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 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

Antiplatelet therapy, most notably aspirin, has been well documented to reduce risks of subsequent cardiovascular disease (CVD) in secondary prevention, acute myocardial infarction (MI), acute occlusive stroke, as well as in primary prevention. In secondary prevention, the most recent Antithrombotic Trialists' Collaboration reviewed 194 published randomized trials of antiplatelet therapy, mostly aspirin, involving more than 212 000 patients (ie, 135 000 using antiplatelet therapy or control and 77 000 using different antiplatelet regimens). In a very wide range of patients who have survived a prior occlusive vascular event-including MI, transient ischemic attacks, occlusive stroke, unstable and stable angina, percutaneous coronary interventions, and coronary artery bypass graft-aspirin prevents about 25% of serious vascular events. Among patients suffering acute Ml or acute occlusive stroke, aspirin begun promptly and continued long-term reduces risks of subsequent MI, stroke, and vascular death. In acute coronary syndromes, clopidogrel added to aspirin further reduces the risk of important vascular events, but not mortality, and causes more side effects, especially bleeding. For patients undergoing percutaneous coronary interventions, the addition of a short-term infusion of a glycoprotein IIb/IIIa receptor antagonist to aspirin prevents additional vascular events during the early in-hospital period but also increases the risk of major bleeding. Ongoing research is investigating other combinations of different antiplatelet drugs. In all these high-risk patients, there is a small excess of major bleeding among those assigned at random to aspirin, which is far outweighed by the magnitude of benefits on CVD. During an acute MI, after a loading dose of 160 mg to 325 mg aspirin, daily doses ranging from 75 to 150 mg daily are as effective as higher doses. For long-term treatment, the effects of doses < 75 mg daily are less certain. Although side effects are dose-related, especially in doses > 325 mg daily, no antiplatelet regimen is more effective than aspirin for long-term use. In primary prevention, 5 randomized trials have been published involving more than 60 000 apparently healthy men and women. Persons randomized to receive aspirin in these trials had significant reductions in risk of a first MI (32%) and important vascular events (15%). Since the numbers of strokes and vascular deaths were insufficient to distinguish between the benefits found in secondary prevention and no effect, use of aspirin in primary prevention should be weighed in light of the cardiovascular risk profile, the side effects of the drug, and its clear benefit in reducing risk of a first MI. Aspirin should be an adjunct, not an alternative, to managing other cardiovascular risk factors. Recently, the US Preventive Services Task Force and the American Heart Association recommended aspirin use for all men and women whose 10-year risks are > 6% and > or = 10%, respectively. In all these patient categories, including secondary prevention, acute MI and acute occlusive stroke, as well as primary prevention, increased and appropriate use of aspirin will prevent large numbers of premature deaths and MIs.
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PMID:Update on aspirin in the treatment and prevention of cardiovascular disease. 1251 36

Is a "routine invasive" or "selective invasive" strategy the best approach for patients with non-ST-segment elevation acute coronary syndrome (ACS)? A "selective invasive" strategy incorporates ischemia-guided use of aggressive medical therapy followed by angiography and revascularization for angina or stress-induced myocardial ischemia. The "routine invasive" strategy (cardiac catheterization followed by percutaneous coronary intervention within 24 to 48 h of symptom-onset) is frequently employed, but no randomized, controlled trials have demonstrated improved clinical outcomes. Recently, the second Fragmin and fast Revascularization during InStability in Coronary artery disease (FRISC-II) and the Treat angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis in Myocardial Infarction (TACTICS TIMI-18) trials found significant reductions in death, recurrent myocardial infarction, or hospitalization for biomarker-positive ACS. Also, the third Randomized Intervention Trial of unstable Angina (RITA-3) recently reported a halving of refractory angina and reduction in the use of antianginal medication with early intervention. Early trials failed to demonstrate the superiority of the "routine invasive" approach, presumably because of fewer revascularizations, unavailability of stents, and more recent use of glycoprotein IIb/IIIa inhibitors and low-molecular-weight heparins. The FRISC-II, TACTICS TIMI-18, and RITA-3 studies indicate that higher-risk patients benefit from early revascularization, but that aggressive antiplatelet, antithrombin, and anti-ischemic therapy are also important. While all three trials support an "early invasive" approach in intermediate- and high-risk patients, other trials support a more "conservative" approach in those without electrocardiographic changes or enzyme elevations. Optimal management should incorporate both strategies.
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PMID:"Routine invasive" versus "selective invasive" approaches to non-ST-segment elevation acute coronary syndromes management in the post-stent/platelet inhibition era. 1264 49

