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Biomedical subjects

E Magnus Ohman

Publications and source records attributed to E Magnus Ohman.

At least 109 records · Page 6Linked to original sources

Significance of atrial fibrillation during acute myocardial infarction, and its current management: insights from the GUSTO-3 trial.

The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)-3 atrial fibrillation (AF) substudy assessed the prognostic significance of AF during acute myocardial infarction (AMI), the use of antiarrhythmic therapies, and whether different antiarrhythmic therapies were associated with different outcomes. The timing of the onset of AF relative to other post-AMI complications was recorded in the study. Of the 13,858 patients who were in sinus rhythm at the time of enrolment into GUSTO-3, 906 (6.5%) developed AF and 12,952 did not. Worsening heart failure, hypotension, third-degree heart block, and ventricular fibrillation were independent predictors of new-onset AF. The risks of 30-day and 1-year mortality were increased among patients with AF versus patients without AF before (odds ratio [OR] 2.74, 95% confidence interval [CI] 2.56-3.34; and OR 2.93, 95% CI 2.48-3.46, respectively) and after adjustment for baseline factors and pre-AF complications (OR 1.49, 95% CI 1.17-1.89; and OR 1.64, 95% CI 1.35-2.01, respectively). A total of 1,138 patients had data available on the management of their AF, including 117 with a history of paroxysmal AF and 138 with chronic AF prior to AMI. Of these 1,138 patients, 317 (28%) received antiarrhythmic therapies: class I antiarrhythmic drugs in 12%, sotalol in 5% and amiodarone in 15%. Electrical cardioversion was attempted in 116 patients (10%). Sinus rhythm was restored in 72% of patients given class I drugs, 67% of those given sotalol, 79% of those given amiodarone, and 64% of those who underwent electrical cardioversion. After adjustment for baseline characteristics and pre-AF complications, none of the specific antiarrhythmic therapies was associated with a higher chance of having sinus rhythm at discharge or before deterioration to in-hospital death. However, the use of class I antiarrhythmic drugs or sotalol was associated with lower unadjusted 30-day and 1-year mortality rates. After adjustment for baseline factors and pre-AF complications, the ORs for 30-day and 1-year mortality were 0.42 (95% CI 0.19-0.89) and 0.58 (95% CI 0.33-1.04), respectively, with class I agents, and 0.31 (95% CI 0.07-1.32) and 0.31 (95% CI 0.09-1.02), respectively, with sotalol. In contrast, there was no association between the use of amiodarone or electrical cardioversion and 30-day or 1-year mortality. New AF is often secondary to other post-AMI complications, but is in itself an independent predictor of a worse outcome. Clinical management of AF is variable, but in GUSTO-3 there was a strong trend towards lower mortality associated with the use of class I antiarrhythmic agents or sotalol. Randomized trials are needed to investigate this observation further.

Anti-Arrhythmia Agents↗

Distance from the coronary ostium to the culprit lesion in acute ST-elevation myocardial infarction and its implications regarding the potential prevention of proximal plaque rupture.

BACKGROUND: Shorter distances from the coronary ostia to culprit lesions have been associated with a higher incidence of adverse outcomes in ST elevation acute myocardial infarction (STEMI). As drug-eluting stents are associated with low rates of restenosis and formation of a stable intima, we sought to develop a mathematical model to estimate how far down the coronary artery a drug-eluting stent would have to be placed to theoretically mitigate the risk of proximal plaque rupture. OBJECTIVES AND METHODS: Distances from the ostia to the end of the culprit lesions were planimetered in 1,914 patients from the TIMI 14, INTEGRITI, FASTER and ENTIRE/TIMI 23 trials. RESULTS: The first 60 mm of the coronary artery contained 75% of STEMI culprit lesions. The median distance from the vessel ostium to the end of the culprit lesion was 43 mm (mean 50 +/- 34) and the relative distance from the vessel ostium to the end of the lesion was 29% (mean 33 +/- 17%) of the total culprit artery length. Diabetes was the only baseline clinical characteristic associated with a longer absolute distance to the end of the culprit lesion (46 mm vs. 43 mm, p = 0.03) as well as relative to total artery length (31% vs. 29%, p = 0.04). Median distances from the artery ostium to the end of the culprit lesion were shortest among the left anterior descending culprits (40 mm), followed by circumflex lesions (43 mm) and then right coronary artery lesions (47 mm, 3-way p < 0.0001). CONCLUSION: The majority of culprit lesions in STEMI are contained within the proximal 30% of the major epicardial coronary arteries, but the distance varies depending upon which epicardial artery is involved. Cumulative distribution functions are presented to allow estimation of the percent of culprit lesions lying proximal to any given distance from the ostium to model the feasibility of prophylactic drug-eluting stenting to minimize the risk of subsequent proximal plaque rupture.

