This was a retrospective single-center observational cohort study that enrolled consecutive patients with a diagnosis of STEMI who underwent primary PCI at the University Clinical Hospital of Santiago de Compostela, Spain, between January 2008 and December 2015 (n=1499). About 40.8% (n=611) patients had MVD. To analyze the impact of multivessel vs culprit vessel-only PCI, patients with MVD and the following characteristics were excluded: a) Killip class IV at admission (n=58), b) a prior history of coronary artery bypass grafting (n=5), and c) planned coronary artery bypass grafting after primary PCI (n=13), as illustrated in Figure 1. The study population consisted of 535 patients with MVD, of which 55.0% (n=294) underwent multivessel PCI and 45.0% (n=241) underwent culprit vessel-only PCI. The decision to perform nonculprit coronary artery percutaneous revascularization and its timing were left to the discretion of the interventional cardiologist and clinical cardiologist or to the Heart Team, when appropriate. The factors influencing this decision were recorded.

Figure 1.

Study flow chart. CABG, coronary artery bypass grafting; MVD, multivessel disease; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation acute myocardial infarction.

(0.13MB).

Primary PCI was undertaken according to the European Society of Cardiology guidelines10,11 and the operators’ routine practice and could include aspiration thrombectomy, heparin, or glycoprotein IIb/IIIa inhibitor administration. Antiplatelet therapy included aspirin and a P2Y12 inhibitor (clopidogrel in the first few years and ticagrelor and prasugrel more recently).

Demographic, clinical, echocardiographic, coronary angiographic, and laboratory data at admission were collected and recorded in a computerized database, in accordance with the protocol in our department for patients with STEMI undergoing primary PCI. Glomerular filtration rate was calculated at admission using the Cockgrauft-Gault formula.

Diagnosis of STEMI was made according to current guidelines.11,12 Ischemia time was defined as the time between symptom onset and reperfusion (guide wire passage in the culprit artery during primary PCI). The MVD was defined as at least 1 lesion in a noninfarct-related artery deemed angiographically significant (more than 50% luminal narrowing diameter). Culprit vessel-only PCI was defined as revascularization of only the infarct-related artery, and multivessel PCI as revascularization of at least 1 more lesion of a different vessel during the index procedure or scheduled for the following 30 days. Major acute cardiovascular events (MACE) during follow-up were composed of all-cause mortality, myocardial infarction, heart failure requiring hospitalization, and unplanned repeat revascularization.

The primary aim of this study was to compare the clinical outcomes during follow-up (all-cause mortality and MACE) of multivessel PCI vs culprit vessel-only PCI in patients with STEMI undergoing primary PCI and MVD, after adjustment with propensity score matching.

Follow-up was performed through consultation of the electronic registries available in the autonomous community of Galicia (IANUS program); all medical evaluations and hospital registries were reviewed. Median follow-up was 2.36 years (interquartile range, 0.68-4.67 years).

Univariate analysis was performed of categorical variables using the chi-square test, with results expressed as percentages and of continuous variables using the Student t test, with results expressed as means±standard deviation. As this was a nonrandomized observational study, propensity score matching was conducted to match the study populations (multivessel PCI vs culprit vessel-only PCI patients) and to reduce the bias due to confounding variables that could influence treatment decisions and clinical outcomes.13 Matching was performed using the following variables: age, sex, body mass index, hypertension, diabetes, dyslipidemia, smoking, ischemic cardiomyopathy, ischemia time, STEMI localization (anterior vs other), infarct-related artery, use of drug-eluting stents, use of glycoprotein IIb/IIIa inhibitors, number of diseased vessels (2-vessel vs 3-vessel coronary artery disease), glomerular filtration rate, creatinine, troponin I peak, hemoglobin, glucose, heart rate, systolic blood pressure, Killip class, left ventricular ejection fraction, GRACE score, CRUSADE score, and the year of the patient's entry. To estimate the propensity score of each patient, matching was based on the nearest neighbor technique without replacement by means of a probit model using all the variables mentioned above. This method is based on the identification of patients inside the common support area of the 2 groups. The degree of overlap in the area of common support for the propensity score matching was very high, as shown in Figure 2, which allowed the inclusion of 215 patients in each group. There were no statistically significant differences in baseline characteristics between multivessel and culprit vessel-only PCI patients. The goodness-of-fit of the propensity matching score was adequate (Hosmer-Lemeshow test chi-square=476.44) and the variables used showed no problems of multicollinearity (mean variance inflation factor=2.01).

Figure 2.

Overlap in the area of common support for the propensity score matching, according to revascularization decision (culprit-only vs multivessel PCI). PCI, percutaneous coronary intervention.

(0.07MB).

