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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.amjmed.2004.12.035 Byline: Michael S. Chen (a), Deepak L. Bhatt (a), Derek P. Chew (b), David J. Moliterno (c), Stephen G. Ellis (a), Eric J. Topol (a) Keywords: Percutaneous coronary intervention; Revascularization; African American; Race; Coronary artery disease Abstract: We aimed to determine whether African Americans and whites have different outcomes after percutaneous coronary intervention (PCI). Author Affiliation: (a) Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio (b) Flinders Medical Centre Adelaide, Australia (c) Gill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky.

PURPOSE: As cocaine abuse has become widespread, catastrophic cocaine-associated cardiovascular events have been noted with increasing frequency. Although these incidents are thought to be caused by drug-induced vasoconstriction and/or arterial thrombosis, the influence of cocaine on the plasma constituents involved in endogenous thrombosis and thrombolysis has not been characterized. PATIENTS AND METHODS: In 22 patients (8 men, 14 women, ages 32 to 62 years) undergoing cardiac catheterization, blood samples were procured before and 15 minutes after the administration intranasal saline (n = 8, controls) or cocaine, 2 mg/kg (n = 14), and the plasma concentrations of fibrinogen, plasminogen, and lipoprotein(a), as well as tissue plasminogen activator activity and plasminogen activator inhibitor (PAI-1) activity, were measured. RESULTS: No variable changed with the use of intranasal saline, whereas the use of cocaine resulted in an increase in PAI-I activity (0.48 + 0.06 (mean + SD] nmol\L at baseline, 0.53 + 0.05 nmol/L after cocaine, P = 0.011). CONCLUSION: Intranasal cocaine administration is associated with an increase in plasma PAI-1 activity. This may be important in recreational users of cocaine who experience vascular thrombosis.

PURPOSE: Although labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown. PATIENTS AND METHODS: In 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9). RESULTS: Of 40 coronary arterial segments analyzed, cocaine induced a 13% [+ or -] 10% (mean [+ or -] standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 [+ or -] 14 mm Hg after cocaine, 110 [+ or -] 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 [+ or -] 1.37 [mm.sup.2] after cocaine, 3.37 [+ or -] 1.32 [mm.sup.2] after labetalol; p = NS). CONCLUSION: Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

The optimal antithrombotic treatment regimen for patients with atrial fibrillation undergoing percutaneous coronary intervention with stent implantation represents a challenge in clinical practice. In 2016, an updated opinion of selected experts from the United States and Canada on the treatment of patients with atrial fibrillation undergoing percutaneous coronary intervention was reported. After the 2016 North American consensus statement on the management of antithrombotic therapy in patients with atrial fibrillation undergoing percutaneous coronary intervention, results of pivotal clinical trials assessing the type of oral anticoagulant agent and the duration of antiplatelet treatment have been published. On the basis of these results, this focused update on the antithrombotic management of patients with atrial fibrillation undergoing percutaneous coronary intervention recommends that a non–vitamin K antagonist oral anticoagulant be preferred over a vitamin K antagonist as the oral anticoagulant of choice. Moreover, a double-therapy regimen (oral anticoagulant plus single antiplatelet therapy with a P2Y12inhibitor) by the time of hospital discharge should be considered for most patients, whereas extending the use of aspirin beyond hospital discharge (ie, triple therapy) should be considered only for selected patients at high ischemic/thrombotic and low bleeding risks and for a limited period of time. The present document provides a focused updated on the rationale for the new expert consensus–derived recommendations on the antithrombotic management of patients with atrial fibrillation treated with oral anticoagulation undergoing percutaneous coronary intervention.

