Prehospital triage in the ambulance reduces infarct size and improves clinical outcome.

BACKGROUND: We evaluated the effect of prehospital triage (PHT) in the ambulance on infarct size and clinical outcome and studied its relationship to the distance of patient's residence to the nearest percutaneous coronary intervention (PCI) center. METHODS: All consecutive ST-segment elevation myocardial infarction patients who were transported to the Isala klinieken from 1998 to 2008 were registered in a dedicated database. Of these, 2,288 (45%) were referred via a spoke center and 2.840 (55%) via PHT. RESULTS: PHT patients were more often treated within 3 hours after symptom onset (46.2% vs 26.8%, P < .001), more often had a post-procedural thrombolysis in myocardial infarction (TIMI) 3 flow (93.0% vs 89.7%, P < .001) had a smaller infarct size (peak creatine kinase 2,188 ± 2,187 vs 2,575 ± 2,259 IU/L, P < .001) and had a lower 1-year mortality (4.9% vs 7.0%, P = .002). After multivariate analysis, PHT was independently associated with ischemic time less than 3 hours (OR 2.45, 95% CI 2.13-2.83), a peak creatine kinase less than the median value (OR 1.19, 95% CI 1.04-1.36) and a lower 1-year mortality (OR 0.67, 95% CI 0.50-0.91). The observed differences between PHT patients and the spoke group were more pronounced in the subgroup of patients living >38 km from the PCI center. CONCLUSION: PHT in the ambulance is associated with a shorter time to treatment, a smaller infarct size and a more favorable clinical outcome, especially with longer distance from the patient's residence to the nearest PCI center. Therefore, PHT in the ambulance may reduce the negative effect of living at a longer distance from the PCI center.

The relation between the atrial blood supply and the complexity of acute atrial fibrillation.

BACKGROUND: Patients with a history of myocardial infarction and coronary artery disease (CAD) have a higher risk of developing AF. Conversely, patients with atrial fibrillation (AF) have a higher risk of developing myocardial infarction, suggesting a link in underlying pathophysiology. The aim of this study was to assess whether coronary angiographic parameters are associated with a substrate for AF in patients without a history of AF. METHODS: During cardiac surgery in 62 patients (coronary artery bypass grafting (CABG;n = 47), aortic valve replacement (AVR;n = 9) or CABG + AVR (n = 6)) without a history of clinical AF (age 65.4 ± 8.5 years, 26.2% female), AF was induced by burst pacing. The preoperative coronary angiogram (CAG) was assessed for the severity of CAD, and the adequacy of atrial coronary blood supply as quantified by a novel scoring system including the location and severity of right coronary artery disease in relation to the right atrial branches. Epicardial mapping of the right atrium (256 unipolar electrodes) was used to assess the complexity of induced AF. RESULTS: There was no association between the adequacy of right atrial coronary blood supply on preoperative CAG and AF complexity parameters. Multivariable analysis revealed that only increasing age (B0.232 (0.030;0.433),p = 0.03) and the presence of 3VD (B3.602 (0.187;7.018),p = 0.04) were independently associated with an increased maximal activation time difference. CONCLUSIONS: The adequacy of epicardial right atrial blood supply is not associated with increased complexity of induced atrial fibrillation in patients without a history of clinical AF, while age and the extent of ventricular coronary artery disease are.

Impact of vessel size on distal embolization, myocardial perfusion and clinical outcome in patients undergoing primary angioplasty for ST-segment elevation myocardial infarction.

BACKGROUND: Mounting interest has emerged on the role of distal embolization as a major explanation of poor myocardial perfusion among patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary angioplasty. The aim of the current study was to evaluate the relationship between vessel size, distal embolization, myocardial perfusion and clinical outcome in patients with STEMI treated by primary angioplasty. METHODS: Our population is represented by 1969 patients with STEMI undergoing primary stenting from 1997 to 2002. All clinical, angiographic, and follow-up data were prospectively collected. RESULTS: Vessel size was linearly associated with gender, diabetes, anterior infarction location, shorter time-delay, the rate of stenting and glycoprotein IIb-IIIa inhibitors. Small vessel size was associated with poor perfusion, despite lower rates of distal embolization. These data were confirmed after correction for confounding factors. The higher risk profile and poor myocardial perfusion contribute to explain the worse outcome observed in patients with smaller vessel size. CONCLUSIONS: This study shows that in patients undergoing primary angioplasty for STEMI, small vessel size is associated with poor myocardial perfusion, despite less distal embolization, that contributes to explain the worse outcome observed among patients with small infarct related arteries.

