Coronary flow reserve varies depending upon the location within the artery it is assessed and the TIMI myocardial perfusion grade: a PROTECT TIMI-30 analysis.

Coronary flow reserve (CFR) is a measure of the capacity of the epicardial coronary artery and the microvasculature to achieve maximal blood flow in response to hyperemic stimulation. It is not known whether the CFR varies along the length of the artery. Likewise, the interaction between CFR and the thrombolysis in myocardial infarction (TIMI) myocardial perfusion grade (TMPG) is unknown. CFR was measured using the number of cineframes required for the contrast to traverse the same length of the coronary artery before and following the administration of intracoronary adenosine. Following percutaneous coronary intervention (PCI), CFR was assessed both proximal and distal to the lesion in 192 consecutive patients with non-ST-segment elevation acute coronary syndrome (NSTEACS) from the PROTECT TIMI-30 trial. TMPG was also assessed. The difference between the distal and proximal CFR for patients with TMPG 0/1 (n = 76) was 0.11 (95% CI 0.01-0.20, P = 0.026), while among those with TMPG 2/3 (n = 114) it was -0.02 (95% CI -0.09-0.06, P = 0.65). The difference in the CFR between the distal and proximal segments among patients with TMPG 0/1 and TMPG 2/3 was significant (P interaction = 0.044). Following PCI among patients with impaired TMPG (0/1) in the setting of NSTEACS, CFR varies significantly between the proximal and distal segment of coronary arteries and is associated with higher (greater) distal CFR.

Effect of prasugrel versus clopidogrel on outcomes among patients with acute coronary syndrome undergoing percutaneous coronary intervention without stent implantation: a TRial to assess Improvement in Therapeutic Outcomes by optimizing platelet inhibitioN with prasugrel (TRITON)-Thrombolysis in Myocardial Infarction (TIMI) 38 substudy.

BACKGROUND: Prasugrel led to a significant reduction in ischemic cardiovascular events among patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) with stent implantation compared to clopidogrel. Whether this benefit extends to patients undergoing PCI without stent implantation is unknown. METHODS: In TRial to assess Improvement in Therapeutic Outcomes by optimizing platelet inhibitioN with prasugrel (TRITON)-Thrombolysis in Myocardial Infarction (TIMI) 38, patients (n = 13 608) undergoing PCI for ACS were randomized to aspirin plus clopidogrel or prasugrel. This postrandomization analysis of a prespecified subgroup was restricted to patients who underwent PCI without stent implantation (n = 569). RESULTS: Patients who underwent PCI without stent implantation were older and had a higher incidence of hypertension, diabetes, prior myocardial infarction (MI), prior coronary artery bypass (CABG) surgery, and renal dysfunction than patients who underwent stent implantation. In the group that did not undergo stent implantation, baseline characteristics were similar between patients receiving clopidogrel and prasugrel. The composite of cardiovascular death, nonfatal MI, and nonfatal stroke occurred in 14.2% of patients receiving prasugrel and 17.1% of patients receiving clopidogrel (HR 0.82, P = .27). There were significant reductions favoring prasugrel in the rates of urgent target vessel revascularization (TVR; HR 0.46, P = .040) and any TVR (HR 0.40, P = .009) and a trend toward a reduction in the incidence of nonfatal MI (HR 0.65, P = .11). CABG-related TIMI major bleeding was more frequent among patients receiving prasugrel. There were no significant interactions between treatment and PCI type. CONCLUSION: Among ACS patients who underwent PCI without stent implantation, prasugrel therapy tended to reduce clinical ischemic events and to increase bleeding events to a similar magnitude as among patients who received stents.

Timing and duration of myocardial ischemia on Holter monitoring following percutaneous coronary intervention and their association with clinical outcomes (a PROTECT-TIMI 30 Substudy Analysis).

