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Plaque Prolapse After Stent Implantation in Patients With Acute Myocardial Infarction

An Intravascular Ultrasound Analysis

Heart Center of Chonnam National University Hospital, Cardiovascular Research Institute, Chonnam National University, Gwangju, Korea.

	Abstract

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Objectives: The aim of this study was to assess the incidence, predictors, and outcome of plaque prolapse (PP) after stent implantation in acute myocardial infarction.

Background: The imaging characteristics of PP in patients with acute myocardial infarction are not well known.

Methods: Intravascular ultrasound (IVUS) imaging was performed in 310 patients immediately following stenting for their first acute myocardial infarction. Multiple clinical, angiographic and IVUS derived variables were compared among patients with and without intrastent PP.

Results: The PP was detected in 27% of the 310 lesions examined. Stent length was longer (31 ± 13 mm vs. 21 ± 8 mm, p < 0.001), and positive remodeling (48% vs. 32%, p = 0.008), plaque rupture (51% vs. 31%, p = 0.001), and thrombus (40% vs. 21%, p = 0.001) were significantly more common in PP lesions compared with non-PP lesions. The creatine kinase-myocardial band (CK-MB) was significantly greater after stenting in PP lesions compared with non-PP lesions ( = +12.3 ± 32.0 U/l vs. –4.9 ± 46.1 U/l, p = 0.002). During a 1-month follow-up, the incidence of stent thrombosis was not significantly different between PP and non-PP lesions [2/85 (2.4%) vs. 2/225 (0.9%), p = 0.308]. Multivariate analysis showed that PP (odds ratio [OR]: 7.34, p < 0.001), plaque rupture (OR: 1.95, p = 0.023), and thrombus (OR: 1.84, p = 0.026) were independently associated with post-stenting CK-MB elevation, and stent length (OR: 2.39, p = 0.003), plaque rupture (OR: 1.96, p = 0.015), and positive remodeling (OR: 1.72, p = 0.044) were independently associated with the development of PP.

Conclusions: PP occurs in one-fourth of infarct-related arteries after stent implantation. Lesion characteristics such as plaque rupture and positive remodeling, together with longer stent predict PP. Although long-term follow-up is pending, PP is associated with more myonecrosis after stenting in patients with acute myocardial infarction.

Key Words: myocardial infarction • ultrasonics • angioplasty

Abbreviations and Acronyms   AMI = acute myocardial infarction   CK-MB = creatine kinase-myocardial band   CSA = cross-sectional area   EEM = external elastic membrane   IVUS = intravascular ultrasound   P&M = plaque plus media   PP = plaque prolapse   STEMI = ST-segment elevation myocardial infarction   TIMI = Thrombolysis In Myocardial Infarction

	Methods

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Patient population.   From January 9, 2001, to July 31, 2007, we identified a total of 310 patients with a first AMI. All underwent pre-intervention IVUS within 24 h of symptom onset, were stented successfully, and received post-intervention IVUS imaging. Patients excluded were those with prior MI, subacute or late stent thrombosis, restenosis after stenting, and coronary artery bypass graft failure. Patients studied with IVUS more than 24 h after symptom onset and/or patients in whom adequate IVUS images could not be obtained were also excluded.

The presence of ST-segment elevation myocardial infarction (STEMI) was identified by >30 min of continuous chest pain, a new ST-segment elevation 2 mm on at least 2 contiguous electrocardiographic leads, and >3 times the normal level of creatine kinase-myocardial band (CK-MB). The presence of non-STEMI was diagnosed by chest pain and a positive cardiac biochemical marker without new ST-segment elevation. Infarct-related arteries were identified using a combination of electrocardiographic findings, abnormalities of left ventricular wall motion on angiogram or echocardiogram, and coronary angiographic findings. All 310 infarct lesions were treated with stent implantation: 138 with sirolimus-eluting stents (Cypher stent, Cordis, Johnson and Johnson, Miami Lakes, Florida), 49 with paclitaxel-eluting stents (Taxus stent, Boston Scientific, Boston, Massachusetts), and 123 with bare-metal stents.

Laboratory analysis.   Venous blood samples were obtained within 24 h of stenting. The blood samples were centrifuged, and serum was removed and stored at –70°C until the assay could be performed. Absolute CK-MB levels were determined by radioimmunoassay (Dade Behring Inc., Miami, Florida). Cardiac-specific troponin I levels were measured using paramagnetic particles and a chemiluminescent immunoenzymatic assay (Beckman, Coulter Inc., Fullerton, California). The serum levels of total cholesterol, triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were measured using standard enzymatic techniques.

