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* From the Division of Cardiology (Drs. Yip, Chen, Hang, Hsieh, Fang, and Wu), Chang Gung Memorial Hospital, Kaohsiung; and Department of Biological Sciences (Dr. Chang), National Sun Yat-Sen University, Kaohsiung, Taiwan, ROC.
Correspondence to: Chiung-Jen Wu, MD, Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, 123, Ta Pei Rd, Niao Sung Hsiang, Kaohsiung Hsien, 83301, Taiwan, ROC; e-mail: cjenwu{at}seed.net.tw
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Abstract |
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1 flow) reperfusion after d-PCI.
Methods and results: Between May 1993 and September 2000, d-PCI was performed in 794 consecutive patients with acute myocardial infarction. Coronary blood flow failed to normalize in 120 patients (15.1%). The incidence of failure to achieve TIMI 3 flow in the IRAs was significantly higher in patients with vs those without the following distinctive prerevascularization angiographic morphologic features: cutoff pattern of occlusion in the IRA (52.4% vs 10.3%, p < 0.001), accumulated thrombus (> 5 mm) proximal to the occlusion (37.5% vs 3.4%, p < 0.001), presence of floating thrombus (66.7% vs 12.7%, p < 0.001), persistent dye stasis distal to the obstruction (51.9% vs 13.8%, p < 0.001), reference lumen diameter (RLD) of the IRA 
4 mm (46.3% vs 9.6%, p < 0.001), and incomplete obstruction with presence of accumulated thrombus more than three times the RLD of the IRA (51.7% vs 3.9, p < 0.0001). Each of these six angiographic morphologic features indicated "high-burden thrombus formation." Multiple stepwise logistic regression analysis demonstrated that each of six angiographic morphologic features was an independent predictor of combined slow-flow and no-reflow phenomenon in the IRAs after d-PCI (p < 0.05). In contrast, early reperfusion time (< 240 min, p = 0.0017), prerevascularization TIMI flow grade 2 (p = 0.0006), and the taper pattern of occlusion in the IRA (p = 0.0284) were independent predictors of freedom from slow-flow or no-reflow phenomenon in the IRAs after d-PCI. The 30-day overall mortality was 8.7% (69 of 794 patients). The 30-day mortality was significantly higher in patients with combined slow-flow and no-reflow phenomenon than in patients with normal coronary blood flow after d-PCI (27.5% vs 5.3%, p < 0.001).
Conclusions: Early reperfusion reduces the incidence of slow-flow or no-reflow phenomenon in the IRA and overall 30-day mortality. The specific angiographic morphologic features in the IRAs can be used as a simple and efficacious method to predict slow-flow or no-reflow phenomenon. These findings provide apparently clinically useful information for the selection of patients who are potential candidates for subsequent prepercutaneous coronary intervention adjunctive therapy.
Key Words: acute myocardial infarction • angiography • no-reflow reperfusion • thrombus
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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1 flow) is associated with relatively more extensive myocardial necrosis,11
and consequently left ventricular dilatation with poor regional and global contractile function and an untoward clinical outcome.3
6
12
The mechanisms of slow-flow and no-reflow phenomenon have been debated extensively.13
14
15
However, no specific and efficacious method has been suggested to promptly reverse slow-flow or no-reflow phenomenon in the IRA after d-PCI. The short-term clinical outcomes of d-PCI have been improved by adjunctive pharmacologic therapy with platelet glycoprotein IIb/IIIa blockade.9
16
17
However, if complete reperfusion of the IRA is considered a successful therapeutic end point, the results were not different between balloon angioplasty alone and balloon angioplasty plus abciximab in the ReoPro and Primary PTCA Organization and Randomized Trial (RAPPORT)9
or between stenting alone and stenting plus abciximab in the Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) trial18
and in another clinical trial.17
This suggests that there are other unidentified confounders. Recently, Cura et al19
demonstrated that the clinical characteristics of advanced age and elevated heart rate, the angiographic evidence of thrombus, and the absence of coronary flow before intervention are the independent predictors of TIMI grade 2 flow after d-PCI in patients with AMI.19
However, their study did not provide further information regarding prerevascularization angiographic morphologic features to identify "high-burden thrombus formation," and to predict slow-flow or no-reflow phenomenon after d-PCI in patients with AMI. In this study, we provide a simple clinical tool that effectively predicts slow-flow or no-reflow phenomenon after d-PCI in patients with AMI. |
Materials and Methods |
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Procedure and Protocol
The procedure and protocol have been described previously in detail.20
Before stents were available in our country, primary balloon angioplasty was performed in the patients; however, after stents were available in our country, primary stenting was performed in most of the patients. Patients were treated with ticlopidine for 2 weeks if stent deployment was performed. Aspirin, 100 mg/d po, was administered indefinitely to each patient. Platelet glycoprotein IIb/IIIa inhibitors were not used in any of our patients because they were not available in our country during this study period.