Enoxaparin (E) is a low-molecular-weight heparin which has been proven more effective than unfractionated heparin (UFH) for the treatment of non-ST-segment elevation acute coronary syndromes. Limited and inconclusive on the other hand, are the data on the use of E in acute myocardial infarction with persistent ST-segment elevation (STEAMI). Therefore, we performed a review of the literature in order to evaluate the level of evidence relative to the efficacy and safety of E in such a clinical setting. The effect of E in STEAMI has been evaluated in 7 clinical studies, including a total of about 9500 patients. Compared to placebo, E resulted more effective on the incidence of the combined end-point of death, re-infarction and recurrent angina in the study by Glick et al. and on the patency of the infarct-related artery in the AMI-SK study. Compared to UFH, E resulted more effective on the incidence of the combined end-point of death, reinfarction and unstable angina in the study by Baird et al. and of in-hospital re-infarction and refractory ischemia rates in both ASSENT-3 and ASSENT-3 PLUS, while the effect on the patency of the infarct-related artery, which was evaluated in HART-II and ENTIRE-TIMI 23, resulted non univocal. Overall, bleeding complications were more frequent than with placebo and comparable to UFH, with the exception of ASSENT-3 PLUS where pre-hospital administration of E was associated with a doubled incidence of intracranial bleeding (although only in patients older than 75 years). In conclusion, the administration of E, in association with aspirin and thrombolytics, already appears a possible therapeutic option for the treatment of STEAMI, due to its good efficacy and safety profile, along with its easiness of use. However, prior to have its use recommended, the current B level of evidence of a superior efficacy and safety compared to UFH needs to be reinforced. Further-more, some open issues relative to the use of E in particular settings (aged patients, in association with glycoprotein IIb/IIIa inhibitors and during percutaneous coronary revascularization) need to be clarified.
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PMID:Enoxaparin for the treatment of acute myocardial infarction with persistent ST-segment elevation. 1455 16

Patients presenting with unstable angina pectoris or non-Q-wave myocardial infarction (MI), if treated inadequately, are at a high risk of MI and subsequent mortality. The use of intravenous small molecule glycoprotein IIb/IIIa inhibitors along with standard therapeutic management options improves outcome. Since the publication of the Thrombolysis in Myocardial Ischemia IIIB, Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) and Fragmin and Fast Revascularization during InStability in Coronary artery disease II (FRISC II) studies, there is great debate about the advantages of following an early 'invasive' treatment option with coronary angiography and revascularization after initial medical therapy compared with the 'conservative' approach, where angiography is reserved for those who remain symptomatic. The Treat angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy--Thrombolysis in Myocardial Infarction 18 (TACTICS-TIMI 18) study has helped to resolve some of the controversies since it was designed with more current medical (early and routine use of tirofiban) and revascularization (use of stents during percutaneous coronary interventions) options as part of the invasive treatment protocol. This study indicated that an early invasive strategy in risk stratified patients combined with early use of tirofiban with standard medical therapy significantly improves outcome and appears well tolerated.
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PMID:Current management of unstable angina: lessons from the TACTICS-TIMI 18 trial. 1472 69

