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Biomedical subjects

Marc S Sabatine

Publications and source records attributed to Marc S Sabatine.

At least 37 records · Page 2Linked to original sources
PubMed2006

Appropriate invasive and conservative treatment approaches for patients with ST-elevation MI.

The combination of aspirin, heparin, and fibrinolytics was established in the late 1980s and early 1990s as the foundation for pharmacologic reperfusion therapy for ST-elevation myocardial infarction (STEMI). Since that time, many attempts have been made to improve on this regimen with limited success. In the late 1990s, primary percutaneous coronary intervention emerged as an invasive approach for reperfusion that offered superior outcomes to fibrinolytic therapy. However, timely access to experienced cardiac catheterization laboratories remains problematic for the majority of patients with STEMI. Meanwhile, recent advances in adjunctive antiplatelet and anticoagulation therapies have improved outcomes in patients undergoing pharmacologic reperfusion.

Journal Article↗
PubMed2006

Combination of quantitative ST deviation and troponin elevation provides independent prognostic and therapeutic information in unstable angina and non-ST-elevation myocardial infarction.

BACKGROUND: ST deviation and troponin are indicators of risk in unstable angina/non-ST-elevation myocardial infarction with related but distinct pathophysiology. We hypothesized that a combination of the two would offer complementary information regarding the benefit of an invasive strategy. METHODS AND RESULTS: Electrocardiogram and troponin data were gathered in 1846 patients in TACTICS-TIMI 18. Adjusting for baseline characteristics, the independent odds ratio (OR) (95% CI) for death or myocardial infarction by 6 months was 1.29 (0.78-2.13) for 0.05 to 0.09 mV ST deviation, 1.83 (1.22-2.75) for > or = 0.10 mV ST deviation, 1.69 (0.96-2.97) for troponin T 0.01 to 0.10 ng/mL, and 2.32 (1.52-3.53) for troponin T > 0.10 ng/mL. There was a significant interaction between the magnitude of ST deviation and treatment strategy (P(interaction) = .04). After adjusting for troponin and other baseline characteristics, an early invasive strategy was associated with a 27% greater reduction in the odds of death or myocardial infarction in those with 0.05 to 0.09 mV of ST deviation (OR(interaction) 0.73, 95% CI 0.27-2.02) and a 64% greater reduction in those with > or = 0.10 mV (OR(interaction) 0.36, 95% CI 0.16-0.84) compared with in those without ST deviation. CONCLUSIONS: The magnitude of ST deviation and degree of troponin elevation are graded independent predictors of outcome in unstable angina/non-ST-elevation myocardial infarction. ST deviation complements troponin elevation in selecting patients for early invasive management.

Angina, Unstable↗
PubMed2006

Predicting a late positive serum troponin in initially troponin-negative patients with non-ST-elevation acute coronary syndrome: clinical predictors and validated risk score results from the TIMI IIIB and GUSTO IIA studies.

BACKGROUND: Troponin testing is useful for evaluating patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS); however, a significant percentage of patients are troponin negative at presentation and develop late rise of the marker. METHODS: Patients in the TIMI IIIB study were assessed with respect to their troponin I (TnI) status at presentation and 12 hours. Multivariable analysis identified independent clinical factors associated with TnI rise at 12 hours among subjects initially TnI negative. A score predicting late TnI rise in TIMI IIIB was developed using these factors and validated among patients in the GUSTO IIA study. RESULTS: Of 1342 subjects in TIMI IIIB, 200 (14.9%) were negative at baseline, but developed an elevated TnI (> or = 0.4 ng/mL) at 12 hours. Six independent predictors of late TnI rise were identified: ST-segment deviation (odds ratio [OR] 3.52, 95% CI 2.38-5.23, P < .001), presentation < 8 hours from symptom onset (OR 2.91, 95% CI 1.92-4.40, P < .001), no prior percutaneous coronary intervention (OR 2.88, 95% CI 1.54-5.39, P = .001), no prior beta-blocker use (OR 1.74, 95% CI 1.15-2.63, P = .008), unheralded angina (OR 1.65, 95% CI 1.12-2.42, P = .01), and a history of myocardial infarction (OR 1.59, 95% CI 1.06-2.37, P = .02). ST deviation, presentation < 8 hours from symptoms, and no prior percutaneous coronary intervention were given a score of 2 points, whereas a score of 1 point was assigned to the other factors. Among baseline TnI-negative patients, a rising score was paralleled by an increasing prevalence of late TnI rise from 0% (with a score of 0) to 69% (with a score of 9) (P < .001). In confirmation, the score was able to similarly predict late troponin T rise among 855 patients in the GUSTO IIA study (P < .0001). CONCLUSION: Development of late troponin rise is common in non-ST-segment elevation acute coronary syndromes. Six easily ascertained variables may be used to identify those at higher risk for late rise in troponin levels after an initially negative presentation.