Angiographic Analysis
Coronary angiographic morphology of the IRA classified by at least two best projections immediately after the angiograms, and TIMI flow grade21
were assessed and consensus was reached immediately after d-PCI by two interventional cardiologists. Quantitative angiographic analysis of the percentage of minimal lumen diameter (MLD) stenosis, lesion length, and reference lumen diameter (RLD) were performed by using a digital edge-detection algorithm22
and selecting end-diastolic frames demonstrating the stenosis in its most severe and nonforeshortened projection. With the contrast-filled guiding catheter used as the calibration standard, the RLDs and MLDs were calculated before and after angioplasty.
Coronary Angiographic Morphologic Features
The angiographic features of the IRAs were morphologically classified as follows on the basis of quantitative and qualitative analyses: (1) incomplete obstruction with the presence of angiographic thrombus; an angiographic thrombus with the greatest linear dimension three times or less of the RLD was defined as a type I lesion (Fig 1
, A1), and an angiographic thrombus with the greatest linear dimension more than three times the RLD was defined as type II lesion (Fig 1
, A3); (2) taper pattern (lesion morphology with a tapered end before occlusion; Fig 2
, B1); (3) tapered cutoff pattern (lesion morphology with proximal tapering and distal abrupt cutoff pattern filled with some thrombus before the occlusion (Fig 2
, B4); (4) cutoff pattern (lesion morphology with an abrupt cutoff without taper before the occlusion (Fig 3
, C1); (5) presence of accumulated thrombus (> 5 mm of linear dimension) proximal to the occlusion (Fig 3
, C4); (6) presence of floating thrombus proximal to the occlusion (Fig 4
, D1); (7) persistent dye stasis distal to the obstruction (Fig 4
, D4); (8) RLD of the IRA 4.0 mm.
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1 mm or definite T-wave inversion or both, and an elevation of creatine kinase with creatine kinase-MB fraction > 4% on at least one occasion. Reperfusion time was defined as the time from onset of chest pain to first balloon inflation. Procedural success was defined as a reduction to residual stenosis of < 50% by balloon angioplasty or successful stent deployment at the desired position with a residual stenosis < 30% followed by TIMI grade 3 flow in the IRA. Slow flow was defined as TIMI grade 2 flow, and no reflow was defined as TIMI grade 1 flow in the distal IRA in the absence of an occlusion at the treatment site or evidence of distal embolization. Angiographic thrombus was defined as the presence of luminal filling defect in the IRA. Each of the six angiographic features—type II lesion, cutoff pattern, accumulated thrombus (> 5 mm) proximal to occlusion, floating thrombus proximal to occlusion, persistent dye stasis distal to obstruction, and RLD of IRA 4.0 mm—indicated high burden thrombus formation in the IRA. Distal embolization was defined as the presence of filling defects in or cut off of a distal branch or vessel.
Data Collection
Detailed in-hospital and follow-up data, including age, sex, coronary risk factors, Killip score on hospital admission, reperfusion time, preintervention and postintervention TIMI flow grades, angiographic morphologic features and results, number of diseased vessels, and in-hospital adverse events, were obtained. These data were collected prospectively and entered into a computerized database.
Statistical Analysis
Data were expressed as mean ± SD. Continuous variables were compared using Wilcoxon rank-sum test. Categorical variables were compared using 
2 or the Fisher exact test. Stepwise logistic regression analysis was used to determine independent predictors of combined slow-flow and no-reflow phenomenon after d-PCI. The test of homogeneity of proportions was used to test the significance of the difference in the incidence of combined slow-flow and no-reflow phenomenon among the four different reperfusion intervals, and 2 trend test was used to test whether the trend of increasing incidence of combined slow-flow and no-reflow phenomenon correlated with increasing reperfusion intervals. Statistical analysis was performed using ASA statistical software for Windows (Version 6.12; SAS Institute; Cary, NC). A probability value < 0.05 was considered statistically significant.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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4.0 mm was also significantly higher in combined RCA and LCX than in LM and LAD (65.0% vs 44.4%, p = 0.003) [Tables 2 , 3
].
