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

The structural homology between plasminogen and apolipoprotein (a), the specific glycoprotein of Lp(a) lipoprotein, raises the possibility of a relationship between this lipoprotein and the plasma fibrinolytic system. The present study examines this proposal by studying 66 patients with angina pectoris. As compared to normal controls, the patients had raised concentrations of Lp(a): B lipoprotein particles. No correlation was found between circulating Lp(a): B and the fibrinolytic system. The pathogenic role of Lp(a): B lipoprotein seems therefore not mediated by its effect on the plasma fibrinolytic system.
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PMID:The increased plasma Lp(a): B lipoprotein particle concentration in angina pectoris is not associated with hypofibrinolysis. 214 23

Increased glycosylation of various proteins in diabetic patients has been reported by many authors. In the present study, the extent of non-enzymatic glycosylation in diabetic patients with or without chronic complications was investigated. Eighty-five diabetic patients were studied, 20 were without any clinical evidence of chronic complications while the remainder were suffering from cataract (n = 18), retinopathy (n = 16), peripheral neuropathy (n = 16) and cardiovascular complications like angina pectoris, myocardial infarction and hypertension (n = 15). All patients were selected on clinical grounds. Fifteen apparently healthy subjects of similar age and weight were studied as control subjects. Fasting plasma glucose was increased in all diabetic patients and correlated significantly with glycosylated hemoglobin, glycosylated plasma protein and serum fructosamine concentrations. There was no significant difference between diabetic patients with or without chronic complications in the levels of fasting plasma glucose, glycosylated plasma proteins, glycosylated hemoglobin, serum fructosamine, mucoprotein, hexosamine, sialic acid and fucose. Alpha-2 globulin fraction was increased in both uncomplicated and complicated diabetic patients and albumin was found to be decreased in patients with cataract, peripheral neuropathy and cardiovascular diseases. Alpha-1 and beta globulins were significantly decreased in patients with cardiovascular diseases and retinopathy respectively while gamma globulin was increased in retinopathy patients. In uncomplicated diabetic patients alpha-1 glycoprotein was decreased and gamma glycoprotein was increased. In diabetic patients with retinopathy, alpha-1 glycoprotein was elevated significantly while beta glycoprotein was decreased.
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PMID:Changes in glycosylated proteins in long-term complications of diabetes mellitus. 216 68

CCB are a diverse group of drugs that bind to specific glycoprotein receptors associated with the cell membrane that are most likely identical to the voltage-sensitive calcium channel. By inhibiting the influx of calcium into myocardial, pacemaker, and conducting tissues and vascular smooth muscle, these agents modify excitation-contraction coupling in muscle and electrical impulse transmission in the heart. The vasodilating and electrophysiologic actions of these drugs have been harnessed for the treatment of coronary vasospasm, angina pectoris, and supraventricular arrhythmias. They also have great potential for the treatment of hypertension, cerebrovascular disorders, and Raynaud's phenomenon. Their utility in hypertrophic cardiomyopathy, congestive heart failure, myocardial preservation, and primary pulmonary hypertension has not been convincingly established. Future second-generation CCB may offer greater selectivity, improved side effect profiles, and an even wider range of actions.
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PMID:Calcium channel blocking drugs. Part II: Clinical applications. 241 54

In patients with various forms of ischemic heart disease the following indices were examined by radial immunodiffusion: alpha-1-acid glycoprotein, alpha-1-antitrypsin, haptoglobin, alpha-2-glycoprotein, beta-2-glycoprotein, immunoglobulin, C3 and C4 complement fractions. The changes in the serum glycoproteins during the acute phase of myocardial infarction are pointed out. The changes in the immunoglobulins and the complement fractions in patients with ischemic heart disease are discussed. Their determination in patients with stenocardia and past myocardial infarction is of no diagnostic value.
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PMID:[Ischemic heart disease--clinical, biochemical and immunobiological parallels]. 321 29

