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  • Title: Aldosterone receptor antagonists induce favorable cardiac remodeling in diastolic heart failure patients.
    Author: Orea-Tejeda A, Colín-Ramírez E, Castillo-Martínez L, Asensio-Lafuente E, Corzo-León D, González-Toledo R, Rebollar-González V, Narváez-David R, Dorantes-García J.
    Journal: Rev Invest Clin; 2007; 59(2):103-7. PubMed ID: 17633796.
    Abstract:
    BACKGROUND: Serum levels of aldosterone in heart failure are increased up to 20 times compared to normal subjects. After an acute myocardial infarction, aldosterone increases progressively as well as interstitial fibrosis and collagen synthesis from cardiac fibroblasts, forming a patchy heterogeneous interstitial collagen matrix that affects ventricular function. Even if angiotensin converting enzyme inhibitors (ACEI) or angiotensin II receptor antagonists (ARA) can reduce aldosterone levels early during treatment, they increase again after a 12 week treatment. The aim of this study was to evaluate the changes in structure and function of the left ventricle in symptomatic (NYHA I-III) diastolic heart failure patients receiving an aldosterone receptor antagonist. METHODS: Twenty-eight subjects with diastolic heart failure, on BB, ACEI and/ or ARA were randomized to receive spironolactone (group A) on a mean dose of 37.5 mg once a day (n = 14, age 63.7 +/- 21.6 years and body mass index, BMI 27.5 +/- 9.4), or not (group B, n = 14, Age 64.8 +/- 11.9, BMI 26.9 +/- 4.7). All patients were followed-up for a mean of 13.79 +/- 0.99 months. RESULTS: Group A showed a 42.8% ischemic origin of heart failure, while in group B was 55% (p = 0.2). No other co-morbidities were significativelly different among both groups. Mean percentage of changes by echocardiogram was as follows: Interventricular septum (IVS) -12.2 +/- 11% vs. 1.3 +/- 15.2 (p = 0.03), pulmonary systolic artery pressure (PSAP was 0.99 +/- 3.8% vs. 10.5 +/- 9.1, p = 0.05). Other parameters did not show statistically significant differences. CONCLUSION: Aldosterone receptor antagonists reduce or avoid increasing of PSAP and inducing a favorable remodeling of the left ventricle, especially in the IVS in diastolic heart failure patients.
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