Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy.

Abnormal left ventricular (LV) diastolic relaxation is an early sign of hypertensive heart disease. Whether LV diastolic dysfunction is caused directly by raised blood pressure, or by structural changes related to LV hypertrophy remains controversial. We examined 115 hypertensive patients with LV hypertrophy, and two age- and gender-matched groups (38 hypertensive patients without LV hypertrophy and 38 normotensive subjects) by echocardiography to assess determinants of LV diastolic function, and the relation between diastolic function and LV geometric pattern. Diastolic function was evaluated by the E/A-ratio, E wave deceleration time (E-dec), isovolumic relaxation time (IVRT), and the atrioventricular plane displacement method (AV-LA/AV-mean). A multivariate analysis (including gender, age and body mass index) shows diastolic function to be inversely related to blood pressure, LV wall thickness and LV mass, but not to LV end diastolic diameter. The E/A-ratio generally showed the strongest relations. Only the E/A-ratio and AV-LA/AV-mean were related to heart rate. By stepwise regression analysis, age was the strongest determinant for the E/A-ratio, E-dec and AV-LA/AV-mean, followed by systolic blood pressure, heart rate and LV wall thickness. For IVRT, however, LV wall thickness appeared strongest, followed by systolic blood pressure and age. In conclusion, blood pressure and LV wall thickness both have independent influence on LV diastolic function. Age and blood pressure are the most important factors to determine the E/A-ratio and E-dec, whereas LV geometry and blood pressure are most important when IVRT is used. AV-LA/AV-mean may not be useful in hypertensive LV hypertrophy.

Regression of left ventricular hypertrophy in human hypertension with irbesartan.

BACKGROUND: The Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA). OBJECTIVE: Angiotensin II induces myocardial hypertrophy. We hypothesized that blockade of angiotensin II subtype 1 (AT1) receptors by the AT1-receptor antagonist irbesartan would reduce left ventricular mass (as measured by echocardiography) more than conventional treatment with a beta blocker. DESIGN AND METHODS: This double-blind study randomized 115 hypertensive men and women with left ventricular hypertrophy to receive either irbesartan 150 mg q.d. or atenolol 50 mg q.d. for 48 weeks. If diastolic blood pressure remained above 90 mmHg, doses were doubled, and additional medications (hydrochlorothiazide and felodipine) were prescribed as needed. Echocardiography was performed at weeks 0, 12, 24 and 48. RESULTS: Baseline mean blood pressure was 162/ 104 mmHg, and mean left ventricular mass index was 157 g/m2 for men and 133 g/m2 for women. Systolic and diastolic blood pressure reductions were similar in both treatment groups. Both irbesartan (P < 0.001) and atenolol (P< 0.001) progressively reduced left ventricular mass index, e.g. by 26 and 14 g/m2 (16 and 9%), respectively, at week 48, with a greater reduction in the irbesartan group (P = 0.024). The proportion of patients who attained a normalized left ventricular mass (i.e. < or = 131 g/m2 for men and < or = 100 g/m2 for women) tended to be greater with irbesartan (47 versus 32%, P = 0.108). CONCLUSIONS: Left ventricular mass was reduced more in the irbesartan group than in the atenolol group. These results suggest that blocking the action of angiotensin II at AT1-receptors may be an important mechanism, beyond that of lowering blood pressure, in the regulation of left ventricular mass and geometry in patients with hypertension.

Influence of age and cardiovascular factors on regional pulsed wave Doppler myocardial imaging indices.

AIMS: To describe the influence of age and other cardiovascular factors on regional pulsed wave Doppler myocardial imaging (DMI), and to compare DMI with conventional transmitral echocardiography and the atrioventricular plane displacement (AVPD) method. METHODS AND RESULTS: Eighty-eight healthy subjects aged 20-81 years were examined by DMI, performed in the intraventricular septum just below the mitral annulus and in the corresponding lateral region, by transmitral pulsed wave Doppler echocardiography, and by AVPD. The DMI peak velocity during the left ventricular (LV) early filling phase (e), decreased with age from 12.3 +/- 2.3 cm/s in the youngest to 7.0 +/- 1.7 cm/s in the oldest tercentile (r=- 0.76, P<0.001). The DMI peak velocity during atrial contraction (a), increased from 7.5 +/- 2.2 cm/s in the youngest to 9.7 +/- 1.7 cm/s in the oldest tercentile (r=0.41, P<0.001). The DMI systolic peak velocity (s), decreased with age from 8.2 +/- 1.1 (youngest tercentile) to 6.9 +/- 1.1 (oldest tercentile), r=-0.39, P<0.001 cm/s, while the fraction shortening of the LV increased from 33.7 +/- 4.1 to 38.2 +/- 5.9% (r=0.36, P<0.01). The DMI e/a correlated with the transmitral early/atrial (E/A) (r=0.83, P<0.001) and with the AVPD measurement of diastolic function AV-LA/AV-mean (r=0.82, P<0.001). The DMI e velocity correlated with the transmitral E velocity (r=0.38, P<0.001). In the multiple regression analysis of DMI e, age was the strongest factor and LV mass index correlated inversely and independently with e. No DMI variables were influenced by gender, while transmitral E correlated with gender. The LV dimension variables explained 35% (R2 adjusted) of the DMI e velocity changes; only 7% of the transmitral E changes were explained by those variables. CONCLUSION: Regional DMI indices are highly age-dependent. In comparision with conventional echocardiography, regional DMI might be more influenced by LV geometry and by myocardial structural changes. These findings suggest a complementary role for regional DMI to conventional echocardiography for the assessment of myocardial function.