Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As part of the WHO MONICA project three population-representative surveys were conducted in the study region of Augsburg since 1984/85 to describe time trends of classical cardiovascular risk factors. These surveys provide relevant baseline-information for prospective health outcome studies. Three independent study populations were recruited in 1984/85 (S1: age 25 - 64 years), 1989/90 (S2: age 25 - 74 years), and 1994/95 (S3: age 25 - 74 years) by a two-stage cluster sampling, with random sampling for the city of Augsburg, and a random selection of 16 communities by community size in the two adjacent counties. In the three surveys, 13,427 persons have had 13,818 study participations, since some subjects were by chance sampled for more than one survey. From 1984 to 1995, no trends in hypertension could be observed, but an increase of 15 % (men) resp. 30 % (women) in dyslipidaemia (total/HDL cholesterol ratio > or = five). Cigarette smoking decreased in 55 to 64 year old men und increased in 35 to 64-year old women. The predictive impact for incident Acute Myocardial Infarction (AMI) per 100,000 person years is highest for cigarette smoking (men 880, women 360), followed by dyslipidemia (men 739, women 318) and systolic blood pressure > or = 160 mm Hg (men 658, women 276). By 31st December 2002 1,551 persons (1,031 men, 520 women) had died. The surveys will be used for further gender-specific cross-sectional and longitudinal analyses with special focus on classical, new laboratory and genetic risk factors as determinants of mortality, incident AMI and incident type 2 diabetes, to improve preventive strategies.
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PMID:The MONICA Augsburg surveys--basis for prospective cohort studies. 1603 12

Acute coronary syndromes (ACS) consist of unstable angina or acute myocardial infarction and are associated with a high risk of early recurrent ischemic events. Revascularization procedures do not modify underlying pathophysiology and only modestly reduce early ischemic events after an index episode of ACS. Although statins improve dyslipidemia and cardiovascular risk over the long term, efforts to identify new ACS treatments are focusing on the ability of statins to modify the arterial wall-blood interface and reduce the risk of early recurrent ischemic events. Statins have been shown to reduce circulating markers of inflammation within days of an acute ischemic event. Short-term statin therapy also has been associated with improved coronary endothelial function, reversal of prothrombotic states, and reduction in atherosclerotic plaque volume. Findings from 6 randomized, controlled intervention trials were evaluated to determine if risk reduction is associated with the intensity of statin therapy. In addition, the predictive ability of baseline lipid levels and inflammatory markers were examined. High-intensity statin therapy (atorvastatin 80 mg) reduced early recurrent ischemic events after ACS compared with moderate-intensity treatment (eg, pravastatin 40 mg) or placebo. Moderate-intensity regimens (simvastatin 40 mg, pravastatin 20 to 40 mg, fluvastatin 80 mg, cerivastatin 0.4 mg) provided minimal benefit compared with placebo. Although there was no apparent relation between low-density lipoprotein (LDL) cholesterol levels before or during randomized treatment and short-term (4-month) risk of recurrent events, the degree of LDL cholesterol reduction with statin treatment after ACS may be related to longer-term event reduction. Moreover, evidence suggests that anti-inflammatory effects of high-intensity statin treatment are associated with clinical benefit.
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PMID:The case for intensive statin therapy after acute coronary syndromes. 1612 23

Epidemiological reports show that about half of all adults suffer from hypertension, and the incidence of diabetes mellitus, dyslipidemia and obesity is markedly increasing in Japan. Recent progress in gene determination has shown that lifestyle-related diseases, including hypertension, are multigenetic diseases. In particular, renin-angiotensin genes play an important role in the pathogenesis of hypertension. Upregulation of the transcription of angiotensinogen and angiotensin-converting enzyme genes increases blood pressure and cardiovascular organ damage through increased levels of angiotensin II. In this review, I first introduce the history of the recognition, understanding and the development of treatment for hypertension. Secondly, the basic relationship of the pathogenesis between hypertension and the new concept of metabolic syndrome will be shown, and the usefulness of angiotensin II receptor antagonist for hypertensive patients with obesity and/or metabolic syndrome. Finally, I will reveal the utility of gene diagnosis for acute myocardial infarction and cerebral infarction by detecting the polymorphism of renin-angiotensin genes. On the other hand, the positive correlation between blood pressure and body mass index is affected by the Gln27Glu genotype of the beta2-adrenoceptor gene. These studies investigating the gene-environmental relationship will contribute to the development of tailor-made medicine in the future.
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PMID:[Increasing menace of cardiovascular diseases in the era of obesity]. 1654 38

