Methods

We conducted an observational analysis based on a large registry of patients who underwent p-PCI at the Catheterization Laboratories of Padova University from 2006 to 2011. Data from 1,200 patients who underwent p-PCI within 12 hours from symptom onset of STEMI at our institution were prospectively collected. Inclusion criteria for patient selection in the current analysis were continuous chest pain for at least 20 minutes, presentation within 12 hours of onset of pain, and ST-segment elevation ≥1 mm (0.1 mV) in ≥2 contiguous leads on the 12-lead electrocardiogram or new-onset left bundle branch block. Exclusion criteria for the present analysis were (1) manual or mechanical thrombus aspiration or utilization of distal protection devices and (2) contraindication to dual antiplatelet therapy. P-PCI was performed with standard technique by radial approach or femoral approach in patients unsuitable for radial catheterization. The infarct-related artery (IRA) was the only target of the procedure, and deployment of coronary bare metal stents or drug-eluting stents were left at operator’s discretion. All patients received 250 mg acetylsalicylic acid (intravenous bolus) before the procedure and thereafter 100 to 325 mg/day orally; heparin (70 U/kg) was given to maintain the activated clotting time >250 seconds during the procedure. Clopidogrel was given as soon as possible after hospital admission at loading dose of 600 mg orally and then at a daily dose of 75 mg. Abciximab was given as 0.25 mg/kg intravenous bolus followed by intravenous infusion >12 hours according to operator’s choice. At the time of study execution, prasugrel and ticagrelor, and also bivalirudin, were not available in our facility. All patients expressed written informed consent to the procedure.

Two experienced interventional cardiologists assessed all angiographic and procedural parameters. Both reviewers were blinded to clinical outcomes. Consensus was achieved in all patients. Half of the angiograms were randomly selected and re-analyzed by the same analysts for intraobserver variability and by a third experienced interventional cardiologist for interobserver variability. Intracoronary thrombus at baseline was angiographically identified and scored in 5 according to the Thrombolysis In Myocardial Infarction (TIMI) Thrombus Score (TTS). In patients with occluded IRA at baseline angiography, TTS was reassessed after positioning of the wire: if wire positioning restored antegrade flow, TTS 5 was reclassified as TTS 1 to 4 according to thrombus burden; otherwise, the case was classified as TTS 5 and associated with TTS 1 for statistical analysis. In cases without flow restoration after wire placement, we did not take into account angiography after pre-dilation to avoid the potential contribution of balloon pre-dilation to DE. The angiographic pattern of coronary occlusion, when present, was defined on baseline angiogram as follows: (1) cut-off pattern, when there was an abrupt occlusion of the epicardial vessel; (2) tapered occlusion, when there was a vessel tapering just before the occlusion; and (3) persistent dye pattern, when there was a dye staining just proximally and/or distally to the occlusion. TIMI flow and myocardial blush grade were assessed as previously reported. DE was defined as a distal filling defect with an abrupt “cutoff” in ≥ peripheral coronary branches of IRA, distal to the PCI site. Angiographic no-reflow was defined as substantial coronary antegrade flow reduction (TIMI <3) without mechanical obstruction. Quantitative coronary analysis was performed at baseline and after procedure as previously described.

Major adverse events occurring during hospitalization, including death, nonfatal re-infarction, heart failure, and stroke, were collected. Diagnosis of nonfatal re-infarction was based on typical chest pain and/or new ST-segment changes with troponin I level re-elevation as previously described. Heart failure was defined as development of signs of congestion and/or hemodynamic instability. Stroke was defined by development of new cognitive or neurologic impairment confirmed by computed tomography or magnetic resonance imaging.