Background: Vorapaxar is effective in the prevention of secondary atherothrombotic events, although the efficacy/safety balance appears less favorable in the treatment of patients with non-ST-segment elevation (NSTE) acute coronary syndrome (ACS). We hypothesized that patients with NSTE ACS already receiving thienopyridine prior to the ACS event may show differential efficacy/safety effects with vorapaxar vs. placebo added to their standard care.Methods: We studied 12,944 patients from the Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRACER) trial with respect to thienopyridine use before admission for the index NSTE ACS event. The primary endpoint was a composite of cardiovascular death, myocardial infarction, stroke, rehospitalization for ischemia, and urgent revascularization. The key secondary endpoint was a composite of cardiovascular death, myocardial infarction, and stroke. Safety endpoints were bleeding complications.Results: Only 1513 patients (11.7%) were receiving thienopyridine before admission for the index NSTE ACS event. In these patients, Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) moderate/severe bleeding occurred in 5.7% treated with vorapaxar and 5.3% treated with a placebo (hazards ratio (HR) 1.10, 95% confidence interval (CI) 0.70–1.71); in thienopyridine-naïve patients, the rates were 5.7% and 4.1%, respectively (HR 1.32, 95% CI 1.11–1.57; Pint=0.45). GUSTO severe bleeding in the prior thienopyridine group occurred in 0.5% of patients treated with vorapaxar and 1.3% of patients treated with placebo (HR 0.34, 95% CI 0.09–1.30); in thienopyridine-naïve patients, the rates were 2.0% and 1.0%, respectively (HR 1.89, 95% CI 1.36–2.62; Pint=0.01). No interaction was observed between vorapaxar efficacy and prior thienopyridine use on the primary (adjusted Pint=0.53) or key secondary endpoints (Pint=0.61).Conclusions: TRACER was largely conducted in thienopyridine-naïve patients with unknown tolerance to multiple antiplatelet treatments. Patients receiving thienopyridine before the index event may have had an attenuated increase in bleeding when adding vorapaxar, whereas concomitantly adding vorapaxar and thienopyridine in naïve patients may have uncovered a latent susceptibility to bleeding.

IMPORTANCE: In the current therapeutic era, the risk for sudden cardiac death (SCD) after non–ST-segment elevation acute coronary syndrome (NSTE ACS) has not been characterized completely. OBJECTIVE: To determine the cumulative incidence of SCD during long-term follow-up after NSTE ACS, to develop a risk model and risk score for SCD after NSTE ACS, and to assess the association between recurrent events after the initial ACS presentation and the risk for SCD. DESIGN, SETTING, AND PARTICIPANTS: This pooled cohort analysis merged individual data from 48 286 participants in 4 trials: the Apixaban for Prevention of Acute Ischemic Events 2 (APPRAISE-2), Study of Platelet Inhibition and Patient Outcomes (PLATO), Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRACER), and Targeted Platelet Inhibition to Clarify the Optimal Strategy to Medically Manage Acute Coronary Syndromes (TRILOGY ACS) trials. The cumulative incidence of SCD and cardiovascular death was examined according to time after NSTE ACS. Using competing risk and Cox proportional hazards models, clinical factors at baseline and after the index event that were associated with SCD after NSTE ACS were identified. Baseline factors were used to develop a risk model. Data were analyzed from January 2, 2014, to December 11, 2015. MAIN OUTCOMES AND MEASURES: Sudden cardiac death. RESULTS: Of the initial 48 286 patients, 37 555 patients were enrolled after NSTE ACS (67.4% men; 32.6% women; median [interquartile range] age, 65 [57-72] years). Among these, 2109 deaths occurred after a median follow-up of 12.1 months. Of 1640 cardiovascular deaths, 513 (31.3%) were SCD. At 6, 18, and 30 months, the cumulative incidence estimates of SCD were 0.79%, 1.65%, and 2.37%, respectively. Reduced left ventricular ejection fraction, older age, diabetes mellitus, lower estimated glomerular filtration rate, higher heart rate, prior myocardial infarction, peripheral artery disease, Asian race, male sex, and high Killip class were significantly associated with SCD. A model developed to calculate the risk for SCD in trials with systematic collection of left ventricular ejection fraction had a C index of 0.77. An integer-based score was developed from this model and yielded a calculated SCD probability ranging from 0.1% to 56.7% (C statistic, 0.75). In a multivariable model that included time-dependent clinical events occurring after the index hospitalization for ACS, SCD was associated with recurrent myocardial infarction (hazard ratio [HR], 2.95; 95% CI, 2.29-3.80; P &lt; .001) and any hospitalization (HR, 2.45; 95% CI, 1.98-3.03; P &lt; .001), whereas coronary revascularization had a negative relationship with SCD (HR, 0.75; 95% CI, 0.58-0.98; P = .03). CONCLUSIONS AND RELEVANCE: In the current therapeutic era, SCD accounts for about one-third of cardiovascular deaths after NSTE ACS. Risk stratification can be performed with good accuracy using commonly collected clinical variables. Clinical events occurring after the index hospitalization are underappreciated but important risk factors.

