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Atorvastatin improves cardiac function and remodeling in chronic non-ischemic heart failure: A clinical and pre-clinical study
Author(s) -
Ibrahim Elmadbouh,
Magda Mansour,
Mohamed Nabeh,
Walaa Faried,
Ahmed Abdelsabour,
Adel Omar
Publication year - 2015
Publication title -
the egyptian heart journal /the egyptian heart journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.212
H-Index - 9
eISSN - 2090-911X
pISSN - 1110-2608
DOI - 10.1016/j.ehj.2014.11.003
Subject(s) - medicine , atorvastatin , heart failure , ejection fraction , cardiology , cardiac function curve , troponin complex , doxorubicin , troponin , myocardial infarction , chemotherapy
AimsThe aim was to evaluate the cardio-protective effect of atorvastatin in combination with standard chronic heart failure (CHF) therapy that might improve cardiac function, remodeling, and further delay the progression of CHF in patients and rats.Methods and resultsCHF patients (n=20 per group) with left ventricular ejection fraction (LV-EF) <45% were randomized into: standard anti-failure treatment alone (controls) and standard anti-failure treatment plus atorvastatin (40mg/day) for 6weeks. After 6weeks, the patients were assessed using echocardiography. Laboratory evaluation for lipid profiles, high sensitive C-reactive protein (hs-CRP), cardiac troponin-T (cTnT) and malondialdehyde (MDA) were performed in all patients. In parallel, rats (n=10 per group) received treatment for 4weeks and were divided as follows: saline treated (control, 1ml intraperitoneal, IP), doxorubicin treated (2.5mg/kg, IP), atorvastatin–doxorubicin treated (10mg/kg, orally), and digoxin–doxorubicin treated (0.02mg/kg, orally). The same laboratory analysis including histopathology of heart tissues was performed on the rats.In patients, atorvastatin improved heart function (increased LV-EF%, LV-fraction shorting (LV-FS%), and E/A velocity ratio; decreased LV-end diastolic diameter (LV-EDD) and LV-end systolic diameter (LV-ESD)) and significantly reduced serum lipid profiles, cTnT, hs-CRP and MDA versus patient controls. In rats, atorvastatin improved signs of CHF, systolic blood pressure, reduced serum lipid profiles, cTnT, hs-CRP and tissue MDA; less cardiac necrosis and fibrosis with enhancement of neo-vascularization versus other doxorubicin-treated rats.ConclusionsAtorvastatin with standard CHF therapy improved cardiac function and remodeling. Cardio-protective “pleiotropic” actions of atorvastatin are anti-inflammatory, anti-fibrotic and anti-oxidative. Thus, atorvastatin has a potential therapeutic value in the management of CHF patients

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