ST-segment Elevation Myocardial Infarction Population Research Articles

Bleeding Events After ST-segment Elevation Myocardial Infarction in Patients Randomized to an All-comer Clinical Trial Compared With Unselected Patients

Most studies reporting bleedings in patients with ST-segment elevation myocardial infarction (STEMI) are reports from clinical trials, which may be unrepresentative of incidences in real-life. In this study, we investigated 1-year bleeding and mortality incidences in an unselected STEMI population, and compared participants with nonparticipants of a randomized all-comer clinical trial (The Third DANish Study of Optimal Acute Treatment of Patients with STEMI (DANAMI-3)). Hospital charts were read and bleedings classified according to thrombolysis in myocardial infarction (TIMI) and Bleeding Academic Research Consortium (BARC) criteria in 2,490 consecutive STEMI patients who underwent primary percutaneous coronary intervention in a single, large, and tertiary heart center. Thrombolysis in myocardial infarction minor and/or major bleeding (TMMB) occurred in 4.4% day 0 to 30 and 2.1% day 31 to 365. DANAMI-3 nonparticipants (n = 887) had significantly higher 30-day bleeding rates than DANAMI-3-participants (n = 1,603) (7.2% vs 2.9%, p <0.0001), but not thereafter (p = 0.8). DANAMI-3 nonparticipation was significantly associated with 30-day TMMB (hazard ratio, 1.8, 95% confidence interval, 1.2 to 2.8, p = 0.007), but this did not persist after adjusting for resuscitated cardiac arrest, Killip-class>2 and anemia. Patients with cardiac arrest, Killip-class>2, and anemia accounted for 70.0% of 30-day TMMBs, and the majority of these patients were DANAMI-3 nonparticipants. TMMB day 0 to 30 was associated with increased 30-day mortality (hazard ratio 3.1, 95% confidence interval 1.9 to 5.2, p <0.0001) but not thereafter (p = 0.9). In conclusion, we found that clinical trial (DANAMI-3) nonparticipants had significantly more TMMBs within 30 days than participants. Patients with resuscitated cardiac arrest, anemia, and Killip-class>2 were accountable for a high rate of TMMBs. Bleeding incidences from clinical trials cannot be translated to an unselected STEMI population.

Subacute cardiac rubidium-82 positron emission tomography (82Rb-PET) to assess myocardial area at risk, final infarct size, and myocardial salvage after STEMI

BackgroundDetermining infarct size and myocardial salvage in patients with ST-segment elevation myocardial infarction (STEMI) is important when assessing the efficacy of new reperfusion strategies. We investigated whether rest 82Rb-PET myocardial perfusion imaging can estimate area at risk, final infarct size, and myocardial salvage index when compared to cardiac SPECT and magnetic resonance (CMR). MethodsTwelve STEMI patients were injected with 99mTc-Sestamibi intravenously immediate prior to reperfusion. SPECT, 82Rb-PET, and CMR imaging were performed post-reperfusion and at a 3-month follow-up. An automated algorithm determined area at risk, final infarct size, and hence myocardial salvage index. ResultsSPECT, CMR, and PET were performed 2.2 ± 0.5, 34 ± 8.5, and 32 ± 24.4 h after reperfusion, respectively. Mean (± SD) area at risk were 35.2 ± 16.6%, 34.7 ± 11.3%, and 28.1 ± 16.1% of the left ventricle (LV) in SPECT, CMR, and PET, respectively, P = 0.04 for difference. Mean final infarct size estimates were 12.3 ± 15.4%, 13.7 ± 10.4%, and 11.9 ± 14.6% of the LV in SPECT, CMR, and PET imaging, respectively, P = .72. Myocardial salvage indices were 0.64 ± 0.33 (SPECT), 0.65 ± 0.20 (CMR), and 0.63 ± 0.28 (PET), (P = .78). Conclusions82Rb-PET underestimates area at risk in patients with STEMI when compared to SPECT and CMR. However, our findings suggest that PET imaging seems feasible when assessing the clinical important parameters of final infarct size and myocardial salvage index, although with great variability, in a selected STEMI population with large infarcts. These findings should be confirmed in a larger population.

Impact of left ventricular hypertrophy on myocardial injury in patients with ST-segment elevation myocardial infarction.

