Hyperlipidemias: Sacco RL

Adams RJ, Albers G, Alberts MJ, Benavente O, Furie K, Goldstein LB, Gorelick P, Halperin J, Harbaugh R, Johnston SC, Katzan I, Kelly-Hayes M, Kenton EJ, Marks M, Sacco RL, Schwamm LH, Anonymous00005, Anonymous00006. · No affiliation provided · Stroke. · Pubmed #18322260 links to  free full text

This publication has no abstract.

Goldstein LB, Adams R, Becker K, Furberg CD, Gorelick PB, Hademenos G, Hill M, Howard G, Howard VJ, Jacobs B, Levine SR, Mosca L, Sacco RL, Sherman DG, Wolf PA, del Zoppo GJ. · No affiliation provided · Stroke. · Pubmed #11136952 links to  free full text

This publication has no abstract.

Goldstein LB, Adams R, Becker K, Furberg CD, Gorelick PB, Hademenos G, Hill M, Howard G, Howard VJ, Jacobs B, Levine SR, Mosca L, Sacco RL, Sherman DG, Wolf PA, del Zoppo GJ. · No affiliation provided · Circulation. · Pubmed #11136703 links to  free full text

This publication has no abstract.

Rincon F, Sacco RL. · Department of Neurology, The Neurological Institute of New York, Columbia University Medical Center, New York, NY 10034, USA. · J Cardiovasc Nurs. · Pubmed #18158505 No free full text.

Abstract: Stroke is the most common life-threatening neurological disorder. Based on limited acute therapies, clinicians have opted to focus on preventive strategies to limit its recurrence. Targets for prevention include modifiable risk factors such as hypertension, diabetes mellitus, dyslipidemia, cigarette smoking, obesity, alcohol use, and physical inactivity among others. The American Stroke Association and American Heart Association guideline for the secondary prevention of stroke published in 2006 provides comprehensive and timely evidence-based recommendations on the prevention of ischemic stroke among survivors of stroke or transient ischemic attack. This guideline helps healthcare providers who have arrived at a potential explanation of the cause of stroke in an individual patient to select therapies that reduce the risk of recurrent events and other vascular events. The purpose of this review is to highlight the recently published American Stroke Association/American Heart Association guidelines for the secondary prevention of stroke.

Sacco RL, Liao JK. · Neurological Institute, Columbia University College of Physicians and Surgeons, Mailman School of Public Health, New York, NY, USA. · Nat Clin Pract Cardiovasc Med. · Pubmed #16258569 No free full text.

Abstract: Stroke is the third leading cause of death in the US and a common cause of long-term disability worldwide. Ischemic strokes, which are often atherothrombotic, account for more than 80% of all strokes. Current stroke prevention focuses on optimizing the treatment of modifiable risk factors, such as hypertension, diabetes and dyslipidemia. The epidemiologic association between serum cholesterol levels and adjusted stroke rates is not as strong as the link between serum cholesterol levels and coronary heart disease. Clinical trials of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins), which are potent inhibitors of cholesterol synthesis, have demonstrated, however, a marked reduction in stroke risk in hypercholesterolemic and atherosclerotic individuals, with benefits extending to normocholesterolemic individuals. These findings suggest that statins might have additional effects in stroke protection beyond cholesterol reduction. Because statins inhibit the synthesis of isoprenoid intermediates in the cholesterol biosynthetic pathway, which are important lipid attachments for intracellular signaling molecules, they might have direct noncholesterol-dependent effects on inflammatory and endothelial cells. Here we discuss data from clinical trials assessing the effects of statins on stroke risk, as well as outline the mechanisms underlying the cholesterol-independent effects of statins and provide evidence-based recommendations for stroke prevention, based on achieved serum cholesterol levels in patients at risk of stroke.

Elkind MS, Tai W, Coates K, Paik MC, Sacco RL. · Department of Neurology, College of Physicians and Surgeons, Columbia University, and Columbia-Presbyterian Medical Center, New York Presbyterian Hospital, New York, NY, USA. · Cerebrovasc Dis. · Pubmed #19018137 No free full text.

Abstract: BACKGROUND: Mass levels of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), a leukocyte-derived enzyme involved in the metabolism of low-density lipoprotein to pro-inflammatory mediators, are associated with prognosis after stroke. Lp-PLA(2) mass correlates only moderately with levels of Lp-PLA(2) activity. The relationship of Lp-PLA(2) activity to risk of stroke recurrence is unknown. We hypothesized that Lp-PLA(2) activity levels would predict risk of recurrence. METHODS: In the population-based Northern Manhattan Stroke Study, first ischemic stroke patients >or=40 years were followed for recurrent stroke. Levels of Lp-PLA(2) activity were assessed in 467 patients, and categorized by quartile. Cox proportional hazard models were used to calculate hazard ratios (HR) and 95% confidence intervals (95% CI) for risk of recurrent stroke associated with marker quartiles after adjusting for demographics, vascular risk factors, and high-sensitivity C-reactive protein (hsCRP). RESULTS: Mean age was 68.9 +/- 12.7 years; 54.6% were women; 53.3% Hispanic, 27.2% black, and 17.8% white. Median follow-up was 4.0 years, and there were 80 recurrent strokes. Compared to the lowest quartile of Lp-PLA(2) activity, those in the highest had an increased risk of recurrent stroke (adjusted HR 2.54, 95% CI 1.01-6.39). CONCLUSION: Stroke patients with Lp-PLA(2) activity levels in the highest quartile, compared to those in the lowest quartile, had an increased risk of recurrence after first ischemic stroke. Further studies are warranted to determine whether this biomarker has clinical utility in determining high-risk populations of stroke survivors, and whether anti-inflammatory strategies that reduce levels of activity of Lp-PLA(2) reduce the risk of stroke recurrence.

Labovitz DL, Boden-Albala B, Hauser WA, Sacco RL. · Department of Neurology, New York University School of Medicine, New York, NY 10016, USA. · Neurology. · Pubmed #17310033 No free full text.

Abstract: Lacunar infarcts (LACs) and deep intracerebral hemorrhages (DICHs) occur in the same structures and may result from the same pathology. It is unclear why one patient has an LAC while another has DICH. We compared LAC to DICH cases derived from a population-based incidence study. In multivariate analysis, LAC cases were significantly older, more likely to have diabetes, and had higher cholesterol than DICH cases.