We reviewed epidemiological findings of acute coronary syndrome (ACS) in Japan. Japan has the lowest mortality and morbidity of ACS in the world. However, the crude mortality of acute myocardial infarction in 2003 increased approximately as twice as that in 1970, most likely due to an aging of population. More importantly, several Japanese prospective studies have failed to demonstrate the decline of the age-adjusted incidence of ACS despite the obvious reduction of ACS incidence caused by the intervention to the risk factors. Particularly, one study implied the increase of ACS patients aged more than 80. Given that the prevalence of dyslipidemia, diabetes, and obesity has increased in Japan, we should endeavor to modify these risk factors, especially in the elderly.
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PMID:[Epidemiology of acute coronary syndrome]. 1661 78

Patients with advanced stages of chronic kidney disease (CKD) have an increased risk of death from cardiovascular disease (CVD). Dyslipidemias are associated with atherosclerotic vascular changes and the risk of occurrence of acute myocardial infarction in hemodialysis patients. However, management of dyslipidemia in hemodialysis patients does not appear to be actively carried out in routine practice. Presumably, there are three reasons for this reluctance to lipid-lowering in hemodialysis patients. First, there are epidemiological data showing the inverse relationship between cholesterol and mortality rate; a high cholesterol predicts a better survival. Second, lipids are not usually measured using standard fasting serum, but a non-fasting specimen. Third, although hypertriglyceridemia is the most common abnormality, fibrates are contraindicated in patients with renal failure because of a high risk of rhabdomyolysis. These issues are discussed in the current review article. Based on published work, lipid lowering would not increase the death rate if carried out without worsening malnutrition. The National Kidney Foundation K/DOQI Clinical Practice Guidelines recommend a reduction in fasting LDL-C below 100 mg/dL for the prevention of CVD in dialysis patients. Practically, however, the use of non-HDL-C measured by casual blood samples might be sufficient for the risk assessment in many hemodialysis patients. Statins are a good choice for lipid-lowering in dialysis patients. Furthermore, lipoprotein profile might be improved by an inventive use of dialyzer membranes, dialysate solutions, and other dialysis-related medications. For severe hypercholesterolemia, LDL-apheresis is another choice for consideration. Further studies are needed to clearly prove the benefit of lipid reduction in hemodialysis patients and those with CKD at earlier stages.
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PMID:Plasma lipoprotein abnormalities in hemodialysis patients--clinical implications and therapeutic guidelines. 1691 Nov 82

The interplay between demographic and epidemiologic evolutions is presented exemplified for cardiovascular diseases in Germany. The actually 82 million inhabitants of Germany build the frame for disease occurrence; currently, 2.1 million men and 4.4 million women are > or = 75 years old. The ongoing increase of life expectancy to 75.6 years in men and 81.3 years in women was associated with a remarkable decrease of cardiovascular and ischemic heart disease (IHD) mortality and an increasing disease-specific mean age of death. Each third male and each fourth female death from IHD could be prevented, whereas the absolute number of nonfatal acute myocardial infarction (AMI) increased in the younger ages and decreased in the higher age groups. Since 1985, the total number of fatal and nonfatal cases of AMI has decreased by 24% in men and by 22% in women; two thirds of male and one third of female cases occur before the 75th year of age. These positive trends are mainly the result of a more effective acute and long-term therapy after AMI onset. Actually, 35% of all AMI patients do not survive the first day after acute onset and in up to 90% of them classic risk factors (hypertension, dyslipidemia, diabetes, cigarette smoking) were present. Therefore, the theme number 1 for the population must be intensified activities of primary prevention.
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PMID:[Epidemiology and demographic evolution exemplified for cardiovascular diseases in Germany]. 1703 23

Atherothrombosis results from direct interaction between the atherosclerotic plaque and arterial thrombosis, and underlies most forms of cardiovascular disease (CVD). The pathophysiology of atherosclerosis is now recognised to involve endothelial dysfunction and dyslipidemia with cholesterol accumulation, as well as critical immuno-inflammatory and apoptotic dimensions. Erosion or rupture of a vulnerable, lipid-rich, inflammatory atherosclerotic plaque triggers the formation of a platelet-rich thrombus that may partially or completely occlude the artery, with resultant clinical scenarios including stable and unstable angina, acute myocardial infarction (MI) and ischaemic stroke. Insight into the pathophysiology of atherothrombosis indicates that an integrated risk factor approach, focusing particularly on management of dyslipidaemia (with a statin) and thrombosis (with aspirin), may constitute an optimal therapeutic approach. Both agents have established roles in secondary prevention. Statin action on atherogenic lipoproteins mediates plaque stabilisation, modification of plaque morphology and attenuation of inflammation, and may lead to plaque regression, while aspirin reduces platelet activation and aggregation, decreases release of inflammatory cytokines at sites of vascular injury and attenuates vasoconstriction. Given these complementary modes of action, this combination would be a logical choice for reducing atherothrombotic risk in patients with CVD. Meta-analysis of 5 major clinical studies has demonstrated that the combination of pravastatin plus aspirin was significantly more effective than either agent alone in reducing the relative risk of key cardiovascular endpoints including MI and ischaemic stroke. This combination may therefore represent an important, cost-efficient therapeutic approach to reduction of cardiovascular risk and prevention of recurrent events in stable CVD.
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PMID:From pathophysiology to targeted therapy for atherothrombosis: a role for the combination of statin and aspirin in secondary prevention. 1707 Sep 23