In patients with unstable angina, evidence of myocardial ischemia on Holter monitoring is associated with an adverse prognosis. However, the association of duration and timing of ischemia on Holter monitoring with outcomes after percutaneous coronary intervention (PCI) in patients with non-ST-segment elevation acute coronary syndromes (NSTEACSs) has not been systematically evaluated. PROTECT-TIMI 30 randomized 857 patients with NSTEACSs undergoing PCI to eptifibatide plus a heparin product or bivalirudin monotherapy. Patients underwent continuous Holter monitoring following PCI, and the association between ischemia and clinical outcomes was evaluated retrospectively. Forty-three patients (5.0%) had ischemia on Holter after PCI. Any ischemia was associated with a significant increase in the incidence of death or myocardial infarction (MI) within 48 hours (32.6% vs 6.1%, odds ratio 7.5, 95% confidence interval 3.70 to 15.10, p <0.001). In patients who developed ischemia, there was a 1.44-fold increase in the odds for death or MI for every 30 minutes of ischemia (95% confidence interval 1.12 to 1.84, p = 0.004). Duration of ischemic events was related to their timing, such that ischemic events that occurred within the first 4 hours after PCI (median duration 141 minutes, interquartile range 36 to 227.5) were significantly longer than events occurring 4 to 24 hours after PCI (median duration 32.8 minutes, interquartile range 17.5 to 118, p = 0.041). In conclusion, early ischemia after PCI for NSTEACS is of longer duration, and longer duration of ischemia recognized by Holter monitoring is associated with an increased incidence of death or MI. Holter monitoring may be a useful surrogate end point in clinical trials.

Efficacy of ranolazine in patients with chronic angina observations from the randomized, double-blind, placebo-controlled MERLIN-TIMI (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Segment Elevation Acute Coronary Syndromes) 36 Trial.

OBJECTIVES: We aimed to evaluate the efficacy and safety of ranolazine in a larger and more diverse group of patients with angina than previously studied. BACKGROUND: Ranolazine is an antianginal shown to reduce angina and improve exercise performance in selected patients with early-positive exercise testing and those with frequent angina. METHODS: We investigated the antianginal effects of ranolazine in the subgroup of patients with prior chronic angina (n = 3,565, 54%) enrolled in the randomized, double-blind, placebo-controlled MERLIN-TIMI (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST Elevation Acute Coronary Syndromes) 36 trial of patients with acute coronary syndrome. Follow-up was a median of 350 days. RESULTS: Patients with prior angina received evidence-based therapy (95% aspirin, 78% statins, 89% beta-blockers, average 2.9 antianginal agents). The primary end point (cardiovascular death, myocardial infarction, recurrent ischemia) was less frequent with ranolazine (hazard ratio [HR]: 0.86; 95% confidence interval [CI]: 0.75 to 0.97; p = 0.017), due entirely to a significant reduction in recurrent ischemia (HR: 0.78; 95% CI: 0.67 to 0.91; p = 0.002). Ranolazine also reduced worsening angina (HR: 0.77; 95% CI: 0.59 to 1.00; p = 0.048) and intensification of antianginal therapy (HR: 0.77; 95% CI: 0.64 to 0.92, p = 0.005). Exercise duration at 8 months was greater with ranolazine (514 s vs. 482 s, p = 0.002). Cardiovascular death or myocardial infarction did not differ between treatment groups (HR: 0.97; 95% CI: 0.80 to 1.16; p = 0.71). Symptomatic documented arrhythmias (2.9% vs. 2.9%, p = 0.92) and total mortality (6.2% vs. 6.4%, p = 0.96) were similar with ranolazine or placebo. CONCLUSIONS: In this largest study of ranolazine in patients with established coronary artery disease, ranolazine was effective in reducing angina with favorable safety in a substantially broader group of patients with angina than previously studied. (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST Elevation Acute Coronary Syndromes; NCT00099788).