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The incidence of prerevascularization angiographic TIMI grade flow 2 in the IRA in this study was 23.1%. Patients with prerevascularization angiographic TIMI grade flow 2 had significantly lower incidence of combined slow-flow and no-reflow phenomenon than those who had prerevascularization angiographic TIMI grade 1 flow in IRA after d-PCI.
The overall mean reperfusion time was 284 min. The mean reperfusion time was significantly higher in patients with combined slow-flow and no-reflow phenomenon than in patients with normal coronary flow immediately after d-PCI (p = 0.0023). When d-PCI was performed within 6 h after onset of AMI, the test of homogeneity of proportions demonstrated that the difference in the incidence of combined slow flow and no reflow among the four different reperfusion intervals (< 2 h, 2 to 4 h, 4 to 6 h and > 6 h) was significant (p = 0.03). Furthermore, the 2 trend test demonstrated that the trend of increasing incidence of combined slow flow and no reflow was significantly correlated with increasing reperfusion intervals (p = 0.007; Fig 5
). Therefore, the incidence of slow-flow or no-reflow reperfusion after d-PCI in patients with a reperfusion time 240 min was significantly higher than that in those with a reperfusion time < 240 min (18.8% vs 11.6%, p = 0.021). However, the incidence of combined slow flow-and no-reflow reperfusion after d-PCI did not change thereafter when reperfusion time was > 240 min (p = 0.972).
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240 min (27.7% vs 29.2%, p = 0.636). However, in the 226 patients with high-burden thrombus formation, the incidence of combined slow-flow and no-reflow phenomenon of the 108 patients with reperfusion time < 240 min was significantly lower than that of the 118 patients with reperfusion time 240 min (31.5% vs 51.7%, p = 0.002). Therefore, normal coronary flow could be achieved if reperfusion occurred earlier, even in the subgroup of patients with high-burden thrombus formation. Moreover, the incidence of distal embolization in patients with high-burden thrombus formation was significantly higher than in patients without this problem: 46.46% (105 of 226 patients) vs 4.23% (24 of 568 patients) [p = 0.001].
Multiple stepwise logistic regression analysis (all significant univariate predictors in Tables 3
, 4
were included in the analysis) demonstrated that prerevascularization angiographic TIMI flow grade 2 flow (odds ratio, 0.172; 95% confidence interval, 0.059 to 0.500; p = 0.0005) and reperfusion time < 240 min (odds ratio, 0.543; 95% confidence interval, 0.331 to 0.889; p = 0.0143) were independent predictors of TIMI 3 flow after d-PCI.
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Relationship Between Coronary Angiographic Features and Slow-Flow or No-Reflow Phenomenon
As shown in Table 4
, the incidence of combined slow-flow and no-reflow phenomenon after d-PCI was significantly higher in patients with type II lesions (p < 0.001), RLD of the IRA 4 mm (p < 0.001), a cutoff angiographic pattern (p < 0.001), presence of accumulated thrombus > 5 mm proximal to the occlusion, presence of a floating thrombus (p < 0.001), and persistent dye stasis distal to the obstruction (p < 0.001). In contrast, the incidence of combined slow-flow and no-reflow phenomenon after d-PCI was significantly lower in patients with a tapered angiographic pattern (p = 0.002). However, there was no significant difference of combined slow-flow and no-flow phenomenon between patients with and without a tapered cutoff angiographic pattern.
Multiple stepwise logistic regression analysis (all significant univariate predictors in Table 4
were included in the analysis) demonstrated that each of the six angiographic features (type II lesion, cutoff angiographic pattern, presence of accumulated thrombus, presence of floating thrombus proximal to occlusion, presence of persistent dye staining distal to obstruction, and RLD of the IRA 4.0 mm) were independent predictors of slow-flow or no-reflow phenomenon after d-PCI (Table 5
), whereas a tapered angiographic pattern (odds ratio, 0.560; 95% confidence interval, 0.332 to 0.944; p = 0.0284) was an independent predictor of TIMI 3 flow after d-PCI.
