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)

In two patients with primary Type V hyperlipoproteinemia with typical clinical features including recurrent bouts of abdominal pain a myocardial infarction was diagnosed. In both cases coronary angiography revealed a severe three vessel disease. The case reports demonstrate that the incidence of ischemic heart disease in patients with Type V hyperlipoproteinemia is higher than reported in the literature. In each case of severe abdominal pain, even in younger Type V patients, a myocardial infarction has to be excluded, In both patients a selective depression in the activity of lipoprotein lipase was found. The possible pathogenetic implication of this finding will be discussed.
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PMID:[Coronary heart disease in patients with primary type V hyperlipoproteinemia (author's transl)]. 20 63

Silent myocardial ischemia (SI), an asymptomatic manifestation of coronary artery disease (CAD), was identified in 10% of apparently healthy nonsmoking, nondiabetic older (60 +/- 7 years, mean +/- SD) men with normal plasma cholesterol levels. We hypothesized that in the absence of other major risk factors for CAD, the men with SI would have reduced plasma levels of high density lipoprotein (HDL) and HDL2 subspecies due to an upper-body fat distribution (waist-to-hip ratio [WHR]), hyperinsulinemia, and abnormal postheparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) activities. Compared with 47 normal control subjects of similar age, obesity, and maximal aerobic capacity, the 18 men with SI had higher plasma triglyceride (TG) (162 +/- 71 versus 102 +/- 39 mg/dl, p less than 0.001) and lower HDL-C (33 +/- 6 versus 37 +/- 7 mg/dl, p less than 0.02) levels with no difference in low density lipoprotein cholesterol level. The HDL2b and HDL2a subspecies measured by gradient gel electrophoresis were also lower in the men with SI (p less than 0.01). The plasma glucose and insulin responses during an oral glucose tolerance test were the same in both groups. Postheparin plasma HL activity was significantly higher in 12 men with SI than in 41 control subjects (34 +/- 8 versus 27 +/- 10 mumol/ml.hr-1, p less than 0.03) and was correlated with log insulin area (r = 0.36, p less than 0.05) and WHR (r = 0.32, p less than 0.05) in the control subjects but not in the men with SI. In the control group, the percent HDL2b subspecies was correlated inversely with postheparin plasma HL activity (r = -0.46, p less than 0.01, n = 41) as well as WHR (r = -0.49, p less than 0.001, n = 47) and log insulin area (r = -0.37, p less than 0.05, n = 47) but not in the men with SI. Postheparin LPL activity was the same in both groups of men and did not correlate with HDL, WHR, insulin, or plasma TG levels. As the control subjects and men with SI had comparable degrees of abdominal obesity and hyperinsulinemia, these results suggest that the reduced HDL-C levels in men with SI may be related to elevations in HL activity. Thus, abdominal obesity, hyperinsulinemia, elevated TG levels, and low HDL-C and HDL2 subspecies levels may predispose these older men to atherosclerosis.
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PMID:Reduced HDL2 cholesterol subspecies and elevated postheparin hepatic lipase activity in older men with abdominal obesity and asymptomatic myocardial ischemia. 161 6

Non-insulin-dependent diabetic (NIDDM) subjects exhibit abnormalities in their plasma lipid and lipoprotein profiles that increase the risk of ischemic heart disease. This study was designed to examine the metabolic behavior of very-low-density (VLDL), intermediate-density (IDL), and low-density (LDL) lipoproteins in NIDDM patients before treatment and after 4 wk of insulin therapy. Basal turnover studies of 131I-labeled VLDL1 (svedberg units [Sf] 60-400) and 131I-labeled VLDL2 (Sf 20-60) apolipoprotein B (apoB) were conducted in a group of seven NIDDM patients who had been off oral therapy for 1 wk. The subjects exhibited higher than normal transport rates for VLDL1 and a diminished input of apoB into the VLDL2 density range. These observations are concordant with the hypothesis that NIDDM patients overproduce VLDL triglyceride but not apoB. VLDL1 and VLDL2 were converted to IDL and ultimately to LDL at approximately normal rates, although the delipidation pathway by which apoB-containing particles were processed exhibited different properties from that seen in control subjects. Insulin therapy reduced plasma triglyceride by 38%, and this was associated with a 41% fall in VLDL1 mass (P less than 0.01). VLDL2 was less affected (19% reduction, P less than 0.05), IDL was unchanged, and LDL fell 17% (P less than 0.05). Repeat metabolic studies revealed that the major effects of insulin were to reduce VLDL1-apoB transport (from 811 to 488 mg/day) and increase the direct input of VLDL2 into the plasma (from 182 to 533 mg/day, P less than 0.05). These alterations in VLDL production led to normalization of apoB kinetics in IDL and LDL. The fractional catabolic rate of LDL increased 19% (P less than 0.05), whereas direct input into this fraction, which had been high before treatment, was reduced. Postheparin plasma lipoprotein lipase (LPL) and hepatic lipase levels were unaffected by insulin, although the hormone did increase LPL in adipose tissue. This lack of effect on lipase activities correlated well with the observation that the rates of catabolism of apoB in VLDL1, VLDL2, and IDL were not significantly affected by insulin therapy.
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PMID:Effect of insulin therapy on metabolic fate of apolipoprotein B-containing lipoproteins in NIDDM. 220 Jul 27