Association of non-steroidal anti-inflammatory drugs with outcomes in patients with ST-segment elevation myocardial infarction treated with fibrinolytic therapy: an ExTRACT-TIMI 25 analysis.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) may be prothrombotic, may worsen hypertension or congestive heart failure and obstruct access to the binding site of aspirin to cyclooxygenase-1 and thereby interfere with aspirin's mechanism of action in reducing death and recurrent myocardial infarction (MI). We hypothesized that treatment with NSAIDs prior to an index MI would be associated with an increase in the risk of death, heart failure and recurrent MI among patients with ST-segment elevation MI (STEMI) treated with fibrinolytic therapy. METHODS: In ExTRACT-TIMI 25, patients with STEMI were treated with aspirin and fibrinolytic therapy and randomized to either enoxaparin or unfractionated heparin. We included patients who had received NSAIDs within 7 days of enrollment and evaluated the incidence of MI, the composite of death and MI and the composite of death, MI, severe heart failure and shock through 30 days. RESULTS: Of 20,479 patients enrolled, 572 (2.8%) received an NSAID within 7 days of enrollment. NSAID treatment prior to entry was associated with a higher incidence of 30-day death or nonfatal recurrent MI (15.9% vs. 10.8%, univariate P < 0.001). In multivariable models adjusting for randomization group and differences in baseline characteristics, NSAID use was associated with higher odds of MI (adjusted odds ratio [OR(adj)] 1.44, 95% confidence interval [CI] 1.01-2.07, P = 0.047), the composite of death and MI (OR(adj) 1.29, 95% CI 1.00-1.66, P = 0.051), and the composite of death, MI, severe heart failure and shock (OR(adj) 1.29, 95% CI 1.02-1.65, P = 0.037). CONCLUSIONS: Among STEMI patients treated with a fibrinolytic agent and aspirin, use of NSAIDs in the week preceding the incident event was associated with a higher incidence of MI, the composite of death and MI as well as the composite of death, MI, severe heart failure and shock at 30 days.

Use of the TIMI frame count in the assessment of coronary artery blood flow and microvascular function over the past 15 years.

Since its introduction, the TIMI frame count method has contributed to the understanding of the pathophysiology of coronary artery disease. In this article, the evolution of the TFC method and its applicability in the assessment of various therapeutic modalities are described.

Transfusion associated microchimerism: a heretofore little-recognized complication following transfusion.

Potent antiplatelet and antithrombotic agents have significantly reduced mortality in the setting of acute coronary syndromes and percutaneous coronary intervention. However these agents are associated with increased bleeding which is in turn associated with adverse clinical outcomes. In many centers, transfusion is often used to correct for blood loss. Blood transfusion in the setting of acute coronary syndrome has been associated with adverse clinical outcomes including increased mortality. Transfusion associated microchimerism (TA-MC) is a newly recognized complication of blood transfusion. There is engraftment of the donor's hematopoietic stem cells in patients who then develop microchimerism. This article discusses the association of bleeding/blood transfusion with adverse outcomes and the potential role of TA-MC in clinical outcomes.

Intracoronary pharmacotherapy in the management of coronary microvascular dysfunction.

Although percutaneous coronary intervention restores optimal epicardial blood flow in most cases, abnormal myocardial perfusion may still persist. This might be as a result of macro and microembolization, neutrophil plugging, vasoconstriction, myocyte contracture, local intracellular and interstitial edema, intramural haemorrhage, and endothelial blistering. Local delivery of intracoronary pharmacotherapy via the coronary arteries may increase local drug concentration several fold, and may improve drug efficacy. Several pharmacological agents such as adenosine, calcium channel blockers, alpha blockers, beta2 receptor activators, vasodilators, antithrombotics, and antiplatelet agents have been used to treat coronary microvascular dysfunction. This article reviews the results of trials of intracoronary pharmacotherapy to date.

Occurrence and frequency of arrhythmias in hypertrophic cardiomyopathy in relation to delayed enhancement on cardiovascular magnetic resonance.

OBJECTIVES: Our aim was to determine whether myocardial fibrosis, detected by cardiovascular magnetic resonance (CMR), represents an arrhythmogenic substrate in hypertrophic cardiomyopathy (HCM). BACKGROUND: Myocardial fibrosis is identified frequently in HCM; however, the clinical significance of this finding is uncertain. METHODS: We studied prevalence and frequency of tachyarrhythmias on 24-h ambulatory Holter electrocardiogram (ECG) with regard to delayed enhancement (DE) on contrast-enhanced CMR in 177 HCM patients (age 41 +/- 16 yrs; 95% asymptomatic or mildly symptomatic). RESULTS: Premature ventricular contractions (PVCs), couplets, and nonsustained ventricular tachycardia (NSVT) were more common in patients with DE than those without DE (PVCs: 89% vs. 72%; couplets: 40% vs. 17%; NSVT: 28% vs. 4%; p < 0.0001 to 0.007). Patients with DE also had greater numbers of PVCs (202 +/- 655 vs. 116 +/- 435), couplets (1.9 +/- 5 vs. 1.2 +/- 10), and NSVT runs (0.4 +/- 0.8 vs. 0.06 +/- 0.4) than non-DE patients (all p < 0.0001); DE was an independent predictor of NSVT (relative risk 7.3, 95% confidence interval 2.6 to 20.4; p < 0.0001). However, extent (%) of DE was similar in patients with and without PVCs (8.2% vs. 9.1%; p = 0.93), couplets (8.5% vs. 8.4%; p = 0.99), or NSVT (8.3% vs. 8.5%; p = 0.35). CONCLUSIONS: In this large HCM cohort with no or only mild symptoms, myocardial fibrosis detected by CMR was associated with greater likelihood and increased frequency of ventricular tachyarrhythmias (including NSVT) on ambulatory Holter ECG. Therefore, contrast-enhanced CMR identifies HCM patients with increased susceptibility to ventricular tachyarrhythmias.

