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)

Carotid duplex ultrasonography is the noninvasive procedure of choice for evaluating ECAD. However, carotid angiography should be performed before doing carotid endarterectomy. Multivariate logistic regression analysis showed that significant prognostic variables for ECAD in an elderly population are (1) cigarette smoking, (2) serum total cholesterol, (3) serum HDL cholesterol (inverse association), (4) diabetes mellitus, and (5) prior CAD. Patients with 80-100% ECAD develop a higher incidence of ABI and TIA than patients with 40-80% ECAD. Patients with 40-80% ECAD develop a higher incidence of ABI and TIA than patients with 0-40% ECAD. Patients with ECAD have a higher prevalence of prior CAD and develop a higher incidence of new coronary events than patients without ECAD. In patients with ECAD, significant prognostic variables for new coronary events are (1) silent ischemia, (2) prior CAD, (3) serum HDL cholesterol (inverse association), and (4) cigarette smoking. Risk factors for ECAD and CAD should be treated in patients with ECAD. Cigarette smoking must be stopped. Hypertension, dyslipidemia, and diabetes mellitus should be treated. Aspirin, 325 mg/d, should be administered to patients with ECAD. Ticlopidine hydrochloride, 250 mg two times per day should be considered in patients with ECAD who are unable to tolerate aspirin or who develop cerebrovascular events on aspirin. Carotid endarterectomy should be considered in symptomatic patients with 70-99% ECAD.
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PMID:Extracranial carotid arterial disease. 818 62

Secondary prevention of arteriosclerosis tries to inhibit progression of the atherosclerotic process. Therapeutic measures focus on modification of cardiovascular risk factors and antithrombotic treatment. Hypercholesterolemia is the main risk factor for coronary artery disease. The risk of a coronary event is correlated to the plasma cholesterol level. Lowering plasma cholesterol results in reduction of vascular morbidity and mortality. Cigarette smoking is the predominant risk factor for peripheral arterial occlusive disease (PAOD). Smoking cessation reduces progression of PAOD and lowers cardiovascular morbidity and mortality. The preventive effect of antihypertensive therapy in hypertensive patients is most pronounced for cerebrovascular events. Antihypertensive measures improve prognosis after stroke and myocardial infarction. The increased cardiovascular risk in diabetics is in part explained by hyperglycemia and hyperinsulinemia, but also depends on coexisting dyslipidemia and hypertension. Intensive treatment of elevated blood glucose levels, dyslipidemia and hypertension are important preventive measures. Aspirin is highly effective in secondary prevention of vascular events. For the coronary arteries, low-dose aspirin is well established. Whether low-dose aspirin is equally effective for reducing progression of arteriosclerosis in the cerebrovascular and in the peripheral vessels is questionable. Ticlopidine serves as an alternative to aspirin; however, neutropenia may occur, which requires supervision of the patient.
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PMID:[Secondary prevention of arteriosclerosis]. 892 4

Platelet activation, impairment of fibrinolysis and dyslipidemia are important factors in the pathogenesis and progression of ischemic heart disease. Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1). The present study was performed in 57 patients with ischemic heart disease (IHD), divided into groups depending on coexistent hyperlipoproteinemia (HLP) and aspirin treatment. The control group included 21 healthy individuals, matched for age and sex. Parameters of hemostasis (SPA, PF4, PAI-1) and concentration of lipid fractions (TC, TG, LDL, HDL) were measured in plasma. Increased PF4 levels were found in all groups with IHD, irrespective of hyperlipoproteinemia or aspirin treatment. Enhanced SPA and higher PAI-1 were limited to group IHD-HLP without aspirin. Highest PAI-1 activities were observed after stimulation of platelets in vitro. In conclusion, patients with IHD and hyperlipoproteinemia presented most pronounced platelet activation and impairment of fibrinolysis. Aspirin had a beneficial effect on these changes. Lower activities of PAI-1, in patients treated with aspirin, can be ascribed to its reduced release from platelets. Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.
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PMID:[Evaluation of platelet function and tissue plasminogen activator activity in ischemic heart disease depending on concurrence with hyperlipoproteinemia and aspirin therapy]. 964 79

Aspirin has been used for more than 100 years, but its mechanisms of action have only been understood in the past 20 years. Aspirin interferes with arachidonic acid metabolism in platelets and endothelial cells and thereby reduces thromboxane A2 and prostacyclin. It also has other mechanisms of action, including anti-inflammatory roles, protection from oxidative stress, enhancement of fibrinolysis, and suppression of plasma coagulation and platelet-dependent inhibition of thrombin generation. It has been used for primary and secondary prevention of myocardial ischemia, and for primary and secondary prevention of cerebrovascular ischemia. We review the 5 pivotal studies relating to primary prevention for cardiovascular risk and the many studies relating to secondary prevention of myocardial ischemia. We also review the utility of aspirin in primary prevention of myocardial infarction and stroke. We conclude that aspirin is one of the most potent drugs ever discovered and that its effects extend well beyond those of cycloxoxygenase enzyme inhibition. Aspirin treatment does not preclude control of underlying and comorbid conditions such as diabetes mellitus, hypertension, and dyslipidemia. For most patients, a daily dose of 325 mg is optimal. Patients must understand the potential for gastrointestinal upset and hemorrhagic complications. The utility of aspirin is greater in coronary artery disease prevention than in cerebrovascular prevention.
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PMID:Aspirin in the prophylaxis of coronary artery disease. 1235 34

