The clinical benefit of percutaneous coronary intervention (PCI) is controversial in stable early latecomers with ST-segment elevation myocardial infarction (STEMI). We evaluated the efficacy of PCI in 2,344 stable patients with STEMI presenting 12 to 72 hours after symptom onset. Patients who had impaired hemodynamics or who had undergone fibrinolysis or immediate or urgent PCI were excluded. The patients were divided into the PCI group (n = 1,889) and medical treatment group (n = 455). The 12-month clinical outcome was compared between the 2 groups. After adjustment using propensity score stratification, the PCI group had lower mortality (3.1% vs 10.1%; hazard ratio 0.31; 95% confidence interval 0.20 to 0.47; p <0.001) and a lower incidence of composite death/myocardial infarction (3.8% vs 11.2%; hazard ratio 0.36; 95% confidence interval 0.25 to 0.53; p <0.001) at 12 months. The benefit of PCI was consistent across all subgroups, including patients presenting without chest pain. In conclusion, in stable patients with STEMI presenting 12 to 72 hours after symptom onset, PCI was associated with significant improvement in the 12-month clinical outcome.
The clinical benefit of reperfusion is controversial for stable patients with ST-segment elevation myocardial infarction (STEMI) presenting >12 to 24 hours after the onset of symptoms and largely unrelated to myocardial salvage. However, viable myocardium can be found even after ischemia of >12 hours and the period to salvage viable myocardium can extend to several days. The accepted definition of “early latecomers” refers to patients with STEMI presenting >12 to 72 hours after the onset of symptoms. Several recent studies evaluating the efficacy of percutaneous coronary intervention (PCI) in early latecomers have shown conflicting results. In the present study, we sought to assess the benefit of PCI in stable, early latecomers with STEMI using the database of the Korea Acute Myocardial Infarction Registry.
Methods
The Korea Acute Myocardial Infarction Registry is the first nationwide, population-based, multicenter data collection registry in Korea designed to track the outcomes of patients presenting with acute myocardial infarction (MI). The diagnosis of acute MI was determined by a typical increase and decrease in biochemical markers of myocardial necrosis (including creatine kinase-MB and troponin I and T), with ≥1 of the following: ischemic symptoms, electrocardiographic changes indicative of ischemia (ST-segment elevation or depression), and the development of pathologic Q waves on the electrocardiogram. The study population was derived from patients in the Korea Acute Myocardial Infarction Registry enrolled from November 2005 to January 2008. We included patients (aged ≥18 years) with persistent ST-segment elevation >0.1 mV in ≥2 contiguous precordial leads or ≥2 adjacent limb leads or new or presumably new left bundle branch block. From this population, we excluded patients with cardiac arrest, ventricular arrhythmia, advanced atrioventricular block, systolic blood pressure <90 mm Hg, heart rate >100 beats/min, or Killip class III-IV at presentation. We also excluded patients who had undergone fibrinolysis. Of the 7,885 patients who presented within 72 hours after symptom onset, 2,640 patients presenting >12 to 72 hours were selected:2,185 underwent PCI and 455 received conservative medical treatment. Of the 2,185 patients in the invasive cohort, 236 underwent immediate PCI (median interval from arrival 59 minutes), 60 underwent urgent PCI during conservative treatment (median interval from arrival 68 hours), and 1,889 underwent elective PCI (median interval from arrival 23 hours). Because it was difficult to capture the fluctuation of chest pain and/or ST-segment elevation from our registry—to compensate for the potential selection bias associated with this—we excluded patients receiving immediate and urgent PCI, and compared the 12-month clinical outcomes of patients who underwent elective PCI (n = 1,889) versus those who received medical therapy (n = 455). The median interval from arrival to PCI was 23 hours (range 13 to 47). The present study was conducted according to the Declaration of Helsinki. The institutional review board of all participating centers approved the study protocol (approval no. 05-49 of Chonnam National University Hospital). All the participating patients provided written informed consent. The primary end point was the occurrence of death or recurrent MI at 12 months between the PCI and medical therapy groups. Death was defined as death from any cause. Recurrent MI was defined as the recurrence of symptoms or the presence of electrocardiographic changes in association with an increase in the cardiac biomarker levels greater than the upper limit of normal.