Relation of hyperemic epicardial flow to outcomes among patients with ST-segment elevation myocardial infarction receiving fibrinolytic therapy.

In patients with ST-segment elevation myocardial infarction (STEMI), the restoration of normal epicardial flow following fibrinolytic administration is associated with improved clinical outcomes. The goal of this analysis was to examine the relation between hyperemic flow and outcomes following fibrinolytic administration for STEMI. In Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis In Myocardial Infarction 28 (CLARITY-TIMI 28), patients with STEMI (n=3,491) treated with fibrinolytic therapy were scheduled to undergo angiography 48 to 192 hours after randomization. Corrected TIMI frame count (CTFC) and TIMI myocardial perfusion grade (TMPG) were assessed, and their associations with outcomes at 30 days were evaluated. When evaluating initial angiography of the infarct-related artery, there was a nearly linear relation between CTFC and 30-day mortality, with faster flow (lower CTFC) associated with improved outcomes. Conversely, in patients who underwent percutaneous coronary intervention (PCI), very fast flow (CTFC<14) after intervention was associated with worse outcomes. Post-PCI hyperemic flow (CTFC<14) was associated with a higher incidence of mortality (p=0.056), recurrent myocardial infarction (p=0.011), and a composite of death or myocardial infarction (p<0.001) compared with normal flow (CTFC 14 to 28). When post-PCI CTFC was further stratified by TMPG, there was a U-shaped relation between mortality and CTFC in patients with poor myocardial perfusion (TMPG 0 or 1). This relation appeared to be linear in patients with TMPG 2 or 3. In conclusion, in patients who undergo PCI after fibrinolytic therapy for STEMI, hyperemic flow on coronary angiography is associated with an increased incidence of adverse outcomes. Hyperemic flow with associated impaired myocardial perfusion may be a marker of more extensive downstream microembolization.

Measuring noncalcified coronary atherosclerotic plaque using voxel analysis with MDCT angiography: phantom validation.

OBJECTIVE: This purpose of this study was to evaluate the accuracy and reproducibility of a voxel analysis technique for measuring noncalcified plaque in the coronary arteries. MATERIALS AND METHODS: Polyethylene phantoms representing noncalcified plaque were scanned in both MDCT and micro-CT scanners and inter- and intrareader variability of volume calculation was performed. RESULTS: Volume measurements by both MDCT and micro-CT were comparable to the true volume as measured by micrometry (< 3%, p = 0.05). CONCLUSION: There appears to be no significant difference (< 3%) between MDCT and micro-CT measurements.

Significance of papillary muscle abnormalities identified by cardiovascular magnetic resonance in hypertrophic cardiomyopathy.