Aged↗
PubMed2006

Clopidogrel use in coronary artery disease.

Platelet adhesion, activation and aggregation are central to the pathophysiology of the acute coronary syndromes. Clopidogrel, an oral thienopyridine derivative, is a platelet adenosine diphosphate receptor antagonist capable of inhibiting platelet activation. During the last decade, the utility of clopidogrel has been evaluated in several common clinical scenarios in a large number of patients. The benefits of clopidogrel in patients with stable coronary artery disease undergoing elective percutaneous coronary interventions and in patients presenting with acute coronary syndromes are now well established. This review outlines the pharmacology of clopidogrel, highlights the results of clopidogrel trials in the setting of acute coronary syndromes, and presents areas of uncertainty and potential future work.

Clopidogrel↗
PubMed2005

Prognostic value of serial B-type natriuretic peptide testing during follow-up of patients with unstable coronary artery disease.

CONTEXT: Elevated concentrations of B-type natriuretic peptide (BNP) at presentation in patients with acute coronary syndrome (ACS) are associated with long-term mortality. Few data exist regarding serial assessment of BNP levels during follow-up. OBJECTIVE: To determine whether concentrations of BNP at study entry (prior to hospital discharge for ACS) and at outpatient follow-up at 4 months and 12 months are associated with subsequent clinical outcomes. DESIGN, SETTING, AND PATIENTS: Prospective observational substudy of 4497 patients with non-ST-elevation or ST-elevation ACS who were enrolled in phase Z of the A to Z trial, which was conducted in 41 countries at 322 acute care hospitals between 1999 and 2003. MAIN OUTCOME MEASURE: Death from any cause or new onset of congestive heart failure (CHF) through 2 years. RESULTS: Levels of BNP were available in 4266 patients at study entry (prior to hospital discharge), 3618 patients at 4 months, and 2966 patients at 12 months. During follow-up there were 230 deaths and 163 incident cases of CHF. Adjusting for age, sex, index event, renal function, hypertension, prior heart failure, and diabetes, elevated levels of BNP (>80 pg/mL) were associated with subsequent death or new CHF when measured at study entry (111 [21%] vs 246 [7%]; adjusted hazard ratio [HR], 2.5; 95% confidence interval [CI], 2.0-3.3), at 4 months (34 [19%] vs 125 [4%]; adjusted HR, 3.9; 95% CI, 2.6-6.0), and at 12 months (19 [11%] vs 37 [1%]; adjusted HR, 4.7; 95% CI, 2.5-8.9). Patients with newly elevated levels of BNP at 4 months were at increased risk of death or new CHF (10 [15%] vs 105 [3%]); HR, 4.5; 95% CI, 2.3-8.6). Patients with elevated levels of BNP at study entry and with BNP levels lower than 80 pg/mL at 4 months tended to have only modestly increased risk (HR, 1.7; 95% CI, 1.0-2.9) compared with patients with BNP levels lower than 80 pg/mL at both visits. CONCLUSIONS: Serial determinations of BNP levels during outpatient follow-up after ACS predict the risk of death or new CHF. Changes in BNP levels over time are associated with long-term clinical outcomes and may provide a basis for enhanced clinical decision making in patients after onset of ACS.Clinical Trials Registration ClinicalTrials.gov Identifier: NCT00251576.

Coronary Disease↗
PubMed2005

Metabolomic identification of novel biomarkers of myocardial ischemia.

