European Heart Journal Advance Access originally published online on January 19, 2009
European Heart Journal 2009 30(3):305-313; doi:10.1093/eurheartj/ehn594
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Predictors and time-related impact of distal embolization during primary angioplasty
1 Cardiac Catheterization Laboratories and Interventional Cardiology, Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, 2 via Giustiniani, 35100 Padova, Italy
2 Department of Environmental Medicine and Public Health, University of Padova, Italy
Received 7 January 2008; revised 7 November 2008; accepted 22 December 2008; online publish-ahead-of-print 19 January 2009.
* Corresponding author. Tel: +39 0498211844, Fax: +39 0498761764, Email: massimo.napodano{at}gmail.com
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Abstract |
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Aims: We sought to identify predictors of distal embolization (DE) occurring during primary percutaneous coronary intervention (p-PCI) as well as to assess its impact on both myocardial reperfusion and necrosis, according to time-to-treatment.
Methods and results: Clinical and angiographic characteristics were prospectively assessed in 400 consecutive patients who underwent p-PCI, in order to identify predictors of DE. The impact of DE on Thrombolysis in Myocardial Infarction (TIMI) flow, myocardial blush, and troponin I (TnI) was assessed according to symptom onset-to-balloon time. DE occurred in 64 (16%) patients and did not change with time-to-treatment (P = 0.87). The occlusion pattern of infarct-related artery (IRA), treatment of right coronary artery, higher TIMI thrombus score, longer lesion, and large IRA diameter were predictors of DE. The rate of TIMI 0/1 and myocardial blush 0/1 was higher in patients exhibiting DE when time-to-treatment was 
6 h (P < 0.0001), while TnI was higher in patients with DE when time-to-treatment was <3 h.
Conclusion: DE during p-PCI occurs more often in the presence of high thrombus burden lesion. It reduces the effectiveness of myocardial reperfusion within 6 h and enhances myocardial damage within 3 h after symptom onset. Afterwards, it does not affect myocardial reperfusion or the extent of myocardial damage.
Key Words: Distal embolization • Myocardial infarction • Myocardial reperfusion • Primary angioplasty • Thrombus
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Introduction |
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Primary percutaneous coronary intervention (p-PCI) has emerged as the preferred treatment of ST-elevation myocardial infarction (STEMI) when logistically feasible,1 and it has been proved to be very effective in obtaining patency of the infarct-related artery (IRA).2 However, distal embolization (DE) of thrombus and plaque debris, as assessed by angiography, has been identified as one of the major drawbacks of p-PCI in STEMI, limiting the effectiveness of myocardial reperfusion and leading to larger myocardial damage and worse prognosis.3 Recently, several mechanical adjunctive devices, such as thrombectomy catheters and distal protection devices, have been developed to prevent DE in coronary circulation, showing their effectiveness in reducing the detrimental effects of thrombus and plaque debris embolization, when used in the setting of high-thrombus burden or saphenous vein graft lesions.4,5 Nevertheless, large multicentre randomized trials have shown no benefit in terms of myocardial reperfusion or myocardial salvage, using both intracoronary thrombectomy and distal protection devices during p-PCI.6–9 However, these studies evaluated the impact of adjunctive mechanical devices in a non-selective fashion, enrolling patients regardless of the angiographic characteristics of IRA and time-to-reperfusion. Indeed, recent evidences have shown that the effectiveness of p-PCI is mainly limited by time-to-treatment, showing that the extent of both myocardial necrosis and microvascular damage increase with the duration of ischaemia.10,11 The aim of this study was to identify angiographic determinants of DE as well as to assess the impact of this complication on both myocardial reperfusion and necrosis according to time-to-treatment.