Increased thickness of the left ventricular (LV) wall is the predominant feature of the hypertrophic cardiomyopathy (HC) phenotype. The structural characteristics of the LV papillary muscles (PMs) have received little attention. In this study, cardiovascular magnetic resonance (CMR) was used to characterize PM morphology in a large HC population. Cine and delayed enhancement (DE) CMR images were obtained in 201 patients with HC and 43 control subjects. PM number and mass index were greater in patients with HC compared with controls (2.5 vs 2.1, p <0.001, and 6 +/- 2 vs 3 +/- 2 g/m(2), p <0.001, respectively), including 109 (54%) with PM mass > or =7 g/m(2) (> or =2 SDs above the mean for controls). Greater LV wall mass index was associated with more substantial PM mass (r = 0.09, p <0.001). Furthermore, 12 patients with HC (19%) had normal LV mass with localized wall thickness but increased PM mass. In patients with HC with LV outflow obstruction at rest, PMs were positioned closer to the ventricular septum (displaced anteriorly: 58% vs 42% for subjects without obstruction, p = 0.02), with more marked hypertrophy (9 +/- 5 vs 6 +/- 4 g/m(2), p <0.001). Preoperative CMR identified 3 patients with accessory, anteriorly displaced PMs judged to contribute to outflow obstruction, which were resected during septal myectomy. DE of the PMs was identified in 13 patients with HC (6%), including 3 with DE confined to PMs. In conclusion, CMR demonstrates LV PMs to be part of the cardiomyopathic process in HC, with increases in number and mass, and not uncommonly associated with remodeling with DE. The identification of accessory PMs may be useful in planning preoperative strategy.

Association of impaired thrombolysis in myocardial infarction myocardial perfusion grade with ventricular tachycardia and ventricular fibrillation following fibrinolytic therapy for ST-segment elevation myocardial infarction.

OBJECTIVES: The goal of this analysis was to evaluate the association of impaired Thrombolysis In Myocardial Infarction myocardial perfusion grade (TMPG) with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). BACKGROUND: Impaired TMPG after successful restoration of epicardial flow among patients treated with fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) has been associated with adverse clinical outcomes, but its relationship to VT/VF has not been evaluated. METHODS: In the CLARITY-TIMI 28 (Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis In Myocardial Infarction 28) study, 3,491 patients underwent angiography a median of 3.5 days after fibrinolytic administration for STEMI; TMPG was assessed, and its association with VT/VF was evaluated. RESULTS: We observed VT/VF in 4.8% of patients. Impaired myocardial perfusion (TMPG 0/1/2) was associated with an increased incidence of VT/VF (7.1% vs. 2.6% with TMPG 3; log-rank p < 0.001). Among patients with restoration of normal epicardial flow (Thrombolysis In Myocardial Infarction flow grade 3), the incidence of VT/VF was increased among patients with impaired TMPG (4.7% vs. 2.7%; p = 0.02). Among patients with left ventricular ejection fraction >or=30%, impaired TMPG remained associated with an increased incidence of VT/VF (4.7% vs. 2.5%; p = 0.03). We found that VT/VF was associated with increased mortality (25.2% vs. 3.5%; p < 0.0001). Furthermore, among patients with VT/VF, impaired TMPG was associated with increased mortality (17.1% vs. 2.3%; p = 0.02). All but 1 death among patients who had VT/VF were among patients with impaired myocardial perfusion. CONCLUSIONS: Despite restoration of normal epicardial flow or a left ventricular ejection fraction >or=30%, impaired myocardial perfusion on angiography 3.5 days after fibrinolytic administration for STEMI is associated with an increased incidence of VT/VF.

Angiographic perfusion score in patients treated with PCI at late angiography following fibrinolytic administration for ST-segment elevation myocardial infarction is associated with morbidity and mortality at 30 days.

BACKGROUND: Among patients with ST-segment elevation myocardial infarction (STEMI), evidence of restoration of both normal epicardial arterial flow and myocardial perfusion early after the administration of fibrinolytic agents has been associated with improved clinical outcomes. In STEMI patients treated with fibrinolytic therapy and scheduled for angiography later during hospital admission, however, the association of later indices of flow and perfusion with clinical outcomes has not been assessed. METHODS: Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in Myocardial Infarction (CLARITY-TIMI) 28 enrolled 3,491 STEMI patients treated with fibrinolytic therapy. Angiography was scheduled 48-192 h (median 84) after randomization. The Angiographic Perfusion Score (APS) (the sum of the TIMI Flow Grade and Myocardial Perfusion Grade before and after percutaneous coronary intervention (PCI), range of 0-12) was assessed in the 1,460 patients treated with PCI at late angiography, and its association with morbidity and mortality at 30 days was examined. RESULTS: Full perfusion, defined as an APS of 10-12, was associated with the lowest mortality (0.8%), while partial perfusion (APS 4-9) (2.3%) and failed perfusion (APS 0-3) (18.0%) were associated with a higher incidence of mortality at 30 days (P < 0.001 for full perfusion vs. partial perfusion, P < 0.0001 for overall trend). In addition, full perfusion was associated with a lower incidence of recurrent myocardial infarction (MI), a composite of death and MI, recurrent myocardial ischemia, ventricular tachyarrhythmia, congestive heart failure and shock (P < 0.05 for all trends). CONCLUSION: Among STEMI patients treated with late PCI following fibrinolytic therapy, higher APS is associated with reduced morbidity and mortality.