BACKGROUND: Recognition of myocardial ischemia is critical both for the diagnosis of coronary artery disease and the selection and evaluation of therapy. Recent advances in proteomic and metabolic profiling technologies may offer the possibility of identifying novel biomarkers and pathways activated in myocardial ischemia. METHODS AND RESULTS: Blood samples were obtained before and after exercise stress testing from 36 patients, 18 of whom demonstrated inducible ischemia (cases) and 18 of whom did not (controls). Plasma was fractionated by liquid chromatography, and profiling of analytes was performed with a high-sensitivity electrospray triple-quadrupole mass spectrometer under selected reaction monitoring conditions. Lactic acid and metabolites involved in skeletal muscle AMP catabolism increased after exercise in both cases and controls. In contrast, there was significant discordant regulation of multiple metabolites that either increased or decreased in cases but remained unchanged in controls. Functional pathway trend analysis with the use of novel software revealed that 6 members of the citric acid pathway were among the 23 most changed metabolites in cases (adjusted P=0.04). Furthermore, changes in 6 metabolites, including citric acid, differentiated cases from controls with a high degree of accuracy (P<0.0001; cross-validated c-statistic=0.83). CONCLUSIONS: We report the novel application of metabolomics to acute myocardial ischemia, in which we identified novel biomarkers of ischemia, and from pathway trend analysis, coordinate changes in groups of functionally related metabolites.

Adenosine Monophosphate↗
PubMed2005

Angiographic and clinical outcomes in patients receiving low-molecular-weight heparin versus unfractionated heparin in ST-elevation myocardial infarction treated with fibrinolytics in the CLARITY-TIMI 28 Trial.

BACKGROUND: Low-molecular-weight heparin (LMWH) offers pharmacological and practical advantages over unfractionated heparin (UFH). Whether these advantages translate into greater infarct-related artery patency and fewer adverse clinical events in patients with ST-elevation myocardial infarction (STEMI) receiving fibrinolytic therapy remains under study. METHODS AND RESULTS: We compared angiographic and clinical outcomes in patients treated with LMWH (n=1429) versus UFH (n=1431) in CLARITY-TIMI 28, a randomized trial of clopidogrel versus placebo in STEMI patients aged 18 to 75 years undergoing fibrinolysis. After comprehensive adjustment for baseline characteristics, therapeutic interventions, and a propensity score, treatment with LMWH was associated with a significantly lower rate of a closed infarct-related artery or death or myocardial infarction before angiography (13.5% versus 22.5%, adjusted OR 0.76, P=0.027). Treatment with LMWH was also associated with a significantly lower rate of cardiovascular death or recurrent myocardial infarction through 30 days (6.9% versus 11.5%, adjusted OR 0.68, P=0.030). The lower event rates were observed in patients allocated to clopidogrel and in those who underwent percutaneous coronary intervention. Rates of TIMI major bleeding through 30 days (1.6% versus 2.2%, P=0.27) and intracranial hemorrhage (0.6% versus 0.8%, P=0.37) were similar in the LMWH and UFH groups. Patients who received both clopidogrel and LMWH, in addition to a standard fibrinolytic and aspirin, had a particularly high rate of infarct-related artery patency (90.9%) and particularly low rates of cardiovascular death (3.2%), recurrent myocardial infarction (3.0%), and major bleeding (1.8%). CONCLUSIONS: In patients with STEMI receiving fibrinolytic therapy, use of LMWH with other standard therapies, including clopidogrel and aspirin, is associated with improved angiographic outcomes and lower rates of major adverse cardiovascular events.

Adolescent↗
PubMed2005

Evaluation of the paraoxonases as candidate genes for stroke: Gln192Arg polymorphism in the paraoxonase 1 gene is associated with increased risk of stroke.

BACKGROUND AND PURPOSE: The paraoxonases are involved in protecting low-density lipoprotein (LDL) from lipid oxidation. Paraoxonase 1 (PON1) was implicated in susceptibility to coronary artery disease and stroke in previous studies. We evaluated, in a comprehensive way, all 3 paraoxonase genes for association with stroke observed in the Cholesterol and Recurrent Events (CARE) trial. METHODS: Over 2500 subjects enrolled in the CARE trial were genotyped for 14 single nucleotide polymorphisms, including 7 newly identified in this study, in the 3 paraoxonase genes. RESULTS: A glutamine (Gln)/arginine (Arg) polymorphism at amino acid residue 192 in PON1 was significantly associated with stroke (P=0.003 in multivariate analysis, including age, sex, LDL, hypertension, diabetes, smoking, and pravastatin treatment as covariates). The odds ratios were 2.28 (95% CI, 1.38 to 3.79) for Gln/Arg heterozygotes and 2.47 (95% CI, 1.18 to 5.19) for Arg/Arg homozygotes compared with Gln/Gln homozygotes. These results are consistent with 2 of 3 other published studies. In combined analysis of all 4 studies, the association between Gln192Arg SNP and stroke was highly significant (chi2(8df)=45.58, P<0.000001). Sequence analysis of the PON1 gene from seventy stroke cases revealed a novel nonsense mutation at codon 32 in one stroke case, which was not detected in over 2500 unaffected individuals. Polymorphisms in the PON2 and PON3 genes were not associated with stroke. CONCLUSIONS: These results suggest that Gln192Arg genotype is an important risk factor for stroke.