The platelet glycoprotein (GP) IIb/IIIa receptor can bind fibrinogen, von Willebrand factor, and other adhesive ligands; this binding is the final common pathway mediating platelet aggregation. The purpose of this study was to evaluate the safety and platelet inhibitory characteristics of the Fab fragment of the murine monoclonal anti-GPII/IIIa 7E3 antibody (m7E3 Fab) when administered intravenously as a single bolus dose, as a single and repeat bolus dose, and as a single bolus dose followed by continuous infusions of varying duration. Various dosage regimens of m7E3 Fab were studied in 74 patients with stable angina. Dosage regimens included single doses of m7E3 Fab from 0.1 to 0.3 mg/kg, a single dose of 0.20-0.30 mg/kg, and a repeat dose of 0.05 mg/kg, or a loading dose followed by a continuous infusion of m7E3 Fab for up to 36 hours. To assess the effect of m7E3 Fab on platelet function, quantitative blockade of GPIIb/IIIa receptors, inhibition of ex vivo platelet aggregation, and template bleeding time were measured in all patients. Dose-dependent inhibition of platelet function was evident in response to escalating bolus doses of m7E3 Fab, with maximum inhibition observed at 0.25-0.30 mg/kg body weight; at the 0.30 mg/kg dose, mean (+/- SE) GPIIb/IIIa receptor blockade was 81 +/- 3%, ex vivo platelet aggregation in response to 20 microM ADP was 14 +/- 6% of baseline, and the median bleeding time was > 20 minutes. Although platelet function gradually recovered following a single bolus injection, platelet inhibition could be sustained by continuous, low-dose infusion of the antibody. Platelet inhibition occurred within minutes, but m7E3 Fab that did not bind to platelets cleared rapidly from circulation. Sixteen percent of the m7E3 Fab-injected subjects exhibited low titer, human anti-murine antibody responses. No significant bleeding or allergic reactions were observed in any patients. One of the 74 patients developed transient thrombocytopenia soon after receiving m7E3 Fab. These studies establish that m7E3 Fab can be administered safely at doses that cause profound inhibition of platelet function.
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PMID:Blockade of the human platelet GPIIb/IIIa receptor by a murine monoclonal antibody Fab fragment (7E3): potent dose-dependent inhibition of platelet function. 857 49

The CD36 molecule is a multifunctional membrane type receptor glycoprotein that reacts with thrombospondin, collagen, oxidized LDL and long-chain fatty acids (LCFA). LCFA are one of the major cardiac energy substrates, hence LCFA metabolism may have an important role in cardiac diseases. In this study, we analyzed CD36 expression in 200 patients with heart diseases [44 patients with hypertrophic cardiomyopathy (HCM), 16 with dilated cardiomyopathy (DCM), 26 with old myocardial infarction (OMI), 55 with angina pectoris (AP) and 59 with other miscellaneous heart diseases] using a flow cytometer. 123I-beta-methyl-p-iodophenylpentadecanoic acid (BMIPP) myocardial accumulation was also examined in some patients. Eight patients (2 with HCM, 1 with DCM, 2 with OMI, and 3 with AP) were diagnosed as having type I CD36 deficiency (neither platelets nor monocytes expressed CD36). Sixteen patients (3 with HCM, 1 with DCM, 1 with OMI, 8 with AP, and 3 with other heart diseases) showed type II CD36 deficiency (monocytes expressed CD36 but platelets did not). In all 8 patients with type I CD36 deficiency, there was no BMIPP accumulation in the heart. However, in 13 patients with type II CD36 deficiency, focally reduced BMIPP accumulation was observed, but there were no patients without BMIPP accumulation. CD36 deficiency was observed in a higher proportion (12%) of patients with heart disease in this study than in a reported control study. Type I CD36 deficiency is associated with absence of BMIPP accumulation in the heart, hence it may have an important role in LCFA metabolic disorders and some types of cardiac hypertrophy as well as other heart diseases.
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PMID:[Different patterns of 123I-BMIPP myocardial accumulation in patients with type I and II CD36 deficiency]. 949 34

The era of platelet glycoprotein (GP) IIb/IIIa receptor inhibition in cardiology was inaugurated in 1994 with the publication of the Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC) trial results. EPIC demonstrated that the GP IIb/IIIa blocker abciximab, administered as a bolus and 12-hour infusion, afforded protection against ischemic complications in high-risk patients undergoing angioplasty and atherectomy, including those with unstable angina or evolving myocardial infarction (MI). A significant reduction in the incidence of death, acute MI, or revascularization was apparent at 30 days and also sustained at 6-month and 3-year follow-up. The subsequent Evaluation in PTCA to Improve Long-Term Outcome with Abciximab GP IIb/IIIa Blockade (EPILOG) study extended these findings to the full spectrum of coronary intervention patients, confirming that abciximab provided similar benefits in low-risk patients as well. The EPILOG trial also proved that any excess bleeding risk associated with potent antiplatelet therapy could be brought down to placebo levels through the use of a low-dose, weight-adjusted heparin regimen, early vascular sheath removal, and elimination of routine postprocedural heparinization. The potential for an advantage of GP IIb/IIIa blockade in patients with refractory unstable angina/non-Q-wave MI was demonstrated in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial, which showed that a 24-hour preprocedural abciximab infusion effectively stabilized these patients, thereby enhancing the safety of intervention and reducing the 30-day incidence of ischemic events. A similar pattern of benefit has emerged from clinical trials of such other GP IIb/IIIa inhibitors as eptifibatide, lamifiban, and tirofiban. Trials are currently underway to clarify the benefits of GP IIb/IIIa blockers in patients undergoing stenting and as an adjunct to thrombolytic therapy or primary angioplasty in patients with acute MI (ST-segment elevation).
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PMID:An overview of the results of clinical trials with glycoprotein IIb/IIIa inhibitors. 953 95