Usefulness of clopidogrel in abolishing the increased risk of reinfarction associated with higher platelet counts in patients with ST-elevation myocardial infarction (results from CLARITY-TIMI 28).

Previous studies have demonstrated an association between increased baseline platelet counts and poorer clinical and angiographic outcomes in patients with ST-elevation myocardial infarction (STEMI). We hypothesized that antiplatelet therapy would mitigate the effect of high baseline platelet counts on clinical outcomes. Data were obtained from 3,491 patients with STEMI in the CLARITY-TIMI 28 trial. Patients were categorized into 3 groups based on their baseline platelet counts: <200 x 10(3)/microl (group 1), 200 to 300 x 10(3)/microl (group 2), and >300 x 10(3)/microl (group 3). Among placebo-treated patients, reinfarction rates increased in a stepwise fashion as platelet counts increased (3.6%, 5.4%, and 9.0%, respectively, p for trend = 0.0025). When confounders of high platelet counts and correlates of reinfarction were adjusted for in a multivariate model, high platelet counts remained independently associated with increased rates of reinfarction at 30 days in placebo-treated patients; using group 1 as a reference group, multivariate odds ratios were 1.45 (95% confidence interval 0.91 to 2.31, p = 0.119) for patients in group 2 and 1.78 (95% confidence interval 1.03 to 3.08, p = 0.038) for patients in group 3. In contrast, among clopidogrel-treated patients, there was no increase in the risk of reinfarction as the platelet count increased (3.2%, 4.1%, and 3.3%, respectively; p for trend = 0.9073, p for interaction=0.064). In conclusion, among patients with STEMI who are treated with aspirin and a fibrinolytic agent, high platelet counts on presentation are independently associated with increased rates of reinfarction. Clopidogrel therapy abolishes this increase in the risk of reinfarction as platelet counts increase. These data are consistent with a putative role of platelets in reinfarction.

Prognostic utility of heart-type fatty acid binding protein in patients with acute coronary syndromes.

BACKGROUND: Heart-type fatty acid binding protein (H-FABP) is a cytosolic protein that is released rapidly from the cardiomyocyte in response to myocardial injury. Although it has been investigated as an early marker of acute myocardial infarction, its prognostic utility in acute coronary syndromes has not been established. METHODS AND RESULTS: We measured H-FABP in 2287 patients with acute coronary syndromes from the OPUS-TIMI 16 trial. H-FABP was elevated (> 8 ng/mL) in 332 patients (14.5%). Patients with an elevated H-FABP were more likely to suffer death (hazard ratio [HR], 4.1; 95% CI, 2.6 to 6.5), recurrent myocardial infarction (HR, 1.6; 95% CI, 1.0 to 2.5), congestive heart failure (HR, 4.5; 95% CI, 2.6 to 7.8), or the composite of these end points (HR, 2.6; 95% CI, 1.9 to 3.5) through the 10-month follow-up period. H-FABP predicted the risk of the composite end point both in patients who were troponin I negative (HR, 2.1; 95% CI, 1.3 to 3.4) and in those who were troponin I positive (HR, 3.3; 95% CI, 2.0 to 5.3). In a Cox proportional-hazards model that adjusted for baseline variables, including demographics, clinical characteristics, creatinine clearance, ST deviation, index diagnosis, and troponin I, elevated H-FABP remained a significant predictor of the composite end point (HR, 1.9; 95% CI, 1.3 to 2.7), as well as the individual end points of death (HR, 2.7; 95% CI, 1.5 to 4.9) and CHF (HR, 2.4; 95% CI, 1.2 to 5.0). In a multimarker approach, H-FABP, troponin I, and B-type natriuretic peptide provided complementary information. CONCLUSIONS: Elevation of H-FABP is associated with an increased risk of death and major cardiac events in patients presenting across the spectrum of acute coronary syndromes and is independent of other established clinical risk predictors and biomarkers.