Primary percutaneous coronary intervention (PCI) is the best reperfusion strategy in patients with ST-elevation acute myocardial infarction (AMI).1 This is mainly because it achieves a very high rate of successful recanalization of the infarct vessel in a wide variety of clinical and angiographic situations,2 but also by virtually eliminating the risk of intracranial bleeding and reducing the incidence of mechanical complications.3 Nearly half of patients with AMI referred for PCI have at least one other diseased vessel apart from the infarct vessel, and these patients have higher rates of mortality, severe mitral regurgitation, conduction abnormalities, severe bleeding and the need for new revascularization procedures.4 The prognostic impact of chronic occlusion in an artery other than the infarct vessel has not been studied in detail. The aim of this study was to elucidate the impact on the prognosis of the presence of a chronic occlusion in a noninfarct-related coronary artery among patients with multivessel disease undergoing PCI for AMI. Patients and Methods Study population. The study population is comprised of 630 patients with AMI who were consecutively treated with PCI within 12 hours after symptom onset at our institution before 2003. The inclusion criteria were: 1) chest pain lasting > 30 minutes; 2) ST-segment elevation (greater than or equal to 1 mm in greater than or equal to 2 adjacent ECG leads); and 3) cardiac catheterization and PCI performed within 12 hours after symptom onset. Patients in cardiogenic shock and those with previous thrombolytic therapy were not excluded from the study. Cardiac catheterization. Cardiac catheterization was performed via the femoral approach using a 6 Fr guiding catheter in most patients. Coronary stents, glycoprotein (GP) IIb/IIIa inhibitors, intra-aortic balloon counterpulsation pump (IABP), and thrombectomy and distal protection devices were used according to the operator’s discretion. Patients received heparin 100 IU/kg at the beginning of the procedure and additional doses when necessary to maintain an activated clotting time > 300 seconds. In patients receiving GP IIb/IIIa inhibitors, both the initial bolus of heparin (50–70 IU/kg) and the target activated clotting time (ACT) (200–250 seconds) were lower. Aspirin (250–500 mg as the initial dose, and 100–300 mg/day afterwards) was given to all patients. After coronary stent implantation, ticlopidine (500 mg as a loading dose and 250 b.i.d. for 1 month) or clopidogrel (300–600 mg as a loading dose and 75 mg/day for 1 month) were also prescribed. The nonculprit vessel was catheterized first, followed by the infarct-related artery. In patients with multivessel disease, only the culprit vessel was treated, except in some patients who had persistent ischemia and hemodynamic instability. Multivessel disease was defined as the presence of > 70% coronary stenosis by visual estimation (> 50% by quantitative coronary analysis) in greater than or equal to 2 major coronary arteries. Left main disease was also codified as multivessel disease. In patients with complete coronary occlusion in > 1 vessel, the infarct-related artery and the chronic coronary occlusion were identified, taking into consideration clinical and electrocardiographic data, as well as angiographic features. The angiographic result was considered successful when Statistical analysis. The SPSS version 11.5 software statistical package (Chicago, Illinois) was used. Continuous variables are expressed as mean ± standard deviation and are compared with the Student’s t-test. Qualitative variables are expressed as percentages and compared using the c2 test and Fisher’s corrections when appropriate. Cumulative survival was estimated using the Kaplan-Meier survival curves, and compared using the Log-Rank and Breslow tests. A multivariate analysis was performed among patients with multivessel disease in order to identify independent predictors for mortality. Variables evaluated in the multivariate analysis included those with significant association in the univariate analysis and also those without statistical significance in the univariate analysis, but with prognostic impact demonstrated in previous studies. Associations were considered statistically significant when p Clinical and angiographic differences among groups. Table 1 shows baseline clinical and angiographic differences between patients with single- versus multivessel disease, as well as between Groups 2 and 3. Unlike