Accelerated atherosclerosis and the increased risk of thrombotic vascular events in diabetes may result from dyslipidemia, endothelial dysfunction, platelet hyperreactivity, an impaired fibrinolytic balance, and abnormal blood flow. There is also a correlation between hyperglycemia and cardiovascular (CV) events. The importance of platelets in the atherothrombotic process has led to investigation of using antiplatelet agents to reduce CV risk. A meta-analysis conducted by the Antiplatelet Trialists' Collaboration demonstrated that aspirin reduced the risk of ischemic vascular events as a secondary prevention strategy in numerous high-risk groups, including patients with diabetes. Based on results from placebo-controlled randomized trials, the American Diabetes Association recommends low-dose enteric-coated aspirin as a primary prevention strategy for people with diabetes at high risk for CV events. Clopidogrel is recommended if aspirin allergy is present. There is occasionally a need for an alternative to aspirin or for additive antiplatelet therapy. Aspirin in low doses inhibits thromboxane production by platelets but has little to no effect on other sites of platelet reactivity. Agents such as ticlopidine and clopidogrel inhibit ADP-induced platelet activation, whereas the platelet glycoprotein (Gp) IIb/IIIa complex receptor antagonists block activity at the fibrinogen binding site on the platelet. These agents appear to be useful in acute coronary syndromes (ACSs) in diabetic and nondiabetic patients. A combination of clopidogrel plus aspirin was more effective than placebo plus standard therapy (including aspirin) in reducing a composite CV outcome in patients with unstable angina and non-ST segment elevation myocardial infarction. In a meta-analysis of six trials in diabetic patients with ACSs, intravenous GpIIb-IIIa inhibitors reduced 30-day mortality when compared with control subjects. Results from controlled prospective clinical trials justify the use of enteric-coated low-dose aspirin (81-325 mg) as a primary or secondary prevention strategy in adult diabetic individuals (aged >30 years) at high risk for CV events. Recent studies support the use of clopidogrel in addition to standard therapy, as well as the use of GpIIb-IIIa inhibitors in ACS patients.
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PMID:The platelet in diabetes: focus on prevention of ischemic events. 1283 32

This study surveyed all cardiologists in a large coalition of cardiology groups. A 1-page, 25-item anonymous questionnaire containing 3 sections (demographics, medical history, and current medications and supplements) was used. Data from returned questionnaires were analyzed and compared with those in national databases. Eight hundred surveys were sent, and complete data were available for analysis on 471 (59%). The average age of the participants was 48.6 years; 7.1% were women. The average body mass index (BMI) was 25 kg/m(2), and 8% were obese (BMI > or =30 kg/m(2)); 1.3% were active smokers; 89% exercised > or =1 time/week; and 72% had > or =1 alcoholic drink/week. Red wine was the most frequently consumed alcoholic beverage. Associated cardiovascular risks included dyslipidemia (28%), hypertension (14%), and diabetes mellitus (0.6%). Four percent had experienced coronary events. Compared with matched cohorts from the United States (US) population, cardiologists reported lower rates of hypertension, dyslipidemia, and diabetes mellitus, and the rates of smoking and obesity were 1/18 and 1/3 those of the US population, respectively. Aspirin and statins were each taken daily by about 1/3 of the participants. A cardiologist with dyslipidemia was 5 times as likely to be treated and a cardiologist with hypertension was almost twice as likely to be treated as an American adult man with either of these disorders, respectively. In conclusion, cardiologists appear to follow healthier lifestyles than the general adult US population.
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PMID:Personal health habits of American cardiologists. 1656 24