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Background: This study characterized a medically managed population in a non-ST-segment elevation acute coronary syndrome (NSTEACS) cohort and evaluated prognosis and outcomes of vorapaxar vs. placebo.Methods: In the TRACER study, 12,944 NSTEACS patients were treated with standard care and vorapaxar (a novel platelet protease-activated receptor-1 antagonist) or placebo. Of those, 4194 patients (32.4%) did not undergo revascularization during index hospitalization, and 8750 (67.6%) underwent percutaneous coronary intervention or coronary artery bypass grafting. Patients managed medically were heterogeneous with different risk profiles, including 1137 (27.1%) who did not undergo coronary angiography. Patients who underwent angiography but were selected for medical management included those without evidence of significant coronary artery disease (CAD), with prior CAD but no new significant lesions, and with significant lesions who were not treated with revascularization.Results: Cardiovascular event rates were highest among those without angiography and lowest in the group with angiography but without CAD. In the medically managed cohort, 2-year primary outcome (cardiovascular death, myocardial infarction, stroke, recurrent ischaemia with rehospitalization, urgent coronary revascularization) event rates were 16.3% with vorapaxar and 17.0% with placebo (HR 0.99, 95% CI 0.83–1.17), with no interaction between drug and management strategy (p=0.75). Key secondary endpoint (cardiovascular death, myocardial infarction, stroke) rates were 13.4% with vorapaxar and 14.9% with placebo (HR 0.89, 95% CI 0.74–1.07), with no interaction (p=0.58). Vorapaxar increased GUSTO moderate/severe bleeding numerically in medically managed patients (adjusted HR 1.46, 95% CI 0.99–2.15).Conclusions: NSTEACS patients who were initially medically managed had a higher risk-factor burden, and one-third had normal coronary arteries. Outcome in the medically managed cohort was significantly related to degree of CAD, highlighting the importance of coronary angiography. Efficacy and safety of vorapaxar appeared consistent with the overall trial results.

Dual antiplatelet therapy (DAPT) cessation increases the risk of adverse events after percutaneous coronary intervention (PCI). Whether risk changes over time, depends on the underlying reason for DAPT cessation, or both is unknown. We assessed associations between different modes of DAPT cessation and cardiovascular risk after PCI.

Ischemic heart disease remains the number one cause of death in the world despite advances in invasive and pharmacologic therapies. An ongoing area of research is the central role of platelets in atherothrombosis. Many therapeutic strategies have been developed over the last few decades affecting different platelet receptors to alter platelet-mediated thrombosis including targeting the receptors for thromboxane A2, adenosine diphosphate, and fibrinogen. However, despite the use of pharmacologic agents directed at these pathways, residual morbidity and mortality still exist. Therefore, identifying agents that more favorably balance a reduction in ischemic events while minimizing bleeding events is an ongoing mission. Thrombin is known to be the most potent stimulant of platelet-mediated thrombosis whose action on the platelet is through a family of receptors known as the protease-activated receptors (PARs). Activation through the PAR-1 receptor, in particular, results in an early and intense response by the platelet to thrombin, and it is the primary thrombin receptor on platelets, thus making it a potentially desirable target for therapy. Most recently, two PAR-1 antagonists, atopaxar and vorapaxar, have been tested in clinical trials. Generally, the results show a reduction in ischemic event rates, but an increase in bleeding event rates. This article will summarize the current state of the literature and consider the role these drugs might play in the future for the prevention of ischemic heart disease events.

The optimal regimen of the anticoagulant and antiplatelet therapies in patients with atrial fibrillation who have had a coronary stent is unclear. It is well recognized that “triple therapy” with aspirin, clopidogrel, and warfarin is associated with an increased risk of bleeding. National guidelines have not made specific recommendations, given the lack of adequate data. In choosing the best antithrombotic options for a patient, consideration needs to be given to the risks of stroke, stent thrombosis, and major bleeding. This executive summary describes these risks, provides specific recommendations concerning vascular access, stent choice, concomitant use of proton pump inhibitors, and the use and duration of triple therapy after stent placement, based on the risk assessment.