Left ventricular hypertrophy (LVH) has been suggested as a determinant of outcome in patients with ST-segment elevation myocardial infarction (STEMI). However, available data are inconclusive and the underlying mechanisms remain unclear. Therefore, the aim of this study was to evaluate the impact of LVH on myocardial injury and clinical outcome in a large multicenter STEMI population. Cardiovascular magnetic resonance was performed in 795 patients within 10days after STEMI to assess left ventricular (LV) mass and parameters of myocardial injury. Gender-specific cutoff values of indexed LV mass were used to define LVH (67g/m2 for men and 61g/m2 for women). Rates of major adverse cardiac events (MACE) were determined at 12-month follow-up. LVH was present in 438 patients (55%) and associated with a significantly larger infarct size [18.3% of LV mass (%LV) versus 14.0%LV; p < 0.01], a lower myocardial salvage index (47.8 versus 54.4; p < 0.01), larger extent of microvascular obstruction (0.4 versus 0%LV; p < 0.01) and lower LV ejection fraction (47.9 versus 53.2%; p < 0.01) compared to STEMI patients without LVH. The effect of LVH on LV ejection fraction, infarct size and myocardial salvage index remained statistically significant after adjustment for baseline characteristics (p < 0.01 for all). MACE rates at 12 months were numerically higher in patients with versus without LVH without reaching statistical significance (7.5 versus 5.6%; p = 0.32). In STEMI patients, LVH is associated with more pronounced structural and functional alterations in CMR imaging as an indicator for adverse clinical outcomes in STEMI survivors.

First serial optical coherence tomography assessment at baseline, 12 and 24 months in STEMI patients treated with the second-generation Absorb bioresorbable vascular scaffold

The aim of the study was to assess the vascular healing response after Absorb bioresorbable vascular scaffold (BVS) implantation in patients with ST-segment elevation myocardial infarction (STEMI) utilising truly serial optical coherence tomography (OCT) examination at baseline, 12 and 24 months. This was a single-centre, prospective, longitudinal study with baseline, 12- and 24-month OCT evaluation of 18 STEMI patients treated with 22 Absorb BVS. The healing pattern was evaluated based upon lumen area, neointimal hyperplasia, strut coverage and apposition. The lumen area decreased at 12 months compared to baseline (8.52±1.69 mm² vs. 7.0±1.70 mm², p<0.01), but it did not change from that point onwards up to 24 months (7.0±1.70 mm² vs. 6.94±1.65 mm², p=0.92). At 12 months after the index procedure, the mean neointimal thickness was 217±69 μm and further neointimal hyperplasia was observed between 12 and 24 months though less pronounced (Δ62±44 μm, p<0.0001). Full circumferential coverage of the vessel wall by neointima was observed in 92% of frames at 24 months. The low number of malapposed struts at the index procedure (<5%) further decreased over the observation period and was found in only one patient at 12 and 24 months. The ratio of uncovered struts was low at both 12 and 24 months. This serial OCT analysis of the second-generation everolimus-eluting BVS in a STEMI population confirmed a favourable healing pattern as expressed by moderate neointimal growth, preserved lumen area and no late acquired malapposition.

Absence of a correlation between the ABO blood group and thrombus burden in patients with ST-segment elevation myocardial infarction.

ABO antigens are highly abundant in many human cell types, including platelets, vascular endothelium, and red blood cells. The presence of a thrombus is associated with adverse clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). We reviewed the relationship between ABO blood groups and thrombus burden in patients with STEMI. We carried out a retrospective study of 396 patients with STEMI who did not have an ABO blood group or thrombus burden. The ABO blood type of all participants was determined. First, angiographic characteristics ranging from a nonexistent thrombus to total occlusion were defined as grades 0, 1, 2, 3, 4, and 5, respectively, using the thrombolysis in myocardial infarction (TIMI) scoring system. After wiring and/or small balloon dilation, the patients were split into two groups according to the TIMI grade: large thrombus burden (LTB) (TIMI 4, n=66) and small thrombus burden (STB) (TIMI 0-3, n=330). The prevalence rates of ABO blood and Rh types were similar between the groups (P>0.05). Moreover, no relationship was found between thrombus burden and the ABO blood group. The ABO blood group was not an independent predictor of large thrombus burden. The present study showed that although previous studies have reported a relationship between the ABO blood type and thrombus burden in the STEMI population, we found no such relationship in our study.

Implementation of an ST-Segment Elevation Myocardial Infarction Bypass Protocol in the Northern United Arab Emirates.