The study was designed to assess blood platelet sensitivity to acetylsalicylic acid and its associations with dyslipidaemia and inflammation in coronary artery disease patients. Platelet non-responsiveness to aspirin is associated with an increased risk of serious cardiovascular events. Several environmental and hereditary factors are reportedly involved in sub-optimal acetylsalicylic acid response. Forty-five coronary artery disease patients and 45 non-coronary artery disease controls received acetylsalicylic acid at a daily dose of 75-150 mg. Controls were examined twice: on the day of entering the study and 10 days later. Urinary 11-dehydrothromboxane B2 was assessed as the marker of platelet thromboxane generation. Aggregation was studied in platelet-rich plasma using turbidimetric aggregometry with collagen and arachidonic acid. Fifty to seventy percent of coronary artery disease patients showed an extent of collagen-induced aggregation above the upper quartile of the reference range compared with 8-15% in controls (P<0.003). For arachidonic acid-activated aggregation these proportions were 45-50% in coronary artery disease versus 7% in controls (P<0.007). In coronary artery disease patients, the acetylsalicylic acid-mediated platelet inhibition positively correlated with increased triglycerides (in arachidonic acid-stimulated platelets, r=0.30, P=0.0018), total cholesterol (r=0.33, P<0.0001 in coll and arachidonic acid-activated platelets) and elevated serum C-reactive protein (CRP) (r=0.27, P=0.0024). In coronary artery disease patients urine 11-dehydrothromboxane B2 concentrations were significantly increased compared to controls after 10 day acetylsalicylic acid intake (563; 313-728 pg/mg creatinine versus 321; 246-488 pg/mg creatinine, P=0.04). The incidence of suboptimal acetylsalicylic acid response incidence was more common in patients with coronary artery disease. Acetylsalicylic acid inhibition of blood platelet reactivity and thromboxane generation was less effective in these patients. Dyslipidaemia and chronic inflammatory states may promote suboptimal acetylsalicylic acid response in coronary artery disease patients.
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PMID:Reduced blood platelet sensitivity to aspirin in coronary artery disease: are dyslipidaemia and inflammatory states possible factors predisposing to sub-optimal platelet response to aspirin? 1663 10

Cardiovascular disease is the leading cause of morbidity and mortality in Western countries, and hypertension-related cardiovascular events affect about 37 million people per year worldwide. In this perspective, treatment of hypertension is a reference illustrating strategies of cardiovascular prevention. Hypertensive patients are at increased risk of undergoing a cardiovascular event throughout their lives, and treatment of high blood pressure is one of the most effective strategies to reduce global cardiovascular risk. However, due to its multifactorial pathophysiology and frequent association with other important risk factors and clinical conditions such as dyslipidemia, diabetes, left ventricular dysfunction, and renal impairment, treatment of hypertension requires an integrated approach, including life-style measures, antihypertensive drugs and other therapies (statins, ASA, etc.). Nonetheless, worldwide, general practitioners continue to focus on managing a single risk factor, e.g. blood pressure, rather than on overall cardiovascular risk profiles. Another debated issue is whether it matters how blood pressure is lowered in hypertensive patients at high risk. In other words, are the latest antihypertensive drugs more effective than older blood pressure strategies in terms of reduction of cardiovascular events? The recent results of the ASCOT Study address these controversial issues and throw new light on the management of cardiovascular risk in hypertension.
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PMID:Integrated cardiovascular risk management for the future: lessons learned from the ASCOT trial. 1664 Jan 73

The number of diabetics will increase almost 70% in developed countries during the next 20 years: peripheral arterial disease is a common and costly complication. The incidence of cardiovascular disease (mortality and morbidity) due to atherosclerosis, is higher among patients with diabetes than in those without diabetes. Intensive management of diabetes, including glycaemic control, treatment of hypertension and dyslipidemia, as well as nonpharmacological interventions, decreases both micro- and macrovascular complications. Aspirin and clopidogrel have less antiplatelet effect in patients with diabetes. Metformin therapy is considered a risk factor for lactic acidosis if not withdrawn 2 days before angiography, but this risk is extremely low in patients with normal renal function. Peri-operative hyperglycaemia and large fluctuations in plasma glucose increase postoperative mortality and morbidity and careful measures are required to minimise these effects.
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PMID:Diabetes care for patients with peripheral arterial disease. 1736 40

Aspirin (acetylsalicylic acid) is one of the main therapeutic medications used in the prevention of thromboembolic vascular events. Aspirin exhibits its antiplatelet action by irreversibly inhibiting platelet cyclooxygenase-1 enzyme, thus preventing the production of thromboxane A2 (TXA2). Aspirin resistance, as measured in vitro, is the inability of aspirin to reduce platelet activation and aggregation by failure to suppress the platelet production of TXA2. Laboratory tests of platelet TXA2 production or platelet function dependent on TXA2 can detect aspirin resistance in vitro. The clinical implication of this laboratory definition has not yet been elucidated via prospective trials that have controlled for confounders, such as hypertension, diabetes and dyslipidemia. Large meta-analyses have found low-dose aspirin to be as effective as high-dose aspirin in preventing vascular events, making a dose-dependent improvement in laboratory response clinically irrelevant. Possible causes of aspirin resistance include poor compliance, inadequate dose, drug interactions, genetic polymorphisms of cyclooxygenase-1, increased platelet turnover and upregulation of non-platelet pathways of thromboxane production. However, there is currently no standardized approach to the diagnosis and no proven effective treatment for aspirin resistance. Further research exploring the mechanisms of aspirin resistance is needed in order to better define aspirin resistance, as well as to develop a standardized laboratory test that is specific and reliable, and can correlate with the clinical risk of vascular events. The intent of this paper is to review the literature discussing possible mechanisms, diagnostic testing and clinical trials of aspirin resistance and to discuss its clinical relevance as it pertains to cerebrovascular and cardiovascular disease.
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PMID:Clinical implications of aspirin resistance. 1786 25


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