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Methods |
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Study population and procedure
We prospectively evaluated 424 patients who underwent p-PCI for STEMI at our institution, between January 2003 and December 2005. Inclusion criteria for patient selection were continuous chest pain for at least 20 min and within 12 h of onset of pain and (i) ST-segment elevation
1 mm (0.1 mV) in two or more contiguous leads on the 12-lead electrocardiogram or (ii) persistent ST-segment depression in precordial leads V1–V4, with or without ST-segment elevation in inferior or lateral leads or (iii) new onset left bundle branch block. After initial assessment, 16 patients were excluded: 8 patients because of symptom lasting more than 12 h, 6 patients because of non-diagnostic electrocardiogram at baseline (pace-maker induced rhythm in four and absence of significant ST shift in two), and 2 patients refused to participate in the study. Of the 408 patients initially selected, 8 were excluded because of lack of analysable angiograms with respect to myocardial blush. Thus, 400 patients were included and compose the cohort of this study. Since we reached a sample size compatible to obtain satisfying results, according to previous study,12 patients selection was stopped. p-PCI was performed with standard technique by femoral approach in all patients. The IRA was the only target of the procedure and coronary bare-metal stents were used without restriction. The procedure was considered successful if Thrombolysis in Myocardial Infarction (TIMI) 3 in the target vessel and a residual stenosis <20% at target site were obtained. Before the procedure, all patients received aspirin 250 mg intravenously, thereafter 100–325 mg/die; heparin (70 U/kg) was given to maintain the activated clotting time >250 s. Clopidogrel was given as soon as possible after hospital admission at bolus dose of 300 mg iv and then at a dose of 75 mg once daily. Abciximab was given according to the judgement of the operator in catheterization laboratories. All patients gave written informed consent to the procedure. The study complies with the Declaration of Helsinki, and the Ethics Review Board of our institution approved the study protocol.
Angiographic analysis
Coronary angiograms were acquired by using digital technique (Integris 5000, Philips Medical Systems, Best, The Netherlands). The angiographic analysis was performed off-line by two experienced operators (M.N., G.T.) blinded to clinical data; a third operator (A.R.) decided in case of disagreement. TIMI flow grade and myocardial blush grade were assessed as described previously.13,14 In order to better define the thrombus burden in case of IRA occlusion, the angiographic pattern of coronary occlusion, when present, was defined on baseline angiogram as follows: (i) cut-off pattern, when there was an abrupt occlusion of the epicardial vessel; (ii) tapered occlusion, when there was a vessel tapering just before the occlusion; (iii) persistent dye pattern, when there was a dye staining just proximally and/or distally to the occlusion.15 Intracoronary thrombus at baseline was angiographically identified and scored in five degrees according to TIMI thrombus score.16 Quantitative coronary analysis was performed at baseline and after procedure, using the Coronary Quantification Package (Philips Medical Systems): minimal lumen diameter, reference vessel diameter, per cent of stenosis in diameter were provided; lesion length was also assessed at baseline angiography, or after vessel reopening (by either wire positioning or balloon pre-dilatation) in patients with occluded IRA at baseline. DE was defined as a distal filling defect with an abrupt ‘cut-off’ in one or more peripheral coronary branches of IRA, distal to the PCI site; in particular, we did not consider as DE the occurrence of TIMI flow impairment, at any stage of the procedure, without evidence of distal filling defect.3
Electrocardiographic analysis
In each patient, a 12-lead electrocardiogram was recorded at admission and 60 ± 30 min after the procedure. The sum of ST-segment elevation was assessed at 20 ms from J-point in the leads V1–V6, I, and aVL for anterior infarction and in the leads II, III, aVF, V5, and V6 for non-anterior infarction; in the latter, the ST-segment depression in leads V1–V4 was also analysed, as a sign of transmural ischaemia of the posterior wall. The two electrocardiograms were compared and the ST-segment elevation was classified as normalized if there was no residual ST-segment elevation after the procedure, improved if a regression 50% was seen, and unchanged if the ST-segment elevation sum appeared unchanged, worsened, or regressed <50%.17
Measures of outcome
Major adverse events occurring during the hospitalization, including death, non-fatal re-infarction, and stroke, were collected. Diagnosis of non-fatal re-infarction was based on typical chest pain and/or new ST-segment changes with troponin I (TnI) level re-elevation. Stroke was defined by development of a new cognitive or neurological deficit confirmed by computed tomography or magnetic resonance imaging. The extent of myocardial necrosis was estimated by measurements of serum concentration of TnI. The TnI levels were reported in micrograms per litre and were assessed every 6 h in the first 48 h after admission, and then twice daily up to discharge. Peak value release from eight serial measurements up to 48 h after admission was reported. All patients underwent 2D-transthoracic echocardiographic examination (Sonos 5500 Hewlett-Packard, Andover, MA, USA) before discharge. End-diastolic volume index, end-systolic volume index, and left ventricular ejection fraction were calculated using the area–length method in the apical four-chamber view and the apical two-chamber view.18
Statistical analysis
Categorical data are expressed as numbers and percentages and were compared using the 
2 or Fisher's exact test, as appropriate. Continuous variables are expressed as mean ± standard deviation for normally distributed variables, and as median (25–75th percentiles) for not normally distributed variables, and compared using the ANOVA and Mann–Whitney U tests, respectively. The potential angiographic predictors of DE occurrence were evaluated one variable at a time with logistic regression. Variables that showed significant association with DE on univariable analysis (P 0.10) were entered in a multivariable logistic regression model. In the multivariable analysis, P 0.05 was considered as statistically significant. The results of the univariable and multivariable analyses are reported as P-values, odds ratios (ORs), and relative 95% confidence interval (CI). The linear relationship between the logit of the endpoint and the explanatory variables was tested at the 10% level using the Box–Tidwell transformation.
