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Beneficial effects of add‐on hydrochlorothiazide in rats with myocardial infarction optimally treated with quinapril
Author(s) -
Westendorp Bart,
Schoemaker Regien G.,
Buikema Hendrik,
Zeeuw Dick,
Boomsma Frans,
Gilst Wiek H.,
Veldhuisen Dirk J.
Publication year - 2005
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2004.12.002
Subject(s) - quinapril , medicine , hydrochlorothiazide , myocardial infarction , cardiology , proteinuria , ace inhibitor , heart failure , endocrinology , urology , plasma renin activity , angiotensin converting enzyme , renin–angiotensin system , blood pressure , kidney
Background: The antihypertensive and renoprotective effects of ACE inhibitor (ACEi) therapy are enhanced by inducing a negative sodium balance. Whether this strategy also improves outcome of chronic ACEi treatment after myocardial infarction (MI) is unknown. Therefore, we investigated whether hydrochlorothiazide (HCTZ) or dietary sodium restriction further improves survival in ACEi‐treated rats with MI. Methods: MI was induced by coronary ligation. After 2 weeks rats were randomised to quinapril (QUI), HCTZ added to quinapril (QUI+HCTZ), or low sodium diet added to quinapril (QUI+LS). Survival was monitored for 62 weeks, after which left ventricular (LV) pressures were measured and blood for neurohumoral characterisation was collected. A separate group of rats, subjected to the same procedure, was evaluated after 35 weeks. Results: After 62 weeks, mortality was comparable in all groups. However, survival was improved by HCTZ until 35 weeks. This effect on survival was paralleled by decreased proteinuria and LV end‐diastolic pressures in QUI+HCTZ rats at 35, but not 62 weeks. Plasma renin activity was significantly decreased in QUI+HCTZ rats at 35 weeks. Contrary to HCTZ, LS added to QUI caused no benefit. Conclusions Adding HCTZ, but not LS, to quinapril improved survival, neurohumoral status, and proteinuria during the early chronic phase of experimental post‐MI LV dysfunction. Since no adverse effects were observed, HCTZ may safely be used to improve ACEi therapy.