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Eric J Topol

Publications and source records attributed to Eric J Topol.

At least 235 records · Page 13Linked to original sources
PubMed2002

Evidence that angiotensin-converting enzyme inhibitor use diminishes the need for coronary revascularization after stenting.

Restenosis after stenting, in contrast to balloon angioplasty, is predominantly due to neointima formation. Angiotensin-converting enzyme (ACE) inhibitors diminish neointima formation in animal models of arterial injury. In an observational study, 1,598 patients who were treated from 1994 to 1997 with coronary stents and prospectively followed for clinical events were divided into 2 groups: those receiving ACE inhibitors at the time of stenting (n = 345) and those who did not (n = 1,253). Multivariate logistic regression was used to adjust for imbalances between populations with regard to elements relevant to risk of 12-month coronary revascularization, which was the primary study end point. After adjustment, ACE inhibitor usage remained significantly protective against revascularization (odds ratio [OR] 0.46, 95% confidence interval 0.29 to 0.73, p = 0.001). Protection was not observed in patients treated with balloon angioplasty alone during the same period (OR 1.06, p = 0.33), which is consistent with the results of prior randomized trials. ACE inhibitors appear to decrease late revascularization, possibly due to a reduction in restenosis after coronary stenting.

Aged↗
PubMed2002

Early and sustained survival benefit associated with statin therapy at the time of percutaneous coronary intervention.

BACKGROUND: Long-term administration of statin therapy has been shown to reduce major coronary events and cardiac mortality within randomized clinical trials. In addition to lowering lipids, statins favorably affect platelet adhesion, thrombosis, endothelial function, inflammation, and plaque stability, which may potentially improve outcome after percutaneous coronary intervention (PCI). Therefore, we hypothesized that statin therapy has an early beneficial effect among patients undergoing PCI. METHODS AND RESULTS: Each year from 1993 to 1999, we prospectively collected data among the first 1000 patients undergoing PCI. Patients who presented with acute or recent myocardial infarction or cardiogenic shock were excluded from the analysis. Baseline, procedural, and 6-month data of statin-treated and non-statin-treated patients were compared. Propensity score and multivariate survival analysis were used to adjust for heterogeneity between the two groups. Of 5052 patients who completed follow-up, 26.5% were treated with statin at the time of the procedure. Statin therapy was associated with a mortality reduction at 30 days (0.8% versus 1.5%; hazard ratio, 0.53; P=0.048) and at 6 months (2.4% versus 3.6%; hazard ratio, 0.67; P=0.046). After adjusting for the propensity to receive statin therapy before the procedure and other confounders, statin therapy remained an independent predictor for survival at 6 months after coronary intervention (hazard ratio, 0.65; 95% CI, 0.42 to 0.99; P=0.045). CONCLUSIONS: In this large study cohort, statin therapy among PCI patients seems to be associated with a significant mortality advantage at early and intermediate-term follow-up.

Aged↗
PubMed2002

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↗
PubMed2002

Outcomes of patients with acute coronary syndromes and prior coronary artery bypass grafting: results from the platelet glycoprotein IIb/IIIa in unstable angina: receptor suppression using integrilin therapy (PURSUIT) trial.

BACKGROUND: Patients with prior CABG with a subsequent non-ST-segment elevation acute coronary syndrome (ACS) pose an increasingly important clinical problem. Although GP IIb/IIIa inhibitors have improved the outcome of patients with ACS, their efficacy in patients with prior CABG has not been previously evaluated. Methods and Results- We analyzed the 30- and 180-day outcomes of patients with prior CABG enrolled in the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial. In this trial, which evaluated the efficacy of eptifibatide in patients with ACS, 1134 patients (12%) with prior CABG and 8321 without prior CABG were enrolled. After adjusting for differences in baseline characteristics and treatment, patients with prior CABG had a significantly higher mortality rates at 30 days (hazard ratio [HR], 1.45 [95% CI, 1.06 to 1.98]; P=0.019) and at 180 days (HR, 1.32 [95% CI, 1.04 to 1.67]; P=0.021). At 30 days, there was a similar effect on the primary end point of death or myocardial infarction in the eptifibatide group versus the placebo group in prior CABG patients (unadjusted HR, 0.90 [95% CI, 0.67 to 1.20]) and in patients without a history of CABG (unadjusted HR, 0.89 [95% CI, 0.80 to 0.99]). CONCLUSIONS: Patients with prior CABG with non-ST-segment elevation ACS have a significantly worse prognosis than do patients without a history of CABG. The treatment effect of eptifibatide in the prior CABG group was similar to the effect seen in patients without prior CABG.

