Introduction and objectives: Sleep apnea-hypopnea syndrome (SAHS) is associated with significant effects on the heart, which can be assessed using noninvasive methods such as transthoracic echocardiography. However, it is not clear whether these effects are due to the condition itself or are influenced by associated factors, such as high blood pressure (HBP). The objective of this study was to investigate the echocardiographic alterations observed in SAHS patients and how they are affected by the presence of concomitant HBP.
Methods: The study involved 103 consecutive patients (49 with HBP and 54 without) with SAHS and an indication for continuous positive airways pressure treatment and 24 controls matched for age and body mass index. Doppler echocardiography was performed in a blinded manner. Both morphology (i.e., wall thickness, and diameters) and function (i.e., ejection fraction, peak E and A wave velocities, mitral deceleration time, and Tei index) were assessed. Results were compared using ANOVA and Bonferroni's test.
Results: Hypertensive patients had larger morphological changes characteristic of left ventricular hypertrophy (i.e., increased septal and posterior wall thicknesses) than nonhypertensive patients, who in turn had larger changes than controls (septal thickness: HBP-SAHS, 12 [2] mm; non-HBP SAHS, 11 [2] mm, and controls, 9.5 [5] mm; 1 vs. 2, P=.038; 1 vs. 3, P=.0001, 2 vs. 3, P=.034) (posterior wall thickness: HBP-SAHS, 11 [2] mm; non-HBP SAHS, 10 [1] mm, and controls, 9 [1.5] mm; 1 vs. 2, P=.5; 1 vs. 3, P=.0001; 2 vs. 3, P=.001). In addition, there were also greater changes in ventricular filling patterns on the left (HBP-SAHS, 92%; non-HBP SAHS, 72%, controls, 29%; P=.0001) and on the right (HBP-SAHS, 72%; non-HBP SAHS, 58%; controls, 25%; P=.001). There was a trend towards a larger left ventricular Tei index (HBP-SAHS, 0.56 [0.2]; non-HBP SAHS, 0.54 [0.12]; controls, 0.5 [0.1]; 1 vs. 2, P=.8; 1 vs. 3, P=.09; 2 vs. 3, P=.7).
Conclusions: From the time of diagnosis, SAHS was associated with left ventricular hypertrophy and impaired biventricular filling, even in the absence of concomitant HBP. The abnormalities observed were more severe when HBP was present.