Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-density lipoprotein (LDL) apheresis is a last-resort treatment for hypercholesterolemic patients resistant to conservative lipid-lowering therapy. In the extracorporeal circuit, LDL, Lp(a) and coagulation factors are selectively eliminated, while the beneficial proteins like high-density lipoprotein, albumin and immunoglobulins are returned to the patient. Clinical effects of LDL apheresis comprise improvement of symptoms like angina and exercise tolerance, reduction of clinical coronary events like unstable angina, need for angioplasty or bypass operation, myocardial infarction and ultimately coronary mortality. The reduction of atherogenic lipoproteins and of coagulation factors by LDL apheresis (LA) positively influences hemorheology, endothelial function and coronary reserve. In the controlled LAARS, LA significantly improved the electrocardiographic signs of myocardial ischemia in the treadmill test. In angiographically controlled trials such as LARS and L-CAPS, a reduction of progression of coronary lesions was observed; in favorable cases, regression of the stenoses could be documented. In addition, in the LDL apheresis coronary morphology trial, LA decreased the coronary plaque area. The Hokuriku trial documented a 72% decrease of coronary events (MACE) in the LA group vs. controls treated only by statins. In longitudinal studies, the incidence of MACE after regular LA decreased compared with the preapheresis period in the same patients. Apart from coronary heart disease, recent studies indicate a positive effect of LA also on carotid artery stenoses and peripheral vascular disease. Prospective randomized studies showed the beneficial effects of cascade filtration on age-related macular degeneration and of heparin-induced LDL precipitation apheresis on acute inner ear deafness.
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PMID:State of the art of low-density lipoprotein apheresis in the year 2003. 1525 20

Patients with chronic renal failure are prone to cardiovascular complications. The mechanisms and the assessment of the risk of cardiovascular diseases (CVD) in this population are of interest. The purpose of this study was to investigate the traditional and potential risk factors for the development of CVD and their contribution to ischemic heart disease (IHD) and variation in carotid intima media thickness (IMT) in hemodialyzed patients (HD). Twenty-one chronically HD patients and nineteen healthy volunteers were recruited. Studied parameters were intima-media thickness, body mass index (BMI), mean arterial blood pressure (MAP), hemoglobin, fibrinogen (Fbg), serum lipids, lipoprotein (a) [Lp(a)], total homocysteine (tHcy). Mean carotid IMT, tHcy, Fbg and Lp(a) were higher in HD patients compared to the control group. There were no differences in cholesterol (tCh) and triglycerides between these groups. Patients with ischemic heart disease were older and they had higher values of carotid IMT, tCh, triglycerides, Fbg and Lp(a). There were no differences in MAP, time on dialysis and tHcy between the two subgroups (with vs without IHD). Carotid IMT correlated positively with age (r = 0.68, p = 0.001), BMI (r = 0.50, p = 0.02), tCh (r = 0.58, p < 0.01), LDL- cholesterol (r = 0.55, p = 0.01) and Fbg (r = 0.57, p < 0.01) but not with tHcy or Lp(a) in the patients group. Carotid intima media thickness thus reflects the risk for ischemic heart disease in hemodialyzed patients. Elevated fibrinogen concentration and dyslipidemia influence arterial remodelling.
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PMID:Intima media thickness of common carotid arteries is associated with traditional risk factors and presence of ischaemic heart disease in hemodialysis patients. 1564 38

Silent myocardial ischemia (SMI) and silent coronary stenoses (CS) are two to seven times more frequent in diabetic patients than in non-diabetic patients. In addition to this, they have a higher predictive value for cardiovascular events than the classical cardiovascular risk factors, either taken alone or combined. Coronary arterial disease is the leading cause of mortality and morbidity in the diabetic population. Altogether, these data suggest that screening for SMI and silent CS is an important issue. We assume that detecting SMI and silent CS improves patient management, and leads to optimised follow-up, action taken on nutrition, exercise and lifestyle, management of the cardiovascular risk factors, and revascularisation procedures whenever possible. However, screening for SMI and silent CS is expensive and may induce morbidity. Selecting the patients with a high a priori risk of SMI and silent CS is therefore of major concern. Carotid or lower limb peripheral arterial disease, proteinuria, male gender, an age greater than 60 years, and two or more cardiovascular risk factors among smoking, microalbuminuria, dyslipidemia, hypertension, a family history of premature cardiac disease, and cardiac autonomic neuropathy have been demonstrated to be the best current predictors of SMI and silent CS. New markers, such as adhesion molecules, Lp(a), inflammation parameters or homocysteine, and endothelium function assessment might be of further help in the future.
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PMID:Markers for silent myocardial ischemia in diabetes. Are they helpful? 1595 27