Acute Disease↗
PubMed2002

Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: a meta-analysis of all major randomised clinical trials.

BACKGROUND: Platelet glycoprotein IIb/IIIa inhibitors have been shown to reduce cardiac complications in patients undergoing percutaneous coronary intervention. The clinical efficacy of these drugs in acute coronary syndromes, however, is still unclear. We did a meta-analysis of all large randomised trials designed to study the clinical efficacy and safety of glycoprotein IIb/IIIa inhibitors in patients with acute coronary syndromes who were not routinely scheduled to undergo early coronary revascularisation. METHODS: Inclusion criteria were: randomisation of patients with acute coronary syndromes but without persistent ST elevation; comparison of a glycoprotein IIb/IIIa inhibitor with placebo or control therapy; non-recommendation of early coronary revascularisation during study-drug infusion; and enrollment of at least 1000 patients. Data on individual patients were obtained from all participants in these trials. FINDINGS: Six trials, enrolling 31402 patients, fulfilled the inclusion criteria. 30 days after randomisation, 3530 (11.2%) patients died or developed a myocardial infarction. At 30 days, a 9% reduction in the odds of death or myocardial infarction was seen with glycoprotein IIb/IIIa inhibitors compared with placebo or control (10.8% [1980/18297] vs 11.8% [1550/13105] events; odds ratio 0.91 [95% CI 0.84-0.98]; p=0.015). The relative treatment benefit was similar in subgroups of patients according to important clinical baseline characteristics; hence, the absolute treatment benefit was largest in high-risk patients. An unexpected and significant interaction was seen between sex and allocated treatment, with a treatment benefit in men (0.81 [0.75-0.89] but not in women (1.15 [1.01-1.30]). However, once patients were stratified according to troponin concentration, there was no evidence of a sex difference in treatment response, and a risk reduction was seen in men and women with raised troponin concentrations. Major bleeding complications were increased by glycoprotein IIb/IIIa inhibitors (2.4% [445/18297] vs 1.4% [180/13105]; p<0.0001), but intracranial bleeding was not (16 [0.09%] vs 8 [0.06%]; p=0.40). INTERPRETATION: Glycoprotein IIb/IIIa inhibitors reduce the occurrence of death or myocardial infarction in patients with acute coronary syndromes not routinely scheduled for early revascularisation. The event reduction is greatest in patients at high risk of thrombotic complications. Treatment with a glycoprotein IIb/IIIa inhibitor might therefore be considered especially in such patients early after admission, and continued until a decision about early coronary revascularisation has been made.

Aged↗
PubMed2002

Long-term mortality benefit with the combination of stents and abciximab for cardiogenic shock complicating acute myocardial infarction.

