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The effect of valsartan on left ventricular myocardial functions in hypertensive patients with left ventricular
Nagehan Kucukler1, Ibrahim H Kurt, Caner Topaloglu
1Department of Cardiology, Mustafa Kemal University School of Medicine, Antioch, Turkey. drnagehan@gmail.com
Insights
Valsartan therapy significantly improved cardiac function in hypertensive patients with left ventricular hypertrophy (LVH). The drug reduced blood pressure and LVH, enhancing myocardial contractility and relaxation.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Management
Background:
- Hypertension-induced left ventricular hypertrophy (LVH) impairs cardiac function.
- Angiotensin receptor blockers are known to reduce LV mass and improve diastolic function.
Purpose of the Study:
- To evaluate the effect of angiotensin receptor blockage on midwall mechanics and myocardial dynamics in hypertensive patients with LVH.
- To assess the cardioprotective effects of valsartan beyond blood pressure reduction.
Main Methods:
- 38 untreated hypertensive patients with LVH received valsartan (80-160 mg) for 6 months.
- Left ventricular midwall mechanics and tissue Doppler velocities were measured at baseline and study end.
Main Results:
- Valsartan significantly reduced blood pressure (152/92 to 131/83 mmHg) and left ventricular mass index (135 to 114 g/m²).
- Midwall fractional shortening and myocardial tissue velocities increased, indicating improved contractility.
- Circumferential end-systolic wall stress and E/Em ratio decreased, signifying enhanced relaxation and reduced diastolic dysfunction.
Conclusions:
- Valsartan demonstrates significant blood pressure-lowering effects.
- The drug promotes regression of LVH and improves left ventricular myocardial contractility and relaxation.
- Valsartan offers cardioprotective benefits in hypertensive patients with LVH.
Background:
It has been shown by various diagnostic methodologies that angiotensin receptor blockage reduces left ventricular mass, improves diastolic function and increases contractility in hypertensive left ventricular hypertrophy (LVH). We planned to detect the effect of angiotensin receptor blockage on midwall mechanics and myocardial dynamics in hypertensive patients with LVH.
Methods:
Angiotensin 2 type 1 receptor blocker (valsartan 80-160 mg) was administered to 38 previously untreated hypertensive patients with LVH for 6 months. Left ventricular midwall mechanics and tissue Doppler velocities were measured at baseline and at the end of the study.
Results:
Mean blood pressure was reduced from 152 ± 14/92 ± 8 to 131 ± 14/83 ± 9 mmHg (P < 0.05). Left ventricular mass index was decreased from 135 ± 15 to 114 ± 14 g/m(2) (P < 0.001). Midwall fractional shortening was increased from 19.0 ± 4 to 22.4 ± 3% (P < 0.05). Circumferential end-systolic wall stress was decreased from 131 ± 44 to 119 ± 37 × 10(3) dyn/cm(2) (P < 0.05). Left ventricular interventricular septal myocardial tissue peak systolic velocity was increased from 6.7 ± 1 to 8.1 ± 0.9 cm/s (P < 0.001) and lateral wall myocardial tissue peak systolic velocity was increased from 7.5 ± 1 to 9.0 ± 1 cm/s (P < 0.001), and E/E(m) ratio was significantly decreased (11.0 ± 0.3 to 8.90 ± 0.1, P < 0.05) with 6-month valsartan therapy.
Conclusion:
This study suggests that valsartan exhibits not only blood pressure-lowering qualities but also cardioprotective actions in patients with hypertension because it enhances regression of LVH and improves left ventricular myocardial contractility and relaxation.
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