The key 'statin trials' focussed on the beneficial effect of lowering the circulating concentrations of low-density lipoprotein cholesterol (LDL). However, epidemiological surveys, mainly based on healthy populations, indicate that other lipid-related variables, such as high-density cholesterol (HDL), triglycerides (TG), dense LDL subfraction distribution, and possibly lipoprotein (a) (Lp(a)), are also predictors of vascular events. Furthermore, TG and HDL levels influenced outcome within some of the statin trials. Plasma fibrinogen levels have also been shown to be powerful predictors of vascular risk in healthy subjects and patients with established ischaemic heart disease. The fibrates exert beneficial effects on all these variables that predict vascular events. The results from recent trials, the Bezafibrate Infarction Prevention (BIP) study and the Veterans Administration HDL Intervention Trial (VA-HIT) have revived our interest in fibrates. These trials involved bezafibrate and gemfibrozil that have a relatively poor LDL-lowering capacity. Therefore, the benefits reported in BIP and VA-HIT must be attributed to actions on variables other than a reduction in LDL quantity. Ciprofibrate and fenofibrate have significantly greater LDL-lowering capacity than bezafibrate or gemfibrozil. This advantage may render them more effective, especially since they retain the additional beneficial actions associated with this class of lipid-lowering drugs.
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PMID:Treatment of dyslipidaemias in patients with established vascular disease: a revival of the fibrates. 1642 31

Stroke represents a major health burden in our country. Ischaemic stroke has got several risk factors associated with increased chance of atherosclerosis. A small hospital-based study was done to look into the risk factors associated with ischaemic stroke. Forty patients with CT-confirmed cerebral infarction were taken for the study and detailed history and clinical findings were obtained. Investigations like complete haemogram, fasting blood glucose, urea, creatinine, lipid profile, serum Lp(a), homocysteine, fibrinogen, ECG, chest x-ray, echocardiography, MRI/MRA where indicated, were done to identify the risk factors as well. Results indicated that hypertension was the most prevalent (87.5%) risk factor followed by ischaemic heart disease (35%) and diabetes. Dyslipidaemia was also found in a significant number of cases, mostly elevated LDL, low HDL and elevated Lp(a). Fibrinogen and homocysteine were of less significance.
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PMID:Risk factor analysis in ischaemic stroke: a hospital-based study. 1657 Jul 59

Evidences suggest that lipoprotein(a) [Lp(a)] is an important risk factor for cardiovascular disease. However, literature has been controversial in confirming its role as an independent risk factor for cardiovascular disease. The objective of the present study is to evaluate the association between serum levels of Lp(a) and ischemic heart disease as well as other cardiovascular risk factors in a population-based study conducted on a local cohort of the Brazilian population. Lp(a) serum levels were measured in 400 individuals selected from a larger sample of a populational survey carried out in Ouro Preto, a city in the southeast of Brazil. Lipid profile, fasting blood glucose, anthropometric and clinical parameters were analyzed. Lp(a) levels were significantly associated with the presence of ischemic heart disease. In relation to other cardiovascular risk factors, it was verified that Lp(a) levels were statistically associated with age, total cholesterol, LDL-cholesterol and percentage of body fat determined by bioelectric impedance. Lp(a) was also highly associated with the Framingham risk score (p=0.003). In a multivariate analysis two significant interactions were revealed; one involving ischemic heart disease, sex and age and other associating ischemic heart disease, age and total cholesterol. In summary, in the present analysis Lp(a) serum levels were correlated with the occurrence of ischemic heart disease and other cardiovascular risk factors.
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PMID:Lipoprotein(a) as a risk factor associated with ischemic heart disease: Ouro Preto Study. 1684 71

Elevated plasma lipoprotein (a) (Lp(a)) and total homocysteine (tHcy) concentrations, as well as fat distributions, are associated with cardiovascular disease (CVD) risk. The purpose of this study was to evaluate plasma Lp(a), tHcy, percentage body fat, anthropometric indices, and blood pressure (BP) and their relationships with each other in well-defined, hospital-based, CVD patients in a Nigerian African community. One hundred seventy patients suffering from hypertensive heart disease, hypertension, ischaemic heart disease, and myocardial infraction with the mean age of 45.3 +/- 1.3 years and 58 apparently healthy volunteers with the mean age of 44.8 +/-1.2 years were selected. Anthropometric indices and BP were measured. Percentage body fat, body mass index, and waist-to-hip ratio (WHR) were calculated. Plasma Lp(a) and tHcy concentrations were determined. The results showed significant increases in BP, skinfold thickness (SFT) variables, and WHR in all of the CVD patients. Plasma Lp(a) was also significantly increased (p < 0.001), whereas the slight increase in the mean tHcy was not statistically significant. Positive significant correlations were found between systolic BP, triceps, SFT, and percentage body fat (p < 0.01), whereas significant correlations were found between some body composition variables, tHcy, and systolic BP (p < 0.05). Our findings provide supportive evidence for altered plasma Lp(a) concentration in addition to some other traditional CVD risk factors in Nigerians. The role of homocysteine is not well defined.
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PMID:Plasma lipoprotein (a), homocysteine, and other cardiovascular disease (CVD) risk factors in Nigerians with CVD. 1834 83