A single high fat meal diet (66 gm fat) was given to 30 healthy males and 20 male patients of ischaemic heart disease (IHD). Ten minutes prior to the 4th postprandial hour, 500 units of heparin--a lipoprotein lipase (LPL) activator--was given, and its effect seen on serum triglyceride (STG) levels observed. Besides higher fasting STG levels, the decline in 4 hour post-prandial STG level was significantly lower in patients of IHD. One explanation for higher fasting STG values and prolonged postprandial lipaemia in these subjects could be deficient LPL activity.
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PMID:Post heparin lipoprotein lipase activity in patients of ischaemic heart disease and in controls. 226 79

Twenty-five CAPD patients were given gemfibrozil in increasing doses for a total of 14 weeks. Parameters of lipid metabolism including serum total cholesterol, LDL cholesterol, HDL cholesterol, HDL2 cholesterol, HDL3 cholesterol triglyceride, apolipoprotein A-1, apolipoprotein B, postheparin lipoprotein lipase, and hepatic lipase activities were measured before the commencement, at every increment in the dose of gemfibrozil and 4 weeks after discontinuation of therapy. Gemfibrozil normalized the deranged parameters of lipid metabolism. Thus, with treatment, serum triglyceride, and total cholesterol, LDL cholesterol and apo B decreased, whereas serum HDL cholesterol, HDL2, and HDL3 (predominantly the latter subfraction), hepatic lipoprotein lipase activities increased. Apo A-1 did not change significantly. Even in normotriglyceridemic patients serum HDL cholesterol increased. The side effects consisted of muscle aches and a significant rise in serum CPK. Gemfibrozil produced a significant decrease in gamma-GT activities. A possible mechanism for the interconversion between HDL2 and HDL3 that resulted in a preferential increase in the latter was discussed. It was concluded that gemfibrozil, in a dose not exceeding 300 mg twice a day favorably improved the risk factor for ischemic heart disease in CAPD patients.
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PMID:Gemfibrozil improves abnormalities of lipid metabolism in patients on continuous ambulatory peritoneal dialysis: the role of postheparin lipases in the metabolism of high-density lipoprotein subfractions. 250 77

There is a very high probability that lipoprotein metabolism plays a central role in the etiology of coronary heart disease. In sedentary persons one way to favorably alter lipoprotein metabolism and possibly delay the progression of coronary atherosclerosis is by an increase in their habitual physical activity. More physically active persons tend to have lower plasma triglycerides and very low density lipoprotein concentrations, and a greater high-density lipoprotein mass due to higher concentrations of the subfraction HDL2 and apoprotein A-I. Plasma low-density lipoprotein concentrations usually are not significantly reduced by exercise unless accompanied by weight loss, but there may be important changes in the distribution among the low-density subfractions. These exercise effects are most likely mediated by alterations in the activity of enzymes involved in the synthesis, transport and catabolism of the various lipoproteins including lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase. In healthy persons as well as in patients with ischemic heart disease, diabetes and renal failure, an increase in moderate-intensity, endurance-type activity requiring an expenditure of approximately 4 MJ (1,000 kcal) per week usually produce favorable lipoprotein changes. Above this level a dose-response relationship exists, with greater changes occurring up to energy expenditures of 19 MJ (4,500 kcal) per week.
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PMID:The influence of exercise training on plasma lipids and lipoproteins in health and disease. 353 12

Since reports that increased high-density lipoprotein cholesterol levels are a negative risk factor for ischemic heart disease, high-density lipoprotein cholesterol has become an important parameter to evaluate. We have shown that hypertensive patients have normal plasma high-density lipoprotein cholesterol levels, that these are higher in women than in men, and that they are significantly decreased in patients with coronary heart disease. Recently, studies have shown that the beta blocker propranolol unfavorably decreases high-density lipoprotein cholesterol levels and increases triglycerides, whereas the selective alpha 1-blocker prazosin increases high-density lipoprotein cholesterol and decreases triglycerides. A randomized 12-week multicenter trial was conducted to clarify the effects of prazosin and propranolol on serum lipids in essential hypertensive patients (WHO I, II, and III without severe end-organ damage) with blood pressures of at least 160 mm Hg systolic and 95 mm Hg diastolic after a minimum of four weeks treatment with trichlormethiazide (or an equivalent diuretic). Both drugs showed equally good antihypertensive effects. After 12 weeks of therapy, patients receiving prazosin (0.5 mg three times a day, titrated to a maximum dose of 12 mg per day) showed no change in high-density lipoprotein cholesterol, a significant decrease in triglycerides (169 to 129 mg/dl, p less than 0.001) and an increase in lecithin cholesterol acyltransferase (73 to 83 mg/dl). However, the opposite trend was apparent in patients receiving propranolol (10 mg three times a day, titrated to a maximum dose of 120 mg per day); there were decreases in high-density lipoprotein cholesterol, increases in triglycerides, and decreases in lecithin cholesterol acyltransferase, although these changes were not statistically significant. We postulate that the mechanism by which triglyceride is decreased during prazosin therapy is via activation of lipoprotein lipase, which results in a decrease in very low-density lipoprotein, and ultimately triglyceride. Conversely, the increase in lecithin cholesterol acyltransferase seen with prazosin is thought to be related to an increase in the activity of the high-density lipoprotein-lecithin cholesterol acyltransferase cycle, low-density lipoprotein pathway, and very low-density lipoprotein/high-density lipoprotein pathway, which results in elevated high-density lipoprotein cholesterol levels. In hypertensive patients receiving diuretics, prazosin and propranolol have opposing effects on lipid metabolism with prazosin having the more favorable profile.
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PMID:Effects of alpha- and beta-blocker antihypertensive therapy on blood lipids: a multicenter trial. 614 45