In regard to risk score development, we randomly divided the pooled data set in a 2:1 fashion into a derivation cohort and a validation cohort and considered the incidence of DE for the primary analysis. Demographic, clinical, and angiographic characteristics were compared between patients with and without DE in the derivation cohort and between derivation and validation cohort, with the Student’s t test for quantitative variables and the chi-square test for categorical variables. Univariable and multivariable analyses for prediction of DE were performed using a logistic regression model in the derivation cohort. To prevent overfitting, in the multivariable analysis, we included covariates independently related to DE in previous studies with a p value <0.05 in the univariable analysis: reference vessel diameter (RVD), occlusion pattern of the IRA, TTS, absence of flow improvement after wire positioning, lesion length ≥20 mm, TIMI 2/3 flow at baseline, diameter of stenosis, anterior myocardial infarction, and gender; the model was built using a backward selection procedure. Each significant covariate in this model was assigned an integer score based on the regression coefficients. Risk score was calculated in each patient by adding the points for each risk factor present. The rate of DE within each score category was derived per integer score and then per low-, intermediate-, or high-risk classification. A significant p value for trend was considered at the p <0.05 level. Overall model performance was assessed by the C-statistic.

To test the validity of these findings, we investigated the association of the derived risk score with the DE rate observed in the validation cohort. Rates of DE per risk score category were derived and compared for trend. Overall model performance was assessed by the C-statistic. A secondary analysis was performed with inclusion of major adverse cardiovascular events occurring during hospitalization (death, nonfatal re-infarction, heart failure, and stroke) in both data sets (derivation and validation) to provide information on prediction of adverse events. Clinician blinded to angiographic and procedural data adjudicated major adverse cardiovascular events, as previously described. All analyses were carried out using SAS 9.2 (SAS Institute Inc., Cary, North Carolina) for Windows.

Results

The study included 1,200 subjects, of whom 173 (14.4%) had DE during p-PCI. Study population was randomly split in a 2:1 fashion into derivation (n = 814) and validation (n = 386) cohorts. Baseline characteristics of derivation cohort are reported in Table 1 . There were no significant differences in risk factors and clinical history between patients with and without DE. At angiographic analysis, patients in the DE group showed a higher rate of cut-off pattern of occluded IRA and more often TIMI flow 0/1 at baseline with no-flow improvement after wire positioning, longer and tighter culprit lesion, and larger RVD than patients without DE. Moreover, patients with DE showed significant differences in effectiveness of reperfusion, as assessed by TIMI flow and myocardial blush grade; angiographic no-reflow was also more frequent in the DE group ( Table 1 ). There were no differences in baseline clinical, angiographic, and procedural data between derivation and validation cohorts except for lesion length ( Table 2 ).

Table 3 lists univariate correlates of DE in the derivation cohort. At multivariate analysis, presence of cut-off occlusion pattern of IRA at baseline angiography, TTS, RVD ≥3.5 mm, and lesion length ≥20 mm resulted in independent predictors of DE ( Table 4 ). These variables entered in the risk score calculation, by assigning a 0 to +2 points according to strength of statistical association. Table 4 lists ORs and the corresponding integer assignments for calculation of the risk score; risk score was calculated in each patient by adding the points for each risk factor present. Derivation cohort risk scores ranged from 0 to 7, with most subjects distributing in the intermediate scores. The distribution of the integer risk score and corresponding probability of DE are shown in Figure 1 , respectively: DE rate ranged from 3.9% in integer group 0% to 55.6% in group 7 ( Figure 1 ), and C-statistic for the risk score was 0.67 (p value for trend <0.0001). From observation of these data, 3 categories of DE risk were defined: risk scores 0 to 1 were considered low risk, 2 to 4 intermediate risk, and 5 to 7 high risk. The distribution of risk score categories and corresponding probability of DE are shown in Figure 1 , respectively: the rate of DE was 5.6% in low-risk, 15.8% in intermediate-risk, and 40.0% in the high-risk group (p value for trend <0.0001). C-statistic for the risk score was 0.70 (p value trend <0.0001).

Table 3

Univariate predictors of distal embolization in the derivation cohort

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