Cardiogenic shock secondary to ischemic heart disease is associated with a high mortality rate, and recent trials have established the benefit of an early invasive approach. However, the role of adjunctive abciximab and stenting for cardiogenic shock has not been established. We prospectively examined collected data from 96 consecutive patients who underwent emergent percutaneous coronary intervention for cardiogenic shock over the past 7 years. Patients were classified as receiving stent plus abciximab, stent alone, percutaneous transluminal coronary angiopplasty (PTCA) plus abciximab, or PTCA alone. Baseline characteristics of the 4 groups were similar. During 2.5 years of follow-up, the mortality rates for stent plus abciximab, stent only, PTCA plus abciximab, and PTCA alone were 33%, 43%, 61%, and 68%, respectively (log-rank p = 0.028). Achievement of postprocedural Thrombolysis In Myocardial Infarction 3 flow was higher with stent plus abciximab than with the other interventions (85% vs 65%, p = 0.048). By multivariate analysis, absence of stent use (hazard ratio 2.58, 95% confidence interval 1.36 to 4.90, p = 0.004) and left ventricular ejection function </=30% (hazard ratio 3.89, 95% confidence interval 1.53 to 9.87, p = 0.004) were independent predictors for mortality during 2.5 years of follow-up. In conclusion, treatment with the combination of stent and abciximab resulted in higher procedural Thrombolysis In Myocardial Infarction 3 flow rates and a long-term mortality benefit in patients with cardiogenic shock complicating acute myocardial infarction.

Abciximab↗
PubMed2002

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↗
PubMed2002

Meta-analysis of randomized and registry comparisons of ticlopidine with clopidogrel after stenting.

OBJECTIVES: We sought to determine whether clopidogrel is at least as efficacious as ticlopidine. BACKGROUND: Several trials have supported the enhanced safety and tolerability of clopidogrel compared with ticlopidine after coronary stent deployment. However, none of these individual trials were powered to detect possible differences in the efficacy for reducing ischemic end points. METHODS: Published data from trials and registries that compared clopidogrel with ticlopidine in patients receiving coronary stents were pooled, and a formal meta-analysis was performed. The rate of 30-day major adverse cardiac events (MACE), as defined in each trial, was used as the primary end point. RESULTS: There were a total of 13,955 patients. The pooled rate of major adverse cardiac events was 2.10% in the clopidogrel group and 4.04% in the ticlopidine group. After adjustment for heterogeneity in the trials, the odds ratio (OR) of having an ischemic event with clopidogrel, as compared with ticlopidine, was 0.72 (95% confidence interval [CI] 0.59 to 0.89, p = 0.002). Mortality was also lower in the clopidogrel group compared with the ticlopidine group-0.48% versus 1.09% (OR 0.55, 95% CI 0.37 to 0.82; p = 0.003). CONCLUSIONS: Based on all available evidence from randomized clinical trials or registries, clopidogrel, in addition to better tolerability and fewer side effects, is at least as efficacious as ticlopidine in reducing MACE. This finding may be due to the more rapid onset of an antiplatelet effect seen with the loading dose of clopidogrel, which was used in most of these studies, or to better patient compliance with clopidogrel therapy. Therefore, clopidogrel plus aspirin should replace ticlopidine plus aspirin as the standard antiplatelet regimen after stent deployment.

Aspirin↗
PubMed2002

Reduction in vascular access site bleeding in sequential abciximab coronary intervention trials.

We analyzed vascular access site bleeding from the EPIC, EPILOG, and EPISTENT trials to quantify the decrease in vascular bleeding complications in these three trials, especially those attributable to abciximab. The incidence of combined major and minor vascular access site bleeding in nonabciximab (heparin plus placebo) patients progressively decreased from EPIC (8.2%) to EPILOG (2.9%) to EPISTENT (1.7%; P < 0.001). Combined major and minor vascular access site bleeding in abciximab (heparin plus abciximab) patients decreased from EPIC (20%) to EPILOG (5.8%) to EPISTENT (2.2%; P < 0.001). There were more major vascular access site bleeds with abciximab compared to placebo in EPIC (odds ration 3.2; P < 0.001) but not in EPILOG or EPISTENT. Modified abciximab and heparin dosing and improved vascular access site management strategies have decreased the risk of vascular access bleeding during coronary intervention and have essentially eliminated the excess access site bleeding associated with abciximab.

Abciximab↗
PubMed2002

Economics and quality of care for patients with acute coronary syndromes: the impending crisis.

