STATINS AND HEART FAILURE
Authors: Camelia C. DIACONU
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Chronic heart failure is a syndrome that appears in the evolution of a large majority of cardiovascular diseases. The main risk factors for chronic heart failure are arterial hypertension, coronary heart disease, diabetes mellitus, obesity, dyslipidemia etc. Over the years, researchers have been intensively studied new approaches and treatments to prevent the development of heart failure, to slow the evolution or to increase survival in patients with this syndrome. Dyslipidemia is a risk factor for chronic cardiovascular diseases, especially coronary heart disease. HMG-CoA reductase inhibitors (statins) are largely used for the treatment of hypercholesterolemia and coronary heart disease. Considering the beneficial effects of statins for the prevention and treatment of cardiovascular diseases, some studies suggested that these drugs can be beneficial in the context of chronic heart failure1-3. However, a “cholesterol paradox” has been recognized in patients with heart failure: although hypercholesterolemia is a risk factor for coronary artery disease, low cholesterol seems to be associated with a poor prognosis in patients with already installed heart failure, as compared with those without heart failure4-6. This is named “the cholesterol paradox”. There are multiple possible explanations for this paradox. Cholesterol is a marker of nutritional status in patients with mild to moderate heart failure. The congestive hepatopathy of patients with chronic heart failure may lead to decreased liver synthesis of cholesterol2. Also, the intestinal congestion in these patients may impair the absorption of cholesterol7. Studies have found that low serum cholesterol is secondary to the severity of the heart failure, as in other chronic diseases. However, it is not yet known if low cholesterol is the cause of a worse prognosis in heart failure or it is only a marker of more severe disease.
On one hand, statins have pleiotropic effects that could be beneficial in heart failure, such as stabilization of atheromatous plaques, inhibition of proinflammatory cytokine activity and even antiarrhythmic effect8. On the other hand, statins may be harmful in patients with heart failure, raising their susceptibility to infections, because lipoproteins remove bacterial endotoxins from the circulation9. Treatment with statins reduces the level of coenzyme Q10, which plays a role in the mitochondrial respiration and influences the contractile activity of the myocardium10. The serum level of coenzyme Q10 is inversely correlated to mortality of patients with heart failure10.
A meta-analysis of 15 studies including 45,110 patients with heart failure, from whom 22,471 were treated with statins, revealed that patients who received a statin had a lower all-cause mortality rate and rehospitalization for heart failure11. Two studies, CORONA and GISSI-HF, suggested that patients with systolic heart failure do not benefit from initiation of statin therapy12,13. CORONA trial suggested that rosuvastatin might be beneficial in patients with ischemic heart disease and systolic heart failure, with NT-proBNP value <868 pg/mL12. The negative results of these two studies are in contrast with numerous other small studies which have demonstrated the beneficial effects of statins in heart failure patients14. The clinical trials did not search if patients already taking a statin, who develop heart failure, benefit from continuation of statin treatment. Until further studies will clarify these issues, it seems reasonable that patients already on statin for another strong indication, developing heart failure, should continue the statin. Patients with systolic heart failure, with a left ventricle ejection fraction <35%, should receive a statin, according to CORONA trial results12. The decision to start a statin in patients with heart failure with preserved ejection fraction is usually based upon other indication, such as high LDL-cholesterol values or documented atherosclerotic vascular disease.