The baseline differences between the 2 groups were compared using the Mann–Whitney U test for continuous variables and the chi-square test or Fisher’s exact test for categorical variables. Unadjusted hazard ratios and their 95% confidence intervals were calculated for the outcome variables. To adjust for the bias inherent in the decision of choosing PCI or medical therapy, propensity scores were used. The propensity scores were estimated for the likelihood of receiving PCI using a multiple logistic regression model that contained all covariates listed in Tables 1 and 2 , except for diastolic blood pressure, total cholesterol, and procedures. Model discrimination was measured by the c-statistic, and calibration was assessed using the Hosmer–Lemeshow goodness-of-fit test (c-statistic 0.82, Hosmer–Lemeshow, p = 0.68). The propensity scores were divided into quintiles to eliminate bias due to an imbalance in the measured covariates between the 2 groups. The degree to which the propensity score balanced the measured covariates was assessed by comparing the standardized differences in the mean values of each covariate. After adjustment by stratification on the propensity score, the standardized differences of all covariates were <0.25, suggesting that all the measured covariates were well balanced between the 2 groups. The treatment effect was estimated separately within each quintile, and a pooled average treatment effect was obtained by combining the estimates across the quintiles. Statistical analyses were conducted using SPSS, version 18.0 (SPSS, Chicago, Illinois) and R, version 2.13.1 (R Foundation for Statistical Computing, Vienna, Austria). All statistical tests were 2-sided, with a significance level of p <0.05.
| Variable | PCI (n = 1,889) | Medical Therapy (n = 455) | p Value |
|---|---|---|---|
| Age (years) | 66 (55–73) | 69 (57–76) | <0.001 |
| Men | 1,314 (69.6%) | 269 (59.1%) | <0.001 |
| Smoker | 1,078 (57.1%) | 221 (48.6%) | 0.001 |
| Hypertension | 1,021 (54.0%) | 236 (51.9%) | 0.40 |
| Diabetes mellitus | 506 (26.8%) | 129 (28.4%) | 0.50 |
| Dyslipidemia | 193 (10.2%) | 42 (9.2%) | 0.53 |
| Chronic kidney disease | 35 (1.9%) | 24 (5.3%) | <0.001 |
| Myocardial infarction | 86 (4.6%) | 46 (10.1%) | <0.001 |
| Angina pectoris | 87 (4.6%) | 41 (9.0%) | <0.001 |
| Percutaneous coronary intervention | 75 (4.0%) | 34 (7.5%) | 0.001 |
| Coronary bypass | 10 (0.5%) | 4 (0.9%) | 0.49 |
| Heart failure | 18 (1.0%) | 32 (7.0%) | <0.001 |
| Stroke | 129 (6.8%) | 54 (11.9%) | <0.001 |
| Peripheral artery disease | 17 (0.9%) | 12 (2.6%) | 0.003 |
| Presentation data | |||
| Interval from symptom onset (hours) | 22 (15–34) | 23 (16–35) | 0.84 |
| Chest pain | 1,521 (80.5%) | 312 (68.6%) | <0.001 |
| Systolic blood pressure (mm Hg) | 130 (110–146) | 130 (110–150) | 0.57 |
| Diastolic blood pressure (mm Hg) | 80 (70–90) | 80 (70–87) | 0.50 |
| Heart rate (beats/min) | 76 (66–86) | 78 (68–92) | <0.001 |
| Killip class | <0.001 | ||
| I | 1,555 (82.3%) | 338 (74.3%) | |
| II | 334 (17.7%) | 117 (25.7%) | |
| Preinfarct angina pectoris | 876 (46.4%) | 199 (43.7%) | 0.31 |
