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)

Platelet activation and thrombus formation within the coronary artery are major factors in acute myocardial infarction (AMI) and unstable angina (UA), and continuing platelet activation is associated with an adverse prognosis. We assessed platelet activation by using flow cytometry to measure platelet surface expression of P-selectin and glycoprotein IIb/IIIa in 20 patients with AMI and 20 with UA, all of whom were treated with aspirin. Platelet studies were repeated after the infusion of a nitric oxide donor (glyceryl trinitrate or S-nitrosoglutathione) that produced a fall in mean arterial pressure of no more than 10 mm Hg. P-selectin was expressed on 2.5% (range, 1.4% to 6.3%) of platelets from AMI and 2.3% (range, 1.6% to 3.3%) from UA subjects compared with 1.0% (range, 0.6% to 1.9%) of platelets from 20 control volunteers without angina (P < .001). Glycoprotein IIb/IIIa expression was 101.6 +/- 2.7 arbitrary units of relative fluorescence in AMI and 100.2 +/- 3.3 in UA compared with 87.8 +/- 2.5 in control subjects (P < .01). In both AMI and UA, S-nitrosoglutathione reduced P-selectin (P < .001) and glycoprotein IIb/IIIa (P < .05) expression, as did glyceryl trinitrate (P < .02 and P < .01, respectively). In 3 of 20 patients receiving glyceryl trinitrate the lowest dose was not tolerated due to headache or hypotension. These findings show that platelet activation persists in AMI and UA despite aspirin treatment and that this can be inhibited by using glyceryl trinitrate or S-nitrosoglutathione. S-nitrosoglutathione is better tolerated at the doses required.
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PMID:Platelet activation in acute myocardial infarction and unstable angina is inhibited by nitric oxide donors. 854 26

Platelet membrane glycoproteins play a crucial role in ischemic complications after coronary stenting. Glycoprotein IIb-IIIa blockade reduces adverse clinical events after angioplasty but is associated with rare but profound thrombocytopenia that might increase hemorrhagic complications. Changes in platelet membrane glycoproteins of patients with angina who underwent coronary stenting and were treated with the GPIIb-IIIa antagonist abciximab (n=20) or with heparin (n=23) were studied. GPIb-IIIa receptor blockade and membrane glycoproteins were evaluated with immunological markers in venous blood samples taken before. 10, 24, 48, 72, and 96 h after initial treatment with either abciximab or heparin. Patients receiving abciximab therapy showed a rapid inhibition of binding of fluorochrome-conjugated mAb CD41 and c7E3 concomitant with a reduction in platelet aggregation which was restored in part in the days after termination of abciximab infusion. Induction of ligand-induced binding sites on GPIIb-IIIa was increased in patients receiving abciximab. The expression of ligand-induced binding sites correlated inversely with platelet count. No significant change in platelet membrane markers were found in the heparin group. In vitro studies showed that abciximab induces ligand-induced binding sites on isolated platelets and on nuclear cells bearing recombinant GPIIb-IIIa. Abciximab rapidly achieves GPIIb-IIIa receptor blockade after coronary stent placement that might be beneficial in high-risk settings to bridge the delayed action of ticlopidine. Significant alterations of platelet membrane glycoproteins during GPIIb-IIIa antagonism might contribute to development of acute profound thrombocytopenia.
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PMID:Effect of glycoprotein IIb-IIIa receptor antagonism on platelet membrane glycoproteins after coronary stent placement. 986 73