Prognostic importance of creatine kinase and creatine kinase-MB after primary percutaneous coronary intervention for ST-elevation myocardial infarction.

BACKGROUND: Although the prognostic significance of creatine kinase (CK) and creatine kinase-MB (CK-MB) after myocardial infarction has been established after thrombolysis or no reperfusion therapy, there is limited evidence of the prognostic importance after primary percutaneous coronary intervention (PCI). METHODS: In this prospective, observational study, individual data from all patients who survived at least 2 days after primary PCI between 1991 and 2004 in our hospital were recorded. The association between enzymatic infarct size (examined by peak CK and peak CK-MB levels, each divided into tertiles) and both left ventricular ejection fraction (LVEF) and 1-year mortality was evaluated. RESULTS: In the study group of 4670 patients, mean peak CK was 2327 U/L (SD 2008) and mean peak CK-MB was 244 U/L (SD 208). Both increased CK and CK-MB were associated with a lower LVEF. A total of 252 patients (5.4%) died between 2 days and 1 year after admission. Both peak CK and peak CK-MB were higher in those who died. Particularly, patients in the highest tertile of either peak CK or peak CK-MB had increased mortality, whereas the differences between the lower tertiles were not significant. In 2738 patients, after multivariable analysis including LVEF, the hazard ratio for 1-year mortality in patients in the highest CK tertile was 2.28 (95% CI 1.32-3.91) and for CK-MB, 1.91 (95% CI 1.11-3.26), compared to those in the other tertiles. CONCLUSIONS: According to this large-scale study, peak CK and peak CK-MB are comparable independent predictors of LV function and 1-year mortality in patients after primary PCI.

Comparison of usefulness of C-reactive protein versus white blood cell count to predict outcome after primary percutaneous coronary intervention for ST elevation myocardial infarction.

White blood cell (WBC) count and high-sensitive C-reactive protein (hs-CRP) are both used as markers of inflammation and prognosis after an ST elevation myocardial infarction (STEMI), but it is unknown whether they have independent prognostic value. We investigated the association and independent prognostic importance of WBC and hs-CRP after STEMI. In this subanalysis of the On-TIME trial, in 490 of 507 (97%) patients, either WBC count or CRP, and in 362 (71%) patients, both WBC count and CRP, were measured on admission before primary percutaneous coronary intervention. There was no significant correlation between WBC count and CRP (R = 0.080). Higher levels of CRP were associated with a reinfarction or death within 1 year (mean hs-CRP 14.2 +/- 20.4 vs 6.1 +/- 14.2, p = 0.006), but CRP was not associated with enzymatic infarct size (lactate dehydrogenase, LDHQ48) or left ventricular ejection fraction. A higher baseline WBC count was associated with larger LDHQ48 and lower left ventricular ejection fraction but not with 1-year reinfarction or death. In conclusion, although both WBC count and CRP are markers of inflammation and predictors of outcome after STEMI, we did not find a correlation between baseline WBC count and CRP levels in patients treated with primary percutaneous coronary intervention for STEMI. The mechanisms by which WBC counts predict outcome were related to myocardial infarct size whereas CRP were not.

Six months versus 12 months dual antiplatelet therapy after drug-eluting stent implantation in ST-elevation myocardial infarction (DAPT-STEMI): randomised, multicentre, non-inferiority trial.