Objective:The aim was to evaluate the translation of an ST-segment elevation myocardial infarction (STEMI) bypass protocol to the outcomes of patients with acute coronary syndrome in the Emirate of Ras al-Khaimah in the United Arab Emirates (UAE).Methods:A prospective cohort study was conducted, which included all patients who had a prehospital 12-lead electrocardiogram (ECG) performed by ambulance crews. Analysis of those who were identified as having STEMI and who subsequently underwent percutaneous coronary intervention (PCI) was performed.Results:A total of 152 patients had a 12-lead ECG performed during the pilot study period (February 24, 2016–August 31, 2016) with 118 included for analysis. Mean patient age was 52 years. There were 87 male (74%) and 31 female (26%) patients. Twenty-nine patients suffered a STEMI, and data were available for 11 who underwent PCI. There was no mortality, and no major adverse cardiac events were reported. The median door-to-balloon (D2B) time was 73 min (range 48–124), and 81% of patients had a D2B time < 90 min. Discharge data were available for six patients: All were discharged home with no impediments to rehabilitation.Conclusion:This pilot study has demonstrated agreement with the existing literature surrounding prehospital ECG and PCI activation in an unstudied STEMI population and in a novel clinical setting. It has demonstrated a D2B time of < 90 min in over 80% of STEMI patients, and a faster mean D2B time than self-presentations (mean 77 min vs. 113 min), with no associated mortality or major adverse cardiac events.

A Prospective Evaluation of a Pre-Specified Absorb BVS Implantation Strategy in ST-Segment Elevation Myocardial Infarction: The BVS STEMI STRATEGY-IT Study

ObjectivesThe aim of this study was to assess the feasibility and clinical results following a pre-specified bioresorbable scaffold (Absorb BVS) implantation strategy in patients with ST-segment elevation myocardial infarction (STEMI). BackgroundConcerns were raised about the safety of Absorb because a non-negligible rate of thrombosis was reported within 30 days and at midterm follow-up after primary percutaneous coronary intervention. MethodsThis was a prospective, multicenter study of patients with STEMI (<75 years of age with symptom onset <12 h) undergoing primary percutaneous coronary intervention with Absorb following a dedicated implantation protocol. The primary endpoint was a device-oriented composite endpoint of cardiac death, target vessel myocardial infarction, and ischemia-driven target lesion revascularization within 30 days. ResultsDuring the study period, 505 patients with STEMI (16.9% of the overall STEMI population) were treated with the Absorb BVS. The mean age was 56.6 ± 9.4 years, and 487 patients (96.4%) were in Killip class I or II at admission. According to the study protocol, direct Absorb implantation was feasible in 47 patients (9.3%), whereas post-dilatation was performed in 468 cases (92.7%). Procedural success was attained in 94.8% of the cases. Dual antiplatelet therapy with ticagrelor or prasugrel was administered at discharge in 481 patients (95.1%). At 30-day follow-up, the hierarchical device-oriented composite endpoint rate was 0.6% (0.4% cardiac death, 0.2% target vessel myocardial infarction and ischemia-driven target lesion revascularization). One episode (0.2%) of probable scaffold thrombosis was reported. ConclusionsA pre-specified Absorb implantation strategy in real-world patients with STEMI undergoing primary percutaneous coronary intervention was feasible and associated with a low 30-day device-oriented composite endpoint rate. Mid- and long-term follow-up is strongly needed to eventually confirm these early results. (Use of BVS in ST-Segment Elevation Myocardial Infarction [STEMI]: The BVS STEMI STRATEGY-IT Prospective Registry [STRATEGY-IT]; NCT02601781)

Temporal Trends in the Clinical Acuity of Patients with ST-Segment Elevation Myocardial Infarction

BackgroundDespite advances in ST-segment elevation myocardial infarction (STEMI) systems of care over the last decade, studies have shown no improvement in risk-adjusted mortality. It has been hypothesized that the population presenting to the catheterization laboratory has become sicker over time, in ways not accurately captured by current mortality models. The objective of this study was to examine changes in the clinical characteristics and in-hospital case fatality rate of the STEMI population treated with early percutaneous coronary intervention (PCI). MethodsWe conducted a retrospective analysis of a nationwide inpatient database for the period 2004-2012. All patients with a diagnosis of STEMI who underwent PCI within 24 hours of admission were identified. The primary outcome was in-hospital mortality. ResultsFrom 2004 to 2012 there was a consistent increase in unadjusted in-hospital mortality (3.9% in 2004 and 4.7% in 2012, odds ratioyear 1.03; 95% confidence interval 1.01-1.04). During this time there was an increase in the proportion of patients with ≥3 Elixhauser comorbidities (14.8% vs 29.0%, Ptrend < .001). Intubation or cardiac arrest on presentation increased from 3.2% to 7.8% (Ptrend < .001) and had a strong, independent association with mortality. After multivariable adjustment using a model that incorporated the increasing trend in intubation/cardiac arrest, mortality decreased over time (odds ratioyear 0.95; 95% confidence interval 0.94-0.97). ConclusionsDuring a period that corresponds to improvement in STEMI quality of care, risk-adjusted in-hospital mortality declined. An increase in comorbidities, and more importantly in the proportion of patients presenting with extreme-risk features, may explain the overall “null” effect regarding in-hospital mortality despite improvements in timely reperfusion.