Kaplan-Meier analysis with a modified log-rank test was used to illustrate 4-year cumulative all-cause mortality for patients depending on the revascularization strategy (culprit vessel-only vs multivessel PCI). Kaplan-Meier mortality curves showed some superimposition during the first few months of follow-up and therefore the Peto-Peto-Prentice test, a statistical test assigning more weight to earlier events, was used to confirm the results. Kaplan-Meier analysis with Peto-Peto-Prentice tests was also performed to evaluate differences in MACE during follow-up. To avoid violation of proportionality assumptions both in the analysis of all-cause mortality and MACE, previous studies have proposed a restricted mean survival analysis.14,15 Consequently, we used the model proposed by Royston and Parmar,16 which shows the number of days gained until each event during follow-up and its statistical significance.

Since the nonfatal components of MACE (myocardial infarction, heart failure, and repeat revascularization) and the endpoint of stent thrombosis may compete with all-cause mortality,17,18 we used a competing risk model19 that shows the cumulative incidence function curves for such endpoints and their sub-hazard ratio differences.

All analyses were 2-tailed and differences were considered significant if the P value was<.05. The statistical analysis was carried out using SPSS version 22.0.

The initial cohort was composed of 535 patients with MVD; mean age was 65.8±13.0 years, 77.8% were male, 27.7% had diabetes, and 37.6% presented with anterior STEMI. We compared baseline characteristics between patients who underwent multivessel PCI (55.0%; n=294) and culprit vessel-only PCI (45.0%; n=241). Multivessel PCI was mostly performed as a staged procedure (85.4%; n=251); multivessel revascularization during the primary PCI procedure was accomplished in 43 patients (14.6%). Complete revascularization was achieved in 67.3% patients (n=198) who underwent multivessel PCI. The decision not to perform PCI of nonculprit coronary arteries was influenced by many factors (Table 1). Multivessel PCI patients were younger, had higher levels of hemoglobin at admission, and more often had 3-vessel disease on coronary angiography (Table 2). Patients who underwent multivessel PCI were less likely to have previous history of ischemic cardiomyopathy (8.5% vs 13.7%; P=.055) and were more likely to have higher glomerular filtration rate at admission (87 vs 81mL/min; P=.120), although these differences were not statistically significant. There were no significant differences regarding sex, cardiovascular risk factors, ischemia time, infarct-related artery, use of drug-eluting stents during primary PCI, troponin peak, hemodynamic variables, Killip class, left ventricular ejection fraction, and risk scores (GRACE and CRUSADE), as depicted in Table 2. Pharmacological treatment at hospital discharge was similar between groups.

The clinical adverse events during follow-up are displayed in Table 3. After propensity score matching, all-cause mortality (11.6% vs 5.1%; Peto-Peto P=.014; Figure 3), unplanned repeat revascularization (12.6% vs 7.0%; Peto-Peto P=.043; Figure 4) and MACE (30.8% vs 22.0%; Peto-Peto P=.049; Figure 5) remained significantly higher in patients who underwent culprit vessel-only PCI. These patients also had a trend toward a higher incidence of myocardial infarction (6.1% vs 4.2%; Peto-Peto P=.360) and heart failure (5.1% vs 2.8%; Peto-Peto P=.187). Tests to evaluate the robustness of the data confirmed the former results (Table 4). The restricted mean survival analysis demonstrated a significant gain in days until the occurrence of MACE, all-cause mortality, and repeat revascularization. The competing model demonstrated that repeat revascularization was almost halved (subhazard ratio=0.52, P=.044; Figure 4).

Figure 3.

Kaplan-Meier curves for all-cause mortality-free survival. PCI, percutaneous coronary intervention.

(0.13MB).

Figure 4.

Cumulative incidence function curves for repeat revascularization. PCI, percutaneous coronary intervention.

(0.13MB).

Figure 5.

Kaplan-Meier curves for MACE-free survival. MACE, major acute cardiovascular events; PCI, percutaneous coronary intervention.

(0.12MB).

There are several limitations to be considered in the interpretation of our study. First, this was a retrospective observational and nonrandomized study conducted at a single hospital and, as such, has the inherent limitations and bias related to retrospective single-center studies. Although propensity score matching between groups increases the strength of statistical analyses, it is impossible to correct for unmeasured confounding factors and all the selection biases regarding treatment decision, which precludes definite conclusions. Second, the factors that led to the performance of multivessel PCI in each case could not be ascertained and, consequently, it is not possible to define a standard approach to patients with MVD and STEMI. Third, we did not collect data on functional assessment of coronary stenosis in patients who underwent multivessel PCI; it is likely that, in most patients, assessment of nonculprit lesions significance was made only on angiography.