Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum lipoprotein (a) (Lp[a]) has been associated with coronary artery atherosclerosis. Its association with restenosis after percutaneous transluminal coronary angioplasty (PTCA) has not been previously studied. Serum levels of Lp(a), in addition to other lipoproteins, and their components using standard assays, were determined in subjects undergoing cardiac catheterization within 10 months after PTCA. Clinical (e.g., sex, diabetes, angina class) and angiographic (e.g., PTCA percent diameter reduction) factors were not different between the group without (diameter reduction less than 50%; group A) and the group with (diameter reduction greater than or equal to 50%; Group B) restenosis. Total cholesterol, triglycerides, high- and low-density lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein B and Lp(a) were compared. Univariate predictors of restenosis were serum triglycerides (2.50 +/- 1.07 mmol/liter for group A vs 1.72 +/- 0.79 +/- mmol/litre for group B, p = 0.008), and Lp(a) (median: 7.0 mg/dl [range 0 to 44] for group A vs 19 mg/dl [range 1 to 120] for group B; p = 0.006). Stepwise logistic regression revealed the only significant independent predictor of restenosis to be serum Lp(a) (p = 0.018). Each quintile of Lp(a) was associated with a progressively higher risk of restenosis, with the highest quintile (40 to 120 mg/dl) having an odds ratio of 11 (95% confidence interval 9 to 13) compared with the lowest quintile (0 to 3.9 mg/dl) (p = 0.033). A serum Lp(a) of greater than 19 mg/dl was associated with an odds ratio of 5.9 (95% confidence interval 4.6 to 7.2) (restenosis rates of 58% in the group with 0 to 19 mg/dl and 89% in the group with 19 to 120 mg/dl; p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Usefulness of serum lipoprotein (a) as a predictor of restenosis after percutaneous transluminal coronary angioplasty. 144 34

The aim of the study was to examine the relationships of obesity, lipids and apolipoproteins with the risk for subsequent ischaemic heart disease in middle-aged women, using a case-control study nested within a cohort study. A total of 3634 women aged 26-88 were recruited in Guernsey between 1977 and 1985 and followed until June 1986 by abstraction of their general practitioners' records. Fifty-one cases of incident ischaemic heart disease (11 myocardial infarction, 40 angina) were identified. For each case up to 4 controls were selected, matched for age and date at recruitment. Odds ratios for the development of ischaemic heart disease in the middle and upper thirds of the distribution for each variable in the controls, relative to the lowest third (and two-sided P-values for linear trends), were: 3.0, 2.6 (0.015) for Quetelet's index; 3.3, 5.1 (0.003) for total cholesterol; 0.5, 0.6 (0.102) for apolipoprotein A-I; 1.8, 2.4 (0.015) for apolipoprotein B; 1.3, 2.1 (0.155) for apolipoprotein(a). The increased risks associated with increased Quetelet's index and total cholesterol were independent of each other and these variables were more strongly related to myocardial infarction than to angina. The relationships of risk with serum cotinine, fatty acids, dehydroepiandrosterone sulphate and sex hormone binding globulin were weak and did not approach statistical significance.
 ...
PMID:A prospective study of obesity, lipids, apolipoproteins and ischaemic heart disease in women. 163 46

Cardiovascular disease is a frequent complication of insulin-dependent diabetes mellitus (IDDM), but the prevalence, interrelations, and risk factors of its principal components (coronary, cerebrovascular, and lower-extremity arterial disease) and of medial arterial wall calcification are not well understood. To address these issues, data from the Epidemiology of Diabetes Complications Study (n = 657) baseline examination were examined. The term coronary heart disease (CHD) was applied to those with myocardial infarction or angina, whereas lower-extremity arterial disease (LEAD) was applied to those who had undergone amputation of a lower limb or who had an ankle to arm blood pressure ratio less than 0.8 at rest or after exercise. Calcification of the lower-extremity arteries was considered to be present if ankle pressure was more than 100 mm Hg higher than brachial pressure. Although the prevalence of CHD was low, LEAD was significantly more common in women than in men (p less than 0.01), whereas calcification was more frequent in men than in women (p less than 0.01). Ten percent of those with LEAD also had CHD, and 8% with LEAD had calcification. Modeling of potential risk factors (e.g., diabetes duration and glycosylated hemoglobin) revealed that duration, female gender, fibrinogen, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and high density lipoprotein cholesterol to apolipoprotein A-I ratio were independent predictors of LEAD, whereas for CHD only, diabetes duration and hypertension contributed to CHD. Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. The results suggest that although LEAD, CHD, and calcification often coexist, their risk factor profiles differ.
 ...
PMID:Cardiovascular disease and arterial calcification in insulin-dependent diabetes mellitus: interrelations and risk factor profiles. Pittsburgh Epidemiology of Diabetes Complications Study-V. 206 46