Aged↗

Sustained ventricular arrhythmias and mortality among patients with acute myocardial infarction: results from the GUSTO-III trial.

BACKGROUND: In many patients, ventricular arrhythmias will develop early after acute myocardial infarction. We studied the incidence, timing, and outcomes of such arrhythmias in the international Global Utilization of Streptokinase and TPA (alteplase) for Occluded Coronary Arteries (GUSTO)-III trial. METHODS: We identified independent predictors of inhospital ventricular fibrillation (VF) and ventricular tachycardia (VT) and compared 30-day and 1-year mortality rates of patients who did (n = 1121) and did not (n = 13,921) have these arrhythmias during the index hospitalization. RESULTS: Significant independent predictors of inhospital VF were higher Killip class, lower baseline systolic pressure, intravenous preenrollment lidocaine use, shorter time to thrombolysis, and beta-blocker use <2 weeks before enrollment; independent predictors of inhospital VT were lower baseline systolic pressure, intravenous lidocaine use before enrollment, higher Killip class, faster baseline heart rate, and advanced age. The 30-day mortality rate was 31% in patients with VF, 24% in those with VT, 44% in those with both, and 6% in those with neither (P =.001). The corresponding 1-year mortality rates were 34%, 29%, 49%, and 9% (P =.001). The 30-day and 1-year mortality rates were higher for patients with late (>48 hours after enrollment) versus early arrhythmias (< or =48 hours after enrollment). CONCLUSIONS: Despite thrombolysis, inhospital ventricular arrhythmias are associated with higher 30-day and 1-year mortality rates after acute myocardial infarction, particularly when occurring later during the initial hospitalization. Better therapies are needed to improve outcomes of these arrhythmias.

Acute Disease↗

Frequency, patient characteristics, and outcomes of mild-to-moderate heart failure complicating ST-segment elevation acute myocardial infarction: lessons from 4 international fibrinolytic therapy trials.

BACKGROUND: There is a paucity of data on the incidence of mild-to-moderate heart failure (HF) complicating ST-segment elevation acute myocardial infarction (MI) and its impact on short-term outcomes. Our objective was to determine the incidence, timing, and consequences of mild-to-moderate HF complicating acute MI. METHODS: We examined the occurrence of death or death/recurrent MI (re-MI) in patients enrolled in the Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I), the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO IIb), the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-III), and Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT-II) trials, which examined different fibrinolytic therapies for MI. We excluded patients who had cardiogenic shock (n = 2994) or unknown HF status at all time points (n = 13,716). Of the remaining 61,041 patients, 17,949 patients (29.4%) had HF, 1566 (8.7%) only at baseline, 10,339 (57.6%) only after admission, and 6044 (33.7%) at baseline and after. RESULTS: The incidence of HF was 32.5% in the United States and 26.9% elsewhere. At 30 days, death and death/re-MI occurred in 2% and 4% of patients without HF and 8% and 12% of patients with HF, respectively (2% and 4% of patients with HF only at baseline, 7% and 13% of patients with HF only after baseline, and 10% and 13% of patients with HF at baseline and later). By use of multivariable analyses, the presence of HF was associated with 1.55 times greater risk of dying at 30 days (95% CI 1.38-1.74) and 2.15 times greater risk of death/re-MI (95% CI 1.96-2.36). CONCLUSION: Mild-to-moderate HF is a frequent and ominous complication of MI, especially when it does not resolve or develops after admission.

Clinical Trials as Topic↗

Randomized COMparison of platelet inhibition with abciximab, tiRofiban and eptifibatide during percutaneous coronary intervention in acute coronary syndromes: the COMPARE trial. Comparison Of Measurements of Platelet aggregation with Aggrastat, Reopro, and Eptifibatide.