Arginine↗
PubMed2005

Effect of clopidogrel pretreatment before percutaneous coronary intervention in patients with ST-elevation myocardial infarction treated with fibrinolytics: the PCI-CLARITY study.

CONTEXT: The benefit of clopidogrel pretreatment before percutaneous coronary intervention (PCI) remains debated and its use has not been universally adopted. OBJECTIVE: To determine if clopidogrel pretreatment before PCI in patients with recent ST-segment elevation myocardial infarction (STEMI) is superior to clopidogrel treatment initiated at the time of PCI in preventing major adverse cardiovascular events. DESIGN, SETTING, AND PARTICIPANTS: The PCI-Clopidogrel as Adjunctive Reperfusion Therapy (CLARITY) study was a prospectively planned analysis of the 1863 patients undergoing PCI after mandated angiography in CLARITY-Thrombolysis in Myocardial Infarction (TIMI) 28, a randomized, double-blind, placebo-controlled trial of clopidogrel in patients receiving fibrinolytics for STEMI. Patients were enrolled at 319 sites in 23 countries from February 2003 through October 2004. INTERVENTIONS: Patients received aspirin and were randomized to receive either clopidogrel (300 mg loading dose, then 75 mg once daily) or placebo initiated with fibrinolysis and given until coronary angiography, which was performed 2 to 8 days after initiation of the study drug. For patients undergoing coronary artery stenting, it was recommended that open-label clopidogrel (including a loading dose) be administered after the diagnostic angiogram. MAIN OUTCOME MEASURES: The primary outcome was the incidence of the composite of cardiovascular death, recurrent MI, or stroke from PCI to 30 days after randomization. Secondary outcomes included MI or stroke before PCI and the aforementioned composite from randomization to 30 days. RESULTS: Pretreatment with clopidogrel significantly reduced the incidence of cardiovascular death, MI, or stroke following PCI (34 [3.6%] vs 58 [6.2%]; adjusted odds ratio [OR], 0.54 [95% CI, 0.35-0.85]; P = .008). Pretreatment with clopidogrel also reduced the incidence of MI or stroke prior to PCI (37 [4.0%] vs 58 [6.2%]; OR, 0.62 [95% CI, 0.40-0.95]; P = .03). Overall, pretreatment with clopidogrel resulted in a highly significant reduction in cardiovascular death, MI, or stroke from randomization through 30 days (70 [7.5%] vs 112 [12.0%]; adjusted OR, 0.59 [95% CI, 0.43-0.81]; P = .001; number needed to treat = 23). There was no significant excess in the rates of TIMI major or minor bleeding (18 [2.0%] vs 17 [1.9%]; P>.99). CONCLUSIONS: Clopidogrel pretreatment significantly reduces the incidence of cardiovascular death or ischemic complications both before and after PCI and without a significant increase in major or minor bleeding. These data add further support to the early use of clopidogrel in STEMI and the strategy of routine clopidogrel pretreatment in patients undergoing PCI.

Aged↗
PubMed2005

Association of hemoglobin levels with clinical outcomes in acute coronary syndromes.

