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Published on: April 8, 2013
Atorvastatin improves left ventricular systolic function and serum markers of inflammation in nonischemic heart
Srikanth Sola1, Muhammad Q S Mir, Stamatios Lerakis
1Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia 30303, USA.
Insights
Atorvastatin improved heart function and reduced harmful heart remodeling in patients with nonischemic heart failure. This statin therapy also decreased inflammatory markers, suggesting a potential mechanism for its benefits.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Heart failure (HF) remains a significant cause of morbidity and mortality despite therapeutic advancements.
- Nonischemic forms of cardiomyopathy present unique challenges in treatment and management.
- Understanding the role of inflammation in HF pathophysiology is crucial for developing novel therapies.
Purpose of the Study:
- To investigate the impact of atorvastatin on left ventricular (LV) systolic function in patients with nonischemic heart failure.
- To assess the effect of atorvastatin on vascular markers of inflammation and echocardiographic parameters.
- To explore potential mechanisms by which statins may benefit patients with nonischemic heart failure.
Main Methods:
- A double-blind, randomized trial involving 108 patients with nonischemic HF and LVEF ≤35%.
- Participants received either atorvastatin 20 mg/day or placebo for 12 months.
- Echocardiography assessed LVEF, LVEDD, and LVESD; serum inflammatory and oxidation markers were measured.
Main Results:
- Atorvastatin significantly increased LVEF and reduced LV end-diastolic diameter (LVEDD) and LV end-systolic diameter (LVESD).
- Placebo group showed a decline in LVEF and an increase in LV dimensions.
- Atorvastatin treatment led to increased erythrocyte superoxide dismutase (E-SOD) activity and reduced serum levels of hs-CRP, IL-6, and TNF-alpha RII.
Conclusions:
- Atorvastatin therapy improves LVEF and attenuates adverse LV remodeling in patients with nonischemic HF.
- The observed reduction in inflammatory markers suggests a key mechanism for statin's beneficial effects.
- These findings support the use of statins as an adjunctive therapy in managing nonischemic heart failure.
Objectives:
This study examined the effect of statin therapy on vascular markers of inflammation and echocardiographic findings in patients with nonischemic forms of cardiomyopathy.
Background:
Despite advances in therapy, morbidity and mortality from heart failure (HF) remain high. We wished to determine whether treatment with atorvastatin affects left ventricular (LV) systolic function and markers of inflammation in patients with nonischemic HF.
Methods:
A total of 108 patients with nonischemic HF and a left ventricular ejection fraction (LVEF) < or =35% were randomized to either atorvastatin 20 mg/day or placebo in a double-blinded fashion for a 12-month period. The LVEF and LV end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were determined by echocardiography. Serum markers of inflammation and oxidation were also measured.
Results:
The LVEF increased from 0.33 +/- 0.05 to 0.37 +/- 0.04 (p = 0.01) in the atorvastatin group over the 12-month follow-up period, whereas those patients in the placebo group experienced a decline in ejection fraction during the same time period. In addition, LVEDD was reduced from 57.1 +/- 5.9 mm to 53.4 +/- 5.1 mm (p = 0.007) and LVESD was reduced from 42.4 +/- 3.8 mm to 39.1 +/- 3.8 mm (p = 0.02) in the cohort of patients treated with atorvastatin; these dimensions increased in the placebo group. There was an increase in erythrocyte superoxide dismutase (E-SOD) activity, and there were significant reductions in serum levels of high sensitivity C-reactive protein, interleukin-6 (IL-6), and tumor necrosis factor-alpha receptor II (TNF-alpha RII) in the atorvastatin group.
Conclusions:
The use of atorvastatin in patients with nonischemic HF improves LVEF and attenuates adverse LV remodeling. The effects on soluble levels of several inflammatory markers with atorvastatin suggest, in part, mechanisms by which statins might exert their beneficial effects in nonischemic HF.
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