BACKGROUND: The relative anti-aggregatory effects of currently prescribed platelet glycoprotein IIb/IIIa receptor antagonists during and after percutaneous coronary intervention for acute coronary syndromes have not been established. METHODS AND RESULTS: We randomized 70 acute coronary syndrome patients undergoing percutaneous coronary intervention to receive abciximab, eptifibatide, or tirofiban at doses used in the Evaluation of Platelet IIb/IIIa Inhibitor for STENTing (EPISTENT), Platelet glycoprotein IIb/IIIa in Unstable angina Receptor Suppression Using Integrilin Therapy (PURSUIT), and Platelet Receptor Inhibition in ischemic Syndrome Management in Patients Limited by Unstable Signs and symptoms (PRISM-PLUS)/Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis (RESTORE) trials, respectively. Platelet aggregation (PA) in response to 20 micro mol/L of adenosine diphosphate was measured with turbidimetric aggregometry in both D-phenylalanyl-L-prolyl-L-arginine chloromethylketone and citrate-anticoagulated blood early (15 and 30 minutes) and late (4, 12, and 18 to 24 hours) after drug initiation. At 15 and 30 minutes, PA was significantly less inhibited by the tirofiban-RESTORE regimen compared with abciximab (P=0.028) and eptifibatide regimens (P=0.0001). The abciximab regimen, however, showed increasingly varied anti-aggregatory effects during continued infusion for > or =4 hours. Citrate exaggerated ex vivo platelet inhibition after eptifibatide and tirofiban, but had the opposite effect on abciximab. Of all regimens evaluated, the eptifibatide regimen inhibited PA most consistently throughout both the early and late periods. CONCLUSIONS: Currently recommended drug regimens to inhibit the platelet glycoprotein IIb/IIIa receptor have distinct pharmacodynamic profiles that might affect their relative efficacy in acute coronary syndromes and percutaneous coronary intervention.

Abciximab↗

Prognostic implications of abnormalities in renal function in patients with acute coronary syndromes.

BACKGROUND: Outcomes in patients with mild to moderate renal function (RF) abnormalities presenting with acute coronary syndromes (ACS) are not well defined. METHODS AND RESULTS: A convenience sample of 4 ACS trial databases including all enrolled patients was assessed to determine 30- and 180-day outcomes. The 4 trials were Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) IIb, GUSTO-III, Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT), and Platelet IIb/IIIa Antagonism for the Reduction of Acute coronary syndrome events in a Global Organization Network (PARAGON-A). Patients were stratified into ST-segment elevation (STE) and non-ST-segment elevation (NSE) groups and by the presence or absence of abnormal RF (creatinine clearance <70 mL/min). In the STE group, 7670 of 18 621 patients (41%) had abnormal RF. In the NSE group, 8152 of 19 304 (42%) had abnormal RF. Patients with abnormal RF were older, more often female, and more likely to have adverse baseline characteristics. They had higher mortality and higher mortality/nonfatal myocardial infarction (MI) at both 30 and 180 days, regardless of ST-segment status. Creatinine clearance was independently associated with risk of mortality (hazard ratio 0.79 in the STE group and 0.81 in the NSE group) and with risk of mortality/MI (hazard ratio 0.93) in the NSE group at 180 days. CONCLUSIONS: Patients presenting with ACS frequently have abnormal RF. Abnormal RF is a marker of adverse baseline clinical characteristics and is independently associated with increased risk of death and death/MI.

Acute Disease↗

Thresholds for the electrocardiographic change range of biochemical markers of acute myocardial infarction (GUSTO-IIa data).

The definition of acute myocardial infarction (AMI) is increasingly dependent on levels of biochemical markers, including troponin. We aimed to determine the levels of biochemical markers associated with definite evolutionary electrocardiographic (ECG) changes in patients with ST-segment elevation myocardial infarction. By examining the database of 855 patients from the troponin substudy of GUSTO-IIa, we selected patients with ST-segment elevation at baseline, evidence of evolution of the QRS, T, and ST-segment waveforms on the predischarge electrocardiogram, and 3 measurements of > or =1 of the following: creatine kinase (CK)-MB, troponin T, or troponin I. We identified 222 patients with evolutionary ECG changes. The median QRS score for this population was 5 points; the fifth percentile was 1. For patients with 3 CK-MB measurements, the fifth percentile as a multiple of the upper limit of normal was 2.1 (upper limit of normal 7.0 ng/ml). For patients with troponin T measurements, the fifth percentile as a multiple of the upper limit of normal was 11.0 (upper limit of normal 0.1 ng/ml). For patients with troponin I measurements, the fifth percentile as a multiple of the upper limit of normal was 3.8 (upper limit of normal 1.5 ng/ml). This study revealed that 95% of the patients with definite ECG evidence of AMI had a more than twofold increase in CK-MB and more than a 3- to 11-fold increase in troponin.