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Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The treatment of the no-reflow phenomenon after d-PCI is an unsavory problem and has vexed cardiologists for more than a decade. Interventional cardiologists are still searching for a profitable and promising strategic management for this problem.24 25 Recently, the role of platelets in the initiation of thrombus formation,25 distal embolization and subsequent no-reflow phenomenon,15 early reocclusion of the IRA,9 17 and ischemic complications26 after d-PCI have been well demonstrated and discussed. However, the platelet glycoprotein IIb/IIIa receptor blockade, which affects the final common pathway of platelet aggregation, has undergone extensively clinical testing.9 16 17 26 Although the combined major ischemic events are reduced by abciximab therapy in the RAPPORT9 and CADILLAC trial,18 the percentage of patients achieving TIMI grade 3 flow in the IRA after d-PCI was not significantly increased in those two randomized trials or in a subgroup study in the Evaluation of 7E3 for the Prevention of Ischemic Complications trial.16 The discrepancy between placebo and adjunctive abciximab therapy in terms of different clinical outcomes and similar rates of achieving TIMI grade 3 flow in the IRA after d-PCI in these studies should raise issues regarding the other mechanism of no-reflow reperfusion rather than the present established mechanisms.
Rationale for Angiographic Classification of the IRA To Predict Slow-Flow or No-Reflow Phenomenon After d-PCI
According to the absence or presence of angiographic evident thrombus in the IRA, post-thrombolytic angiographic morphologies have been well analyzed and classified into TIMI thrombus grades 0 to 5.27
However, this classification cannot provide information regarding the prediction of slow-flow or no-reflow phenomenon on subsequent percutaneous coronary intervention. Furthermore, despite extensive studies on the mechanism of the no-reflow phenomenon after d-PCI, preinterventional angiographic morphologic features to identify high-burden thrombus formation, and to predict slow-flow or no-reflow phenomenon after d-PCI in patients with AMI have never been reported. To the best of our knowledge, this is the first study, by quantitative and qualitative analysis, to provide a simple and useful angiographic classification to predict slow-flow or no-reflow phenomenon after d-PCI according to prerevascularization angiographic morphologic features of the IRA.
In the present study, we found that patients with a type II lesion in the IRA had a significantly higher incidence of combined slow-flow and no-reflow phenomenon after d-PCI than those who had a type I lesion. Angiographic findings showed large numbers of thrombi in type II lesions (Fig 1
, A3). Conceivably, the size of the thrombus should have a key role in slow-flow or no-reflow phenomenon after d-PCI. Interestingly, the taper pattern of the IRA had a significantly lower incidence of combined slow-flow or no-reflow phenomenon than without this angiographic pattern of IRA. Angiographic findings demonstrated that rare thrombus accumulated proximally to the occluded level of the taper pattern in the IRA (Fig 2
, B1). Moreover, after opening the obstructive lesion by either wiring or first balloon dilatation, we usually observed no obvious thrombus distal to the obstructive vessel in the taper pattern of the IRA except for the IRA with an RLD 4.0 mm (Fig 2
, B2). The impact of this angiographic observation offered a firm relationship between the taper pattern and a lower thrombus burden, and subsequently yielded a significantly lower incidence of slow-flow or no-reflow phenomenon after d-PCI. However, with and without the tapered cutoff pattern, the IRA had a similar frequency of combined slow-flow or no-reflow phenomenon after d-PCI. Angiographic findings demonstrated that some thrombus accumulated proximally to the occluded level in the tapered cutoff of the IRA (Fig 2
, B4). Moreover, after opening the obstructive lesion by either wiring or first balloon dilatation, heterogeneous distribution (from small to large amount) of thrombus burden distal to the obstructive level was observed in the tapered cutoff pattern of the IRA, and this finding might explain the limited prognostic implication in this angiographic pattern of the IRA.
One of our most important discoveries was that patients with distinctive coronary angiographic morphologies of the cutoff pattern, the presence of floating thrombus and accumulated thrombus proximal to the occluded level, and persistent dye staining distal to the occluded level of the IRA had particularly higher incidences of combined slow-flow and no-reflow phenomenon. The results of these angiographic findings indicated that these IRA always present with high-burden thrombus formation proximal to the occluded level. After the obstruction was opened by either wiring or first balloon dilatation, angiographic results further demonstrated that after the obstructive level the IRA was always filled with a high burden of thrombus (Fig 3 , C1 to C6; Fig 4 , D1 to D6). These findings further supported that high-burden thrombus formation plays a pivotal role in slow-flow or no-reflow phenomenon after d-PCI.