To identify the independent predictors of unsuccessful angiographic reperfusion, defined as myocardial blush 0/1, logistic regression analysis of variables known to be related to these parameters was performed.14,19 The model included age, gender, infarct location, diabetes, Killip class, multivessel disease, occluded IRA at baseline, presence of collaterals, stent use, symptom onset-to-balloon time, and occurrence of DE. The ORs and their corresponding 95% CIs are provided. In order to assess the impact of DE on myocardial reperfusion and outcome according to time-to-treatment, defined as time from symptom onset to first balloon dilatation, patients were divided into three groups as follows: group 1: includes 132 patients treated <3 h from symptom onset; group 2: includes 197 patients with symptom onset-to-balloon time between 3 and 6 h; group 3: includes 71 patients with symptom onset-to-balloon time >6 h. Since baseline clinical and angiographic characteristics did not differ among groups, a secondary analysis to compare DE, TIMI flow, myocardial blush, and measures of clinical outcome was performed in these three groups, by using 2 test for categorical variables and ANOVA or Mann–Whitney U test for continuous variables, respectively. P < 0.05 with the two-tailed test was considered to be statistically significant. Statistical analysis was carried out by SPSS software package, version 13.0 (SPSS, Chicago, IL, USA).
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Angiographic features of distal embolization
Overall, 64 of 400 (16%) patients had DE during p-PCI, 23.4% of which occurred after wire positioning, 54.7% after balloon dilatation, 17.2% after stent deployment, and, interestingly, in 4.7% of cases it was discovered at baseline angiogram. Clinical characteristics are shown in Table 1. Patients with DE had anterior infarction less frequently (Table 1). Angiographic analysis at baseline revealed a higher rate of occluded IRA and more often a cut-off pattern in the DE group (Figure 1A; Table 2). Patients in the DE group also showed longer lesions and larger reference vessel diameter (Table 2). Procedural details were not different between groups; however, abciximab was administered more often in the DE groups (Table 2). At multivariable analysis, the presence of the cut-off pattern or dye-staining pattern of IRA occlusion at baseline angiography, higher TIMI thrombus score, reference vessel diameter
3.5 mm, longer lesion, and treatment of right coronary artery resulted as independent predictors of DE (Table 3). When patients with patent IRA at baseline were excluded from the analysis, TIMI thrombus score did not remain an independent predictor (OR 1.64; CI 0.91–2.96; P = 0.10), whereas reference vessel diameter 3.5 mm (OR 2.98; CI 1.42–6.23; P = 0.004), the presence of cut-off pattern (OR 2.49; CI 1.17–5.31; P = 0.18), and treatment of right coronary artery (OR 2.28; CI 1.19–4.26; P = 0.013) remained determinants of DE. Otherwise, considering only patients with patent IRA at baseline, higher TIMI thrombus score was the only independent predictor of DE (OR 1.82; CI 1.07–3.10; P = 0.03).