Aged↗

Troponin T levels in patients with acute coronary syndromes, with or without renal dysfunction.

BACKGROUND: Among patients with suspected acute coronary syndromes, cardiac troponin T levels have prognostic value. However, there is concern that renal dysfunction may impair the prognostic value, because cardiac troponin T may be cleared by the kidney. METHODS: We analyzed the outcomes in 7033 patients enrolled in the Global Use of Strategies to Open Occluded Coronary Arteries IV trial who had complete base-line data on troponin T levels and creatinine clearance rates. The troponin T level was considered abnormal if it was 0.1 ng per milliliter or higher, and creatinine clearance was assessed in quartiles. The primary end point was a composite of death or myocardial infarction within 30 days. RESULTS: Death or myocardial infarction occurred in 581 patients. Among patients with a creatinine clearance above the 25th percentile value of 58.4 ml per minute, an abnormally elevated troponin T level was predictive of an increased risk of myocardial infarction or death (7 percent vs. 5 percent; adjusted odds ratio, 1.7; 95 percent confidence interval, 1.3 to 2.2; P<0.001). Among patients with a creatinine clearance in the lowest quartile, an elevated troponin T level was similarly predictive of increased risk (20 percent vs. 9 percent; adjusted odds ratio, 2.5; 95 percent confidence interval, 1.8 to 3.3; P<0.001). When the creatinine clearance rate was considered as a continuous variable and age, sex, ST-segment depression, heart failure, previous revascularization, diabetes mellitus, and other confounders had been accounted for, elevation of the troponin T level was independently predictive of risk across the entire spectrum of renal function. CONCLUSIONS: Cardiac troponin T levels predict short-term prognosis in patients with acute coronary syndromes regardless of their level of creatinine clearance.

Abciximab↗

Prognostic significance of elevated troponin I after percutaneous coronary intervention.

OBJECTIVES: We sought to assess the incidence and clinical significance of elevated cardiac troponin I (cTnI) after percutaneous coronary intervention (PCI). BACKGROUND: Elevated creatine kinase-MB (CK-MB) is prognostically important after PCI, but the prognostic significance of elevated cTnI after PCI is uncertain. METHODS: In a prospective substudy of the Sibrafiban Versus Aspirin to Yield Maximum Protection From Ischemic Heart Events Post-acute Coronary Syndromes (SYMPHONY) trials, which randomized patients with acute coronary syndromes (ACS) to receive aspirin or sibrafiban, we measured cTnI (positive, > or =1.5 ng/ml) and CK-MB (positive, > or =7 ng/ml) in 481 patients with PCI. Samples were collected immediately before and at 0, 8 and 16 h after PCI and analyzed by a core laboratory. The primary end point was the Kaplan-Meier estimate of death, myocardial infarction or severe, recurrent ischemia at 90 days. RESULTS: Overall, 230 patients (48%) had elevated cTnI after PCI. Such patients underwent PCI sooner and were more likely to have coronary stenting. Elevated cTnI was associated with nonsignificantly higher risks of the primary end point (11.5% vs. 8.7%; p = 0.15) and of death (1.8% vs. 0.4%; p = 0.4) and a significantly higher risk of death or infarction (10.6% vs. 4.2%; p = 0.005). This pattern was more pronounced for patients who became positive only after PCI: primary end point, 20.7% vs. 10.1% for patients who remained negative after PCI (p = 0.05); death, 5.2% vs. 0% (p = 0.02); death or infarction, 18.1% vs. 4.1% (p = 0.007). CONCLUSIONS: Elevated cTnI, often observed after PCI in patients with ACS, is associated with worse 90-day clinical outcomes. This marker, therefore, is a useful prognostic indicator in such patients.