Cardiac electric therapies effectively terminate tachyarrhythmias. Recent data suggest a possible increase in long-term mortality associated with implantable cardioverter-defibrillator shocks. Little is known about the association between external cardioversion episodes (ECVe) and long-term mortality. We sought to assess the safety of repeated ECVe with regard to cardiovascular mortality and morbidity.

The use of upstream small-molecule glycoprotein (GP) IIbIIIa inhibitors in non–ST-segment elevation acute coronary syndromes (NSTE ACS) has been studied in multiple randomized clinical trials. We systematically reviewed the effect of upstream GP IIbIIIa inhibitor use in NSTE ACS as reported in published clinical trials.

Dual antiplatelet therapy with aspirin and a thienopyridine has been shown to reduce cardiac events after coronary stenting. However, many patients and health care providers prematurely discontinue dual antiplatelet therapy, which greatly increases the risk of stent thrombosis, myocardial infarction and death.

Clopidogrel has become a mainstay in the management of acute coronary syndrome patients over the past decade, as well as an essential component of percutaneous coronary intervention (PCI) pharmacotherapy. Until recently, no prospective study has evaluated the effectiveness of clopidogrel in the setting of an ST-segment elevation myocardial infarction (STEMI). The majority of patients presenting with STEMI receive thrombolytic therapy (aspirin, heparin and a fibrinolytic agent) although many do not achieve or maintain adequate reperfusion of the infarct-related artery. The CLARITY (Clopidogrel as Adjunctive Reperfusion Therapy) study and the PCI–CLARITY substudy were designed to address whether a beneficial effect of clopidogrel, including a loading dose, would be attained among STEMI patients who were being treated with thrombolytic therapy and undergoing coronary angiography during the index hospitalisation. A total of 3491 patients who presented within 12 h after the onset of STEMI were randomly assigned to receive clopidogrel (300-mg loading dose followed by 75 mg daily) or placebo. Patients were scheduled to undergo coronary angiography after 48 h, and those who underwent PCI during the index hospitalisation formed the basis of PCI–CLARITY. This PCI cohort was followed for the combined end point of cardiovascular death, recurrent myocardial infarction and stroke for 30 days.

Chronic kidney disease (CKD) is highly prevalent in patients with cardiovascular disease. We explored the associations of CKD with outcomes using combined data from two large acute coronary syndrome (ACS) trials. We also explored the associations of CKD with prescription patterns for common cardiovascular medications and the association of these prescription patterns with clinical outcomes.

The use of arteriotomy closure devices (CDs) to achieve hemostasis after femoral artery access in percutaneous coronary intervention is steadily increasing. However, the safety information with these devices in the era of triple antiplatelet therapy is limited.

The clinical guidelines for unstable angina UA and nonST elevation myocardial infarction NSTEMI published in 1994 by the Agency for Health Care Policy Research AHCPR were intended to help improve treatment. No large study, however, has evaluated the effect of the guidelines on clinical practice

Fibrinolytic therapy for the treatment of ST‐segment elevation myocardial infarction unquestionably reduces mortality when administered within 12 hours of symptom onset. By promptly restoring antegrade perfusion, infarct size is limited, ventricular function is less compromised, and mortality rates are lowered. Although fibrinolytic therapy initially restores antegrade flow in the infarct vessel in the majority of patients, sustained, tissue‐level reperfusion occurs in only approximately one fourth of patients. Thrombin and platelets associated with a coronary thrombus are not specifically targeted by fibrinolytic agents, but rather have paradoxically increased activity. These components contribute to the tendency for vessel reocclusion after initially successful reperfusion. Thus, adjunctive therapy with antithrombins and antiplatelet agents are essential in the successful treatment of a coronary thrombus. Although aspirin has been shown to reduce mortality in acute myocardial infarction, it is a weak antiplatelet agent that is pathway specific. Glycoprotein IIb/IIIa inhibitors are potent antiplatelet agents that block the final common pathway for platelet aggregation. Thus, the growing evidence of platelet preeminence in the pathophysiology of failed thrombolysis has lead to the study of combination drug therapy with glycoprotein IIb/IIIa inhibition and reduced dose fibrinolytic agents in the treatment of acute ST‐segment elevation myocardial infarction. This article reviews the rationale, results, and clinical implications of the major trials of combination drug therapy in acute myocardial infarction.