Current evidence suggests that routine invasive therapy in the setting of unstable angina/non-ST-segment elevation myocardial infarction (UA/NSTEMI) reduces the incidence of composite end points (i.e., death, myocardial infarction, or angina.). The 2002 American College of Cardiology/American Heart Association guidelines recommend invasive therapy in high-risk patients, although it is unknown if such an approach improves survival. We conducted a meta-analysis on 5 studies in 6,766 UA/NSTEMI patients who were randomized to either routine invasive versus conservative therapy in the era of glycoprotein IIb/IIIa inhibitors and intracoronary stents. Compared with conservative therapy, an invasive approach suggested a reduction in mortality at 6 to 12 months (risk ratio [RR] 0.80, 95% confidence interval [CI] 0.63 to 1.03) and at 24 months (RR 0.77, 95% CI 0.60 to 0.99). The composite end point of death or myocardial infarction was reduced throughout all periods of follow-up: at 30 days (RR 0.61, 95% CI 0.45 to 0.84), at 6 months (RR 0.75, 95% CI 0.63 to 0.89), and at 12 months (RR 0.78, 95% CI 0.65 to 0.92). For the same composite end point at 6 to 12 months, men benefited from invasive therapy (RR 0.68, 95% CI 0.57 to 0.81), as did troponin-positive patients (RR 0.74, 95% CI 0.59 to 0.94). The results for women (RR 1.07, 95% CI 0.82 to 1.41) and troponin-negative patients (RR 0.82, 95% CI 0.59 to 1.14) were equivocal. Routine invasive therapy in UA/NSTEMI patients along with adjunctive use of glycoprotein IIb/IIIa inhibitors and intracoronary stents improves survival. Enhanced risk stratification is needed in women and troponin-negative patients so that invasive therapy may be more effectively recommended in these groups.
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PMID:Invasive therapy along with glycoprotein IIb/IIIa inhibitors and intracoronary stents improves survival in non-ST-segment elevation acute coronary syndromes: a meta-analysis and review of the literature. 1505 Apr 84

Administration of GP IIb/IIIa inhibitors during percutaneous coronary intervention (PCI) has proven clinical benefit, but is administered at a dose allowing for the patients' weight but not other variables. This study of 75 patients evaluated platelet inhibition achieved by standard-dose abciximab therapy during PCI as measured by two point-of-care (POC) instruments, Plateletworks (PW) and whole blood aggregation (WB). Results were related to the decrease of platelet activation produced as well as patients' return of angina within 30 days. Flow cytometric measurement showed abciximab suppressed platelet-monocyte aggregates (P < 0.001) and activated glycoprotein IIb/IIIa (P < 0.001) but not P-selectin. Greater POC-measured inhibition corresponded to less postabciximab expression of platelet-monocyte aggregates (P < 0.01). Patients above the lowest quartile of POC inhibition with PW demonstrated a relative risk of experiencing return of angina within 30 days of 0.48 (0.23-0.99). In conclusion, POC measurements reflect platelet activation suppression, higher PW measurements being associated with a decreased risk of return of angina.
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PMID:Point-of-care testing shows clinically relevant variation in the degree of inhibition of platelets by standard-dose abciximab therapy during percutaneous coronary intervention. 1517 Jul 2

A polymorphism of glycoprotein IIb/IIIa has been associated with myocardial infarction and restenosis after percutaneous coronary intervention. The influence on outcome and the interaction of the Pl(A1) genotype with classic risk factors for coronary artery disease (CAD) were characterized in patients with chronic CAD followed prospectively for 3 years. Pl(A1) genotypes were assessed in 592 patients enrolled in the Medical, Angioplasty, or Surgery Study II, a randomized trial comparing treatments for patients with CAD and preserved left ventricular function. The incidence of the composite end point of cardiac death, myocardial infarction, and refractory angina requiring revascularization were determined in each genotype group. Risk was assessed with the Cox proportional-hazards model. The clinical characteristics and treatment of each genotype were similar. Although the composite end point tended to be more common in patients with the Pl(A2) allele, only smokers with the Pl(A2) allele had a significantly increased incidence of the composite end point (p = 0.01). Moreover, a 2.2-fold increased risk was apparent in smokers with the Pl(A2) allele (p = 0.03). Thus, taken together, these data provide support for the interaction effect between smoking and the Pl(A1) gene variant. Smokers with the Pl(A2) polymorphism of platelet glycoprotein IIIa are at greater risk for subsequent cardiac events in stable coronary disease.
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PMID:Effect of glycoprotein IIIa PlA2 polymorphism on outcome of patients with stable coronary artery disease and effect of smoking. 1519 15