Glycoprotein IIb-IIIa receptor inhibitors are the newest anti-platelets drugs currently used in patients with coronary artery disease. We examined mechanisms of their action and different pharmacokinetic and pharmacodynamic characteristics of the four glycoprotein IIb-IIIa antagonists evaluated in randomized, controlled and multicenter trials. We reviewed results of these trials in the settings of percutaneous revascularizations procedures or unstable coronary syndromes. Platelet glycoprotein IIb-IIIa receptor inhibitors reduced incidence of cardiac death and myocardial infarction during the short- and midterm, and benefit was greater in: a) patients undergoing coronary angioplasty with or without stent implantation, particularly in the presence of unstable angina, diabetes or complex and diffuse coronary artery disease; b) as a direct therapy of unstable coronary syndromes, particularly in patients with refractory angina, diabetes and elevated Troponin; more recently they have been used as adjuvant therapy in acute myocardial infarction. Infusion of these drugs was not associated with higher rates of major bleedings.
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PMID:[Platelet glycoprotein IIB-IIIA receptor inhibitors in patients with ischemic heart disease]. 1110 81

Glycoprotein IIb/IIIa receptor inhibitors can improve vessel patency for patients with myocardial infarction and angina. Patients who receive these drugs can be managed more conservatively, without invasive procedures, and may have less risk of recurrent infarction and death.
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PMID:Beyond aspirin: how glycoprotein inhibitors ease acute coronary syndromes. 1199 1

The objective of this study was to determine the safety of the glycoprotein IIb/IIIa receptor inhibitor eptifibatide in patients at high risk for adverse clinical outcomes and to determine risk factors for eptifibatide-associated bleeding. Consecutive patients (n = 175) who presented with an acute coronary syndrome and who were at high risk for adverse clinical outcomes were prospectively observed for eptifibatide-associated bleeding, which was classified according to Thrombolysis in Myocardial Infarction (TIMI) and Global Use of Strategies to Open Occluded arteries (GUSTO) criteria. High risk was defined as unstable angina or non-Q-wave myocardial infarction with at least one of the following: left ventricular ejection fraction < 40%, diabetes mellitus, ST segment depression or transient ST segment elevation, serum [troponin I] > 2.5 ng/mL, and recurrent angina symptoms after initiation of conventional antianginal therapy. Bleeding incidences in the patients in this study were compared with those in the 4722 eptifibatide-treated patients in the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial. Compared to PURSUIT patients, the population in this study was similar in age but had a higher proportion of females, African Americans, hypertension, diabetes, prior myocardial infarction, heart failure, and revascularization. Bleeding incidences in this study's patients were similar to or lower than those in the PURSUIT population: TIMI major 1.1% versus 10.8%, TAMI minor 12.6% versus 13.1%, GUSTO severe 1.7% versus 1.5%, GUSTO moderate 3.9% versus 11.3%, and GUSTO mild 19.7% versus 26.1%. Renal dysfunction was an independent risk factor for TIMI (odds ratio = 9.1 ([95% CI= 1.6-52.5]) and GUSTO (odds ratio = 6.1 [95% CI = 1.2-30.0]) bleeding. In conclusion, despite being at higher risk for adverse outcomes, patients administered eptifibatide according to this study's institutional guidelines had comparable or lower bleeding rates than in the PURSUIT trial. Renal dysfunction is an independent risk factor for eptifibatide-induced bleeding.
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PMID:Bleeding associated with eptifibatide targeting higher risk patients with acute coronary syndromes: incidence and multivariate risk factors. 1246 32