| Q waves | 372 (19.7%) | 74 (16.3%) | 0.09 |
| Left bundle branch block | 12 (0.6%) | 8 (1.8%) | 0.04 |
| Anterior myocardial infarction | 830 (43.9%) | 166 (36.5%) | 0.004 |
| Left ventricular ejection fraction (%) | 53 (46–60) | 53 (44–60) | 0.13 |
| Laboratory findings | |||
| Total cholesterol (mg/dl) | 182 (157–211) | 171 (143–202) | <0.001 |
| Low-density lipoprotein cholesterol (mg/dl) | 114 (95–141) | 108 (80–128) | <0.001 |
| High-density lipoprotein cholesterol (mg/dl) | 43 (37–51) | 43 (36–53) | 0.51 |
| Triglycerides (mg/dl) | 104 (76–152) | 102 (69–132) | 0.002 |
| Creatinine (mg/dl) | 0.9 (0.8–1.1) | 1.0 (0.8–1.3) | 0.001 |
| Peak troponin I (ng/ml) | 15 (5–39) | 8 (2–17) | <0.001 |
| Glucose at admission (mg/dl) | 130 (109–168) | 131 (108–169) | 0.84 |
| High-sensitivity C-reactive protein at admission (mg/dl) | 1.2 (0.4–3.9) | 1.2 (0.4–3.7) | 0.91 |
| N-terminal pro-B-type natriuretic peptide at admission (pg/ml) | 1,020 (683–1,291) | 1,020 (857–1,854) | 0.002 |
| Variable | PCI (n = 1,889) | Medical Therapy (n = 455) | p Value |
|---|---|---|---|
| Procedure | |||
| Coronary angiography | 1,889 (100%) | 132 (29.0%) | <0.001 |
| Infarct-related artery | 0.39 | ||
| Left main | 43 (2.3%) | 6 (4.5%) | |
| Left anterior descending | 883 (46.7%) | 63 (47.7%) | |
| Left circumflex | 387 (20.5%) | 24 (18.2%) | |
| Right coronary | 576 (30.5%) | 39 (29.5%) | |
| Prepercutaneous coronary intervention Thrombolysis In Myocardial Infarction flow | <0.001 | ||
| 0 | 808 (42.8%) | 35 (26.5%) | |
| 1 | 242 (12.8%) | 15 (11.4%) | |
| 2 | 296 (15.7%) | 20 (15.2%) | |
| 3 | 543 (28.7%) | 62 (47.0%) | |
| Complications during hospitalization | |||
| Cardiogenic shock | 30 (1.6%) | 14 (3.1%) | 0.04 |
| Atrial fibrillation | 6 (0.3%) | 2 (0.4%) | 0.66 |
| Ventricular tachycardia/fibrillation | 20 (1.1%) | 10 (2.2%) | 0.05 |
| Advanced atrioventricular block | 21 (1.1%) | 1 (0.2%) | 0.10 |
| Cardiovascular resuscitation | 15 (0.8%) | 12 (2.6%) | 0.001 |
| Intra-aortic balloon counterpulsation | 36 (1.9%) | 2 (0.4%) | 0.03 |
| Mechanical ventilation | 23 (1.2%) | 14 (3.1%) | 0.004 |
| Temporary cardiac pacing | 33 (1.7%) | 1 (0.2%) | 0.01 |
| Acute kidney injury | 6 (0.3%) | 5 (1.1%) | 0.05 |
| Major bleeding | 5 (0.3%) | 2 (0.4%) | 0.63 |
| Acute stroke | 3 (0.2%) | 4 (0.9%) | 0.03 |
| Medical treatment during hospitalization | |||
| Unfractionated heparin | 1,134 (60.0%) | 258 (56.7%) | 0.19 |
| Low-molecular-weight heparin | 656 (34.7%) | 135 (29.7%) | 0.04 |
| Aspirin | 1,877 (99.4%) | 431 (94.7%) | <0.001 |
| Clopidogrel | 1,862 (98.6%) | 405 (89.0%) | <0.001 |
| Cilostazol | 596 (31.6%) | 27 (5.9%) | <0.001 |
| β Blockers | 1,491 (78.9%) | 300 (65.9%) | <0.001 |
| Calcium channel blockers | 222 (11.8%) | 97 (21.3%) | <0.001 |
| Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker | 1,600 (84.7%) | 344 (75.6%) | <0.001 |
| Diuretics | 471 (24.9%) | 187 (41.1%) | <0.001 |
| Long-acting nitrates | 1,315 (69.6%) | 325 (71.4%) | 0.45 |
| Statin | 1,493 (79.0%) | 277 (60.9%) | <0.001 |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