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Impact of distal embolization on myocardial reperfusion
Patients in the DE group showed lower TIMI flow and myocardial blush at both baseline and at the end of procedure (Figure 1A–D). The inter-observer variability was 8% for TIMI flow and 12% for myocardial blush (myocardial blush 0/1 vs. 2/3). Procedural success occurred in 45 of 64 (70.3%) patients with DE and in 312 of 336 (92.7%) patients without DE (P < 0.0001). Dividing patients into three groups according to time-to-treatment, it clearly appeared that DE was not time-dependent, occurring in 23 of 132 (17.4%) patients treated <3 h, in 30/197 (15.2%) patients treated between 3 and 6 h, and in 11/71 (15.5%) patients beyond 6 h (P = 0.8). However, patients exhibiting DE had more often TIMI 0/1 and myocardial blush 0/1 than patients without DE when symptom onset-to-balloon time was
6 h, whereas after this time-window there was no difference in TIMI 0/1 and MBG 0/1 rate between the two groups (Figure 2A and B). Of 400 patients, 390 showed analysable ST-segment in both the electrocardiogram: ST-segment elevation completely regressed in 26.9%, regressed at least 50% in 42.3%, and unchanged or regressed <50% in 30.8% of patients in DE group, and in 36.5, 34.9, and 28.5% of patients without DE (P = 0.25). Analysing the data according to time-to-treatment, ST-resolution regressed <50% of initial value more often in patients without DE only when time-to-treatment was <3 h, whereas after this time-window there were no differences between the two groups (Figure 2C). At multivariable analysis, symptom onset-to-balloon time (OR 1.002; CI 1.001–1.004; P < 0.0001), age (OR 1.05; CI 1.03–1.06; P < 0.0001), and DE (OR 8.42; CI 4.30–16.48; P < 0.0001) were independent predictors of MBG 0/1.
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Relationship between distal embolization, myocardial damage, and outcome
TnI release was significantly higher in patients exhibiting DE (Figure 3A), particularly in those treated within 3 h, but after this time it did not differ between DE and no-DE patients. Likewise, left ventricular ejection fraction, as assessed before hospital discharge, was lower in patients with DE than in those without DE when patients were treated within 6 h from symptom onset, but not in those treated later (Figure 3B). Wall motion score index was higher in patients with DE: 1.97 ± 0.35 vs. 1.54 ± 0.32 in patients with and without DE, respectively (P = 0.048). In-hospital events were not different between groups, except for stroke that occurred more often in patients having DE (Figure 4). Interestingly, in patients treated early (symptom onset-to-balloon time <3 h), the occurrence of DE significantly increased in-hospital death, but beyond this time window it did not affect the mortality (Figure 4B).
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Discussion |
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Recently, DE of thrombus and plaque debris, as assessed by angiography, has been identified as one of the major drawback of p-PCI in the setting of STEMI, limiting myocardial reperfusion and leading to larger myocardial damage and worse prognosis.3 In the last years, many efforts have been made to improve myocardial reperfusion in STEMI, particularly developing new drugs2,20 and mechanical devices able to limit DE during p-PCI.4–9 Interestingly, in large randomized trials, both intracoronary thrombectomy and distal protection devices have proved to give no benefit in terms of either myocardial reperfusion or myocardial salvage in the setting of p-PCI for STEMI.6–9 However, since these studies enrolled patients regardless of the angiographic features of the IRA, the results of these trials just provided the effect of a non-selective use of mechanical devices during p-PCI. To our knowledge, our study represents the first report on angiographic determinants of DE, showing that this complication occurs more often in the presence of specific angiographic features, identifying a subset of lesions at higher risk of embolization. We identified not only the TIMI thrombus score as major determinant of DE, but also other angiographic features, such as the pattern of IRA occlusion, treatment of right coronary artery, and large IRA diameter. In fact, the TIMI thrombus score represents an useful angiographic tool to weigh thrombus amount in coronary lesions;16 however, its value may be limited in the presence of a thrombotic occlusion, where the score assumes the highest degree and gives no information about the amount of either atheroma or superimposed thrombus. Interestingly, in our study, after the exclusion of patients with patent IRA, TIMI thrombus score did not remain an independent predictor of DE at multivariable analysis, suggesting that in the presence of a thrombotic occlusion the value of TIMI thrombus score in predicting DE is weak and that other angiographic tools, such as the occlusion pattern, reference vessel diameter of IRA, and treatment of right coronary artery, do predict DE. In this scenario, since the rate of occluded IRA in STEMI has been reported in up to 75% of cases,2 the recognition of these angiographic features may play a crucial role in understanding the thrombus amount in the setting of coronary occlusion.15 Moreover, it is important to remark that plaque components other than thrombus may compose the embolization debris,21 thus explaining the independent role of large IRA diameter and right coronary artery in predicting DE22 and suggesting a complex interplay between vessel dimensions, plaque burden and DE.