Identifying Patients at Risk for Prehospital Sudden Cardiac Arrest at the Early Phase of Myocardial Infarction: The e-MUST Study (Evaluation en Médecine d'Urgence des Stratégies Thérapeutiques des infarctus du myocarde).

In-hospital mortality of ST-segment-elevation myocardial infarction (STEMI) has decreased drastically. In contrast, prehospital mortality from sudden cardiac arrest (SCA) remains high and difficult to reduce. Identification of the patients with STEMI at higher risk for prehospital SCA could facilitate rapid triage and intervention in the field. Using a prospective, population-based study evaluating all patients with STEMI managed by emergency medical services in the greater Paris area (11.7 million inhabitants) between 2006 and 2010, we identified characteristics associated with an increased risk of prehospital SCA and used these variables to build an SCA prediction score, which we validated internally and externally. In the overall STEMI population (n=8112; median age, 60 years; 78% male), SCA occurred in 452 patients (5.6%). In multivariate analysis, younger age, absence of obesity, absence of diabetes mellitus, shortness of breath, and a short delay between pain onset and call to emergency medical services were the main predictors of SCA. A score built from these variables predicted SCA, with the risk increasing 2-fold in patients with a score between 10 and 19, 4-fold in those with a score between 20 and 29, and >18-fold in patients with a score ≥30 compared with those with scores <10. The SCA rate was 28.9% in patients with a score ≥30 compared with 1.6% in patients with a score ≤9 (P for trend <0.001). The area under the curve values were 0.7033 in the internal validation sample and 0.6031 in the external validation sample. Sensitivity and specificity varied between 96.9% and 10.5% for scores ≥10 and between 18.0% and 97.6% for scores ≥30, with scores between 20 and 29 achieving the best sensitivity and specificity (65.4% and 62.6%, respectively). At the early phase of STEMI, the risk of prehospital SCA can be determined through a simple score of 5 routinely assessed predictors. This score might help optimize the dispatching and management of patients with STEMI by emergency medical services.

One-year incidence and clinical impact of bleeding events in patients treated with prasugrel or clopidogrel after ST-segment elevation myocardial infarction

Little information is available on the long-term incidence of bleeding events after ST-segment elevation myocardial infarction (STEMI) with the current antithrombotic strategy. To evaluate the effect of bleedings for up to 12months on clinical events and therapeutic compliance in unselected STEMI patients treated with prasugrel or clopidogrel. Patients were treated with clopidogrel or prasugrel according to guidelines. The primary endpoint was first occurrence of a bleeding event from hospital discharge to 12months, assessed by the Bleeding Academic Research Consortium (BARC) classification using a dedicated questionnaire. Topography of bleedings, causes of premature cessation and ischaemic events were compared between clopidogrel- and prasugrel-treated patients. A total of 390patients were enrolled (211 in the prasugrel group, 179 in the clopidogrel group). Elderly, female and low-body weight patients were more likely to receive clopidogrel. At 12months, the incidence of major bleedings (BARC 3) was lower with prasugrel (1% vs 6%; P=0.02), mainly due to fewer transfusions. Elderly age was a risk factor for severe bleeding. Premature treatment cessation was related to ischaemic complications (P=0.03), and occurred more frequently with prasugrel (P=0.001). One-year mortality was very low (1.9 per 100person-years, 95% confidence interval 0.9-4.0), and was higher in the clopidogrel group (P=0.03). In this unselected STEMI population, the rate of major bleedings with prasugrel at 12months was low, but nuisance bleedings were frequent and led to more premature cessations than with clopidogrel. Prevention of bleeding complications, even minor, is necessary to prevent disruption of antithrombotic medication.

Early Intravenous Beta-Blockers in Patients With ST-Segment Elevation Myocardial Infarction Before Primary Percutaneous Coronary Intervention

