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)

The authors administered lovastatin (Mevacor, MSD) to 18 patients with primary hyperlipoproteinaemia (familial and non-familial) with a lipoprotein pattern type IIa and IIb. During treatment a marked reduction of atherogenic indicators of the lipid metabolism occurred, i.e. a decline of total cholesterol (-28.6%), LDL-cholesterol -39%), apolipoprotein B (-18.6%), the index of total cholesterol/HDL-cholesterol (-44.6%) and the index LDL-cholesterol/HDL-cholesterol (-48.2%). At the same time a favourable effect on indicators of the lipid metabolism to which a protective action is ascribed was recorded: a rise of HDL-cholesterol (+13.6%) and apolipoprotein AI (+13%) and AII (+13%). An excellent effect was observed also in four heterozygotes with familial hypercholesterolaemia which is usually rather resistant to other types of hypolipidaemic treatment. The drug was very well tolerated and subjective side-effects of treatment were minimal. Despite the fact that a number of laboratory indicators was followed up, the authors did not observe any undesirable side-effects, only a transient and marginal rise of ALT in one patient. Lovastatin is, due to its potent hypolipidaemic effect, a new hope in the treatment of hypercholesterolaemia. Its usefulness in the prevention of ischaemic heart disease, as well as its safety during prolonged administration are tested at present in long-term investigations.
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PMID:[Personal experience with lovastatin, a HMG-CoA reductase inhibitor (Mevacor, MSD) in the treatment of hypercholesterolemia]. 184 44

In order to establish the possible existence of a cardiac converting enzyme and its role in the pathophysiology of the myocardial ischemia, the direct cardiac effects of IEC and AI or AII were studied on the isolated rat heart perfused through the left atria. Three series of seven hypertensive rats (SHR) were used. The reduction of the aortic flow (QAO) due to ischemia (produced by a left coronary artery ligation of 10 mn) was brought into line with the reduction of the coronary flow (QCORO) and the weight of the heart. This reduction was 2.06 +/- 1.8 for the control, 1.96 +/- 1.27 when captopril (CAP) (10(-5) M) was added to the perfusion liquid and 1 +/- 0.42 when perindopril (PER) (1.2 x 10(-5) M) was added to the perfusion liquid (p less than 0.05 vs CAP). Four series of 10 rat hearts (Sprague Dawley) were used to study the changes on the working heart caused by short perfusions of AI or AII (10(-7) M) in the presence of IEC or saralasin (SAR 10(-7) M). AII caused a reduction of the QCORO of 2.1 +/- 0.26 ml/mn, an increase of the QAO of 2.5 +/- 0.9 ml/mn and an increase of the heart rate (HR) of 9 +/- 3.24 beats/mn. In the presence of CAP or PER the effects of AII were the same, however in the presence of SAR these effects were prevented. AI caused a reduction of the QCOR of 2.5 +/- 0.4 ml/mn, an increase of the QAO of 2.5 +/- 0.8 ml/mn and an increase of the HR of 18 +/- 4 beats/mn.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Direct cardiac effects of angiotensins I and II and 2 converting enzyme inhibitors (captopril and perindopril). Indirect demonstration of a converting enzyme in the rat heart]. 284 75

This work aims to analyze the influence of aminophylline in the pulmonary and hepatic uptake of 99mTc-methoxyisobutil isonitrile (99mTc-MIBI). 72 patients were studied and a myocardial perfusion (MPS) single photon emission computed tomography (SPECT) with 99mTc-MIBI was carried out after the administration of dipyridamole. According to the MPS, the patients were classified into 2 groups: Group A: 45 patients without myocardial ischemia and Group B: 27 with ischemia. Each group was divided into 2 subgroups according to whether they had (I) or had not (II) received intravenous aminophylline. The dipyridamole was administered for 4 minutes at a dose of 0.56 mg/kg. If the patients presented any complication, intravenous aminophylline was administered. At 30 minutes p.i., planar images were obtained during a scintigraphy in the interior projection after the injection of 99mTc-MIBI. The regions of interest in the heart, hepatic cupula, and most active area of the left lung were outlines and the activity rates were calculated: lung/heart (LHR) and liver/heart (LivHR). No statistically significant differences were observed in the uptake of 99mTc-MIBI between subgroups I and II. However, the LHR rates in both subgroups were significantly lower in the patients with normal myocardial perfusion than in the patients with ischemia: LHR group A1 vs B1: 0. 32 +/- 0.08 vs 0.36 +/- 0.06, p = 0.03; group AII vs BII 0.31 +/- 0. 07 vs 0.35 +/- 0.07, p = 0.01 respectively. In conclusion, the administration of aminophylline, after the infusion of dipyridamole for MPS, does not modify the pulmonary or hepatic uptake of 99mTc-MIBI.
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PMID:The effect of aminophylline administration on 99mTc-MIBI lung and liver uptake in patients with or without myocardial ischemia. 1106 Feb 72