Angina, Unstable↗

Eptifibatide and low-dose tissue plasminogen activator in acute myocardial infarction: the integrilin and low-dose thrombolysis in acute myocardial infarction (INTRO AMI) trial.

OBJECTIVES: This study was designed to test the hypothesis that eptifibatide and reduced-dose tissue plasminogen activator (t-PA) will enhance infarct artery patency at 60 min in patients with acute myocardial infarction (AMI). BACKGROUND: Combination fibrin and platelet lysis improves epicardial and myocardial reperfusion in AMI. METHODS: Patients were enrolled in a dose finding (Phase A, n = 344) followed by a dose confirmation (Phase B, n = 305) protocol. All patients received aspirin and weight-adjusted heparin and underwent angiography at 60 and 90 min. In Phase A, eptifibatide in a single or double bolus (30 min apart) of 180, 180/90 or 180/180 microg/kg followed by an infusion of 1.33 or 2.0 microg/kg per min was sequentially added to 25 or 50 mg of t-PA. In Phase B, patients were randomized to: 1) double-bolus eptifibatide 180/90 (30 min apart) and 1.33 microg/kg per min infusion with 50 mg t-PA (Group I); 2) 180/90 (10 min apart) and 2.0 g/kg per min with 50 mg t-PA (Group II); or 3) full-dose, weight-adjusted t-PA (Group III). RESULTS: In Phase A, the best rate of Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 was achieved using 180/90/1.33 microg/kg per min eptifibatide with 50 mg t-PA: 65% and 78% at 60 and 90 min, respectively. In Phase B, the incidence of TIMI flow grade 3 at 60 min was 42%, 56% and 40%, for Groups I through III, respectively (p = 0.04, Group II vs. Group III). The median corrected TIMI frame count was 38, 33 and 50, respectively (p = 0.02). TIMI major bleeding was reported in 8%, 11% and 6%, respectively; intracranial hemorrhage occurred in 1%, 3% and 2% of patients (p > 0.5 for both). The incidences of death (4%, 5% and 7%), reinfarction or revascularization at 30 days were similar among the three treatment groups. CONCLUSIONS: In comparison with standard t-PA regimen, double-bolus eptifibatide (10 min apart) with a 48-h infusion and half-dose t-PA (Group II) is associated with improved quality and speed of reperfusion. The safety profile of this therapy is similar to that of other combination regimens.

Adult↗

The prognostic value of creatine kinase elevations extends across the whole spectrum of acute coronary syndromes.

OBJECTIVES: The study investigated the relationship among creatine kinase (CK) elevations, clinical characteristics and cardiac events across the whole spectrum of acute coronary syndromes (ACS). BACKGROUND: Elevated serum levels of cardiac enzymes have been shown to be a major prognostic determinant in acute myocardial ischemia. Yet prior to this report, the relation between cardiac enzyme levels and other prognostic determinants across the entire spectrum of ACS has not been explored by a large clinical study. METHODS: We evaluated the relation between the maximum CK ratio (CK level/upper limit of normal) in the early hours following admission and cardiac events at six months in 11,725 patients enrolled in a large trial of ACS. RESULTS: Patients with higher risk characteristics, such as older age, female gender, hypertension, diabetes, prior coronary events or heart failure, more frequently presented without ST-segment elevation on the electrocardiogram and tended to develop lesser enzyme elevations. After adjusting for significant baseline predictors of cardiac events, a continuous correlation was observed between the CK ratio and death (chi-square 63.04, p < 0.0001) and (re)infarction or death (chi-square 55.48, p < 0.0001). This correlation was similar for patients with and without ST-segment elevation. The adjusted incidence of cardiac events at follow-up began to rise even for CK levels within the normal range, the steepest part of the curve residing between one and three times the upper limit of normal. In patients with a CK ratio of >1 to 2 compared with those within the normal range, the adjusted odds ratio for death was 1.26 (95% confidence interval [CI] 0.98 to 1.63), and 1.59 (95% CI 1.38 to 1.90) for (re)infarction and death. For all CK levels, the event rate was higher among patients without ST-segment elevation. CONCLUSIONS: Although high-risk patients with ACS often develop lesser CK elevations, this study demonstrated that even minor enzyme elevations appear to have important and independent prognostic implications.

