Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
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PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

Dyslipidemia represents one of the major risk factors for atherosclerosis affecting the arteries of large and medium caliber and consequently causing ischemia in the brain, heart, or legs. Coronary artery disease and cerebral stroke represent the major causes of morbidity and mortality among the elderly and middle aged subjects. The change of lifestyle can reduce the risk of cardiovascular disease but available drug therapy (in particular statins, inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase) is effective in modifying hyperlipidemia and consequently reducing cardiovascular events. The hypolipemic drugs can prevent, slow the progression and sometimes determine the regression of atherosclerotic plaques, therefore significantly reducing the clinical complications of atherosclerotic cardiovascular disease. In this review, we want to point out the role of the different lipoproteins, such as triglycerides, HDL-C, LDLC, Lp(a), in the pathogenesis of stroke and the role of statins in reducing both lipid fractions and stroke risk.
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PMID:Lipoproteins, stroke and statins. 2418 85

Cardiovascular disease predominantly includes coronary heart disease (CHD) and stroke, results in high morbidity and mortality. MicroRNA-143-3p (miR-143-3p) is a tumor suppressor and is involved in many cancers. However, the role and mechanism of miR-143-3p in coronary heart disease is still unclear. In this study, we identified that miR-143-3p was up-regulated in rabbit CHD model. The results of TargetScan and the dual luciferase reporter assay indicated that KLLN (killin, p53 regulated DNA replication inhibitor) was a direct target of miR-143-3p. Besides, we revealed that KLLN was down-regulated in rabbit coronary heart disease model. In addition, we found that the related-markers of CHD such as TC (total cholesterol), TG (triglyceride), and LDLC (low-density lipoprotein cholesterol) in the model group were significantly increased than that in the control group. And compared with the model group, miR-143-3p inhibitor significantly reduced TC, TG, LDLC expression, while miR-143-3p mimic further increased the expression of TC, TG, and LDLC. We next found that miR-143-3p mimic promoted cell viability and migration of vascular smooth muscle cells, inhibited apoptosis; and these changes were reversed by KLLN-plasmid. And miR-143-3p inhibitor had the counter effects. Our study provided a new target for the treatment of CHD and deserves further study.
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PMID:Significant role and mechanism of microRNA-143-3p/KLLN axis in the development of coronary heart disease. 3131 71

Background: The link between low-density lipoprotein cholesterol (LDL-C) and stroke risk remains controversial and few studies have evaluated the effect of LDL-C after stroke survival.Aims: We assessed the hypothesis proposing the effect of LDL-C on the outcome of stroke patients under the influence of previous Aspirin Therapy.Methods: Associations between LDL-C and outcomes. The effect of LDL cholesterol on stoke outcome was evaluated using Kaplan-Meier methodology, log-rank test, Cox proportional hazard models and Bootstrap Analysis.Results: In a cohort of 342 cases, we observed that among stroke patients with no record of previous aspirin therapy LDL-C levels within recommended range (nLDL-C) are associated to a poor overall survival on (p < 0.001, log-rank test) leading to a 4-fold increased mortality risk in both timeframes of 12 (HR 4.45, 95% CI 1.55-12.71; p = 0.004) or 24 months (HR 4.13, 95%CI 1.62-10.50;p = 0.003) after the first event of stroke. Moreover, modelling the risk of a second event after the first stroke in the timeframe of 24 months demonstrated a predictive capacity for nLDL-C plasmatic levels (HR 3.94, 95%CI 1.55-10.05; p = 0.004) confirmed by Bootstrap analysis (p = 0.003; 1000 replications). In a further step, the inclusion of LDL-C in simulating models equations to predict the risk of a second event in the timeframe of 12 months increased nearly 20% the predictive ability (c-index from 0.763 to 0.956).Conclusion: A worse outcome was seen in stroke patients with normal levels of LDLC, but this finding was restricted to patients not under previous aspirin therapy.
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PMID:Low density lipoprotein cholesterol values and outcome of stroke patients: influence of previous aspirin therapy. 3202 49