BACKGROUND: In the setting of an acute coronary syndrome (ACS), anemia has the potential to worsen myocardial ischemia; however, data relating anemia to clinical outcomes in ACS remain limited. METHODS AND RESULTS: We examined the association between baseline hemoglobin values and major adverse cardiovascular events through 30 days in 39,922 patients enrolled in clinical trials of ACS. After adjustment for differences in baseline characteristics and index hospitalization treatments, a reverse J-shaped relationship between baseline hemoglobin values and major adverse cardiovascular events was observed. In patients with ST-elevation myocardial infarction, when those with hemoglobin values between 14 and 15 g/dL were used as the reference, cardiovascular mortality increased as hemoglobin levels fell below 14 g/dL, with an adjusted OR of 1.21 (95% CI 1.12 to 1.30, P<0.001) for each 1-g/dL decrement in hemoglobin. At the other end of the range of hemoglobin, patients with hemoglobin values >17 g/dL also had excess mortality (OR 1.79, 95% CI 1.18 to 2.71, P=0.007). In patients with non-ST-elevation ACS, with those with hemoglobin 15 to 16 g/dL used as the reference, the likelihood of cardiovascular death, myocardial infarction, or recurrent ischemia increased as the hemoglobin fell below 11 g/dL, with an adjusted OR of 1.45 (95% CI 1.33 to 1.58, P<0.001) for each 1 g/dL decrement in hemoglobin. Patients with hemoglobin values >16 g/dL also had an increased rate of death or ischemic events (OR 1.31, 95% CI 1.03 to 1.66, P=0.027). CONCLUSIONS: Anemia is a powerful and independent predictor of major adverse cardiovascular events in patients across the spectrum of ACS.

Acute Disease↗
PubMed2005

Influence of race on death and ischemic complications in patients with non-ST-elevation acute coronary syndromes despite modern, protocol-guided treatment.

BACKGROUND: In the setting of acute coronary syndromes (ACS), nonwhite patients are less likely to undergo invasive cardiac procedures and may have worse clinical outcomes than white patients. Whether the disparate outcomes exist independently of potential biases in treatment patterns remains unclear. METHODS AND RESULTS: We examined the association between race and outcome in the Treat Angina with Aggrastat and Determine Cost of Therapy With an Invasive or Conservative Strategy-Thrombolysis in Myocardial Infarction 18 study (TACTICS-TIMI 18), a randomized trial of invasive versus conservative treatment strategy in patients with non-ST-elevation ACS. There were 1722 white and 461 nonwhite patients. After adjustment for differences in medical characteristics, nonwhite patients were at significantly increased risk for death, MI, or rehospitalization for ACS (hazard ratio [HR], 1.54; P=0.003). Rates of protocol-guided angiography and revascularization were similar in both groups. For non-protocol-guided care, however, we found significant disparities, with nonwhite patients less likely to be taking their cardiac medications at follow-up (odds ratio [OR], 0.59; P=0.0002), to undergo non-protocol-mandated angiography (OR, 0.40; P=0.03), to receive a stent if undergoing percutaneous coronary intervention (OR, 0.55; P=0.045), and to have less procedural success after percutaneous coronary intervention (acute gain, 1.40+/-0.83 versus 1.81+/-0.92 mm; P=0.004). Nonetheless, an invasive strategy was similarly efficacious in white (HR, 0.66; 95% CI, 0.50 to 0.88) and nonwhite (HR, 0.85; 95% CI, 0.52 to 1.39) patients (P(interaction)=0.52), especially in those with troponin elevation or ST deviation. CONCLUSIONS: After adjustment for baseline characteristics, nonwhite patients had a significantly worse prognosis than white patients, regardless of treatment approach. In the absence of protocol guidance, important disparities emerged between the care given the 2 groups. An early invasive strategy is beneficial in and should be considered for all patients, regardless of race.

Black or African American↗
PubMed2005

Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation.