Aged↗

Comparison of outcomes after 8 vs. 9.5 French size intra-aortic balloon counterpulsation catheters based on 9,332 patients in the prospective Benchmark registry.

The Benchmark intra-aortic balloon counterpulsation (IABC) registry maintains prospectively gathered clinical information on a large cohort of IABC patients. The purpose of the present report is to compare in-hospital outcomes and complications in patients treated with the newer 8 vs. 9.5 Fr size catheters. Between January 1997 and August 2000, data on 7,078 9.5 Fr and 2,254 8 Fr IABC insertions were submitted to Benchmark. This was not a randomized comparison but rather a posthoc analysis of prospectively gathered data. There was less limb ischemia with the 8 Fr IABC size catheter. There were no significant differences in bleeding or mortality between the two groups. Smaller IABC catheter size is associated with significantly less limb ischemia, especially in higher-risk patients. The large, population-based, ongoing Benchmark registry provides a useful vehicle for outcomes research concerning the evolving practice of IABC.

Aged↗

Trends in intraaortic balloon counterpulsation complications and outcomes in cardiac surgery.

BACKGROUND: As the proportion of high-risk patients for cardiac surgery increases, use of intraaortic balloon counterpulsation (IABC) has increased, especially in preoperative therapy. Although the efficacy and cost-effectiveness of IABC have been demonstrated, historically higher complication rates have dissuaded some practitioners from using IABC. METHODS: This report describes IABC use in cardiac surgery, examines trends in complications over time, and compares outcomes in preoperative versus postoperative use in a single prospective worldwide registry over the past 3 years. RESULTS: The frequency of IABC use appears to be increasing with time as the complication rates have dramatically fallen. The overall IABC-related complication rate was 6.5% (460/7,101), and the rate of major complications (requiring surgery or transfusion) was 2.1% (148/7,101). Hospital mortality was significantly lower in patients treated preoperatively with IABC compared with patients treated postoperatively (8.8% vs 28.2%, p < 0.0001), although this may be due to a selection bias in the postoperative group. CONCLUSIONS: Preoperative IABC therapy leads to better patient outcomes in high-risk CABG patients. Improved IABC technology and better surveillance have led to increased use with lower complication rates. Although selection bias is inherent in retrospective studies, the Benchmark Counterpulsation Outcomes Registry outcomes are in close concordance to prospective randomized studies previously reported.

Cardiac Surgical Procedures↗

Effect of eptifibatide for acute coronary syndromes: rapid versus late administration--therapeutic yield on platelets (The EARLY Platelet Substudy).

BACKGROUND: Receptors other than GP IIb/IIIa may mediate leukocyte-platelet-endothelial interactions that obstruct the microvasculature in acute coronary syndromes (ACS) and cause microinfarcts. The effect of eptifibatide on these receptors was investigated in a substudy of the EARLY Trial. METHODS: Patients received early (in the Emergency Department, n = 27) or late (12-24 h, n = 28) eptifibatide. Ten platelet receptors by flow cytometry and platelet aggregation (10 micromol/L ADP) were measured serially at baseline, and at 3, 6, 12 and 24 h after randomization. RESULTS: Platelet aggregation was rapidly inhibited by early eptifibatide therapy (baseline, 72 +/- 20%; 3 h post, 7 +/- 9%; p < 0.001). No significant differences were seen in either group for CD 31, CD 63, CD 107a, CD 107b, CD 41 (GPIIb/IIIa expression), or CD 62p. Leukocyte-platelet aggregate formation (mean fluorescense intensity) trended upward after presentation (early baseline, 43.1 +/- 26.0 versus 65.8 +/- 35.6, p =.09). PAC-1 (GP IIb/IIIa activity), CD 51/61 (vitronectin receptor) and CD 42b (GP Ib) were inhibited by eptifibatide (p <.05). CONCLUSIONS: In Emergency Department patients with unstable angina, early eptifibatide rapidly and profoundly inhibits platelet aggregation and reduces GP IIb/IIIa activity and the expression of CD51/61 and CD 42b; the latter two effects may also contribute to the drug's anti-thrombotic effect. However, platelet-leukocyte aggregate formation, a marker of platelet activity rises within 24 h after presentation despite eptifibatide therapy and is a potential mechanism for microvascular obstruction.

Acute Disease↗