patients with single-vessel disease, those with multivessel disease were older, had a greater prevalence of hypercholesterolemia, hypertension, non-anterior location, previous infarction, prior coronary artery bypass graft surgery, and were more frequently in cardiac failure and cardiogenic shock at presentation. Unlike Group 2, patients from Group 3 had a worse Killip class at presentation and tended to be older. Angiographic results. An angiographically successful result was achieved less frequently in patients with multivessel disease than in those with single-vessel disease (92.6% vs. 97.1%; p = 0.010), although no differences were observed between Groups 2 and 3 (Table 2). No significant difference was observed regarding the use of coronary stents and GP IIb/IIIa inhibitors. Infarct vessel reocclusion was documented in 1.8%, 2.4%, and 7.0% of patients included in Groups 1, 2 and 3, respectively, but differences were not statistically significant. Influence on clinical outcomes. Table 2 and Figure 1 show the short- and long-term clinical outcome of patients included in Groups 1, 2 and 3. Clinical outcome was significantly worse in Group 3 than in Group 2, and in Group 2 than in Group 1. The probability of being free from events was lower in patients with multivessel disease than was the case for patients in Group 1 (84 ± 2% vs. 92 ± 1 at 30 days; 71 ± 3 vs. 81 ± 3% at 2 years; Log-Rank: p = 0.001; Breslow: p Multivessel disease and PCI for AMI. Between 43% and 69% of patients with AMI treated with PCI have multivessel disease, and in patients in cardiogenic shock, this proportion may reach approximately 70%.5 In our study, the proportion of patients with multivessel disease was 45%, and these had a two-fold mortality rate compared to those with single-vessel disease. Multivessel disease has been extensively recognized as a prognostic deleterious factor in patients with AMI treated with PCI.6–8 This is especially due to a higher frequency of cardiac failure and cardiogenic shock at presentation,9 but also because of a worse clinical profile, a lower rate of angiographic success, and a higher incidence of recurrent ischemia, new revascularization procedures, and infarct-related complications such as severe mitral regurgitation.4 Prognostic impact of a noninfarct vessel chronic coronary occlusion. The main finding of the present study is that among patients with AMI and multivessel disease undergoing PCI, those with a chronic coronary occlusion in another vessel have worse long-term clinical outcomes. Among patients with multivessel disease, clinical outcome was worse in Group 3 than in Group 2, both at short- and long-term. In Group 3, the mortality rate at 2 years was 1.9-fold greater than in Group 2, and 2.6-fold greater than in Group 1. The potential mechanisms explaining the worse clinical outcomes of patients with a chronic coronary occlusion in another vessel among those with AMI and multivessel disease undergoing PCI may be the following: 1) A chronic coronary occlusion may be associated with a previous infarction in this territory, and this is associated with a worse left ventricular ejection fraction. 2) Collateral circulation visible at coronary angiography is associated with an improved outcome in patients with AMI undergoing PCI.10 The presence of a chronic coronary occlusion prevents the development of collateral circulation to the infarct-related vessel. 3) The infarct-related vessel could have previously supported coronary blood flow to the chronically occluded coronary artery. Thus, the acute occlusion of the infarct vessel could lead to myocardial necrosis, not only in the myocardial area supported by the infarct vessel, but also in areas supplied by the chronic occlusion. Among patients with AMI and multivessel disease referred for primary PCI, multivariate analysis did not reveal the presence of a chronic occlusion in a noninfarct vessel as an independent predictor of mortality. Rather, cardiogenic shock at admission, left main disease and anterior location were independent predictors. Thus, although taking into consideration the relatively small number of patients included in Group 3 (n = 84), the presence of a chronic occlusion in a noninfarct-related artery seems to be a marker for a worse prognosis, rather than a causative factor for mortality. Group 3 patients had a worse Killip class, poorer left ventricular ejection fraction and a greater prevalence of previous coronary artery bypass graft