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Effect of Losartan on left ventricular diastolic function in patients with nonobstructive hypertrophic cardiomyopathy
Aloir Queiroz Araujo1, Edmundo Arteaga, Barbara Maria Ianni
1Cardiomyopathies Division Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil. aloirqueiroz@cardiol.br
Insights
Losartan treatment improved left ventricular diastolic function in patients with hypertrophic cardiomyopathy (HC). Six months of losartan therapy reduced left atrial size and NT-pro-BNP levels, indicating better heart function.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Diastolic dysfunction is a key feature of hypertrophic cardiomyopathy (HC), driven by myocardial hypertrophy and fibrosis.
- Angiotensin II contributes to cardiac hypertrophy and fibrosis; blocking its receptors shows promise in reversing these effects.
Purpose of the Study:
- To evaluate the short-term effects of losartan on left ventricular (LV) diastolic dysfunction in nonobstructive HC.
- To compare the efficacy of losartan versus no treatment in HC patients over six months.
Main Methods:
- A 6-month study involving 20 patients with nonobstructive HC treated with losartan 100 mg/day.
- A control group of 10 HC patients received no treatment.
- Echocardiography and plasma NT-pro-BNP levels were used for evaluation.
Main Results:
- The losartan group showed a significant decrease in left atrial diameter and improved diastolic function (increased Ea, decreased E/Ea ratio).
- Plasma NT-pro-BNP levels significantly decreased in the losartan group.
- No significant changes in LV wall or cavity dimensions were observed in either group.
- A correlation was found between NT-pro-BNP changes and E/Ea ratio improvements.
Conclusions:
- Losartan effectively improved left ventricular diastolic function in patients with nonobstructive HC over a 6-month period.
- The findings suggest losartan as a potential therapeutic option for managing diastolic dysfunction in HC.
Abstract:
In hypertrophic cardiomyopathy (HC), diastolic dysfunction of the left ventricle is a prominent feature caused by myocardial hypertrophy and fibrosis. Angiotensin II has trophic and profibrotic effects on the heart, and the blockade of angiotensin II receptors reverses hypertrophy and fibrosis in human cardiac diseases and in animal HC. This study investigated the short-term (6 months) effects of losartan 100 mg/day in 20 patients with nonobstructive HC, with an emphasis on left ventricular (LV) diastolic dysfunction, compared with 10 patients with HC who were not treated. At the final evaluation, significant changes were observed in the losartan group: a left atrial diameter decrease (p<0.0001), a tissue Doppler early (Ea) mitral annulus diastolic velocity increase (p=0.003) and an E/Ea ratio decrease (p=0.0002), and a significant decrease in plasma levels of the aminoterminal fragment of pro-brain natriuretic peptide (NT-pro-BNP) from a median of 860 to 606 pg/ml (p=0.001). A significant correlation was found between percentage changes in NT-pro-BNP and the E/Ea ratio from baseline to 6 months (r=0.61, p=0.002). In the 2 groups, echocardiographic LV wall and cavity measures did not change. In conclusion, in selected patients with nonobstructive HC, losartan during a 6-month period improved LV diastolic function.
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