The influence of an acute myocardial ischemia on lipoprotein lipase (LPL) activity in the myocardium was studied in open chest dogs. Myocardial ischemia was induced by occlusion of a branch of left descending coronary artery and biopsies were taken from non-ischemic and ischemic myocardium. After 60 min of myocardial ischemia a significantly lower LPL activity was found in full wall biopsies of ischemic than of non-ischemic left ventricular myocardium. The ischemia-induced reduction in LPL activity was most pronounced in the endocardial half of the myocardium. Reduction of LPL activity in the ischemic zone might contribute to limitation of the ischemic injury through reduction of FFA extraction from plasma triglycerides.
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PMID:Myocardial lipoproteins lipase activity during acute myocardial ischemia in dogs. 706 1

Effects of 5-methyl-7-diethylamino-s-triazolo-1, 5-a) pyrimidine (trapidil, Rocornal), a therapeutic agent for ischemic heart disease, on various types of experimental hyperlipemias were studied. With administration of trapidil, elevation of serum high density lipoprotein cholesterol (HDL-C) levels and reduction in serum total cholesterol (TC), low density lipoprotein and very low density lipoprotein cholesterol (LDL-C) and the ratio of HDL-C to LDL-C (LDL-C/HDL-c) were observed in most disease models. Changes in HDL-C levels and LDL-C/HDL-C in the hyperlipemia induced by lipid-enriched diet in mice and in the hyperlipemia induced by high cholesterol diet in Japanese quails were of statistical significance. Also, amelioration of reduction in HDL-C induced by high fat emulsion plus 6-n-propyl-2-thiouracil in rats was observed to be significant. Moreover, trapidil significantly reduced TC, LDL-C levels and LDL-C/HDL-C in the hyperlipemia in hamsters. To investigate possible mechanisms of therapeutic effects of trapidil, blood enzyme activities in Japanese quails with hyperlipemia were assayed. Trapidil showed increases in plasma lipoprotein lipase and serum lecithin-cholesterol acyltransferase activities. These results suggest that trapidil may be an effective chemotherapeutic agent for treating ischemic heart disease.
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PMID:[Effects of 5-methyl-7-diethylamino-s-triazolo-(1, 5-a) pyrimidine (trapidil) on various experimental hyperlipemias (author's transl)]. 720 81

Associations between loss of glucose tolerance, insulin resistance, and ischemic heart disease (IHD) are of great current concern. Considerable controversy and uncertainty relates to the mechanism(s) that underlies these associations. Whilst there is some evidence in prospective studies of an association between hyperinsulinemia and future IHD, it is by no means strong or consistent between different studies. Hypertriglyceridemia is another possible factor involved in the linkage between glucose intolerance and IHD. There is good evidence for an affect of plasma nonesterified fatty acids (NEFA) to increase hepatic output of VLDL. Insulin, contrary to some suggestions, acts to lower plasma VLDL by actions directly on hepatic output and activation of adipose tissue lipoprotein lipase, and indirectly via the hormones affect of lowering plasma NEFA. Glycosylation and oxidation of lipoproteins may enhance their atherogenic potential. It is highly probable that procoagulant changes are also important processes predisposing to IHD. Associations between plasminogen activator inhibitor-1 and insulin, intact and 32,33 split proinsulin hypertriglyceridemia, and insulin resistance have been reported, but a unifying hypothesis explaining these links remains elusive. Epidemiological studies now repeated in a number of centers have shown links between infant mortality and birth weight and risk of IHD, and between birth weight and risk of impaired glucose tolerance and non-insulin-dependent diabetes mellitus (NIDDM). It has been proposed, therefore, that impairment of fetal and infant growth may underlie the associations between loss of glucose tolerance and risk of IHD. Animal models form the basis of much current research to test this concept.
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PMID:Role of insulin and proinsulin in diabetic vascular disease. 747 16


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