Key result
Six-month losartan use linked to lower BP and LVMI without improving abnormal diastolic function.
Why the study?
The effects of angiotensin II type I receptor blockade on left ventricular hypertrophy and diastolic cardiac function in hypertensive patients were controversial and data were scarce.
Does losartan reduce left ventricular hypertrophy and improve diastolic function in patients with moderate primary hypertension?
Observational (n=31)
Does losartan reduce left ventricular hypertrophy and improve diastolic function in patients with moderate primary hypertension?
p-value: p=<=0.02
In patients with moderate primary hypertension, losartan reduces left ventricular hypertrophy proportionally to blood pressure reduction but does not improve diastolic cardiac function.
In contrast to the well-recognized salutary effects of angiotensin-converting enzyme inhibition, the value of angiotensin II type I (ATl)-receptor blockade on left ventricular hypertrophy (LVH) is controversial. In addition, the data on the influence of this therapy on cardiac diastolic function are scarce. Thirty-nine patients with moderate primary hypertension, LVH, and normal systolic function received losartan, 50 to 100 mg daily. Transthoracic echocardiography was performed at baseline and after 6 months of treatment. Thirty-one patients completed and were included in the study (16 males, 61.1 +/- 1.0 years). The patients were divided into responders if mean blood pressure (BP) decreased > 5 mm Hg at the end of the study (20 patients) and non-responders (mean BP decrease < or = 5 mm Hg, 11 patients). The BP and the LVH were significantly reduced (systolic BP by 10.0%, diastolic BP 6.5%, mean BP 8.2%, left ventricular mass index [LVMI] 6.2%, interventricular septum 5.8%, posterior wall 3.0%) (p< or =0.02), attributed to the reduction of BP and LVH in responders; the LVH in non-responders did not alter with treatment. A significant correlation was noted between changes in BP and LVMI (r=0.60, p<0.001). The systolic cardiac function remained normal. The Doppler parameters usually used to assess the diastolic function of the LV (early diastolic filling velocity [E wave], late diastolic filling velocity [A wave], ratio of E/A waves, isovolumic relaxation time), which were abnormal at baseline, did not change with treatment. The size of the left atrium increased (p<0.05) at the end of the study. In conclusion, a 6-month course with losartan decreased BP and LVH. However, the LVH regression was rather associated with the reduction of the hemodynamic stimulus per se, than any trophic effect of the drug in the myocardium. The diastolic cardiac function remained abnormal with treatment.
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Zakynthinos et al. (2004) conducted an observational in Moderate primary hypertension with left ventricular hypertrophy (n=31). Losartan was evaluated on Blood pressure and left ventricular mass index (LVMI) (p=<=0.02). A 6-month course of losartan significantly reduced blood pressure and left ventricular mass index (P<=0.02), but did not improve abnormal diastolic cardiac function.
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