Pravastatin therapy and the risk of stroke

White, Halina; Simes, R. John; Anderson, Neil E.

doi:10.1016/s1062-1458(00)00169-0

Cited by 20 publications

(17 citation statements)

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“…We assumed that patients who had a stroke or CHD event started statins immediately after the event occurred, which is consistent with clinical practice. 25,27,28 In other words, once L CHD = 1 or L S = 1, the action I was taken.…”

Section: Treatment Decisionsmentioning

confidence: 99%

Optimizing Statin Treatment Decisions for Diabetes Patients in the Presence of Uncertain Future Adherence

et al. 2011

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Section: Treatment Decisionsmentioning

confidence: 99%

Optimizing Statin Treatment Decisions for Diabetes Patients in the Presence of Uncertain Future Adherence

et al. 2011

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“…It has been shown that high concentrations of low‐density lipoprotein (LDL) cholesterol increase the risk of ischemic stroke, 2–4 whereas high concentrations of high‐density lipoprotein (HDL) cholesterol possibly decrease the risk of ischemic stroke, particularly small vessel stroke 2,5 . Furthermore, large‐scale randomized clinical trials have revealed that lowering cholesterol concentrations with statins reduces the risk of ischemic and overall stroke, 6–8 despite an increase in hemorrhagic stroke 8 . However, given high phenotypic and genetic correlation across different lipids and apolipoproteins, 9 it remains unclear whether one or more lipid‐related entities account for the observed associations between lipids and stroke.…”

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confidence: 99%

Circulating Lipoprotein Lipids, Apolipoproteins and Ischemic Stroke

Yuan

Tang

Zheng

et al. 2020

Annals of Neurology

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Objective: We conducted a Mendelian randomization (MR) study to disentangle the comparative effects of lipids and apolipoproteins on ischemic stroke. Methods: Single-nucleotide polymorphisms associated with low-and high-density lipoprotein (LDL and HDL) cholesterol, triglycerides, and apolipoprotein A-I and B (apoA-I and apoB) at the level of genomewide significance (p < 5 × 10 −8) in the UK Biobank were used as instrumental variables. Summary-level data for ischemic stroke and its subtypes were obtained from the MEGASTROKE consortium with 514,791 individuals (60,341 ischemic stroke cases, and 454,450 non-cases). Results: Increased levels of apoB, LDL cholesterol, and triglycerides were associated with higher risk of any ischemic stroke, large artery stroke, and small vessel stroke in the main and sensitivity univariable MR analyses. In multivariable MR analysis including apoB, LDL cholesterol, and triglycerides in the same model, apoB retained a robust effect (p < 0.05), whereas the estimate for LDL cholesterol was reversed, and that for triglycerides largely attenuated. Decreased levels of apoA-I and HDL cholesterol were robustly associated with increased risk of any ischemic stroke, large artery stroke, and small vessel stroke in all univariable MR analyses, but the association for apoA-I was attenuated to the null after mutual adjustment. Interpretation: The present MR study reveals that apoB is the predominant trait that accounts for the etiological basis of apoB, LDL cholesterol, and triglycerides in relation to ischemic stroke, in particular large artery and small vessel stroke. Whether HDL cholesterol exerts a protective effect on ischemic stroke independent of apoA-I needs further investigation.

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“…Thus he examines a NEJM article that claimed a 19 percent reduction in stroke risk in a population that took the statin Pravachol, compared to those who had been given a placebo. 19 However, as Abramson reminds us, the percent advantage represents the relative risk, but what matters is the absolute risk. This difference between relative and absolute risk is illustrated in Moynihan and Cassels's Selling Sickness, where they report a presentation given by a University of British Columbia therapeutics team, James McCormack and Bob Rango.…”

Section: Reexamining the Evidencementioning

confidence: 99%

The Other War on Drugs: The Pharmaceutical Industry, Evidence-Based Medicine, and Clinical Practice

Kushner¹

2007

J. Policy Hist.

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Over the past decade, evidence-based medicine (EBM) has become the standard for medical practice.1 Evidence-based practices have been established in general medicine and specialized fields; new evidence-based journals have been launched.2 Although its roots can be found in mid-nineteenth-century medical philosophy, contemporary EBM was largely developed by the clinical epidemiology program at McMaster University in 1992.3 According to the McMaster manifesto published in JAMA, EBM “deemphasizes intuition, unsystematic clinical experience, and pathophysiologic rationale as sufficient grounds for clinical decision-making, and stresses the examination of evidence from clinical research.”4 The most frequently cited definition of EBM is reliance on the “conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients,” based on an integration of “individual clinical expertise with the best available external clinical evidence from systematic research.”5 However, as Stefan Timmermans and Aaron Mauck recently observed, EBM “is loosely used and can refer to anything from conducting a statistical meta-analysis of accumulated research to promoting randomized clinical trials, to supporting uniform reporting styles for research, to a personal orientation toward critical self-evaluation.”6

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Pravastatin therapy and the risk of stroke

Cited by 20 publications

References 0 publications

Optimizing Statin Treatment Decisions for Diabetes Patients in the Presence of Uncertain Future Adherence

Optimizing Statin Treatment Decisions for Diabetes Patients in the Presence of Uncertain Future Adherence

Circulating Lipoprotein Lipids, Apolipoproteins and Ischemic Stroke

The Other War on Drugs: The Pharmaceutical Industry, Evidence-Based Medicine, and Clinical Practice

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