Statin Therapy and Risks for Death and Hospitalization in Chronic Heart Failure

Go, Alan S.; Lee, Wendy Y.; Yang, Jingrong; Lo, Joan C.; Gurwitz, Jerry H.

doi:10.1001/jama.296.17.2105

Cited by 256 publications

(177 citation statements)

References 47 publications

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“…50 Targeted medication use before admission was ascertained on the basis of dispensing information from ambulatory prescriptions found in health plan pharmacy databases using previously described and validated algorithms and methods. [51][52][53][54] …”

Section: Covariatesmentioning

confidence: 99%

Elevated BP after AKI

Hsu

Hsu²,

Yang

et al. 2016

Journal of the American Society of Nephrology

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151

111

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The connection between AKI and BP elevation is unclear. We conducted a retrospective cohort study to evaluate whether AKI in the hospital is independently associated with BP elevation during the first 2 years after discharge among previously normotensive adults. We studied adult members of Kaiser Permanente Northern California, a large integrated health care delivery system, who were hospitalized between 2008 and 2011, had available preadmission serum creatinine and BP measures, and were not known to be hypertensive or have BP.140/90 mmHg. Among 43,611 eligible patients, 2451 experienced AKI defined using observed changes in serum creatinine concentration measured during hospitalization. Survivors of AKI were more likely than those without AKI to have elevated BP-defined as documented BP.140/90 mmHg measured during an ambulatory, nonemergency department visit-during follow-up (46.1% versus 41.2% at 730 days; P,0.001). This difference was evident within the first 180 days (30.6% versus 23.1%; P,0.001). In multivariable models, AKI was independently associated with a 22% (95% confidence interval, 12% to 33%) increase in the odds of developing elevated BP during follow-up, with higher adjusted odds with more severe AKI. Results were similar in sensitivity analyses when elevated BP was defined as having at least two BP readings of .140/90 mmHg or those with evidence of CKD were excluded. We conclude that AKI is an independent risk factor for subsequent development of elevated BP. Preventing AKI during a hospitalization may have clinical and public health benefits beyond the immediate hospitalization.

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Section: Covariatesmentioning

confidence: 99%

Elevated BP after AKI

Hsu

Hsu²,

Yang

et al. 2016

Journal of the American Society of Nephrology

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151

111

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“…34,[37][38][39][40] Coexisting illnesses of interest included diabetes mellitus, hypertension, coronary heart disease, heart failure, and chronic lung or liver disease. Body mass index category 41 and tobacco history were ascertained from ambulatory visit databases.…”

Section: Covariatesmentioning

confidence: 99%

“…Longitudinal medication use was ascertained from ambulatory pharmacy records for common medications potentially associated with cancer risk using previously described algorithms. 37,42 These medications included oral antihypertensive agents 21,22 (b-blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, a-blockers, calcium channel blockers, and aldosterone receptor antagonists), nonstatin lipid-lowering agents, statins, 24,25 and 5-a reductase inhibitors. 23,26 Analytic Approach Analyses were performed using SAS software, version 9.2 (SAS Institute, Cary, NC).Baseline characteristics were compared across GFR categories using ANOVAs for continuous variables and chi-squared tests for categorical variables.…”

Section: Covariatesmentioning

confidence: 99%

CKD and the Risk of Incident Cancer

Lowrance

Ordoñez

Udaltsova

et al. 2014

Journal of the American Society of Nephrology

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231

183

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Previous studies report a higher risk of cancer in patients with ESRD, but the impact of less severe CKD on risk of cancer is uncertain. Our objective was to evaluate the association between level of kidney function and subsequent cancer risk. We performed a retrospective cohort study of 1,190,538 adults who were receiving care within a health care delivery system, had a measurement of kidney function obtained between 2000 and 2008, and had no prior cancer. We examined the association between level of eGFR and the risk of incident cancer; the primary outcome was renal cancer, and secondary outcomes were any cancer and specific cancers (urothelial, prostate, breast, lung, and colorectal). During 6,000,420 person-years of follow-up, we identified 76,809 incident cancers in 72,875 subjects. After adjustment for time-updated confounders, lower eGFR (in milliliters per minute per 1.73 m 2 ) was associated with an increased risk of renal cancer (adjusted hazard ratio [HR], 1.39; 95% confidence interval [95% CI], 1.22 to 1.58 for eGFR=45-59; HR, 1.81; 95% CI, 1.51 to 2.17 for eGFR=30-44; HR, 2.28; 95% CI, 1.78 to 2.92 for eGFR,30). We also observed an increased risk of urothelial cancer at eGFR,30 but no significant associations between eGFR and prostate, breast, lung, colorectal, or any cancer overall. In conclusion, reduced eGFR is associated with an independently higher risk of renal and urothelial cancer but not other cancer types.

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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

538

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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Statin Therapy and Risks for Death and Hospitalization in Chronic Heart Failure

Abstract: Among adults diagnosed with heart failure who had no prior statin use, incident statin use was independently associated with lower risks of death and hospitalization among patients with or without coronary heart disease.

Cited by 256 publications

References 47 publications

Elevated BP after AKI

Elevated BP after AKI

CKD and the Risk of Incident Cancer

Pleiotropic effects of statin therapy: molecular mechanisms and clinical results

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