surgery and proximal occlusion, and tended to be older — all of which are factors that have been associated with unfavorable clinical outcomes among patients with AMI.11 Practical implications. The main practical implication of the present study is that among patients with AMI referred for primary PCI, the presence of a chronic coronary occlusion in a noninfarct vessel allows immediate identification of a very high-risk subgroup of patients. It could be hypothesized that some therapeutic means, such as intra-aortic counterpulsation balloon pump, could be of particular benefit in these patients, although this remains speculative. On the other hand, in patients with a chronic coronary occlusion, not only left ventricular function,12 but also clinical outcome, may be improved after successful recanalization, especially in cases where myocardial viability has been demonstrated.13 One of the mechanisms explaining the long-term benefit after a successful PCI of a chronic coronary occlusion could be partially explained by a protective effect in the event that the patient suffers an AMI. Our findings support the treatment of chronic coronary occlusions in patients with stable ischemic heart disease. The combination of novel therapies, such as specially-designed guidewires and drug-eluting stents will help us to increase the proportion of patients with chronic coronary occlusions in which successful and sustained coronary perfusion is achieved.14,15
1. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: A quantitative review of 23 randomised trials. Lancet 2003;361:13‚Äì20. 2. Moreno R, Garcia E, Soriano J, et al. Coronary angioplasty in the acute myocardial infarction: In which patients is it less likely to obtain an adequate coronary reperfusion? Rev Esp Cardiol 2000;53:1169‚Äì1176. 3. Moreno R, Lopez-Send√≥n JL, Garc√≠a E, et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction. J Am Coll Cardiol 2002;39:598‚Äì603. 4. Moreno R, Garcia E, Elizaga J, et al. Results of primary angioplasty in patients with multivessel disease. Rev Esp Cardiol 1998;51:547‚Äì555. 5. Hibbard MD, Holmes DR, Bailey KR, et al. Percutaneous transluminal coronary angioplasty in patients with cardiogenic shock. J Am Coll Cardiol 1992;19:639‚Äì646. 6. Krikorian RK, James LV, Beauchamp GD. Timing, mode, and predictors of death after direct angioplasty for acute myocardial infarction. Cathet Cardiovasc Diagn 1995;35:192‚Äì196. 7. Kahn JK, Rutherford BD, McConahay DR, et al. Result of primary angioplasty for acute myocardial infarction in patients with multivessel coronary artery disease. J Am Coll Cardiol 1990;16:1089‚Äì1096. 8. Moreno R, Garc√≠a E, Soriano J, et al. Early coronary angioplasty for acute myocardial infarction: Predictors of poor outcome in a non-selected population. J Invasive Cardiol 2001;13:202‚Äì210. 9. Rothbaum DA, Linnemeier TJ, Landin RJ, et al. Emergency transluminal coronary angioplasty in acute myocardial infarction: 3 year experience. J Am Coll Cardiol 1987;10:264‚Äì272. 10. Antoniucci D, Valenti R, Moschi G, et al. Relation between preintervention angiographic evidence of coronary collateral circulation and clinical and angiographic outcomes after primary angioplasty or stenting for acute myocardial infarction. Am J Cardiol 2002;89:121‚Äì125. 11. Moreno R, Lopez de Sa E, Lopez-Sendon JL, et al. Determining whether acute myocardial infarction in patients with previous coronary bypass grafting is the result of narrowing of a bypass conduit or of a native coronary artery. Am J Cardiol 1997;79:670‚Äì671. 12. Sirnes PA, Myreng Y, Molstad P, et al. Improvement in left ventricular ejection fraction and wall motion after successful recanalization of chronic coronary occlusions. Eur Heart J 1998;19:273‚Äì281. 13. Bax JJ, Poldermans D, Elhendy A, et al. Improvement of left ventricular ejection fraction, heart failure symptoms and prognosis after revascularization in patients with chronic coronary artery disease and viable myocardium detected by dobutamine stress echocardiography. J Am Coll Cardiol 1999;34:163‚Äì169. 14. Ng W, Chen WH, Lee PY, Lau CP. Initial experience and safety in the treatment of chronic total coronary occlusions with a new optical coherent reflectometry-guided radiofrequency ablation guidewire. Am J Cardiol 2003;92:732‚Äì734. 15. Hoye A, Tanabe K, Lemos PA, et al. Significant reduction in restenosis after the use of sirolimus-eluting stents in the treatment of chronic total occlusions. J Am Coll Cardiol 2004;43:1954‚Äì1958.