OBJECTIVE: To show that limiting dual antiplatelet therapy (DAPT) to six months in patients with event-free ST-elevation myocardial infarction (STEMI) results in a non-inferior clinical outcome versus DAPT for 12 months. DESIGN: Prospective, randomised, multicentre, non-inferiority trial. SETTING: Patients with STEMI treated with primary percutaneous coronary intervention (PCI) and second generation zotarolimus-eluting stent. PARTICIPANTS: Patients with STEMI aged 18 to 85 that underwent a primary PCI with the implantation of second generation drug-eluting stents were enrolled in the trial. Patients that were event-free at six months after primary PCI were randomised at this time point. INTERVENTIONS: Patients that were taking DAPT and were event-free at six months were randomised 1:1 to single antiplatelet therapy (SAPT) (ie, aspirin only) or to DAPT for an additional six months. All patients that were randomised were then followed for another 18 months (ie, 24 months after the primary PCI). MAIN OUTCOME MEASURES: The primary endpoint was a composite of all cause mortality, any myocardial infarction, any revascularisation, stroke, and thrombolysis in myocardial infarction major bleeding at 18 months after randomisation. RESULTS: A total of 1100 patients were enrolled in the trial between 19 December 2011 and 30 June 2015. 870 were randomised: 432 to SAPT versus 438 to DAPT. The primary endpoint occurred in 4.8% of patients receiving SAPT versus 6.6% of patients receiving DAPT (hazard ratio 0.73, 95% confidence interval 0.41 to 1.27, P=0.26). Non-inferiority was met (P=0.004 for non-inferiority), as the upper 95% confidence interval of 1.27 was smaller than the prespecified non-inferiority margin of 1.66. CONCLUSIONS: DAPT to six months was non-inferior to DAPT for 12 months in patients with event-free STEMI at six months after primary PCI with second generation drug-eluting stents. TRIAL REGISTRATION: Clinicaltrials.gov NCT01459627.

Mortality in patients with left ventricular ejection fraction

Decreased left ventricular (LV) function is a strong predictor of mortality. Although current guidelines recommend prophylactic implantable cardioverter-defibrillator (ICD) implantation after ST-elevation myocardial infarction and a depressed LV ejection fraction for 1 month, the prognoses of these patients may be better than those observed in randomized trials of ICDs (1-year mortality 6.8% to 19%), particularly because reperfusion treatment has improved, and the use of life-saving drugs is higher. To assess 1-year mortality in patients with depressed LV ejection fractions after primary percutaneous coronary intervention, a prospective, observational study was performed. Data from all patients who survived >/=30 days after primary percutaneous coronary intervention and had LV ejection fractions

Are patients with non-ST elevation myocardial infarction undertreated?

BACKGROUND: The worse prognosis in patients without ST-elevation (non-STEMI) as compared to ST-elevation myocardial infarction (STEMI), may be due to treatment differences. We aimed to evaluate the differences in characteristics, treatment and outcome in patients with non-STEMI versus STEMI in an unselected patient population. METHODS: Individual patient data from all patients in our hospital with a discharge diagnosis of MI between Jan 2001 and Jan 2002 were evaluated. Follow-up data were obtained until December 2004. Patients were categorized according to the presenting electrocardiogram into non-STEMI or STEMI. RESULTS: A total of 824 patients were discharged with a diagnosis of MI, 29% with non-STEMI and 71% with STEMI. Patients with non-STEMI were significantly older and had a higher cardiovascular risk profile. They underwent less frequently coronary angiography and revascularization and received less often clopidogrel and ACE-inhibitor on discharge. Long-term mortality was significantly higher in the non-STEMI patients as compared to STEMI patients, 20% vs. 12%, p = 0.006, respectively. However, multivariate analysis showed that age, diabetes, hypertension and no reperfusion therapy (but not non-STEMI presentation) were independent and significant predictors of long-term mortality. CONCLUSION: In an unselected cohort of patients discharged with MI, there were significant differences in baseline characteristics, and (invasive) treatment between STEMI and non-STEMI. Long-term mortality was also different, but this was due to differences in baseline characteristics and treatment. More aggressive treatment may improve outcome in non-STEMI patients.

Heritability in a SCN5A-mutation founder population with increased female susceptibility to non-nocturnal ventricular tachyarrhythmia and sudden cardiac death.