We set out to determine the genotype distributions of the PI(A) polymorphism of platelet glycoprotein IIIa, the HPA-3 polymorphism of platelet glycoprotein IIb, and the variable number tandem repeat (VNTR) polymorphism of platelet glycoprotein Ib in subjects with Type 2 diabetes mellitus (Type 2 DM) with (n = 125) and without (n = 90) a clinical history of macrovascular disease. In 215 white European subjects with Type 2 DM, presence of coronary artery disease was determined as a clinical history of angina, myocardial infarction (MI), coronary angioplasty or coronary artery by-pass grafting. Presence of peripheral vascular disease was defined as a clinical history of intermittent claudication with confirmatory vascular ultrasound or angiography, intermittent claudication with undetectable foot pulses and no history of arthralgia or surgery for leg ischaemia, confirmed by reference to medical case notes. Polymorphisms were detected by polymerase chain reaction amplification of DNA. There was no difference in the genotype distributions of subjects with and without macrovascular disease. In subjects with a first MI before the age of 60 years (n = 26), there was a 38% incidence of PI(A2) compared to 29% in subjects free from clinically evident macrovascular disease, but this difference did not reach statistical significance. This study does not support the hypothesis that polymorphisms of platelet glycoproteins, in particular the PI(A) polymorphism of platelet glycoprotein IIIa, play an important role in the pathogenesis of macrovascular disease in subjects with Type 2 DM.
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PMID:Polymorphisms of platelet glycoproteins in relation to macrovascular disease in type 2 diabetes mellitus. 958 97

The era of platelet glycoprotein (GP) IIb/IIIa receptor inhibition in cardiology was inaugurated in 1994 with the publication of the Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC) trial results. EPIC demonstrated that the GP IIb/IIIa blocker abciximab, administered as a bolus and 12-hour infusion, afforded protection against ischemic complications in high-risk patients undergoing angioplasty and atherectomy, including those with unstable angina or evolving myocardial infarction (MI). A significant reduction in the incidence of death, acute MI, or revascularization was apparent at 30 days and also sustained at 6-month and 3-year follow-up. The subsequent Evaluation in PTCA to Improve Long-Term Outcome with Abciximab GP IIb/IIIa Blockade (EPILOG) study extended these findings to the full spectrum of coronary intervention patients, confirming that abciximab provided similar benefits in low-risk patients as well. The EPILOG trial also proved that any excess bleeding risk associated with potent antiplatelet therapy could be brought down to placebo levels through the use of a low-dose, weight-adjusted heparin regimen, early vascular sheath removal, and elimination of routine postprocedural heparinization. The potential for an advantage of GP IIb/IIIa blockade in patients with refractory unstable angina/non-Q-wave MI was demonstrated in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial, which showed that a 24-hour preprocedural abciximab infusion effectively stabilized these patients, thereby enhancing the safety of intervention and reducing the 30-day incidence of ischemic events. A similar pattern of benefit has emerged from clinical trials of such other GP IIb/IIIa inhibitors as eptifibatide, lamifiban, and tirofiban. Trials are currently underway to clarify the benefits of GP IIb/IIIa blockers in patients undergoing stenting and as an adjunct to thrombolytic therapy or primary angioplasty in patients with acute MI (ST-segment elevation).
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PMID:An overview of the results of clinical trials with glycoprotein IIb/IIIa inhibitors. 959 18

The fact that certain ethnic groups and specific populations residing in certain geographic areas carry an increased risk for thrombosis and that thrombosis occurs in young patients without established risk factors indicates the presence of new, previously unrecognized inherited conditions predisposing to thrombosis. We are now aware that interindividual variations within the loci coding for proteins relevant to lipid and vascular metabolisms as well as blood coagulation are universally found. Platelets play central roles in cerebrovascular diseases and acute coronary syndromes, as demonstrated by histopathological findings and clinical observations showing the efficacy of antiplatelet therapies for these disorders. In this article, we show our recent findings on the association between coronary artery disease (CAD) and polymorphisms in platelet membrane glycoproteins. The glycoprotein (GP) Ib/IX complex is a receptor for von Willebrand factor, which mediates shear stress-dependent platelet activation. It has recently been implicated in the pathogenesis of acute coronary syndromes. We have determined genotypes of the "size-polymorphism" of GPIb alpha--i.e., the variable number (1-4) of a 13 amino acid sequence (399-411)--in angiographically proven Japanese CAD patients with myocardial infarction or angina pectoris as well as in individuals from the general population with no history of angina or other heart diseases and normal resting electrocardiograms (ECG). We have found that the genotypes having at least one 4-repeat allele (4R) are more frequently found in patients than in controls. Logistic regression analyses for the adjustment of age, sex, and other acquired coronary risk factors provided an odds ratio of 7.94 (p=0.0043) for those with 4R vs. those without 4R, suggesting that the presence of 4R is an independent risk factor for CAD. The molecular mechanisms underlying this association are currently under investigation. Relationships between arterial thrombosis and polymorphisms in other platelet GPs (collagen receptor and fibrinogen receptor), blood coagulation factors, fibrinolytic factors, vasoactive substances, and factors relevant for lipid metabolisms are also discussed.
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PMID:Genetic polymorphisms and risk of coronary artery disease. 970 55


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