BACKGROUND: A substantial proportion of patients receiving fibrinolytic therapy for myocardial infarction with ST-segment elevation have inadequate reperfusion or reocclusion of the infarct-related artery, leading to an increased risk of complications and death. METHODS: We enrolled 3491 patients, 18 to 75 years of age, who presented within 12 hours after the onset of an ST-elevation myocardial infarction and randomly assigned them to receive clopidogrel (300-mg loading dose, followed by 75 mg once daily) or placebo. Patients received a fibrinolytic agent, aspirin, and when appropriate, heparin (dispensed according to body weight) and were scheduled to undergo angiography 48 to 192 hours after the start of study medication. The primary efficacy end point was a composite of an occluded infarct-related artery (defined by a Thrombolysis in Myocardial Infarction flow grade of 0 or 1) on angiography or death or recurrent myocardial infarction before angiography. RESULTS: The rates of the primary efficacy end point were 21.7 percent in the placebo group and 15.0 percent in the clopidogrel group, representing an absolute reduction of 6.7 percentage points in the rate and a 36 percent reduction in the odds of the end point with clopidogrel therapy (95 percent confidence interval, 24 to 47 percent; P<0.001). By 30 days, clopidogrel therapy reduced the odds of the composite end point of death from cardiovascular causes, recurrent myocardial infarction, or recurrent ischemia leading to the need for urgent revascularization by 20 percent (from 14.1 to 11.6 percent, P=0.03). The rates of major bleeding and intracranial hemorrhage were similar in the two groups. CONCLUSIONS: In patients 75 years of age or younger who have myocardial infarction with ST-segment elevation and who receive aspirin and a standard fibrinolytic regimen, the addition of clopidogrel improves the patency rate of the infarct-related artery and reduces ischemic complications.

Adult↗
PubMed2005

Correlation between the TIMI risk score and high-risk angiographic findings in non-ST-elevation acute coronary syndromes: observations from the Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) trial.

BACKGROUND: The TIMI risk score for unstable angina and non-ST elevation myocardial infarction is an effective tool for predicting the risk of death and ischemic events among patients with non-ST elevation acute coronary syndromes, as well as for identifying those who are likely to benefit most from low-molecular-weight heparin and glycoprotein IIb/IIIa inhibition. METHODS: To explore the pathobiologic basis for this interaction, we evaluated the relationship between the risk score, assessed at presentation, and angiographic findings among patients with non-ST elevation acute coronary syndromes. Angiographic data regarding thrombus, epicardial flow, and lesion severity were available for 1491 patients from the angiographic substudy of PRISM-PLUS. RESULTS: Patients with risk scores of 5 to 7 (N = 435) were more likely to have a severe culprit stenosis (81% vs 58%, P < .001) and multivessel disease (80% vs 43%, P < .001) compared to those with scores of 0 to 2 (N = 220). The probability of left main disease (P = .01), visible thrombus, and impaired flow in the culprit lesion also increased progressively with rising risk scores (P < .001). Of the risk indicators that comprise the score, history of coronary disease, advanced age, and ST changes showed the strongest association with severe epicardial disease. Positive biomarkers of necrosis, ST changes, and prior aspirin use emerged as stronger correlates of visible thrombus and/or impaired culprit artery flow. CONCLUSIONS: The TIMI risk score identifies patients who are more likely to have intracoronary thrombus, impaired flow, and increased burden of coronary atherosclerosis. These findings likely explain in part the particular benefit of potent antithrombin and antiplatelet agents among patients with higher risk scores.

Aged↗
PubMed2005

Design and rationale of Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in Myocardial Infarction (CLARITY-TIMI) 28 trial.

BACKGROUND: Although fibrinolysis is effective in improving outcomes in ST-elevation myocardial infarction (STEMI), failure to achieve reperfusion and/or reocclusion of the infarct-related artery occur in substantial proportions of patients during their index hospitalization and are associated with a significant increase in mortality. We hypothesize that the addition of clopidogrel to standard fibrinolytic therapy in patients with acute STEMI will improve reperfusion. STUDY DESIGN: CLARITY-TIMI 28 is a multicenter, international, randomized, double-blind, placebo-controlled trial designed to examine the efficacy and safety of clopidogrel when added to standard adjuvant therapy for fibrinolysis. The primary efficacy end point is the composite of an occluded infarct-related artery (defined as TIMI flow grade 0 or 1) on the predischarge angiogram or death or a recurrent myocardial infarction (MI) up to the start of coronary angiography. For subjects who do not undergo angiography, occurrence of death or recurrent MI by day 8 or by hospital discharge, whichever comes first, is used. The primary safety assessment is TIMI major bleeding. Secondary end points include ST resolution at 180 minutes and the clinical composite of death, MI, or recurrent ischemia. Substudies include analyses of biomarkers, DNA, continuous electrocardiogram monitoring, and initiation of treatment in the ambulance. CONCLUSIONS: CLARITY-TIMI 28 will help to define the role of clopidogrel as part of the pharmacologic reperfusion regimen for acute STEMI.

Clopidogrel↗