Acute coronary syndromes (ACS), including those associated with or without ST-segment elevation, share a common pathophysiology mediated by activated platelets and thrombin. It is becoming increasingly appreciated that reperfusion therapies using primary mechanical or pharmacologic strategies result in suboptimal reperfusion at the myocardial tissue level. Complete reperfusion of the coronary microvasculature has recently been shown to be an important predictor for survival following myocardial infarction. Abciximab has well-established clinical benefits in numerous interventional trials. Through its anti-platelet and anti-thrombotic activities, abciximab reduces thrombus formation and hence minimizes risk of thrombotic microvascular embolization and improves tissue-level reperfusion. Several recent landmark trials have evaluated the clinical efficacy of adjunctive abciximab during mechanical or pharmacologic reperfusion therapy in the setting of ACS. This article provides an update of the role of abciximab in the treatment for ACS based on the results of these clinical trials.

OBJECTIVES

Despite the success of abciximab in preventing ischemic events after percutaneous coronary interventions, attempts to develop intravenous, small-molecule glycoprotein IIb/IIIa antagonists and diversify the clinical indications for these agents have produced varied results. The 30-day ischemic event reduction in the percutaneous coronary intervention trials has ranged by over three-fold (16% to 56%) and is greater among the acute coronary syndrome trials. The phase III trials exploring the role of oral glycoprotein IIb/IIIa inhibition have been consistently disappointing, with evolving evidence of increased mortality. Mechanisms contributing to these heterogeneous results may include normal variation in platelet or receptor number, differences in receptor activity, interpatient variation in pharmacological dose-response and the possibility of prothrombotic or nonglycoprotein IIb/IIIa effects. Plausibility of “suboptimal” effect is suggested by several recent studies. Trials investigating the role of intravenous small-molecule IIb/IIIa antagonists highlight the importance of effective dosing. The increase in bleeding and mortality observed in the oral glycoprotein IIb/IIIa studies indicate the consequences of suboptimal dosing on safety on one hand, while raising the possibility of important prothrombotic, counterregulatory or other sudden cardiac events. This article will undertake a review of the relevant platelet biology, discuss the mechanisms that may contribute to suboptimal antiplatelet efficacy with these agents and examine insights from the clinical trials supporting these concepts.

OBJECTIVES

The molecular understanding of platelet function, together with an appreciation of the role of platelet thrombus in the pathogenesis of acute coronary syndromes (ACS) and abrupt vessel closure following coronary intervention, lead to the development of the class of agents now referred to as platelet glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors. Currently three parenteral GP IIb/IIIa inhibitors are licensed for use in patients undergoing coronary intervention or as empirical therapy in non-ST elevation ACS (unstable angina and non-Q wave myocardial infarction). Clinical trials using these agents in patients undergoing coronary interventions have demonstrated a consistent reduction in ischaemic end points at 30 days that is sustained during long-term follow-up. Similar benefits have been found in patients with ACS who are managed medically or who proceed to revacularisation. Studies using prolonged platelet inhibition using oral GP IIb/IIIa inhibitors in patients following coronary intervention or with ACS have produced disappointing results. Further investigation with existing and newer oral agents are ongoing. The use of GP IIb/IIIa inhibitors in combination with fibrinolytic agents for optimal reperfusion in patients with acute ST-elevation myocardial infarction (MI) is an active area of interest. Angiographic outcomes with this approach have been encouraging and clinical outcome data are awaited. Beyond efficacy, GP IIb/IIIa inhibitors have proven to be safe for clinical use. Haemorrhagic complications and thrombocytopenia are the most common adverse events, though infrequent. Unresolved issues regarding drug dosing, monitoring of effect, duration of therapy, head-to-head comparisons of agents, and use of adjunctive therapies are the subject of ongoing studies.

Am Heart J 1999;137:8-11.

Objectives. This study sought to determine whether the duration of pretreatment with the adenosine diphosphate receptor antagonist ticlopidine prior to intracoronary stenting is associated with the incidence of procedure-related non–Q-wave myocardial infarctions (MIs).

