVH) [left ventricular mass index (LVMI) > or = 125 g/m in men, and > or = 110 g/m in women] and cardiac diastolic function (E/A ratio) were determined by echocardiography. RESULTS: The LVMI, prevalence rate of LVH and body mass index (BMI) were higher, and the E/A ratio lower in the subjects with severe OSA (apnoea-hypopnoea index > or = 30/h, n = 146, LVH 80%) than in those with mild to moderate OSA (n = 89, LVH 35%; P < 0.01), although plasma BNP levels were similar in the two groups. Although the log-transformed plasma BNP level showed a negative correlation with BMI, the results of binary logistic regression analysis demonstrated that the quintile value of BNP was an independent significant variable for the identification of LVH (adjusted odds ratio in quintile 5 = 4.01, 95% confidence interval 1.18-13.70, P < 0.01), even after adjusting for obesity and other risk factors. CONCLUSION: An increased likelihood of cardiac structural and functional abnormalities was observed with increasing severity of OSA. Increased plasma levels of BNP do seem to reflect an increased likelihood of LVH in patients with severe OSA.

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OBJECTIVES: Regional myocardial systolic function in hypertensive left ventricular hypertrophy was assessed using the newly developed myocardial strain imaging. METHODS: This study included 17 patients with hypertensive left ventricular hypertrophy (LVH group) and 22 normal subjects (N group). The transmural location of the strain peak value (StPP), and the strain peak value (StPV) in the end-systolic phase were measured at the posterior wall by myocardial strain imaging. Left ventricular mass index was simultaneously measured in both groups. RESULTS: StPV was significantly lower in the LVH group than the N group (1.00 +/- 0.36 vs 1.38 +/- 0.42, p < 0.01) and StPP was significantly moved to the epicardium side compared with the N group (31 +/- 10% vs 11 +/- 5%, p < 0.0001). StPV decreased and StPP increased with greater left ventricular mass index (r = -0.61, p < 0.0001; r = 0.72, p < 0.0001, respectively). CONCLUSIONS: Myocardial systolic impairment in hypertensive left ventricular hypertrophy may occur from the endocardium side, and the impairment may progress with increased left ventricular hypertrophy.

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