Cholesterol Reduction and Stroke Occurrence: An Overview of Randomized Clinical Trials

Mascio, Rocco Di; Marchioli, Roberto; Tognoni, Gianni

doi:10.1159/000016035

Cited by 89 publications

(33 citation statements)

References 51 publications

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“…[1][2][3][4][5][6] Treatment with statins should be initiated in all patients with an ischemic stroke or transient ischemic attack (TIA) who have evidence of or high risk for developing CAD over the next years if their cholesterol concentration is Ͼ5.0 mmol/L or low-density lipoprotein cholesterol (LDL-C) exceeds 3.0 mmol/L. [7][8][9][10][11][12][13] In patients with CAD, the rate of lipid evaluation is low, and statins are underused.…”

mentioning

confidence: 99%

Determination of Lipid Profiles and Use of Statins in Patients With Ischemic Stroke or Transient Ischemic Attack

Lalouschek

Lang

Greisenegger

et al. 2003

Stroke

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Background and Purpose-Statins reduce the risk of myocardial infarction and stroke in patients with vascular disease.Inappropriate serum lipid determination and underuse of statins have been documented in patients with coronary artery disease. Evaluation of hyperlipidemia and treatment with statins in patients with recent ischemic cerebrovascular eventshave not yet been investigated. Methods-We determined the frequency of total cholesterol (TC) and low-density lipoprotein cholesterol measurements and the use of statins in a multicenter prospective cohort study of 1743 patients with acute ischemic stroke or transient ischemic attack (TIA). Using multivariate logistic regression analysis, we determined the influence of several clinical variables on lipid measurements and the prescription of statins at hospital discharge. Results-TC was measured in 90% and low-density lipoprotein cholesterol was measured in 48% of the patients.Differences between the centers accounted for most of the observed variability in a multivariate model. Statin prescription also varied widely between the centers. The prescription of a statin at discharge was most strongly associated with statin intake before the event and with increasing TC levels; elderly patients received statins less often. Coronary artery disease, peripheral artery disease, and other manifestations of atherosclerosis were not independently associated with the use of statins; 68% of the patients with manifest atherosclerosis and TC levels Ͼ200 mg/dL were discharged without a statin. Conclusions-The

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mentioning

confidence: 99%

Determination of Lipid Profiles and Use of Statins in Patients With Ischemic Stroke or Transient Ischemic Attack

Lalouschek

Lang

Greisenegger

et al. 2003

Stroke

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“…[86][87][88] For primary prevention, an earlier study of pravastatin did not demonstrate a reduced risk of stroke among hyperlipidemic subjects. 89 However, atorvastatin was recently shown to decrease the risk of stroke among patients not traditionally deemed hyperlipidemic (total cholesterol < 6.5 mmol/L) but who had multiple vascular risk factors.…”

Section: Lipid-lowering Agentsmentioning

confidence: 99%

Current and future concepts in stroke prevention

O’Rourke

Dean

Akhtar

et al. 2004

Canadian Medical Association Journal

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STROKE IS A MAJOR CAUSE OF MORBIDITY and mortality in an aging population. The current understanding of the pathophysiology of atherosclerotic diseases, the most common cause of stroke, and the evidence for existing therapeutic interventions for the prevention of stroke are presented. Specifically, we review the evidence for antiplatelet agents, anticoagulants, antihypertensive medications, lipidlowering agents and carotid endarterectomy for stroke prevention. primary preventive measure, antiplatelet agents do not reduce the risk of ischemic stroke among patients without vascular disease. They are associated with an increased risk of intracranial hemorrhage (odds ratio [OR] 1.35, 95% confidence interval [CI] 0.88-2.10) 23 and major noncerebral hemorrhage (OR 1.73, 95% CI 1.14-2.63 ). 24 The benefits of ASA in the secondary prevention of stroke have been well documented in the period immediately after a stroke 25 (Table 1). Long-term antiplatelet treatment after stroke shows an even more impressive reduction of 25 nonfatal strokes and 36 serious vascular events per 1000 treated over a 29-month follow-up period. 25 There appears to be no difference in efficacy between low (50 mg) and higher doses (up to 1500 mg) of ASA. 29,30 The combination of dipyridamole and ASA has been shown to reduce the relative risk of recurrent stroke compared with ASA alone 26 (Table 1). Dipyridamole inhibits platelet aggregation by increasing levels of cyclic adenosine monophosphate and cyclic guanosine monophosphate. The limiting factor in the use of the ASAdipyridamole combination is the latter's potential effects on coronary perfusion. Dipyridamole can cause coronary vasodilation, which results in increased blood flow to nonstenosed coronary arteries. The result is that myocardial ischemia may be provoked during exercise. As such, the current American College of Cardiology/American Heart Association guidelines recommend that dipyridamole not be used in patients with chronic stable angina. 31 However, this recommendation was based on shortacting dipyridamole, which also reduced myocardial ischemia in a similar number of patients in the study quoted by these guidelines. 32 With the use of sustained-release dipyridamole, no increase in cardiac events was observed in subjects with prior coronary artery disease. 33 Thienopyridines block adenosine-diphosphate-mediated platelet aggregation. Ticlopidine was the first of this class of drug to be studied for stroke prevention. One clinical trial demonstrated that patients treated with ticlopidine had similar rates of stroke as those treated with ASA 28 (Table 1). However, serious granulocytopenia associated with ticlo- Leukocytes localize in the earliest atherosclerotic lesions, binding to vascular cell adhesion molecules (VCAM-1) on the vascular endothelium and migrating into the intima. This initiates and perpetuates a local inflammatory response. Monocytes mature into lipid-scavenging macrophages and subsequently foam cells. T-lymphocytes express inflammatory cytokines, which cont...

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“…Six metaanalyses, including the above studies, revealed a reduction of about 25% in stroke as a result of statin use [42][43][44][45][46][47], but this information mainly comes from secondary prevention studies. Interestingly, these meta-analyses confirm that, although stroke incidence was reduced by 25%, stroke mortality was not altered by statin treatment.…”

Section: Total Cholesterolmentioning

confidence: 99%

“…Of the six meta-analyses of cholesterol reduction cited above, only three have analysed primary and secondary prevention trials separately [43,44,47]; these revealed a non-significant 15%, 20%, and 4% 1 reduction in stroke, but none of the three included the last trial of primary prevention with 6605 randomised subjects [49]. Moreover, the trials on primary prevention were designed specifically to detect a reduction in coronary heart disease [39,49] or in carotid intimal medial thickening [50][51][52].…”

Section: Total Cholesterolmentioning

confidence: 99%

Approaches to prevention of a first stroke

2001

Swiss Arch Neurol Psychiatr

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Stroke is one of the leading causes of mortality and morbidity worldwide. Despite recent important advances in therapeutic approaches, only a very small proportion of patients receive treatment and treatment is still far from satisfactory. Several conditions and life-style factors have been identified as risk factors for stroke, and strategies aimed at modifying these are the best way to reduce the burden imposed by the disease.We review the available data on the effectiveness of modifying risk factors by means of life-style changes, drugs, and surgery in the primary prevention of stroke. Identification of new risk factors and of markers for individuals at high risk is essential for more efficacious prevention.

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Cholesterol Reduction and Stroke Occurrence: An Overview of Randomized Clinical Trials

Cited by 89 publications

References 51 publications

Determination of Lipid Profiles and Use of Statins in Patients With Ischemic Stroke or Transient Ischemic Attack

Determination of Lipid Profiles and Use of Statins in Patients With Ischemic Stroke or Transient Ischemic Attack

Current and future concepts in stroke prevention

Approaches to prevention of a first stroke

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