Angiographic analysis.   Coronary angiograms were analyzed with a validated quantitative coronary angiography system (Philips H5000 or Allura DCI program, Philips Medical Systems, Eindhoven, the Netherlands). Using the outer diameter of the contrast-filled catheter as the calibration standard, the minimal lumen diameter and reference diameter were measured in diastolic frames from orthogonal projections. Myocardial blush scores were categorized into 4 densitometric grades based on a visual assessment of contrast opacification of the area containing the infarct-related artery, as previously described (8).

Electrocardiogram analysis.   All patients underwent a 12-lead ECG at baseline and again 90 min after the procedure. The ST-segment elevation was manually measured 20 ms from the J-point, as previously described (9). The ST-segment resolution was expressed as a percentage of the initial ST-segment and a value >70% was defined as indicative of successful myocardial reperfusion 90 min after the index procedure.

IVUS imaging and analysis.   All IVUS examinations were performed before and after stenting after intracoronary administration of 300-µg nitroglycerin using a commercially available IVUS system (Boston Scientific Corporation/SCIMed, Minneapolis, Minnesota). The IVUS catheter was advanced distal to the target lesion, and imaging was performed retrograde to the aorto-ostial junction at an automatic pullback speed of 0.5 mm/s.

IVUS analysis was performed according to the American College of Cardiology Clinical expert consensus document on standards for acquisition, measurement, and reporting of intravascular ultrasound studies (10). At pre-intervention, we measured the external elastic membrane (EEM) and lumen cross-sectional area (CSA). Plaque plus media (P&M) CSA was calculated as EEM CSA minus lumen CSA, and plaque burden was calculated as P&M CSA divided by EEM CSA. The lesion was the site with the smallest lumen CSA; if there were multiple image slices with the same minimum lumen CSA, then the image slice with the largest EEM and P&M was measured. Coronary artery remodeling was assessed by comparing the lesion site to the reference EEM CSA. Remodeling index was the lesion site EEM CSA divided by the average of the proximal and distal reference EEM CSA. Positive remodeling was defined as a remodeling index >1.05, intermediate remodeling as a remodeling index between 0.95 and 1.05, and negative remodeling as a remodeling index <0.95 (11). Hypoechoic plaque was less bright compared with the reference adventitia. Hyperechoic, noncalcified plaque was as bright as or brighter than the reference adventitia without acoustic shadowing. Calcium plaque was hyperechoic with shadowing. A calcified lesion contained >90° of circumferential lesion calcium.

A ruptured plaque contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. A fragmented and loosely adherent plaque without a distinct cavity and without a fibrous cap fragment was not considered a plaque rupture. Rupture sites separated by a length of artery containing smooth lumen contours without cavities were considered to represent different plaque ruptures (12,13). Plaque cavity was measured and extrapolated to the ruptured capsule area. Thrombus was an intraluminal mass having a layered or lobulated appearance, evidence of blood flow (microchannels) within the mass, and speckling or scintillation (13,14). A lipid-pool-like image was defined as a pooling of hypoechoic or echolucent material covered with a hyperechoic layer.

At the time of post-intervention assessment, the minimum stent CSA was measured. Percent stent expansion was calculated as the minimum stent CSA divided by the mean reference lumen CSA. The PP was defined as tissue extrusion through the stent strut, assessed post-intervention, and the volume of PP was calculated by subtracting the lumen volume from the stent volume.

Statistical analysis.   The SPSS (Statistical Package for Social Sciences) for Windows, version 15.0 (Chicago, Illinois) was used for all analyses. Continuous variables were presented as the mean value ± standard deviation; comparisons were conducted using Student t test or, if the normality assumption was violated, the nonparametric Wilcoxon test. Discrete variables were presented as percentages and relative frequencies; comparisons were conducted by chi-square statistics or Fisher exact test, as appropriate. Multivariate logistic regression analyses were performed to identify independent predictors of post-stenting CK-MB elevation and PP. Univariate analyses were first conducted to identify potential risk factors for post-stenting CK-MB elevation and PP. The likelihood ratio test was used, and the variables with a p value <0.2 were included in the multivariate model. Finally, a step-down logistic regression was performed. The least significant variable was dropped at each step until only covariates with a p value <0.05 remained. A p value <0.05 was considered statistically significant.

	Results

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Patient characteristics.   The baseline characteristics are summarized in Table 1. There was a tendency for PP to be observed more frequently in lesions from STEMI patients, compared with lesions from patients with non-STEMI. Distal protection devices were used more frequently in PP lesions than in non-PP lesions. Total cholesterol levels were significantly higher, and low-density lipoprotein cholesterol levels tended to be higher in patients with PP compared with patients without PP.