BackgroundThe impact of intravenous (IV) beta-blockers before primary percutaneous coronary intervention (PPCI) on infarct size and clinical outcomes is not well established. ObjectivesThis study sought to conduct the first double-blind, placebo-controlled international multicenter study testing the effect of early IV beta-blockers before PPCI in a general ST-segment elevation myocardial infarction (STEMI) population. MethodsSTEMI patients presenting <12 h from symptom onset in Killip class I to II without atrioventricular block were randomized 1:1 to IV metoprolol (2 × 5-mg bolus) or matched placebo before PPCI. Primary endpoint was myocardial infarct size as assessed by cardiac magnetic resonance imaging (CMR) at 30 days. Secondary endpoints were enzymatic infarct size and incidence of ventricular arrhythmias. Safety endpoints included symptomatic bradycardia, symptomatic hypotension, and cardiogenic shock. ResultsA total of 683 patients (mean age 62 ± 12 years; 75% male) were randomized to metoprolol (n = 336) or placebo (n = 346). CMR was performed in 342 patients (54.8%). Infarct size (percent of left ventricle [LV]) by CMR did not differ between the metoprolol (15.3 ± 11.0%) and placebo groups (14.9 ± 11.5%; p = 0.616). Peak and area under the creatine kinase curve did not differ between both groups. LV ejection fraction by CMR was 51.0 ± 10.9% in the metoprolol group and 51.6 ± 10.8% in the placebo group (p = 0.68). The incidence of malignant arrhythmias was 3.6% in the metoprolol group versus 6.9% in placebo (p = 0.050). The incidence of adverse events was not different between groups. ConclusionsIn a nonrestricted STEMI population, early intravenous metoprolol before PPCI was not associated with a reduction in infarct size. Metoprolol reduced the incidence of malignant arrhythmias in the acute phase and was not associated with an increase in adverse events. (Early-Beta blocker Administration before reperfusion primary PCI in patients with ST-elevation Myocardial Infarction [EARLY-BAMI]; EudraCT no: 2010-023394-19)

Stenting the Non-Culprit Lesion during Primary Angioplasty of the Infarct-Related Coronary Artery: The Long and Winding Road

Submit Manuscript | http://medcraveonline.com J Cardiol Curr Res 2015, 4(3): 00141 treatment of choice for ST-segment elevation myocardial infarction (STEMI) [3]. Considering the fact that patients with multivessel coronary heart disease (CHD) comprise over half of the STEMI population, it is not an uncommon finding to observe a significant non-culprit lesion besides the occluded infarctrelated coronary artery during primary PCI. These patients with multivessel disease in this context have a worse prognosis than patients with single vessel disease [4,5]. Now, the problem is what to do with the non-culprit significant stenosis once the infarctrelated coronary artery was already treated. Should we proceed and stent the non-culprit lesion turning unstable a coronary plaque that was previously stable and jeopardize another wall in a patient that already has an infarcted territory? It seems logical to think that treating all significant coronary stenosis would provide a better clinical outcome. However, although there is recent data in favor of this therapeutic management, the 2013 ACCF/ AHA guidelines for the management of ST-elevation myocardial infarction discouraged this approach due to a significant increase in adverse outcomes for patients undergoing multivessel PCI in the setting of STEMI, and recommended a restrictive approach that discourages treatment of non-culprit lesions during the index PCI, unless the patient is in cardiogenic shock [6]. Moreover, the 2014 ESC/EACTS guidelines on myocardial revascularization are in accordance with the latter approach [7]. They stated that evidence supporting immediate (preventive) intervention in noninfarct-related lesions is a matter of debate [8,9]. On the other hand, patients with extensive CHD in vessels remote from the infarct-related artery have reduced success in reperfusion and an adverse prognosis following primary PCI [8]. They concluded that at present, multivessel PCI during STEMI should be considered in patients with cardiogenic shock in the presence of multiple, critical coronary stenosis, and if there is persistent ischemia after PCI on the supposed culprit lesion [6]. It is well known that patients with stable CHD and multivessel disease benefit from achieving complete revascularization [1013]. The question is if this assumption also holds true in the setting of STEMI if a more aggressive approach leading to more complete revascularization is performed. This is a controversial subject if we analyze current data based on observational studies and compare them to the results of recent randomized clinical trials in the era of drug eluting stents. In fact, observational data suggested that this approach was not beneficial and might be even harmful, with slightly better outcome depending on the timing of the nonculprit PCI [14,15]. On the other hand, recent evidence obtained from randomized trials documented significant reductions in composite ischemic endpoints by performing multivessel revascularization during STEMI [16,17]. However, there had been some inconsistencies in the analysis of the results. For example, the PRAMI (Preventive Angioplasty in Myocardial Infarction) trial [16], was stopped prematurely due to a much higher than expected treatment efficacy. They found a 65% reduction in ischemic events with complete revascularization during the index PCI in 465 patients. It seems a little surprising to achieve such high statistically significant results with a relatively small number of patients and of clinical events raising concerns of a chance finding magnified by the early termination of the trial. In addition, the CVLPRIT (Complete Versus Lesion-Only Primary PCI) trial [17] did not show reductions in hard endpoints, and the benefit demonstrated in the composite endpoint was obtained by repeat revascularizations. This open-label clinical trial randomized 296 patients in 7 UK centers to either inhospital complete revascularization (n: 150), or culprit lesiononly revascularization (n: 146). Complete revascularization was performed in the index hospitalization either at the time of primary PCI or before hospital discharge. The primary endpoint of mortality, recurrent myocardial infarction, heart failure, or ischemia-driven revascularization within 12 months occurred in Editorial

Glycemia Lowering and Risk for Heart Failure: Recent Evidence from Studies of Dipeptidyl Peptidase Inhibition.