BACKGROUND: Heritable cardiac-sodium channel dysfunction is associated with various arrhythmia syndromes, some predisposing to ventricular fibrillation. Phenotypic diversity among carriers of identical-by-descent mutations is often remarkable, suggesting influences of genetic modifiers. OBJECTIVE: The purpose of this study was to identify a unique SCN5A-mutation founder population with mixed clinical phenotypes and sudden cardiac death, and to investigate the heritability of electromechanical traits besides the SCN5A-mutation effect. METHODS: The 16-generation founder population segregating SCN5A c.4850_4852delTCT, p.(Phe1617del), was comprehensively phenotyped. Variance component analysis was used to evaluate the mutation's effects and assess heritability. RESULTS: In 45 p.(Phe1617del) positives, the mutation associated strongly with QTc prolongation (472 ± 60 ms vs 423 ± 35 ms in 26 mutation negatives; P <.001; odds ratio for long-QT syndrome 22.4; 95% confidence interval 4.5-224.2; P <.001) and electromechanical window (EMW) negativity (-29 ± 47 ms vs 34 ± 26 ms; P <.001). Overlapping phenotypes including conduction delay and Brugada syndrome were noted in 19. Polymorphic ventricular tachyarrhythmias occurred mostly in the daytime, after arousal-evoked heart-rate acceleration and repolarization prolongation. Cox proportional hazards regression analysis revealed female gender as an independent risk factor for cardiac events (hazard ratio 5.1; 95% confidence interval 1.6-16.3; P = .006). p.(Phe1617del) was an important determinant of QTcbaseline, QTcmax, and EMW, explaining 18%, 28%, and 37%, respectively, of the trait's variance. Significant heritability was observed for PQ interval (P = .003) after accounting for the p.(Phe1617del) effect. CONCLUSION: This SCN5A-p.(Phe1617del) founder population with phenotypic divergence and overlap reveals long-QT syndrome-related and arousal-evoked ventricular tachyarrhythmias with a female preponderance. Variance component analysis indicates additional genetic variance for PQ interval hidden in the genome, besides a dominant p.(Phe1617del) effect on QTc and EMW.

Hyperglycemia is an important predictor of impaired coronary flow before reperfusion therapy in ST-segment elevation myocardial infarction.

OBJECTIVES: This study was designed to investigate whether elevated glucose is associated with impaired Thrombolysis In Myocardial Infarction (TIMI) flow before primary percutaneous coronary intervention (PCI). BACKGROUND: Reperfusion before primary PCI in patients with ST-segment elevation myocardial infarction (STEMI) is associated with an improved outcome. Hyperglycemia in patients with STEMI is associated with an adverse prognosis. Hyperglycemia may induce a pro-thrombotic state and therefore be of influence on TIMI flow before PCI. METHODS: A total of 460 consecutive patients with STEMI treated with primary PCI were included in this analysis. Hyperglycemia was defined as a glucose > or =7.8 mmol/l (140 mg/dl). RESULTS: Hyperglycemia was observed in 70% and TIMI flow grade 3 before primary PCI in 17% of the patients. Patients with hyperglycemia less often had TIMI flow grade 3 before primary PCI (12% vs. 28%, p < 0.001). After adjustment for differences in baseline variables, hyperglycemia was a strong predictor of absence of reperfusion before primary PCI (odds ratio 2.6, 95% confidence interval 1.5 to 4.5). CONCLUSIONS: Hyperglycemia in patients with STEMI is an important predictor of impaired epicardial flow before reperfusion therapy has been initiated. Investigation of methods improving coronary flow before primary PCI in these patients is warranted.

Impact of statin therapy at discharge on 1-year mortality in patients with ST-segment elevation myocardial infarction treated with primary angioplasty.

BACKGROUND: Statin therapy can reduce long-term mortality in several subgroups of patients with coronary artery disease, but the benefits after primary angioplasty for ST-segment elevation myocardial infarction (STEMI) have yet to be established. The aim of the current study was to determine whether statin therapy is associated with a reduction in mortality in patients with STEMI treated with primary angioplasty. METHODS: Our population is represented by a total of 1513 consecutive in-hospital survivors treated with primary angioplasty for STEMI between April 1997 and October 2001. Patients were divided in two groups according to statin therapy (statin group, n=893; control group, n=620) at discharge. Clinical follow-up was performed at 1 year. A propensity score, built on the basis of variables independently associated with statin prescription, was used to investigate the benefits from statin therapy in subgroups of patients that were homogeneous in terms of baseline clinical and angiographic characteristics. RESULTS: At 1-year follow-up statin therapy was associated with a significantly lower mortality (1.2% versus 7.1%, R(2) [95% CI]=0.16 [0.09-0.32], p<0.0001). These benefits were confirmed in all subgroups according to the propensity score, and at multivariate analysis (adjusted R(2) [95% CI]=0.24 [0.12-0.47], p<0.0001). CONCLUSIONS: Statin therapy at discharge was associated with a significant reduction in 1-year mortality after primary angioplasty for STEMI. Therefore, the use of statins is highly recommended in these patients.