Several factors are placing significant financial burdens on the health care system today. These include the growing older population, the obesity and type II diabetes epidemics, and the attendant increased prevalence of heart disease, which remains the leading cause of death in the United States. In response, cardiovascular medicine is undergoing sweeping change in the use of advanced technology and interventions. In addition, biomarkers, such as troponin, are emerging as critical predictors of responses to therapy, particularly for coronary stenting. Future trends in the treatment of acute coronary syndromes (ACS) will embrace the use of genomic solutions, such as gene expression profiling, to predict therapeutic outcomes. Careful consideration will need to be given to these innovative approaches to ensure they are cost effective.

Acute Disease↗
PubMed2002

Multi-year follow-up of abciximab therapy in three randomized, placebo-controlled trials of percutaneous coronary revascularization.

There is considerable evidence supporting the use of platelet glycoprotein IIb/IIIa inhibitors to reduce ischemic complications of percutaneous coronary revascularization. However, long-term follow-up has been limited. In three large-scale randomized trials that tested abciximab at a uniform bolus dose and 12-hour infusion against placebo, in a double-blind fashion, a total of 5799 patients had their long-term follow-up vital status determined at a minimum of 7 years (EPIC), 4.5 years (EPILOG), or 3 years (EPISTENT) after randomization (median, 4.8 years). The prespecified primary endpoint was all-cause mortality by intention-to-treat analysis at 3 years in patients randomly assigned to a common intervention. Follow-up for 5603 of the 5799 patients was 96.6% complete at 3 years; 320 deaths had occurred by that time. After 3 years of follow-up, mortality was 6.4% in the placebo groups and 5.0% in the abciximab groups (hazard ratio [HR] = 0.78; 95% confidence interval [CI]: 0.63 to 0.98; P = 0.03). A similar reduction in mortality was observed on an intention-to-treat basis when all follow-up information was utilized after a median of 4.8 years of follow-up (n = 652 deaths): 12.6% in the placebo groups and 10.2% in the abciximab groups (HR = 0.82; 95% CI: 0.70 to 0.96; P = 0.01).Abciximab treatment reduced all-cause mortality by about 20% during long-term follow-up after percutaneous coronary intervention. The findings were similar in magnitude and consistent in direction for each of the three trials, and the absolute survival benefit appeared to increase over time. Brief intervention with this monoclonal antibody during percutaneous coronary revascularization is associated with significant improvement of long-term survival.

Abciximab↗
PubMed2002

Effect of anti-tumor necrosis factor-alpha polyclonal antibody on restenosis after balloon angioplasty in a rabbit atherosclerotic model.

Inflammation has been postulated to contribute to restenosis after balloon angioplasty. Tumor necrosis factor (TNF)-alpha is a pleiotropic proinflammatory cytokine involved in many features of inflammation. We examined the tissue expression pattern of TNF-alpha and the inflammatory response to arterial injury, and the effects of a goat anti-rabbit-TNF-alpha polyclonal antibody on tissue TNF-alpha expression, inflammation and restenosis in a rabbit atherosclerotic model. At different time points following air dessication and subsequent balloon injury, fresh rabbit femoral artery tissues were homogenized and analyzed for TNF-alpha levels by quantitative TNF-alpha bioassay. Rabbits were treated with a goat anti-rabbit-TNF-alpha polyclonal antibody, Serum and tissue TNF-alpha neutralization, macrophage infiltration (as an indicator of inflammation), and neointimal areas were determined. Balloon angioplasty increased tissue TNF-alpha expression 100000-fold over baseline, and this increase persisted over 6 days after arterial injury, serum anti-TNF-alpha antibody levels were sufficient to neutralize tissue TNF-alpha activity by 60-75%, macrophage infiltration was suppressed, but did not decrease the neointimal formation. These data indicate that tissue TNF-alpha levels were markedly increased after balloon angioplasty. Anti-TNF-alpha treatment was sufficient to neutralize tissue TNF-alpha activity, reduce inflammation, but did not inhibit neointimal formation following balloon angioplasty in a rabbit atherosclerotic model.