The global epidemic of type 2 diabetes mellitus (T2DM) has substantial implications for cardiovascular disease–related morbidity and mortality.1 The prevalence of T2DM in patients with heart failure (HF) is high, with strong and independent association between T2DM and incident HF observed in multiple prospective studies and in randomized-controlled clinical trials. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), which enrolled subject’s ≥55 years of age with hypertension and ≥1 risk factor, patients with T2DM had a 2-fold risk for HF hospitalization or death after adjustment for other risk factors (RR, 1.95). The association with T2DM was independent of coronary artery disease and at least equivalent in magnitude and greater than that for electrocardiographic left ventricular (LV) hypertrophy.2 All measures of glycemia including fasting, postprandial, measures of insulin resistance, and hemoglobin A1c (HbA1c) have been associated with risk of developing HF, with the association extending to both HF with preserved ejection fraction and to HF with reduced ejection fraction.3,4 A substantial body of evidence from preclinical studies, endomyocardial biopsies in humans and more recently with cardiac MRI, support increased myocardial stiffness in T2DM related to alteration in extracellular matrix. There are multiple proximate mediators that have been hypothesized to play a role including advanced glycation end product deposition and reactive oxygen species that may increase myocardial stiffness during diastole, by cross-linking collagen or by enhancing collagen formation.5,6 Another pernicious proximal mediator is the elevation in postprandial lipids, such as remnant lipoproteins, characteristic of atherogenic dyslipidemia, a highly prevalent abnormality in T2DM, that may result in direct myocellular deposition of lipid, leading to microcirculatory dysfunction, alteration in substrate use and mitochondrial dysfunction.7,8 Indeed, positron emission tomography studies show reduced myocardial glucose uptake in favor of fatty acid …

A regional pharmacoinvasive PCI strategy incorporating selected bleeding avoidance strategies.

Pharmacoinvasive therapy (PIT) is a potential treatment for ST-segment elevation myocardial infarction patients who are not able to achieve primary percutaneous intervention (PCI) within guideline-recommended time limits. The risk for bleeding complications with PIT has not been studied in the setting of routine use of two selected bleeding avoidance strategies (BAS): bivalirudin and vascular closure devices. We analyzed a contemporary multicenter registry (2009-2013) of consecutive patients undergoing PCI as part of a 10-hospital regional algorithm involving one PCI center and nine transfer centers: PIT for hospitals greater than 60 min (N=140), and primary PCI if less than 60-min travel time to the PCI center (N=346). We compared the risk for Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction (HORIZONS) major bleeding among patients undergoing PIT versus primary PCI in the setting of routine use of selected BAS and determined the independent predictors of major bleeding in the entire cohort. The PIT patients had a median travel time of 103±49 min, were more frequently female, had a higher incidence of renal failure, and had a lower frequency of cardiogenic shock compared with the primary PCI group. BAS were routine and similar in both groups. Rates of death, stroke, and ischemic and major bleeding outcomes were similar between the two groups, and the length of stay was shorter in the PIT group. Multivariate logistic models indicated that two independent predictors of major bleeding were cardiac arrest [odds ratio (OR)=3.89, 95% confidence interval (CI): 1.2-12.1, P=0.02] and bailout glycoprotein IIb/IIIa inhibitor utilization (OR=3.29, 95% CI: 1.1-9.6, P=0.03). The PIT strategy in conjunction with selected BAS did not predict major bleeding (OR=2.1, 95% CI: 0.85-5.44, P=0.11). Bleeding and ischemia rates were similar between the PIT and primary PCI strategies in the setting of routine use of selected BAS; further study on a broader range of BAS including the radial approach may be warranted. Cardiac arrest and bailout glycoprotein IIb/IIIa inhibitor, but not PIT in conjunction with selected BAS, are independent predictors of bleeding risk in a regional ST-segment elevation myocardial infarction population.