View larger version (19K): [in this window] [in a new window] [Download PPT slide]   Figure 1 Incidence of PP in Relation to the Stent Length Stent length was divided into 3 groups such as short stent length group (less than 18 mm, n = 137), intermediate stent length group (between 18 and 28 mm, n = 89), and long stent length group (more than 28 mm, n = 84). Plaque prolapse (PP) was most frequently observed in the group with the long stents (>28 mm) compared with the groups with short- (18 mm) or intermediate-length (>18 and 28 mm) stents.

When the incidence of PP was assessed in relation to the presence/absence of plaque rupture, PP was observed more frequently in lesions with plaque rupture than in lesions without plaque rupture (Fig. 2). When the lesions were divided into 3 groups according to their remodeling pattern (positive, intermediate, or negative), PP was most frequently observed in the group showing positive remodeling (Fig. 3). The minimum stent CSA and percent stent expansion were significantly greater in PP lesions than in non-PP lesions.

View larger version (18K): [in this window] [in a new window] [Download PPT slide]   Figure 2 Incidence of PP in Relation to the Presence or Absence of the Plaque Rupture A ruptured plaque contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. A fragmented and loosely adherent plaque without a distinct cavity and without a fibrous cap fragment was not considered a plaque rupture. The PP was observed more frequently in lesions with plaque rupture compared with lesions without plaque rupture.

View larger version (22K): [in this window] [in a new window] [Download PPT slide]   Figure 3 Incidence of PP in Relation to the Remodeling Pattern Remodeling index was defined as the lesion site external elastic membrane (EEM) cross-sectional area (CSA) divided by the average of the proximal and distal reference EEM CSA. Positive remodeling (n = 113) was defined as a remodeling index >1.05, intermediate remodeling (n = 75) as a remodeling index between 0.95 and 1.05, and negative remodeling (n = 122) as a remodeling index <0.95. The PP was most frequently observed in the group showing positive remodeling compared with the groups showing intermediate or negative remodeling.

Post-stenting myocardial blush score and ST-segment resolution in patients with STEMI.   In 125 patients with STEMI, there was a trend for the rates of post-stenting myocardial blush score 2 (PP: 30 of 41 [73.2%]; non-PP: 73 of 84 [86.9%]; p = 0.058), and for the complete ST-segment resolution to be lower in patients with PP than in patients without PP (PP: 29 of 41 [70.7%]; non-PP: 71 of 84 [84.5%]; p = 0.070).

Independent predictors of post-stenting PP.   Multivariate analysis was performed to identify independent predictors of post-stenting PP. The following variables were tested (all with p < 0.2 in univariate analysis): clinical presentation, distal protection device use, ejection fraction, creatinine clearance, total cholesterol, infarct-related artery, TIMI flow grade 0, stent type, number of deployed stents, stent length, inflation pressure, quantitative coronary angiography pre-minimal luminal diameter, IVUS minimum lumen CSA, IVUS plaque burden, plaque rupture, thrombus, lipid-pool-like image, hypoechoic plaque, calcium arc, positive remodeling, and percent stent expansion. Stent length (OR: 2.39; 95% CI: 1.17 to 3.89, p = 0.003), plaque rupture (OR: 1.96; 95% CI: 1.14 to 3.37, p = 0.015), and positive remodeling (OR: 1.72; 95% CI: 1.01 to 2.92, p = 0.044) were each independently associated with the development of PP.

	Discussion

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The present study demonstrates that lesion characteristics identified at pre-intervention IVUS, namely plaque rupture and positive remodeling, together with stent length predict PP. Furthermore, PP is associated with myonecrosis after stenting of an infarct-related artery in patients with AMI.

The PP is characterized by an intraluminal tissue extrusion through the stent struts, and this is easily detectable using IVUS. Several pre-intervention IVUS factors such as soft (rather than fibrous or calcified) plaque, smaller minimal lumen diameter, and larger plaque burden are known to be related to PP, and the risk of PP is known to be higher during aggressive stenting procedures (3,4). Some studies have demonstrated that PP might contribute to the development of stent thrombosis (5–7).

The incidence of PP varies. Hong et al. (4) reported that the incidence of minor PP in 407 native coronary lesions was 23% in 384 patients who underwent IVUS-guided single bare-metal stenting. Kim et al. (15) evaluated the incidence of PP according to the different drug-eluting stent types (41 sirolimus-eluting stents and 42 paclitaxel-eluting stents) and different inflation pressures. In the study by Kim et al. (15), the incidence of PP was 41% (17 of 41 lesions) with the sirolimus-eluting stents versus 24% (10 of 41 lesions) with the paclitaxel-eluting stents with an inflation pressure of 14 atm, and 35% (14 of 40) in sirolimus-eluting stents versus 17.8% (5 of 28) in paclitaxel-eluting stents when an inflation pressure of 20 atm was used. Futamatsu et al. (16) reported that the incidence of PP was 16% (9 of 56) after bare-metal stent implantation, 16% (9 of 57) after sirolimus-eluting stent implantation, and 27% (15 of 55) after paclitaxel-eluting stent implantation. In the present study, PP was detected in 27% of patients and there was a trend toward a higher incidence of PP when paclitaxel-eluting stents were used compared with sirolimus-eluting or bare-metal stents.