The aim of this review is to summarize present evidence of a causal association of lipoprotein(a) with risk of ischemic heart disease (IHD). Evidence for causality includes reproducible associations of a proposed risk factor with risk of disease in epidemiological studies, evidence from in vitro and animal studies in support of pathophysiological effects of the risk factor, and preferably evidence from randomized clinical trials documenting reduced morbidity in response to interventions targeting the risk factor. Elevated and in particular extreme lipoprotein(a) levels have in prospective studies repeatedly been associated with increased risk of IHD, although results from early studies are inconsistent. Data from in vitro and animal studies implicate lipoprotein(a), consisting of a low density lipoprotein particle covalently bound to the plasminogen-like glycoprotein apolipoprotein(a), in both atherosclerosis and thrombosis, including accumulation of lipoprotein(a) in atherosclerotic plaques and attenuation of t-PA mediated plasminogen activation. No randomized clinical trial of the effect of lowering lipoprotein(a) levels on IHD prevention has ever been conducted. Lacking evidence from randomized clinical trials, genetic studies, such as Mendelian randomization studies, can also support claims of causality. Levels of lipoprotein(a) are primarily determined by variation in the LPA gene coding for the apolipoprotein(a) moiety of lipoprotein(a), and genetic epidemiologic studies have documented association of LPA copy number variants, influencing levels of lipoprotein(a), with risk of IHD. In conclusion, results from epidemiologic, in vitro, animal, and genetic epidemiologic studies support a causal association of lipoprotein(a) with risk of IHD, while results from randomized clinical trials are presently lacking.
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PMID:Lipoprotein(a) and ischemic heart disease--a causal association? A review. 2010 78

This study evaluated whether statin therapy changed a diagnostic validity of lipid and inflammatory markers in ischemic heart disease (IHD) patients. Levels of lipids, lipoproteins, apolipoproteins, inflammatory markers, and atherogenic indexes were determined in 49 apparently healthy men and women, 82 patients having stable angina pectoris (SAP), 80 patients with unstable angina (USAP), and 106 patients with acute ST-elevation myocardial infarction (STEMI) treated or not treated with statins. Diagnostic accuracy of markers was determined by ROC curve analysis. Significantly lower apoA-I in all statin-treated groups and significantly higher apoB in statin-treated STEMI group compared to non-statin-treated groups were observed. CRP showed the best ROC characteristics in the assessment of STEMI patients. Lp(a) is better in the evaluation of SAP and USAP patients, considering that Lp(a) showed the highest area under the curve (AUC). Regarding atherogenic indexes, the highest AUC in SAP group was obtained for TG/apoB and in USAP and STEMI patients for TG/HDL-c. Statins lowered total cholesterol, LDL-c, and TG but fail to normalize apoA-I in patients with IHD.
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PMID:Lipoprotein(a) Is the Best Single Marker in Assessing Unstable Angina Pectoris. 2140 66

Study aim was to investigate the association of lipoprotein (a) [Lp(a)] level with the development of cardiovascular complications in long-term follow-up period after coronary artery bypass grafting (CABG). Patients with chronic ischemic heart disease (IHD) (n = 361, 88% men, mean age 55 +/- 9 years) who had had CABG were included in the study. Before surgery we assessed presence of classical risk factors, left ventricular ejection fraction, concentrations of lipids and Lp(a) in blood serum. During follow-up (from 1 to 140, mean 66 +/- 34 months) we registered cardiac deaths, nonfatal myocardial infarctions (MI), strokes, repeat procedures of revascularization, and hospitalizations due to relapse or progression of angina pectoris. Information on prognosis was obtained from 263 patients. In 109 of them we registered 142 serious events including cardiac death n = 20 (14%), nonfatal MI n = 14 (10%), myocardial revascularization (n = 35), 29 (20%) with stenting), repeat CABG n = 6 (4%), hospitalization due to angina pectoris n = 53 (37%), stroke n = 4 (3%), noncardiac outcome n = 16 (10%). In subjects with hyperlipidemia (a) [HLp(a) - Lp(a) > 30 mg/l] survival after CABG was lower (log rank p < 0.001): 11 of 93 (11.3%) and 9 of 170 (5.2%) patients died among those with Lp(a) > 30 and < 30 mg/I, respectively. Relative risk (RR) of any cardiovascular complication was 3.24 (95% confidence interval [CI] 2.18 to 4.83, p < 0.001), of death - 2.89 (95% CI 1.31 to 6.35, p < 0.01), and of MI A 1.01 (95% CI 1.00 to 1.02; p = 0.02). RR of development of MI and cardiac death in patients with HLp(a) in 5 years was 2.61 (95% CI 1.11 to 5.74; p = 0.02), in 10 years - 2.95 (95% CI 1.50 to 5.79; p < 0.001). In patients with chronic IHD high level of Lp(a) can serve as independent predictor of unfavorable events including death and nonfatal MI during 10 years after CABG.
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PMID:[High level of lipoprotein (a) as a predictor of poor long-term prognosis after coronary artery bypass surgery]. 2162 97


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