Angioplasty, Balloon↗
PubMed2002

An automated strategy for bedside aPTT determination and unfractionated heparin infusion adjustment in acute coronary syndromes: insights from PARAGON A.

BACKGROUND: Intravenous unfractionated heparin remains a cornerstone of anticoagulation therapy for patients with acute coronary syndromes, but regulation to a target aPTT is challenging. We assessed unfractionated heparin infusion regulation by bedside, whole-blood aPTT testing and computerized, algorithmic infusion adjustment, and further evaluated the relationship of achieving the target aPTT with clinical outcomes. METHODS AND RESULTS: We studied 1,275 patients randomized to unfractionated heparin in PARAGON-A, which tested lamifiban with or without unfractionated heparin versus unfractionated heparin. All patients had baseline and 6-hour blinded, bedside aPTTs, then aPTTs per algorithm. A central computer translated encrypted values to algorithmic dose-adjustment commands. We assessed the ability to achieve and maintain aPTTs of 50-70 seconds and associations of 6- and 12-hour aPTTs and time-to-target with 30-day outcomes.Overall, the median 6-hour aPTT was 50-70 seconds and remained so throughout infusion. Individually, only 33.6% of patients achieved 6-hour target-range aPTTs, and only 40% of all aPTTs were in-range. After achieving target, only 42% of subsequent measures were in-range. Thirty-day death or myocardial infarction (death/MI) increased non-significantly as time-to-target increased (p = 0.08). Thirty-day mortality was similar if target aPTT was reached, regardless of timing. Death/MI trended lower if target aPTT was reached by 8 hours (p = 0.10). The best clinical outcomes were associated with in-range aPTTs. CONCLUSIONS: This study represents the most systematic monitoring and regulation of unfractionated heparin anticoagulation to date. Although average anticoagulation achieved target range, wide inter- and intra-patient variability may have important implications for clinical outcomes.

Acetates↗
PubMed2002

The determinants of activated partial thromboplastin time, relation of activated partial thromboplastin time to clinical outcomes, and optimal dosing regimens for heparin treated patients with acute coronary syndromes: a review of GUSTO-IIb.

CONTEXT: Unfractionated heparin remains widely utilized in the treatment of acute coronary syndromes (ACS). However, limited data exist on optimal dosing and range of activated partial thromboplastin time (aPTT) in this setting. A large trial of thrombolysis for acute myocardial infarction has reported an association between longer aPTTs and adverse outcomes. OBJECTIVES: Estimate the optimal heparin-dosing regimen in achieving early therapeutic aPTTs (50 to 75 seconds) and determine the association of aPTT and death, reinfarction, and bleeding in population with ACS. DESIGN: Subgroup analysis within a randomized, controlled trial of 5861 patients given unfractionated heparin who had aPTTs at 6, 12, or 24 hours, with outcome analyses by weight categories. SETTING: In 373 hospitals in 13 countries from May 1994 to October 1995. PATIENTS: A total of 12142 patients admitted for ACS, stratified by the presence (n = 4131) or absence (n = 8011) of ST-segment elevation, and randomized to 72 hours of unfractionated heparin. RESULTS: In a simulated weight-adjusted model, based on retrospective grouping by weight, a simulated dose of 60-U/kg bolus and 12-U/kg/h infusion resulted in the highest proportion of therapeutic aPTTs. After adjustment for baseline variables, longer 12-hour aPTT was associated with the composite of 30-day death or reinfarction in patients not treated with thrombolytic therapy (odds ratio, 1.10; 95% CI, 1.00 to 1.22; P = 0.047). Longer aPTT at 6 hours was associated with increased moderate or severe bleeding for the entire cohort. There was also a significant, nonlinear correlation of the 12-hour aPTT with moderate or severe bleeding in thrombolysis-treated patients. CONCLUSIONS: For ACS patients who are treated with heparin, aPTT is highly associated with body weight. Longer aPTT within the first 12 hours is associated with adverse outcomes in ACS. Heparin dosing for ACS should be weight based.