Comparison between stenting and balloon angioplasty in patients undergoing primary angioplasty of small coronary vessels.

BACKGROUND: Primary angioplasty has been shown to improve outcomes in selected patients with ST-segment elevation myocardial infarction. However, no information has been reported so far in small vessels. In the Zwolle-6 randomized trial, consecutive patients with ST-segment elevation myocardial infarction were randomized to stenting or to balloon angioplasty without any exclusion criterion. In this study, we present data on patients with small vessels (< 3.0 mm). METHODS: From April 1997 to October 2001, 798 patients randomized to balloon angioplasty or to stenting before their initial angiogram underwent primary angioplasty of small vessels, defined according to a postprocedural reference diameter < or = 3 mm. One-year follow-up data were available from all patients. RESULTS: Three hundred eighty-seven patients were randomized to stent, whereas 411 were to balloon. The crossover rates from balloon to stent and from stent to balloon were 28% and 13.9%, respectively (P < .001). The groups were comparable in terms of postprocedural TIMI flow, myocardial blush grade, distal embolization, and ST-segment resolution. No difference was observed in 1-year mortality (7.2% vs 5.8%, P = not significant [NS]), target vessel revascularization (17.8% vs 22.1%, P = NS), and major adverse cardiac events (24.8% vs 29.0%, P = NS) between the groups. CONCLUSIONS: As compared with balloon angioplasty, routine stenting does not seem to improve clinical outcomes in patients undergoing primary angioplasty of small vessels. Future trials are certainly needed to evaluate the safety and benefits of drug-eluting stents in this high-risk subset of patients.

Impact of infarct location on left ventricular ejection fraction after correction for enzymatic infarct size in acute myocardial infarction treated with primary coronary intervention.

BACKGROUND: Left ventricular function and infarct size are strong predictors for prognosis after acute myocardial infarction (MI). Anterior MI is associated with greater reduction of left ventricular ejection fraction (LVEF) and worse prognosis. Our objective was to study whether the impact of infarct size on global LVEF is dependent of infarct location. METHODS: We analyzed 888 patients treated with primary percutaneous coronary intervention for acute MI. Enzymatic infarct size and LVEF within 1 week were measured. In 490 patients (55%), LVEF was measured a second time at 6 months. RESULTS: Every 1000 U/L of cumulative lactate dehydrogense release corresponded to a decrease of 4.7% (95% CI 4.1-5.3) in LVEF measured within 1 week post MI for left anterior descending coronary artery (LAD)-related infarcts and to a decrease of 2.4% (95% CI 1.7-3.1) in LVEF measured within 1 week post MI for non-LAD-related infarcts (P < .0001). Left ventricular ejection fraction measured 6 months post MI showed a decrease for every 1000 U/L cumulative lactate dehydrogense release of 4.8% (95% CI 4.2-5.3) for LAD and 2.4% (95% CI 1.7-3.1) for non-LAD-related infarcts (P < .0001). Multivariate correction for relevant clinical and angiographic data did not change these results. CONCLUSION: In patients with a first acute MI treated with primary percutaneous coronary intervention, LAD-related infarcts show for a similar amount of myocardial necrosis as determined by enzymatic infarct size, a lower residual LVEF when compared with non-LAD-related infarcts.

Feasibility and benefit of prehospital diagnosis, triage, and therapy by paramedics only in patients who are candidates for primary angioplasty for acute myocardial infarction.

