MRC/BHF Heart Protection Study

Violi, Francesco; Micheletta, Fausta; Luliano, L.

doi:10.1016/s0140-6736(02)11691-6

Cited by 12 publications

(4 citation statements)

References 4 publications

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“…In primary and secondary prevention studies of populations with multiple atherosclerotic risks or with coronary artery disease, statin use has significantly reduced the risk of cardiovascular outcomes including that of IS [27,28]. A similar benefit of statin drugs has also been shown in patients with previous IS/TIA.…”

Section: Discussionmentioning

confidence: 99%

Optimal Medical Management Reduces Risk of Disease Progression and Ischemic Events in Asymptomatic Carotid Stenosis Patients: A Long-Term Follow-Up Study

Shah¹,

Masoomi²,

Thapa³

et al. 2017

Cerebrovasc Dis

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Background and Purpose: To assess the effect of optimal medical management including atherosclerotic risk factor control on ischemic stroke (IS), transient ischemic attack (TIA), carotid revascularization (CRV), and progression of severity of carotid stenosis (PSCS) in patients with asymptomatic carotid artery stenosis (ACAS). Methods: We conducted a retrospective analysis of patients with ACAS (who had at least 3 serial carotid duplex ultrasounds) for incidence of IS, TIA, and PSCS. Results: Eight hundred sixty-four patients with a mean follow-up duration of 79 ± 36 months were included. IS/TIA and CRV occurred in 12.2% of the patients and PCSS was observed in 21.5% vessels. On univariate analysis it was found that low-density lipoprotein (LDL) levels >100 mg/dL, no statin or low-potency statins, average systolic blood pressure (SBP) ≥140 mm Hg and/or diastolic blood pressure (DBP) ≥90 mm Hg and history of smoking were predictors of the combined endpoint of IS/TIA/CRV and PSCS. On multivariate analysis, it was found that LDL >100 mg/dL, no statin or low-potency statin, SBP ≥140 mm Hg and/or DBP ≥90 mm Hg, and Hx of smoking were independent predictors of PSCS. Similarly no statin or low-potency statin, SBP ≥140 mm Hg and/or DBP ≥90 mm Hg, Hx of atrial fibrillation/flutter, Hx of chronic kidney disease, and PSCS were independent predictors of IS/TIA. No statin or low-potency statin, SBP ≥140 mm Hg and/or DBP ≥90 mm Hg, diabetes mellitus, baseline carotid artery stenosis ≥70%, and PSCS were found to be independent predictors of combined endpoint IS/TIA and CRV. Conclusion: Intensive medical therapy in the patients with ACAS results in lower incidence of IS/TIA, CRV, and PSCS with a significant incremental beneficial effect.

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Section: Discussionmentioning

confidence: 99%

Optimal Medical Management Reduces Risk of Disease Progression and Ischemic Events in Asymptomatic Carotid Stenosis Patients: A Long-Term Follow-Up Study

Shah¹,

Masoomi²,

Thapa³

et al. 2017

Cerebrovasc Dis

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“…For example, in 1975 we had good scientific evidence for antihypertensive therapy in primary stroke prevention 6,7 and were nearing the completion of a secondary prevention study showing the effectiveness of aspirin. 8 At present, we have scientific evidence concerning the effectiveness of 4 antiplatelet drugs for secondary stroke prevention, 9 -13 warfarin for primary and secondary stroke prevention, [12][13][14][15][16] statins for primary stroke prevention, [17][18][19][20] antihypertensive therapy for primary and secondary stroke prevention, 21,22 red blood cell transfusions in sickle cell disease for primary stroke prevention, 23 and carotid endarterectomy for both secondary and primary stroke prevention. 24 -27 Comparison of the effectiveness of carotid stenting with carotid endarterectomy is a very active area of investigation.…”