Impact of distal embolization on myocardial reperfusion and myocardial necrosis
The negative results of large trials testing mechanical adjunctive devices during p-PCI have raised concerns not only about the effectiveness of such devices, but also, and more interestingly, about the impact of DE on myocardial reperfusion and infarct size.6–9 Although experimental and clinical studies have shown that DE may affect myocardial reperfusion, enhancing myocardial necrosis,3,23 the impact of this phenomenon may be difficult to address in a clinical setting, since myocardial reperfusion represents a complex process and the impairment of microcirculation is multifactorial in aetiology.24 Moreover, the effectiveness of myocardial reperfusion seems largely time-dependent, with myocardial necrosis enhancing as time-to-treatment increases.10,11 In this scenario, the impact of DE may be fairly different by time-to-treatment, having only limited relevance or even no impact on reperfusion and infarct size in the late comers, among whom many patients may have already developed transmural infarction at the time of IRA reopening.11 Accordingly, our study was able to demonstrate, for the first time, that, while the occurrence of DE is not time-dependent, its impact on both epicardial flow and microvascular reperfusion is time-dependent, with DE impairing myocardial reperfusion in the first 6 h after symptom onset, but having no additional effect on microvascular damage beyond this time. Furthermore, among patients treated within 3 h, those having DE not only had worse myocardial reperfusion, but also larger necrosis and higher in-hospital mortality, surprisingly higher than that expected in this group,25 reflecting the detrimental effect of this complication on jeopardized myocardium when occurring early and the absence of additional effect on myocardial damage when occurring late in the reperfusion process. These findings could partially explain the disappointing results of mechanical adjunctive devices use on infarct size coming from large randomized trials in which patients were enrolled even beyond the first 3 h from symptom onset.6–9 Furthermore, it seems very important to speculate on the discrepancy observed in our series with regard to the time-window of the impact of DE on reperfusion and myocardial damage, respectively: while DE worsened myocardial reperfusion in the first 6 h, the infarct size was affected by DE within 3 h. These observations are consistent with previous experimental and clinical data, showing that both reperfusion and infarct size are time-dependent and that microvascular damage lagged behind myocardial necrosis.10,11 Moreover, our data emphasize that even if the detrimental effect of DE on myocardial necrosis is strictly confined to the first hours from symptom onset, left ventricular function seems affected beyond this time, showing a dissociation between myocardial necrosis and residual ventricular function, outlining that the extent of necrosis is not the only determinant of ventricular function after reperfused STEMI.26–28 However, since we did not exclude patients with previous infarction from the study, this could have affected this discrepancy. Some limitations of our study should be taken into account, in order to place our findings in proper perspective. First of all, since our study was designed to investigate the predictors and the impact of DE occurring during p-PCI, as evaluated by coronary angiography, we detected only the macro-embolization phenomenon. Moreover, at the time the study was performed, abciximab was administered to a relatively small number of our patients, probably making the potential beneficial effects of this drug on DE insufficiently felt. On the other hand, it is important to emphasize that abciximab, as administered in downstream fashion at the operator's discretion, was given more often in patients with DE; therefore, the occurrence of DE per se may have drawn abciximab administration in some cases, rendering not possible to draw conclusions about the effect of abciximab on DE phenomenon. Finally, since we did not perform an evaluation of infarct size using advanced imaging technology, such as magnetic resonance or nuclear scan, we probably underestimated the impact of DE on the extent of necrosis. However, since TnI serum level has been recognized as a good surrogate of infarct size estimation because of its proven correlation with the extent of necrosis as evaluated by magnetic resonance imaging study,29 the clinical significance of this measurement may be correct.
Clinical implications
Our findings suggest that DE during p-PCI occurs more often in the presence of specific angiographic features of high thrombus-burden lesions, such as high TTS, the occlusion pattern of the IRA, treatment of right coronary artery, and large IRA diameter. These findings may provide useful insights for the selection of patients who may benefit from mechanical adjunctive devices preventing DE during p-PCI, suggesting that future trials evaluating the impact of these devices on myocardial damage and reperfusion should enrol only patients with angiographically documented high thrombus burden at target lesions. However, since the impact of DE on myocardial reperfusion and damage seems largely influenced by time-to-treatment, reducing the effectiveness of myocardial reperfusion within 6 h and enhancing the extent of necrosis within 3 h after symptom onset, it should be pointed out that mechanical adjunctive devices may be useful only in those patients presenting in the first hours after symptom onset.
Conflict of interest: none declared.
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