Myocardial diastolic impairment caused by left ventricular hypertrophy involves basal septum more than other walls: analysis by pulsed Doppler tissue imaging.

OBJECTIVE: To assess regional diastolic function in patients with hypertension with or without left ventricular hypertrophy using Doppler tissue imaging, a new tool that analyzes myocardial wall motion 'on-line'.
METHODS: Ten normotensive subjects, 20 hypertensive patients without hypertrophy and 20 with hypertrophy (left ventricular mass index >50 g/m2.7), all men, underwent Doppler echocardiography and Doppler tissue imaging, which was performed in apical view by placing pulsed sample volume at the level of the basal and middle septum, basal and middle lateral wall, and infero-posterior wall. Peak velocities and time-velocity integrals of myocardial early (Em) and late (Am) waves and their ratios, regional deceleration time and regional relaxation time were measured in each segment.
RESULTS: Transmitral peak E/A ratio was 1.37 in normotensive subjects, 1.01 in hypertensive patients without hypertrophy and 0.77 in those with hypertrophy (P < 0.00001). The myocardial diastolic indexes derived by Doppler tissue imaging worsened at all levels in hypertensive patients without hypertrophy compared with normotensive subjects. In hypertensive patients with hypertrophy, the majority of myocardial diastolic indexes were further impaired at the basal septal level, but only marginal differences were found in other regions, compared with indexes in hypertensive patients without hypertrophy. The main diastolic indexes were found, using separate intra-group analyses, to be more compromised at the basal septum than at other levels only in hypertrophic hypertensive patients. The prevalence of regions having peak Em/Am ratios < 1 increased significantly from normotensive subjects to hypertensive patients without hypertrophy, but not significantly from these to the hypertrophic group. Among pooled hypertensive patients, after adjusting for heart rate and diastolic blood pressure using multivariate models, the septal wall thickness was shown to be an independent determinant of the diastolic indexes of the basal and middle septum.
CONCLUSIONS: In hypertensive patients without hypertrophy, diastolic dysfunction is uniform along the ventricular walls, whereas in those with hypertrophy it is more evident at the basal septal level than in other walls. Overall among hypertensive patients, the diastolic properties of the interventricular septum worsen as the thickness of the septal wall increases, in the presence and in the absence of hypertrophy.