Section: Stroke Preventionmentioning

confidence: 99%

William M. Feinberg Lecture: Stroke Therapy in the Year 2025

Broderick

2004

Stroke

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Background-More than 700 000 strokes occurred in the United States during 2002, of which approximately 500 000 are first-ever strokes and 200 000 recurrent strokes. If we would decrease the enormous burden of stroke throughout the world, we first need to know the barriers that we have to overcome. These are quite similar to the barriers that we have tried to surmount during the last 25 years. Stroke Prevention-We have developed many successful primary and secondary therapies to prevent stroke over the past 25 years and have begun to understand some of the genetic risk factors underlying stroke. Yet, the incidence rate of stroke in Rochester, Minn, remained unchanged from 1975 to the mid-1990s, and mortality rates for Ohio have changed little for men, women, blacks, and whites over the past decade. The primary reason that we have made little progress in decreasing the burden of stroke is that we have made little progress in modifying the primary risk factors for stroke in the population. Other barriers of improved stroke prevention in the future include costs of therapy and aging of blood vessels and brain, which is the most important risk factor for stroke. Acute Stroke-Breakthroughs in acute stroke treatment are likely to follow the steps of cardiology with the primary focus for ischemic stroke on the restoration of oxygenated blood flow to ischemic brain as quickly as possible. To improve acute stroke therapy in the year 2025, we need to have more focused messages sent to the lay public about stroke warning signs, better and safer methods to open arteries quickly, truly effective neuroprotection in the setting of reperfusion, regional organization for acute stroke therapy, and large randomized trials to find clinically important but smaller benefits. A scientifically proven treatment for treatment of acute intracerebral hemorrhage is another major goal. Recovery After Stroke-Brain recovery after stroke is the area of scientific discovery with the largest potential for advances far into the next century. Obstacles that block effective therapies in the recovery from stroke include the extent of initial injury from stroke, the brain plasticity of a given patient, and, most importantly, understanding the "neural code"-how the brain is organized and how cells communicate with one another.

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“…HMG-CoA reductase inhibitors (statins) are commonly used for treatment of dyslipidemia and have been shown to be the most effective available agents for decreasing LDL-C 24–26. In addition, statins have been shown to have a variable response in their ability to reduce the number of small, dense LDL particles and increase their size 27–29…”

Section: Introductionmentioning

confidence: 99%

Combination of niacin extended-release and simvastatin results in a less atherogenic lipid profile than atorvastatin monotherapy

Insull¹,

Tóth²,

Superko³

et al. 2010

VHRM

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Objective:To compare the effects of combination niacin extended-release + simvastatin (NER/S) versus atorvastatin alone on apolipoproteins and lipid fractions in a post hoc analysis from SUPREME, a study which compared the lipid effects of niacin extended-release + simvastatin and atorvastatin in patients with hyperlipidemia or mixed dyslipidemia.Patients and methods:Patients (n = 137) with dyslipidemia (not previously receiving statin therapy or having discontinued any lipid-altering treatment 4–5 weeks prior to the study) received NER/S (1000/40 mg/day for four weeks, then 2000/40 mg/day for eight weeks) or atorvastatin 40 mg/day for 12 weeks. Median percent changes in apolipoprotein (apo) A-1, apo B, and the apo B:A-I ratio, and nuclear magnetic resonance lipoprotein subclasses from baseline to week 12 were compared using the Wilcoxon rank-sum test and Fisher’s exact test.Results:NER/S treatment produced significantly greater percent changes in apo A-I and apo B:A-I, and, at the final visit, apo B < 80 mg/dL was attained by 59% versus 33% of patients, compared with atorvastatin treatment (P = 0.003). NER/S treatment resulted in greater percent reductions in calculated particle numbers for low-density lipoprotein (LDL, 52% versus 43%; P = 0.022), small LDL (55% versus 45%; P = 0.011), very low-density lipoprotein (VLDL) and total chylomicrons (63% versus 39%; P < 0.001), and greater increases in particle size for LDL (2.7% versus 1.0%; P = 0.007) and VLDL (9.3% versus 0.1%; P < 0.001), compared with atorvastatin.Conclusion:NER/S treatment significantly improved apo A-I levels and the apo B:A-I ratio, significantly lowered the number of atherogenic LDL particles and VLDL and chylomicron particles, and increased the mean size of LDL and VLDL particles, compared with atorvastatin.

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MRC/BHF Heart Protection Study

Cited by 12 publications

References 4 publications

Optimal Medical Management Reduces Risk of Disease Progression and Ischemic Events in Asymptomatic Carotid Stenosis Patients: A Long-Term Follow-Up Study

Optimal Medical Management Reduces Risk of Disease Progression and Ischemic Events in Asymptomatic Carotid Stenosis Patients: A Long-Term Follow-Up Study

William M. Feinberg Lecture: Stroke Therapy in the Year 2025

Combination of niacin extended-release and simvastatin results in a less atherogenic lipid profile than atorvastatin monotherapy

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