We tested the hypothesis that selected prothrombotic biomarkers might be associated with early spontaneous coronary recanalization in patients with ST-segment elevation acute myocardial infarction (STEMI). We prospectively enrolled 123 patients with STEMI including 53 patients with spontaneous coronary recanalization (cases) and 70 patients with persistent occlusion (controls) at the time of emergent coronary angiography and before angioplasty. All had received aspirin and heparin. Blood samples were collected immediately before angioplasty to measure soluble P-selectin, circulating microparticles originating from platelets (PMPs), granulocytes (GMPs), endothelial cells (EMPs); tissue factor-associated MP (TF-MP); soluble platelet glycoprotein V (sGPV) and prothrombin F1 + 2; tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1) and plasmin-antiplasmin (PAP). A sub-group of 70 patients (35 cases, 35 controls) was available for flow cytometry analysis of platelet P-selectin and activated GPIIb-IIIa. Baseline clinical characteristics did not differ between groups except for more frequent hypertension and dyslipidemia in controls. Platelet activation markers and PMP did not differ between the two groups. Controls had higher numbers of EMPs and GMPs compared to cases, but the difference was no longer significant when corrected for risk factors. Controls differed from cases by higher plasma levels of sGPV [64 (47-84) ng/ml vs. 53 (44-63) ng/ml] and PAP [114(65-225) ng/ml vs. 88 (51-147) ng/ml]. The difference persisted after adjustment for risks factors (p = 0.031 and 0.037, respectively). Persistent occlusion of the infarct related artery is associated with some markers related to higher thrombin (sGPV) and plasmin (PAP) production but is not associated with markers of platelet activation.
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PMID:Prothrombotic markers and early spontaneous recanalization in ST-segment elevation myocardial infarction. 1772 26

The leading cause of acute myocardial infarction (AMI) in patients with coronary heart disease is plaque rupture. Between 6% and 12% of AMI patients have angiographically normal coronary arteries. However, new procedures have demonstrated the limits of coronarography and challenged the existence of this situation. Angiograms may fail to detect minimal lesions whereas, in many cases, intravascular sonography reveals small atherosclerotic plaques. With the development of intravascular sonography and multislice computed tomography, the prevalence of myocardial infarction with normal coronary arteries has fallen to about 1%. Myocardial infarction with normal coronary arteries may be due to coronary vasospasm, hypercoagulable states, intense sympathetic stimulation, non atherosclerotic coronary disease, alcohol or cocaine abuse, and systemic diseases. In a series of 1205 AMI patients, we found no significant coronary disease in 45 patients, but intravascular sonography showed minimal intracoronary plaque in 21 of these cases. The 24 patients without significant lesions were young, had no risk factors for AMI without a prodrome, low peak creatine release, a small reduction in the left ventricular ejection fraction after thrombolysis or angioplasty, and good outcome at 26 months. The mechanisms of AMI in these 24 patients were coronary spasm, myocardial bridge, a prothrombotic state, contraceptive pill usage, and drug or alcohol abuse. The diferential diagnoses of these cases of AMI are acute myocarditis and stress cardiomyopathy, and apical left ventricular ballooning. Initial management is the same as for "conventional" AMI, including pain relief nitrates, antiplatelet agents, heparin, thrombolysis or angioplasty in the acute phase, and ACE inhibitors. Patients with spasm should receive calcium antagonists rather than beta-blockers. The prognosis of these patients is better than that of patients with atherosclerotic lesions. They nonetheless need close follow-up and strict secondary prevention measures, including smoking cessation and prevention of dyslipidemia and diabetes.
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PMID:[Myocardial infarction with "angiographycally normal coronary arteries" myth or reality?]. 1822 36

We examined 4 groups of patients younger than 70 years with atherosclerosis of coronary and/or cerebral arteries. In 98 patients the disease began as acute myocardial infarction, 65 patient from the very beginning suffered from angina of effort, 33 had ischemic cerebral stroke, and in 26 dyscirculatory encephalopathy was diagnosed. Among patients with ischemic heart disease (IHD) and cerebrovascular damages (CVD) 87 and 89%, respectively, had dyslipidemia (DLP). Disorders of lipid composition of the blood with pronounced hypercholesterolemia prevailed in patients with IHD and elevated level of triglycerides or selective decrease of antiatherogenic fraction of lipoproteides - in patients with CVD (especially in patients with stroke). When treatment is prescribed to patients with IHD and CVD at the background of DLP it is necessary to take into consideration DLP variants in order to obtain most effective action of statins and fibrates.
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PMID:[About dyslipidemic states characteristic for various forms of ischemic heart disease and cerebrovascular damages]. 1826 Sep 3


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