Recently, we reported that an IRA with an RLD 4.0 mm was a strong predictor of no-reflow phenomenon in patients with AMI complicated by cardiogenic shock.20
In the present study, we further demonstrated that an IRA with an RLD 4.0 mm was an independent predictor of combined slow-flow and no-reflow phenomenon after d-PCI in patients with or without cardiogenic shock. The high incidence of combined slow-flow and no-reflow phenomenon in an IRA with an RLD 4.0 mm indicated that larger thrombus formation occurred in these vessels. After balloon dilatation or stent implantation, large thrombi were crushed and they subsequently embolized the distal vasculature. The dislodged thrombi further activated more platelets and, therefore, thrombosis cascade; this ultimately yielded slow-flow or no-reflow phenomenon in the IRA. We also found that the incidence of RLD 4.0 mm in the RCA and LCX was significantly higher than that in the LM and LAD. This could explain why the combined incidence of slow-flow and no-reflow phenomenon of the RCA and LCX was significantly higher than that of the LM and LAD; therefore, the combined incidence of slow-flow and no-reflow phenomena after d-PCI in inferior wall MIs was also significantly higher than that in anterior wall MIs.
Relationship Between TIMI Flow and Reperfusion Time
Our results demonstrated that when d-PCI was performed within 6 h after onset of AMI, the incidence of combined slow-flow and no-reflow phenomenon was significantly increased with increasing reperfusion time (Fig 5)
. Multivariate stepwise logistic regression analysis also showed that early reperfusion (< 240 min) was an independent determinant of improvement in TIMI flow after d-PCI. Theoretically, an ideally linear relationship between reperfusion time and high-burden thrombus formation should be deduced. Surprisingly, there was no significant difference in the incidence of high- burden thrombus formation between reperfusion times of < 240 and 240 min. However, in patients with high-burden thrombus formation, those with a reperfusion time < 240 min had a significantly lower incidence of combined slow-flow and no-reflow phenomenon than those who had a reperfusion time 240 min. Therefore, a higher incidence rate of normal coronary flow could be achieved if reperfusion was performed early, even in the subgroup of the patients with high-burden thrombus formation. This perplexity could probably be explained by the fact that the major component of high-burden thrombi that formed early and rapidly after AMI were platelet-rich, erythrocyte-rich thrombus and contained "red" fibrins, and these could be only partially lysed by combination therapy with abciximab as shown in the TIMI 14 substudy.27
As time goes on, organization of the thrombus occurs and the thrombus becomes more firm. The organized thrombus is broken down into fragmented debris (mixed macroemboli and microemboli) by mechanical devices such as balloons or stents, and these debris cause embolization of branch or distal vessels and can completely plug the microvasculature, resulting in slow-flow or no-reflow phenomenon. This clinical observation provides a pathophysiologic mechanism link between high-burden thrombus formation, mixed macroembolization and microembolization, and development of slow-flow or no-flow phenomenon in the IRA. This chain of events probably cannot be completely prevented or abolished by platelet glycoprotein IIb/IIa receptor blockade agents. This clinical observation might explain why the percentage of patients achieving TIMI grade 3 flow in the IRA after d-PCI and adjunctive abciximab therapy was not significantly increased in the RAPPORT9
and CADILLAC trial.18
There are several limitations in this study. First, although our study conveyed useful information about the slow-flow and no-flow phenomenon after d-PCI from prerevascularization angiographic features, this study did not provide specific treatment of the no-reflow phenomenon. Second, the mechanism for slow-flow or no-reflow phenomenon after d-PCI may include not only embolization of thrombus and debris but also reperfusion injury (microvascular damage, edema etc). As our study was not designed to discuss the basic mechanism of the slow-flow and no-reflow phenomenon after d-PCI, we could not provide evidence other than thrombosis. Third, the angiographic features are arbitrarily classified. However, this unique angiographic classification provides simple and useful clinical predictors to predict no-reflow phenomenon after d-PCI. Finally, myocardial contrast echocardiography, ST-segment resolution, and angiographic "blushing" scores may provide a more meaningful assessment of reperfusion efficacy than TIMI flow grade. However, our study was developed before the development of those assessments of reperfusion methods. Moreover, TIMI flow grade is still the most common assessment for reperfusion.
In conclusion, prerevascularization angiographic features of the IRAs can be used as a simple and efficacious clinical tool with much merit in prediction of slow-flow or no-reflow reperfusion after d-PCI. Early reperfusion reduces the incidence of slow-flow or no-reflow reperfusion in the IRA and the overall 30-day mortality. These are the most important findings, and they convey useful information to facilitate appropriate and early patient triage for possibly subsequently pre-percutaneous coronary intervention adjunctive therapy.
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Footnotes |
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Received for publication January 4, 2002. Accepted for publication April 29, 2002.
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