Recently, much attention has been paid to small sized low density lipoprotein (LDL) as a risk factor for ischemic heart disease. We investigated the effect of celiprolol hydrochloride (CH), which is a beta 1 selective beta-blocker with high intrinsic sympathomimetic activity (ISA), on the LDL particle size. We treated 41 hypertensive patients with CH and studied the change in LDL particle size according to the score of fast beta lipoprotein and LDL relative mobility value (LDL-Rm) measured by lipoprotein polyacrylamide gel disc electrophoresis (PAGE). We also studied changes in blood pressure, total cholesterol (TC), trygiyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and midband on PAGE. Systolic and dyastolic blood pressure and pulse significantly decreased during treatment. TC levels were significantly decreased at 8 weeks in all subjects and at 4, 8 and 12 weeks in patients with a TC value of over 220 mg/dl. TG levels were significantly decreased at 4 and 8 weeks in patients with initial levels of over 150 mg/dl, and significantly increased at 4 and 8 weeks in those with initial levels of under 150 mg/dl of TG. HDL-C levels did not significantly change during treatment. LDL-C levels were significantly decreased at 4, 8 and 12 weeks in patients with initial levels of over 150 mg/dl. Apo AI, AII, B, CII, CIII and E levels did not significantly change during treatment. Fast beta lipoprotein scores did not significantly change overall during treatment, but were significantly decreased at 4 and 8 weeks in patients initial TG levels of over 150 mg/dl and at 4 and 12 weeks in those with initial levels of over 220 mg/dl of TC. LDL-Rm scores did not significantly change during treatment. Midband scores were significantly reduced overall at 8 weeks, and after 4 and 8 weeks in patients with initial TG levels of over 150 mg/dl and at 4, 8 and 12 weeks in those with initial TC levels of over 220 mg/dl. These results indicated that CH did not change LDL particle size. It was suggested that CH might be a beneficial beta-blocker from the standpoint of prevention for atherosclerosis.
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PMID:[The effect of celiprolol hydrochloride for lipid metabolism--especially for the low density lipoprotein particle size]. 1143 90

Atherosclerosis is a vascular inflammatory disease resulting from lipid deposition within vascular wall and changes in structure and function of the vascular wall. Atherosclerosis is accelerated when total and LDL cholesterol are elevated and/or HDL is low. Free radical production is increased in hypercholesterolemia leading to oxidative transformation of both parts of LDL particles, protein and lipid part. Small, dense LDL particles have extreme atherogenic potential; they can be easily oxidized and strongly maintain vascular inflammation. Oxidized LDL particles (oxLDL) support further free radical production. OxLDL are removed by macrophages into sub epithelial space. During that process macrophages produce inflammatory cytokines and induce the production of adhesion molecules, which further cause adherences of new macrophages and further support inflammation. OxLDL also induce sinthesis of endothelial growth factor receptors, which enable transduction of different signals important for: vascular remodeling, cellular migration, mitosis and NF-kappaB activation and increased metalloproteinase activity. HDL particles have an important role in the reverse cholesterol path and protective effects in vascular inflammation and atherogenesis. The ratio of apoprotein AI and AII, amount of CETP, LCAT and paraoxsonase, determine the function of HDL particles. Increased levels of triglycerides in the morning and especially postprandial levels are an independent risk factor for coronary heart disease, and heighten the risk when associated with other lipid disturbances. An increased triglyceride level is associated with the increased PAI I and reduced fibrinolisis. The ratio of total cholesterol/HDL cholesterol, as well as the levels of markers of inflammation such as CRP or IL-6, have great predictive value for the development of ischemic heart disease and cardiovascular diseases.
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PMID:[Vascular inflammation: effect of proatherogenic dyslipidemic trio or quartet]. 1970 14