During percutaneous coronary revascularization, intracoronary stents are effective in the treatment of abrupt vessel closure and improvement of suboptimal angioplasty results, and compared to balloon angioplasty, they reduce stenosis recurrence. Opposing these benefits, subacute thrombosis of stents is associated with a substantial increase in periprocedural morbidity and mortality. To review factors associated with stent thrombosis and to study the impact of evolving procedural techniques on the incidence of stent thrombosis, we reviewed all English articles from MEDLINE (1988 to 1995) with key words “stent” and “thrombosis”. Stent registry data and recent abstracts from scientific meeting were also reviewed. Factors related to the clinical setting, the lesion, the stent and the procedural technique that affect the risk of stent thrombosis were identified. Sixty clinical studies were reviewed and include 7,914 patients receiving intracoronary stents. Studies were separated into those reporting stents placed emergently or electively without adjunct high-pressure balloon inflations, stents placed in saphenous vein graft conduits, and stents placed with high-pressure balloon inflations but without subsequent oral anticoagulants. Overall, subacute thrombosis was substantially higher in stents placed emergently (10.1%) compared to those placed electively (4.3%). Among contemporary trials employing high-pressure balloon inflations, the rate of stent thrombosis appears markedly lower (1.3%) despite reduced postprocedural anticoagulation. Taken together, these studies suggest factors associated with a heightened risk of stent thrombosis, many of which can be avoided with proper case selection and contemporary techniques.

Cocaine induces vasoconstriction of epicardial coronary arteries in patients with and without coronary artery disease, and this vasoconstriction is particularly marked in segments narrowed by atherosclerosis. To assess the effect of nitroglycerin on cocaine-induced coronary vasoconstriction, computer-assisted quanitative analysis was performed on nondiseased and diseased coronary artery segments in 23 patients (18 men, 5 women, aged 43 to 65 years) 1) at baseline, 2) after administration of intranasal saline solution (in 8 patients) or 2 mg/kg of cocaine (in 15 patients), and then 3) after administration of sublingual placebo (in 6 patients) or 0.4 or 0.8 mg of nitroglycerin (in 9 patients) in the 15 patients given cocaine.

Objectives. The purpose of this study was to investigate whether or not there is an association between managed care insurance and the delivery and outcome of care in patients presenting with unstable angina.

Intranasal cocaine, 2 to 3 mg/kg body weight, is a commonly used local anesthetic for rhinolaryngologic procedures, and many persons who abuse it ingest a similar amount. Previous studies in humans showed that this dose of cocaine causes coronary vasoconstriction, and studies in animals showed that larger amounts given intravenously diminish myocardial performance. This study assessed the hemodynamic effects of intranasal cocaine, 2 mg/kg, in humans.

While angina is not uncommonly seen in association with hyperthyroidism, only rare case reports have suggested that myocardial ischemia in this state may be due to coronary artery spasm. The authors review the literature and describe a case in which the repetitive occurrence of episodes of myocardial ischemia due to coronary spasm correlated with repeated transient elevations in thyroid hormone levels, thus clarifying this relationship. The importance of defining thyroid status in patients presenting with coronary vasospasm is emphasized and the effects of thyroid hormone on the heart are reviewed.

Objectives. This study was undertaken to define and better understand the characteristics and outcomes of patients with diabetes treated for acute myocardial infarction with contemporary thrombolysis.

The activated clotting time (ACT) has been used during percutaneous transluminal coronary angioplasty (PTCA) to monitor the extent of thrombin inhibition and anti-coagulation from heparin in an attempt to minimize untoward thrombotic events and hemorrhagic complications. With the introduction of potent platelet inhibitors, such as the chimeric monoclonal antibody c7E3, to interventional cardiology, the utility of measuring and regulating procedural ACT has not been examined. To investigate the possible influence of platelet IIb/IIIa antagonism on procedural ACT, we reviewed data from the Evaluation of c7E3 Fab in the Prevention of Ischemic Complications (EPIC) trial. In the EPIC trial, 2,099 patients undergoing PTCA with a high risk of abrupt vessel closure were randomized to receive placebo (n = 696) or the IIb/IIIa platelet receptor antagonist c7E3 Fab (n = 1,403). Despite receiving less procedural heparin, and fewer patients receiving very high heparin doses (>14,000 U) than the placebo group, those receiving c7E3 had a higher mean (401 vs 367 seconds, p < 0.001) ACT when corrected for body weight. The ACT is increased approximately 35 seconds by the platelet IIb/IIIa receptor antagonist c7E3 Fab. This has important implications for dosing conjunctive heparin therapy and performing PTCA or directional coronary atherectomy in the setting of IIb/IIIa-directed therapy.

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Am Heart J 2003;145:203-5.

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