Acute coronary syndromes are responsible for the deaths of tens of thousands of patients every year. Rupture of coronary atheromatous plaques with resultant luminal thrombosis is the cause in most cases. Although great steps forward have been taken in the management of acute myocardial infarction (MI) and unstable angina (UA), new therapeutic strategies are required to reduce further the incidence and risk of these events. At present, aspirin, nitrates and heparin are the conventional treatments for unstable angina. Aspirin, in combination with a thrombolytic agent or with percutaneous transluminal coronary angioplasty (PTCA), has been shown to be effective in reducing mortality in acute MI. Heparin is conventionally used in all PTCA procedures, whereas its efficacy in enhancing the therapeutic role of thrombolytic agents remains uncertain and may depend on the thrombolytic agent used. PTCA, which is also an effective therapy for stable angina, can be complicated by intimal dissection and thrombosis in a minority of cases, with vessel restenosis leading to recurrent symptoms in approximately 30% of cases. A number of new agents are being evaluated in both acute coronary syndromes and PTCA. These can be classified as adenosine diphosphate (ADP) receptor antagonists, Factor Xa inhibitors (low-molecular weight heparin [LMWH], direct thrombin inhibitors, new thrombolytic agents and glycoprotein IIb/IIIa receptor blockers. Of the latter, the most studied is abciximab, the Fab fragment of the chimeric monoclonal antibody, 7E3. This is a potent inhibitor of platelet aggregation. Four major clinical studies of PTCA in high-risk patients have demonstrated clear efficacy of abciximab in reducing acute ischaemic complications, mainly by reducing the frequency of MI and the need for repeat revascularisation. Unlike other glycoprotein IIb/IIIa receptor blockers, both short- and long-term efficacy have been demonstrated. Its impact on the rate of restenosis after PTCA is unclear. Abciximab's role in an era of intracoronary stent implantation is undergoing further study (with encouraging early results). Its role in other situations, such as the early (non-angioplasty) management of unstable angina and its ability to enhance the efficacy of thrombolytic agents, is under active investigation.
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PMID:Abciximab (Reopro): a clinically effective glycoprotein IIb/IIIa receptor blocker. 1599 12

Coronary angioplasty, eventually followed by stent implantation, represents the gold standard of acute myocardial infarction (AMI) treatment. Optimal reperfusion implies both patency of the infarct-related artery and a good myocardial microrevascularization with normal tissue reperfusion. The so called no-reflow phenomenon mainly occurs in the presence of highly thrombotic lesions, especially during primary angioplasty and it represents a negative prognostic factor of the outcome of AMI patients treated with angioplasty. A 77-year-old high-risk male patient, previous coronary artery bypass graft with the saphenous vein graft to the left anterior descending coronary artery for post-AMI angina in 1984, aided by 118 ambulance for anterior AMI was admitted to our cath-lab for primary coronary angioplasty. During the transport he was given aspirin i.v. 300 mg, heparin 5000 IU and abciximab (9.4 ml bolus plus infusion for 12 hours). The time of treatment (from symptom onset to first inflation) was about 90 min. Coronary angiography showed a massive thrombus occlusion of the vein graft with TIMI 0 distal flow. We employed the Export Catheter for mechanical aspiration of the occluding thrombus. The procedure was completed with direct stent implantation with good angiographic outcome. The use of thrombus aspiration and protection devices (filters or occlusive balloons) associated or not with the use of glycoprotein IIb/IIIa receptor blockers, has reduced the risk of distal embolization and of no-reflow phenomenon.
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PMID:[The use of the Export Catheter device in a patient with acute myocardial infarction for thrombotic occlusion of the venous graft on the left anterior descending coronary artery: a case report]. 1601 34


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