The predictors of PP are not well understood in patients with AMI. Hong et al. (4) reported that the infarct-related artery and a small pre-intervention minimum lumen diameter were factors associated with PP. Typical IVUS features observed following AMI include plaque rupture, thrombus formation, positive remodeling, and only either spotty or deep calcium within the minimum lumen site (17–24). Several studies (25,26) have reported that rupture of a vulnerable plaque and subsequent thrombus formation is the most important mechanism leading to an acute coronary syndrome. These vulnerable plaques, especially those undergoing plaque rupture and positive remodeling (both of which were identified as independent predictors of PP in the present study), might facilitate tissue extrusion through the stent struts.

Multiple or long coronary stents are frequently implanted in long or tandem lesions. Kim et al. (15) reported that implantation of long stents was associated with PP to a greater degree than was implantation of shorter stents. In the present study, more stents were deployed and stent length was greater in patients with PP compared with patients without PP. This higher frequency of PP in patients who underwent long stent implantation might be caused by uneven distribution of inflation pressure along the length of the stent.

Elevation of the serum CK-MB fraction after percutaneous coronary intervention is associated with early and late mortality, even after successful revascularization (27–31). The CK-MB release after native coronary artery intervention is related to the underlying plaque burden, disease severity, and unstable plaque morphometry (positive remodeling and plaque rupture) (32,33). In addition to these pre-intervention IVUS findings, a more aggressive stenting procedure appeared to be associated with elevation of CK-MB (27,33–35) and the development of PP (4). In the present study, PP was independently associated with post-stenting elevation of CK-MB. Although minor PP within stents might not be associated with long-term clinical outcome (4), PP might be related to myonecrosis after stenting, especially for long lesions with unstable plaque morphometry (plaque rupture and positive remodeling).

The potential risk of stent thrombosis associated with PP is another issue. The PP may act as a trigger for thrombus accumulation in an environment that already has a high potential for thrombogenesis. Impaired arterial healing and stent thrombosis have been associated with the prolapse of the necrotic core between stent struts. This is especially relevant in the setting of AMI, because such patients already have an increased risk for this devastating event. However, in the present study, the incidence of stent thrombosis was not significantly different between PP and non-PP lesions, as assessed during the 1-month clinical follow-up (although long-term clinical follow-up data were not collected).

Study limitations.   First, the present study is a retrospective single-center study, so it is subject to the limitations inherent to this type of clinical investigation. Second, the number of PP was relatively small. Thus, some selection bias cannot be entirely excluded. Third, it may be difficult to differentiate between an organized thrombus and a PP. It is possible that some cases identified as having PP actually had thrombus prolapse. Fourth, there may be enough differences between STEMI and non-STEMI to confound the statistical analysis (especially related to CK-MB elevation). Fifth, there are methodologic issues related to the measurement of a single CK-MB within 24 h after stent placement, rather than a methodical and protocol-driven sequence and timing of CK-MB measurements. This may significantly compromise the interpretation of the CK-MB data. Finally, long-term clinical follow-up was not available.

	Conclusions

Top Abstract Methods Results Discussion Conclusions Appendix REFERENCES

 
The incidence of PP after stenting of infarct-related arteries was 27%. Longer stent length and pre-intervention IVUS-detected plaque rupture and positive remodeling can predict PP, and PP is associated with myonecrosis after stenting for infarct-related artery in patients with AMI.

	Appendix

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For an accompanying slide set, please see the online version of this article.

^_* Reprint requests and correspondence: Dr. Myung Ho Jeong, Director of Cardiovascular Research Institute, The Heart Center of Chonnam National University Hospital, 8 Hak-dong, Dong-gu, Gwangju 501–757, Korea. (Email: myungho{at}chollian.net).

Manuscript received February 11, 2008; revised manuscript received March 11, 2008, accepted April 9, 2008.

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Top Abstract Methods Results Discussion Conclusions Appendix REFERENCES

 

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This Article Abstract Figures Only Full Text (PDF) View Cardiosource Slide Set View CVN News Brief Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hong, Y. J. Articles by Kang, J. C. Search for Related Content PubMed Articles by Hong, Y. J. Articles by Kang, J. C. Related Collections Related Article