BACKGROUND: Despite data showing that time to treatment is very important in ST-elevation myocardial infarct patients, unacceptable long delays to reperfusion remain present in daily life practice. We sought to evaluate the feasibility and effect of improving logistics by early infarct diagnosis in the ambulance and immediate triage to a percutaneous coronary intervention (PCI) center performed by paramedics only without interference of a physician. METHODS: In the On-TIME study, 209 patients were included after prehospital infarct diagnosis and triage in the ambulance (ambulance group, n = 209). Infarct diagnosis was made by highly trained paramedics with the help of a computerized electrocardiographic algorithm. The accuracy of diagnosis, time to treatment, left ventricular function, and clinical outcome were compared with the patients who were diagnosed and triaged at a referral non-PCI center (referred group, n = 258). Left ventricular function was assessed before discharge using a nuclear technique. RESULTS: Acute myocardial infarction was accurately diagnosed in 95% of patients in the ambulance group, as compared with 99% in the referred group (P = .01). The percentage of patients in whom pharmacologic pretreatment (heparin, aspirin, tirofiban, or placebo) was initiated in the ambulance within 90 minutes after the onset of symptoms was 59% in the ambulance group versus 43% in the referred group (P < .01). A left ventricular ejection fraction of <40% was present in 25% in the ambulance group, as compared with 38% in the referred group (P = .013). After multivariate analysis, ambulance triage was independently associated with a left ventricular ejection fraction >40% and a favorable long-term clinical outcome. CONCLUSIONS: Early, prehospital infarct diagnosis, triage, and therapy in the ambulance with direct transportation to the nearest PCI center, performed by trained paramedics only, is feasible in 95% of patients. Ambulance triage resulted in earlier diagnosis and initiation of therapy and was independently associated with a better left ventricular function and clinical outcome, as compared with triage and transportation from a referral non-PCI center.

Predictors and clinical implications of early reinfarction after primary angioplasty for ST-segment elevation myocardial infarction.

BACKGROUND: Recurrent infarction after fibrinolytic therapy has been shown to be associated with increased mortality. The aim of this study was to analyze predictors and outcome of reinfarction in a consecutive series of patients undergoing primary angioplasty. METHODS: Our population is represented by a total of 1955 patients with ST-segment elevation myocardial infarction treated by primary angioplasty between 1997 to 2002. All clinical, angiographic, and follow-up data were prospectively collected. Early reinfarction was defined when two clinical criteria were satisfied within 30 days after the procedure: (1) recurrent ischemic symptoms for >15 minutes after resolution of symptoms from initial MI; (2) new ST-T-wave changes or new Q waves; (3) reelevation in creatine kinase (CK) or CK-MB to higher levels than normal (or by another 20% if already higher than normal). RESULTS: Early reinfarction was observed in 75 (3.8%) patients. At multivariate analysis, advanced Killip class (P = .002), poor preprocedural TIMI flow (P = .014), administration of IIb-IIIa inhibitors (P = .02), and diabetes (P = .038) were independent predictors of 30-day reinfarction. A total of 107 (5.6%) patients had died. Early reinfarction was associated with a significantly higher mortality (22.7% vs 4.9%, P < .001), even after adjustment for confounding factors (blood pressure, diabetes, Killip class, preprocedural TIMI flow, coronary stenting, multivessel disease, anterior infarct location, preprocedural stenosis, and administration of IIb-IIIa inhibitors) (HR 3.32, 95% CI 1.88-5.84, P < .0001). CONCLUSIONS: This study showed that, among patients undergoing primary angioplasty for ST-segment elevation myocardial infarction, advanced Killip class at presentation, poor preprocedural TIMI flow, the use of IIb-IIIa inhibitors, and diabetes are independently associated with 30-day reinfarction. Early reinfarction is an independent predictor of 1-year mortality.

Impact of routine stenting on myocardial perfusion and the extent of myocardial necrosis in patients undergoing primary angioplasty for ST-segment elevation myocardial infarction.