Abstract 20119: Incidence and Predictors of Left Ventricular Thrombus in ST Elevation Myocardial Infarction

Introduction: Anticoagulation with coumadin is often employed after anterior ST-segment elevation myocardial infarction (STEMI) complicated by left ventricular (LV) dysfunction to prevent LV thrombus and cardioembolic events. However, the combination of dual antiplatelet therapy used for coronary stents and coumadin has been repeatedly shown to have a high incidence of bleeding. The current guidelines give coumadin a class II recommendation and support an individualized approach to treatment. Hypothesis: Determining the incidence and predictors of LV thrombus in a contemporary STEMI population at high risk for LV thrombus may assist in clinical decision making. Methods: Anterior STEMI patients at our institution between 2006 and 2013 treated with primary percutaneous intervention (PCI) that had an echocardiogram performed within 1 week and an ejection fraction of less than 40% or less than 50% with anterior apical akinesis were retrospectively identified. 687 patients with anterior STEMI were screened and 310 met inclusion. Demographic, clinical, and angiographic data was extracted from the medical record. Patients were categorized in 2 groups according to echocardiographic findings (no LV thrombus or probable/definite LV thrombus). The groups were compared by chi squared or T-test where appropriate. Logistic regression analysis was performed. Results: The mean age of the study population was 61.8% and 71.5% were male. The incidence of LV thrombus was 15% (n=263 no thrombus; n=47 probable/definite thrombus). Patients with LV thrombus were less likely to have hyperlipidemia, and more likely to have post procedure TIMI 0-1 flow and no stent use compared to patient with no LV thrombus. After adjustment, variables associated with LV thrombus risk were cardiac arrest (OR 4.06, 1.3-12.7), unfractionated heparin post PCI (2.43, 1.16-5.1), and stent use (DES 0.22, .06-.77, BMS 0.23 .07-.75, compared to balloon angioplasty). Conclusions: The incidence of LV thrombus in at risk STEMI patients remains high in contemporary practice. Development of a clinical risk score is limited by the lack of a sufficient number of predictive variables. Further investigation is needed to determine the optimal anticoagulation strategy in these patients.

Close, but not close enough.

Close, but not close enough.

Impact of low level of high-density lipoprotein-cholesterol sampled in overnight fasting state on the clinical outcomes in patients with acute myocardial infarction (difference between ST-segment and non-ST-segment-elevation myocardial infarction)

BackgroundDespite good treatment, there are residual risks in acute myocardial infarction (AMI) patients, and low level of high-density lipoprotein-cholesterol (HDL) has drawn attention as a possible cause. However, the impact of low HDL on ST-segment-elevation myocardial infarction (STEMI) compared with non-ST-segment-elevation myocardial infarction (NSTEMI) is not clear. Our aim was to evaluate the impact of low HDL on clinical outcomes in patients with STEMI or NSTEMI. MethodsWe included 9270 AMI patients undergoing successful percutaneous coronary intervention. They were grouped into STEMI and NSTEMI, and subdivided into two groups according to HDL level sampled in overnight fasting state. Primary end point was in-hospital death. Secondary end point was a composite of major adverse cardiac events (MACE) in hospital survivors during one-year follow-up. ResultsIn the STEMI population, low HDL group showed significantly higher in-hospital death rate [4.6% vs. 1.4%, hazard ratio (HR): 2.380, 95% confidence interval (CI): 1.143–4.956, p=0.020] than normal HDL group. In NSTEMI population, there was no significant difference between two groups (1.8% vs. 0.9%, HR: 1.231, 95% CI: 0.649–2.335, p=0.525), but in subgroup analysis, very low HDL subgroup showed higher in-hospital mortality rate compared with normal HDL group (4.0% vs. 0.9%, respectively, p=0.009). In 12-month MACE rates, there was no significant difference between two groups in both populations. ConclusionsLow HDL was associated with significantly higher risk of in-hospital mortality in STEMI patients, but not in NSTEMI patients. Thus, more aggressive treatment should be considered in STEMI patients with low HDL.

Comprehensive Prognosis Assessment by CMR Imaging After ST-Segment Elevation Myocardial Infarction

BackgroundAlthough the prognostic value of findings from cardiac magnetic resonance (CMR) imaging has been established in single-center center studies in patients with ST-segment elevation myocardial infarction (STEMI), a large multicenter investigation to evaluate the prognostic significance of myocardial damage and reperfusion injury is lacking. ObjectivesThe aim of this study was to assess the prognostic impact of CMR in an adequately powered multicenter study and to evaluate the most potent CMR predictor of hard clinical events in a STEMI population treated by primary percutaneous coronary intervention (PCI). MethodsWe enrolled 738 STEMI patients in this CMR study at 8 centers. The patients were reperfused by primary PCI <12 h after symptom onset. Central core laboratory–masked analyses for quantified left ventricular (LV) function, infarct size (IS), microvascular obstruction (MO), and myocardial salvage were performed. The primary clinical endpoint of the study was the occurrence of major adverse cardiac events. ResultsPatients with cardiovascular events had significantly larger infarcts (p < 0.001), less myocardial salvage (p = 0.01), a larger extent of MO (p = 0.009), and more pronounced LV dysfunction (p < 0.001). In a multivariate model that included clinical and other established prognostic parameters, MO remained the only significant predictor in addition to the TIMI (Thrombolysis In Myocardial Infarction) risk score. IS and MO provided an incremental prognostic value above clinical risk assessment and LV ejection fraction (c-index increase from 0.761 to 0.801; p = 0.036). ConclusionsIn a large, multicenter STEMI population reperfused by primary PCI, CMR markers of myocardial damage (IS and especially MO) provide independent and incremental prognostic information in addition to clinical risk scores and LV ejection fraction. (Abciximab i.v. Versus i.c. in ST-elevation Myocardial Infarction [AIDA STEMI]; NCT00712101).