To investigate the prostaglandin I2 (PGI2) half-life regulated by high density lipoprotein (HDL) in patients with coronary artery disease (CAD), we determined the stability of PGI2 and serum apolipoprotein A-I (Apo A-I) and apolipoprotein A-II (Apo A-II) levels in four age-matched groups of patients: controls (n = 17), angina pectoris (n = 18), unstable angina pectoris (n = 17), myocardial infarction (n = 19) (acute phase, 3.6 +/- 1.7 hours from onset; subacute phase, 75 +/- 15 hours from onset in the same patients). Serum PGI2 half-life and total serum Apo A-I levels were lower in the CAD group than in the control group. PGI2 was least stable in patients with unstable angina and the acute phase of myocardial infarction. In these patients, the molar ratio of Apo A-I to Apo A-II and HDL-associated Apo A-I levels were decreased, and free Apo A-I levels were increased. After in vitro incubation of HDL with increasing amounts of Apo A-II, Apo A-I in HDL was displaced by Apo A-II, with the parallel decrease in stability of PGI2. Free Apo A-I cannot stabilize PGI2. HDL-associated Apo A-I, whose amount is affected by Apo A-II, stabilized PGI2 and correlated well with stability of PGI2 in patients with CAD and control patients. Decreased PGI2 half-life may play an important role in the pathogenesis of atherosclerosis and thrombus formation in the coronary arteries, especially thrombus formation during an acute coronary event.
 ...
PMID:Prostaglandin I2 half-life regulated by high density lipoprotein is decreased in acute myocardial infarction and unstable angina pectoris. 211 45

The prevalence of coronary heart disease (CHD), cardiovascular disease (CVD) and associated risk factors was studied in 413 men aged 70-89, the survivors of the Finnish cohorts of the Seven Countries Study. Men were divided into five categories according to manifestations of prevalent CVD: I, history or ECG evidence of previous myocardial infarction (MI; 48 men, 12%); II, typical angina pectoris (AP; 56 men, 14%); III, other ischaemic electrocardiographic (ECG) changes (82 men, 20%); IV, stroke, transient ischaemic attack, intermittent claudication or minor ECG changes (other CVD; 78 men, 19%); V, free of CVD (149 men, 36%). Both systolic and diastolic blood pressures were lowest in men with previous MI and in men free of CVD, and highest in men with other ischaemic ECG changes (P = 0.017). Low HDL-cholesterol (< 0.9 mmol/l) was more prevalent and the total/HDL-cholesterol ratio and triglyceride levels were higher in men with prevalent CHD (P < 0.05). Total and LDL-cholesterol, smoking, body mass index, fibrinogen, coagulation factor VIIc, apolipoprotein A-I, apolipoprotein B and lipoprotein(a) were not associated with prevalent CVD. The results show that manifestations of CHD and CVD are common among elderly Finnish men. Low HDL-cholesterol, total/HDL ratio, triglycerides and hypertension were associated with manifest CVD cross-sectionally.
 ...
PMID:Prevalence of coronary heart disease and associated risk factors among elderly Finnish men in the Seven Countries Study. 814 50

High-density lipoprotein (HDL) and its principal apolipoprotein A-I (ApoA-I) have now been convincingly shown to influence glucose metabolism through multiple mechanisms. The key clinically relevant observations are that both acute HDL elevation via short-term reconstituted HDL (rHDL) infusion and chronically raising HDL via a cholesteryl ester transfer protein (CETP) inhibitor reduce blood glucose in individuals with type 2 diabetes mellitus (T2DM). HDL may mediate effects on glucose metabolism through actions in multiple organs (e.g., pancreas, skeletal muscle, heart, adipose, liver, brain) by three distinct mechanisms: (i) Insulin secretion from pancreatic beta cells, (ii) Insulin-independent glucose uptake, (iii) Insulin sensitivity. The molecular mechanisms appear to involve both direct HDL signaling actions as well as effects secondary to lipid removal from cells. The implications of glucoregulatory mechanisms linked to HDL extend from glycemic control to potential anti-ischemic actions via increased tissue glucose uptake and utilization. Such effects not only have implications for the prevention and management of diabetes, but also for ischemic vascular diseases including angina pectoris, intermittent claudication, cerebral ischemia and even some forms of dementia. This review will discuss the growing evidence for a role of HDL in glucose metabolism and outline related potential for HDL therapies.
...
PMID:HDL and glucose metabolism: current evidence and therapeutic potential. 2658 89