Acute Disease↗
PubMed2002

Persistence of delays in presentation and treatment for patients with acute myocardial infarction: The GUSTO-I and GUSTO-III experience.

STUDY OBJECTIVE: Early treatment with fibrinolytic therapy substantially decreases mortality in acute myocardial infarction (AMI). We examined delays to hospital arrival and treatment in 2 large, multinational, randomized trials of fibrinolytic therapy: Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) and Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-III). METHODS: We evaluated delays to hospital arrival, time from arrival to treatment, and total time to treatment in the 27,849 US patients with AMI enrolled in GUSTO-I or GUSTO-III. Time intervals were defined prospectively for total time to treatment and symptom onset to hospital arrival as 0 to 2 hours (early), 2 to 4 hours, or more than 4 hours (late). Time to fibrinolytic therapy once in hospital was prospectively defined as 0 to 1 hour (early) or more than 1 hour (late). Socioeconomic data were also obtained from patients enrolled in the GUSTO-III trial. RESULTS: In GUSTO-III, as in GUSTO-I, patients who arrived at the hospital later were older (64 years versus 60 years; P =.001) and more often female (35% versus 27%; P =.001), black (6% versus 4%; P =.02), and diabetic (25% versus 16%; P =.001). These groups also received treatment later once in hospital, as did patients with hypertension (48% versus 42%; P =.001), previous angina (46% versus 36%; P =.001), and previous infarction (21% versus 16%; P =.001). Higher levels of education, professional occupations, and private health insurance were associated with significantly earlier arrival and treatment. Although in hospital time to treatment has decreased (66 minutes to 48 minutes; P <.0001), time to arrival has not changed over the past 7 years, averaging 84 minutes. CONCLUSION: Certain groups of patients with AMI, including the elderly, women, diabetic patients, and minorities, exhibit delays to hospital arrival and treatment in the emergency setting. Patients with higher educational levels, professional occupations, and private health insurance arrive at the hospital sooner and receive treatment more quickly. Patients and health care providers must be educated regarding high-risk populations for delay to maximize benefit from fibrinolytic therapy.

Age Distribution↗
PubMed2002

Misreporting of myocardial infarction end points: results of adjudication by a central clinical events committee in the PARAGON-B trial. Second Platelet IIb/IIIa Antagonist for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network Trial.

BACKGROUND: Myocardial (re)infarction (MI), a common trial end point, can be difficult to identify because of inconclusive signs and symptoms. We examined disagreement between investigator and clinical events committee (CEC) reporting of MIs in an international, randomized trial. METHODS: The primary end point of the PARAGON-B trial was a 30-day composite of death, MI (CEC adjudicated), or ischemia-driven intervention. If CEC and investigator determinations of MI differed, we sent investigators event summaries and rationales for CEC decisions and asked whether they now agreed with the CEC assessment. If they still disagreed, they were to provide a rationale and supporting data. Such cases were reviewed, and a final decision was made. RESULTS: Overall, 1736 of 5225 (33%) patients had suspected MIs; the CEC adjudicated 483 of 1736 (28%) as MIs. In 404 patients (23%), investigator and CEC assessments of MI differed; 270 MIs were identified by the CEC but not investigators, and 134 were identified by investigators but not the CEC. Most disagreements concerned periprocedural MIs, but some reflected clinical ischemia and enzyme elevations. Letters for 382 disagreements were sent and returned by investigators, and investigators came to agree with CEC assessments in 307 cases (80%). For the other 75 cases (20%), after review the investigators' assessments were confirmed in 10 cases, and the original CEC decisions were supported in the other 65 cases. CONCLUSIONS: Investigators misreport MI end points, but most later agree with CEC assessments. These data support standard, independent adjudication of suspected MIs for accurate reporting, which may affect evaluations of therapies, sample-size calculations, and event-rate comparisons across trials.

Clinical Enzyme Tests↗