Impact of Diabetes Mellitus on Clinical Characteristics, Management, and In-hospital Outcomes in Patients With Acute Myocardial Infarction (from the NCDR)

Patients with diabetes mellitus (DM) presenting with acute myocardial infarction (AMI) have worse outcomes versus those without DM. Comparative contemporary data in patients presenting with AMI with insulin-requiring diabetes mellitus (IRDM), noninsulin-requiring diabetes mellitus (NIRDM), and newly identified DM (hemoglobin A1C level >6.5%) versus patients without DM are limited. This observational study from the National Cardiovascular Data Registry (NCDR) Acute Coronary Treatment and Intervention Outcomes Network-Get with the Guidelines (ACTION Registry-GWTG consisted of 243,861 patients with AMI from 462 US sites identified from January 2007 to March 2011 entered into the registry. Clinical characteristics, management, and in-hospital outcomes were analyzed. Patients with DM with non-ST-segment elevation myocardial infarction (NSTEMI; n = 53,094, 35%) were less likely to undergo diagnostic angiography or revascularization, whereas those with ST-segment elevation myocardial infarction (STEMI) (n = 21,507, 23%) were less likely to undergo reperfusion therapy compared with patients without DM. There was an increased adjusted risk of in-hospital mortality in the DM group in both the NSTEMI (odds ratio [OR] 1.14, 95% confidence interval [CI] 1.06 to 1.22) and STEMI (OR 1.17, 95% CI 1.07 to 1.27) population. In patients with DM, the risk-adjusted in-hospital mortality was higher in patients with IRDM than those with NIRDM in the NSTEMI group (OR 1.12, 95% CI 1.01 to 1.24) but not in the STEMI group (OR 1.12, 95% CI 0.95 to 1.32). Newly diagnosed patients with DM presenting with AMI had similar unadjusted in-hospital outcomes compared with patients without DM. In conclusion, patients with DM presenting with AMI have a higher mortality risk than patients without DM. In patients with DM, those with IRDM presenting with NSTEMI had an increased mortality than those with NIRDM.

Safety of eptifibatide when added to bivalirudin during ST-segment elevation myocardial infarction

Patients presenting with ST-segment elevation myocardial infarction (STEMI) represent a high-risk group for in-hospital adverse events and bleeding. The safety and outcomes of eptifibatide in addition to bivalirudin in this population have not been determined. Over an 11-year period, we identified 1849 STEMI patients undergoing primary percutaneous coronary intervention (PCI), of which 1639 received bivalirudin monotherapy compared with 210 patients who received both bivalirudin and provisional eptifibatide. Safety of combination therapy was assessed by the occurrence of thrombolysis in myocardial infarction (TIMI) major bleeding. In-hospital event rates of death, Q-wave myocardial infarction (MI), and acute stent thrombosis were evaluated for efficacy. Multivariate analysis was used to adjust for significant differences between groups. Patients treated with bivalirudin plus eptifibatide, when compared with patients with bivalirudin monotherapy, had increased rates of cardiogenic shock (15.7% vs. 9.4%), aspiration thrombectomy (48.5% vs. 23.7%), pre-TIMI flow ≤1 (63.5% vs. 40%), and higher peak troponin I (93.65±92.7 vs. 49.16±81.59; all p <0.01). These, however, were not associated with differences in the primary end point after adjusting for significant baseline and procedural characteristics (OR: 1.63; 95% CI, 0.90-2.96, p=0.12). Importantly, TIMI major bleeding was not significantly different between groups (OR 1.78; 95% CI, 0.79-2.95, p=0.20). The addition of eptifibatide to bivalirudin during primary PCI reflects a high-risk STEMI population. This therapy results in similar in-hospital outcomes without an increase in major bleeding. Therefore, when required, combination therapy may be considered in this population.