Glycoprotein IIb/IIIa receptor inhibition prevents the major cardiac events and improves the prognosis of patients with acute coronary syndromes. The purpose of the study was to evaluate the effects of tirofiban on clinical stabilization parameters in patients with unstable angina (UA) and non-Q-wave myocardial infarction (MI). Eighty-three patients presenting with prolonged ongoing chest pain and ST segment depression were included in the study. Forty-two patients were randomized to aspirin and heparin therapy, and 41 patients to tirofiban therapy in addition to the aspirin and heparin therapy. The interval between the initiation of the treatment and the disappearance of angina, recovery time of ST segment depression, creatine kinase-MB (CK-MB) levels, onset of decrease and normalization of CK-MB, and frequency of in-hospital major cardiac events were compared. The interval between initiation of the treatment and the disappearance of angina was significantly shorter in the tirofiban group (3.5 +/- 4.2 vs 9.1 +/- 8.6 h, P << 0.001). Recovery time of ST depression was also significantly shorter in the tirofiban group (5.1 +/- 7.3 vs 12.3 +/- 11.5 h, P << 0.05). The peak CK-MB values were significantly lower in the non-Q-wave MI and UA subgroups of tirofiban than in the heparin group ( P = 0.04 for both). The onset of the CK-MB decrease was significantly earlier in the tirofiban group (15 +/- 14 vs 24 +/- 15 h, P = 0.02). The normalization time of the CK-MB was relatively shorter in the tirofiban group but without statistical significance (50 +/- 22 vs 60 +/- 25 h). The tirofiban group had a lower frequency of total major cardiac events (26% vs 54%, P = 0.01), acute MI (2.4% vs 19%, P = 0.03), and recurrent angina (26% vs 50%, P = 0.04). The frequency of death and urgent revascularization did not differ between the groups. Tirofiban, in addition to heparin, provides earlier clinical stability and prevents major in-hospital cardiac events in patients with UA and non-Q-wave MI as compared to heparin therapy alone.
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PMID:Effects of glycoprotein IIb/IIIa inhibition on clinical stabilization parameters in patients with unstable angina and non-Q-wave myocardial infarction. 1295 26

Glycoprotein IIb/IIIa receptor antagonists, such as abciximab, are used to reduce major adverse cardiac events (MACEs) in patients undergoing percutaneous transluminal coronary angioplasty. The goal of this study was to evaluate the administration of abciximab in relation to lesion complexity and periprocedural complications. A total of 357 patients with 435 de novo lesions were included in this study. Lesions were divided into simple (type A and type B1) and complex (type B2 and type C) lesions according to the American College of Cardiology/American Heart Association Task Force lesion complexity system. Abciximab was given to unstable complex lesions and simple lesions with a periprocedural unstable complicated course. The overall incidence of MACE during the 9-month follow-up period was 17.0%. Patients treated with abciximab had a higher lesion complexity (P < 0.001), dissections (P = 0.014), stents (P < 0.001), and vessels involved (P < 0.001). in addition, the abciximab group was characterized by a higher angina NYHA class (P = 0.005), lower TIMI flow prior to stenting (P = 0.01), and a longer total inflation time (P = 0.006). Despite these clinical differences, the occurrence of MACE within the abciximab group was slightly less than in the group without abciximab (16.2% and 17.3%, respectively). Lesion complexity was directly related to MACE in the group that did not receive abciximab (simple and stable complex lesions; P = 0.04). On the other hand, in subjects treated with abciximab, lesion complexity was not related to a higher incidence of MACE (P = 0.76). The use of abciximab equalizes the difference in outcome between simple and complex lesions. Therefore, abciximab should be advocated especially in unstable and complex percutaneous coronary interventions.
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PMID:Clinical impact of abciximab on long-term outcome after complex coronary angioplasty. 1457 84

The goal of this study was to compare the clinical presentation and angiographic morphology of patients having an unstable angina pectoris. A total of 321 patients were consecutively studied and underwent cardiac catheterization, mean age 59 + 6 years. According to Braunwald classification, class III was predominant (58%) On coronary angiography, 148 patients had single vessel disease, double-vessel in 92 and triple-vessel in 64. Morphology of coronary artery lesions was classified according to Ambrose's classification, 100 patients had simple lesions (type I or IIA), 204 patients had complex lesions (type IIB, III, intracoronary thrombus or total occlusion). Thoracic rest pain (class III) or postinfarction angina (class C), were associated with the presence of complex lesions. This subgroup of high risk patients would benefit from either Glycoprotein IIb/IIIa blockers with an early revascularisation strategy.
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PMID:[Correlation of clinical and angiographic morphology in unstable angina]. 1512 9