BACKGROUND: Primary stenting for ST-segment elevation myocardial infarction (STEMI) has been shown to improve the outcome because of the benefits in terms of restenosis. However, still controversial are the benefits in terms of reperfusion. In the Zwolle-6 randomized trial, a consecutive cohort of patients with STEMI was randomized to balloon angioplasty or stenting, without exclusion criteria. In this study, we analyzed data on myocardial perfusion and the extent of myocardial necrosis. METHODS: From April 1997 to October 2001, a total of 1683 consecutive patients with STEMI were randomized to stenting or balloon angioplasty. No exclusion criteria were applied. Myocardial perfusion was evaluated by myocardial blush grade and ST-segment resolution. The extent of myocardial necrosis was evaluated by enzymatic infarct size and predischarge ejection fraction. All data were prospectively collected. RESULTS: A total of 785 patients (92.5%) in the stent group and 763 patients (91.5%) in balloon group underwent primary angioplasty. The 2 groups showed similar baseline characteristics. No difference was observed between stent and balloon in myocardial blush grade, complete ST-segment resolution, distal embolization, enzymatic infarct size, and predischarge ejection fraction at both intention-to-treat and actual treatment analysis, even when restricted to patients with anterior infarction. Time delay to treatment (earlier or later than 6 hours) did not affect the results. No difference was observed in 1-year mortality (6.0% vs 5.9%, P = NS). CONCLUSIONS: As compared with balloon angioplasty, routine stenting does not improve myocardial perfusion, the rate of distal embolization, and the extent of myocardial necrosis in a large cohort of unselected patients with STEMI.

Platelet microaggregation inhibition in patients with acute myocardial infarction pretreated with tirofiban and relationship with angiographic and clinical outcome.

BACKGROUND: The relationship between the level of platelet aggregation inhibition in patients with acute myocardial infarction and their clinical outcome is unknown. METHODS: In patients with acute myocardial infarction included in the On-TIME trial and transferred to the primary percutaneous coronary intervention (PCI) center of Zwolle, who were pretreated with tirofiban on top of acetylsalicylic acid and heparin, platelet microaggregation inhibition was assessed on admission and immediately after PCI, using the Sysmex K4500 (Sysmex Corp, Kobe, Japan) platelet microaggregation measurement. The level of platelet microaggregation inhibition was compared with angiographic and clinical outcome. Patients were randomized to early prehospital initiation of tirofiban or to initiation in the catheterization laboratory. Therefore, the effect of tirofiban on platelet microaggregation inhibition could additionally be determined by measuring baseline platelet microaggregation also at entrance into the hospital. RESULTS: In 412 (89%) of 463 patients, platelet microaggregation inhibition was measured after receiving tirofiban. There was no difference between the 4 quartiles of the level of platelet microaggregation inhibition with regard to distal embolization, TIMI-3 flow and blush grade 3 after PCI, mean corrected TIMI frame count, ejection fraction, enzymatic infarct size, and percentage ST-segment resolution (P values .91, .97, .46, .94, .73, .33, and .72, respectively). The baseline platelet microaggregation inhibition in patients treated with tirofiban was 38% +/- 25% (mean +/- SD), and in the patients treated with placebo, 14% +/- 22% (P < .001). CONCLUSIONS: We found no correlation between the level of platelet microaggregation inhibition after tirofiban and outcome, whereas only a modest increase in platelet microaggregation inhibition was observed after a commonly used dose of tirofiban.

Pre-treatment with clopidogrel and postprocedure troponin elevation after elective percutaneous coronary intervention.

Elevated troponin after elective percutaneous coronary intervention (PCI) has been associated with a worse prognosis. Pretreatment with clopidogrel may be beneficial in patients undergoing PCI. Therefore, a prospective observational study was conducted to address the potential role of clopidogrel in reducing troponin release after elective PCI. TroponinT was measured 12 hours after elective PCI in 656 patients without elevated troponin before PCI. To assess the independent association between pre-treatment with clopidogrel and increased troponin, multivariate analyses were performed. Mean age of the 656 patients was 63.5 years (SD 10.2), 194 patients (30%) were female and 114 patients (17.4%) had diabetes. In 217 patients (33%) troponin was increased after PCI. Of the 330 patients who were not pre-treated with clopidogrel, 118 patients (34%) had increased troponin after the PCI compared to 99 patients (30%) of the 326 patients who were treated with clopidogrel longer than 24 hours before the procedure (p = 0.14). Stratified analyses showed that patients with older age (p = 0.03), previous PCI (p = 0.013), angina CCS 4 (p = 0.03) and multivessel disease (p = 0.04) had a significantly lower risk of troponin increase after pre-treatment with clopidogrel compared to patients without pre-treatment. After adjusting for differences in the other variables, patients who were pre-treated with clopidogrel had a significant lower risk of post-PCI increase of troponin T (odds ratio 0.69, 95% confidence interval 0.49-0.99). Pre-treatment with clopidogrel is associated with a significantly lower incidence of increased troponin after elective PCI. Combined with results of other studies, pre-treatment should be advised in patients waiting for elective PCI.

