Statins and Mortality Among Elderly Patients Hospitalized With Heart Failure

Foody, JoAnne M.; Shah, Rahman; Galusha, Deron; Masoudi, Frederick A.; Havranek, Edward P.; Krumholz, Harlan M.

doi:10.1161/circulationaha.105.591446

Cited by 140 publications

(65 citation statements)

References 37 publications

(30 reference statements)

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“…270,271 Furthermore, retrospective analyses of trials in patients with coronary artery disease but without a history of HF demonstrated a reduction in the risk of development of HF and HF hospitalizations in patients taking statins. 272 However, 2 large, prospective, randomized trials failed to confirm these beneficial effects of statins in patients with established HF.…”

Section: Treatment Of Hyperlipidemia In Hf For the Indication Of Hf Amentioning

confidence: 99%

Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure: A Scientific Statement From the American Heart Association

Bozkurt¹,

Aguilar²,

Deswal³

et al. 2016

Circulation

355

220

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CLINICAL STATEMENTS AND GUIDELINESfailed to show a significant reduction of SBP in patients with resistant hypertension. 81 Other strategies such as targeting excessive sympathetic nerve activity by carotid body denervation are awaiting clinical validation in the hypertension and HF populations. Drugs to Avoid in Patients With HFSeveral classes of drugs should be avoided in patients with HFrEF with a history of hypertension. Because of their negative inotropic properties and the increased likelihood of worsening HF symptoms, the nondihydropyridine calcium channel blockers such as diltiazem and verapamil should be avoided. 8 The dihydropyridine calcium channel blocker amlodipine appeared to be safe in patients with severe HFrEF in the PRAISE trial (Prospective Randomized Amlodipine Survival Evaluation), 82 as was felodipine. 73 In the current 2013 HF guidelines, most calcium channelblocking drugs except amlodipine are not recommended. 8Although clonidine is an effective antihypertensive agent, a similar centrally acting drug, moxonidine, was associated with increased mortality in patients with HF; thus, centrally acting norepinephrine-depleting agents may need to be avoided or used with caution in patients with HFrEF. 83In the ALLHAT trial, the α-blocker doxazosin arm of the trial was discontinued because of a 2-fold increase in the risk of developing HF compared with chlorthalidone treatment. 45 Although the ALLHAT study excluded patients with established HF and there are caveats about extrapolating these data to the management of hypertension in patients with established HF, the safety and efficacy of α-blockers in the management of patients with HF with hypertension are currently unclear. Potent direct-acting vasodilators such as minoxidil should also be avoided because of their renin-related salt and fluid-retaining effects. Nonsteroidal anti-inflammatory agents should be used with caution in these patients, given their effects on BP, volume status, and renal function. Treatment of Hypertension in Patients With HF With Preserved LVEFMost patients with HF and preserved LVEF (HFpEF), especially elderly women, have hypertension. A significant proportion of these patients also have evidence of LV hypertrophy, and some may have atrial dilatation, cardiac enlargement, and wall motion abnormalities without LV systolic dysfunction. Patients with HFpEF may respond particularly well to the treatment of hypertension with regression of hypertrophy 84 and improvement in filling pressures. 84,85 Most patients with HFpEF require treatment with cardiac medications for the comorbidities of hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation. The 2013 HF guidelines suggest that the use of β-blocking agents, ACE inhibitors, and ARBs in patients with hypertension is reasonable to control BP in patients with HFpEF. 8 The use of ARBs might also be considered to decrease hospitalizations for patients with HFpEF. recommendations Harmonized With Existing Guidelines for the recognition and Treatment of pa...

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Section: Treatment Of Hyperlipidemia In Hf For the Indication Of Hf Amentioning

confidence: 99%

Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure: A Scientific Statement From the American Heart Association

Bozkurt¹,

Aguilar²,

Deswal³

et al. 2016

Circulation

355

220

View full text Add to dashboard Cite

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“…What is surprising is that statins also improve heart function and survival in patients with non-ischemic heart failure [21][22][23][24]. Patients with severe heart failure without evidence of ischemic etiology have reduced all-cause mortality and are free from urgent transplantation on statin therapy [25].…”

Section: Clinical Trials With Statinsmentioning

confidence: 99%

Pleiotropic effects of statin therapy: molecular mechanisms and clinical results

Wang

Liu

Liao

2008

Trends in Molecular Medicine

537

394

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Statins inhibit the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which is required for cholesterol biosynthesis, and are beneficial in the primary and secondary prevention of cardiovascular disease. Most of the benefits of statin therapy are owing to the lowering of serum cholesterol levels. However, by inhibiting HMG-CoA reductase, statins can also inhibit the synthesis of isoprenoids, which are important lipid attachments for intracellular signaling molecules, such as Rho, Rac and Cdc42. Therefore, it is possible that statins might exert cholesterol-independent or 'pleiotropic' effects through direct inhibition of these small GTP-binding proteins. Recent studies have shown that statins might have important roles in diseases that are not mediated by cholesterol. Here, we review data from recent clinical trials that support the concept of statin pleiotropy and provide a rationale for their clinical importance. [6], have demonstrated the beneficial effects of statin therapy for primary and secondary prevention of cardiovascular disease. Because 60-70% of serum cholesterol is derived from hepatic synthesis and HMG-CoA reductase is the crucial, rate-limiting enzyme in the cholesterol biosynthetic pathway, inhibition of this enzyme by statins results in a dramatic reduction in circulating low-density lipoprotein (LDL)-cholesterol (Figure 1). In addition, reduction of LDL-cholesterol leads to upregulation of the LDL receptor and increased LDL clearance. The lowering of serum cholesterol levels is therefore thought to be the primary mechanism underlying the therapeutic benefits of statin therapy in cardiovascular disease [1]. Pleiotropy of statins: beyond cholesterol loweringStatins, however, might also exert cholesterol-independent or pleiotropic effects. By inhibiting the conversion of HMG-CoA to L-mevalonic acid, statins prevent the synthesis of important isoprenoids, such as farnesylpyrophosphate (FPP) and geranylgeranylpyrophosphate (GGPP), which are precursors of cholesterol biosynthesis [7] (Figure 1). These intermediates serve as important lipid attachments for the post-translational modification of proteins, such as nuclear lamins, Ras, Rho, Rac and Rap [8]. These isoprenylated proteins constitute approximately 2% of total cellular proteins [9]. Protein isoprenylation (see Glossary) enables proper subcellular localization and trafficking of intracellular proteins. Given that isoprenylated proteins might

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“…Similar results were found by another report looking at hospital discharge diagnosis and prescription data gathered on Medicare patients; those heart failure patients who filled their prescriptions for statins had significantly lower morality rates. 17 An association of statins with lower mortality rates was also noted in the EuroHeart Failure survey. 18 The Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) 15 was recently published.…”

Section: Reviewmentioning

confidence: 73%

Statins as Anti‐Arrhythmics: A Systematic Review Part II: Effects on Risk of Ventricular Arrhythmias

Abuissa

O’Keefe

Bybee

2009

Clinical Cardiology

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BackgroundRecent studies have demonstrated that statins may possess anti‐arrhythmic properties in addition to their lipid‐lowering effects.MethodsStudies which reported the association of statins with the incidence of ventricular arrhythmias were identified through a systematic review of the published literature.ResultsStatins have been associated with a significant reductions in ventricular arrhythmia in cardiomyopathy patients with an implantable cardioverter defibrillator, although randomized trials have not been completed.ConclusionsPublished data suggests that statins may possess anti‐arrhythmic properties that reduce the propensity for ventricular arrhythmias. Most of this data is observational; more randomized, placebo‐controlled trials are needed. Copyright © 2009 Wiley Periodicals, Inc.

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Statins and Mortality Among Elderly Patients Hospitalized With Heart Failure

Cited by 140 publications

References 37 publications

Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure: A Scientific Statement From the American Heart Association

Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure: A Scientific Statement From the American Heart Association

Pleiotropic effects of statin therapy: molecular mechanisms and clinical results

Statins as Anti‐Arrhythmics: A Systematic Review Part II: Effects on Risk of Ventricular Arrhythmias

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