Incidence and predictors of subacute thrombosis in patients undergoing primary angioplasty for an acute myocardial infarction.

Subacute thrombosis (SAT) is a major concern in patients undergoing percutaneous coronary intervention (PCI). So far, only little data has been available on characteristics and outcome of patients with SAT after primary PCI for ST elevation myocardial infarction (STEMI). From 1997-2001, 1,548 unselected consecutive patients underwent primary PCI for STEMI as part of a randomized controlled trial stenting vs. balloon angioplasty. All patients received acetylsalicylic acid (500 mg i.v.) and heparin (5,000 IU) before the procedure. After stenting, all patients received ticlopidine 250 mg daily (before July 1999) or clopidogrel 75 mg daily (after July 1999) for one month. Five percent of patients received glycoprotein IIb/IIIa blockers. We prospectively recorded incidence and characteristics of patients with SAT during one year follow-up. SAT occurred in 4.1% (63/1548) and reinfarction in 6.0% of patients. The incidence of SAT did not change over time (1997: 8/175[4.6%],1998: 8/325 [2.5%],1999: 13/358 [3.6%], 2000: 22/426 [5.2%], 2001: 12/264 [4.5%]). SAT occurred in 39/63(62%) patients during hospital stay. The incidence did not differ between patients after ticlopidine 23/681 (3.4%) or clopidogrel 40/867 (4.6%, p = 0.222). Univariate predictors of SAT were: patients with an LAD stenosis (5.4% vs. 2.9%, p = 0.016), with Killip class >1 at presentation (8.6% vs. 3.7%, p = 0.007) and in patients who received a stent (5.1% vs. 2.7%, p = 0.022). After multivariate analysis, Killip class >1 on admission was the only independent predictor of SAT(OR 2.26, 95% CI 1.14-4.47, p = 0.019). SAT was associated with a higher mortality at long-term follow-up (15% vs. 7%, p = 0.026). In a prospectively recorded, unselected consecutive series of patients undergoing PCI for STEMI, SAT occurred in 4.1% of patients at one-year follow-up. Signs of heart failure on admission, anterior myocardial infarction and stenting were predictors of SAT.

Effect of coronary occlusion site on angiographic and clinical outcome in acute myocardial infarction patients treated with early coronary intervention.

In acute myocardial infarction that is treated with thrombolysis, proximal coronary artery occlusion is associated with worse prognosis, irrespective of the infarcted artery. Primary percutaneous coronary intervention (PCI) is currently the treatment of choice for ST-segment elevation acute myocardial infarction. Therefore, we evaluated the prognostic significance of proximal versus distal coronary artery occlusion in patients with acute myocardial infarction that was treated with primary PCI. Between 1994 and 2001, patients with a first acute myocardial infarction that was treated with primary PCI were analyzed. A lesion was considered proximal if it was located proximal to the first diagonal branch in the left anterior descending coronary artery (LAD), the first marginal obtuse branch in the left circumflex coronary artery, and the first right acute marginal branch in the right coronary artery. Lesions distal of these side branches were considered distal. In total, 1,468 patients were analyzed. Left ventricular ejection fraction (LVEF) for proximal LAD lesions was lower than that for distal ones (37 +/- 11% vs 42 +/- 11%, p <0.0001). Adjusted relative risk of 3-year mortality for proximal versus distal LAD was 4.04 (95% confidence interval 1.95 to 8.38). In patients with infarcts related to the right or left circumflex coronary artery, no significant association between lesion location and LVEF or mortality was seen. No difference was seen in adjusted 3-year mortality between distal LAD and non-LAD-related infarcts (p = 0.145). In conclusion, our analysis shows that, even in patients with acute myocardial infarction that is treated with primary PCI, infarcts related to the proximal LAD have the worst 3-year survival and lowest residual LVEF compared with distal LAD or non-LAD-related infarcts.