Author + information
- Received September 22, 2009
- Revision received December 22, 2009
- Accepted January 8, 2010
- Published online May 1, 2010.
- Mitsuaki Endo, MD⁎,
- Kiyoshi Hibi, MD⁎,⁎ (, )
- Tomoaki Shimizu, MD‡,
- Naohiro Komura, MD⁎,
- Ikuyoshi Kusama, MD⁎,
- Fumiyuki Otsuka, MD⁎,
- Takayuki Mitsuhashi, MD⁎,
- Noriaki Iwahashi, MD⁎,
- Jun Okuda, MD⁎,
- Kengo Tsukahara, MD⁎,
- Masami Kosuge, MD⁎,
- Toshiaki Ebina, MD⁎,
- Satoshi Umemura, MD† and
- Kazuo Kimura, MD⁎
- ↵⁎Reprint requests and correspondence:
Dr. Kiyoshi Hibi, Division of Cardiology, Yokohama City University Medical Center, 4-57 Urafune-cho, Minami-ku, Yokohama 232-0024, Japan
Objectives The aim of this study was to assess whether ultrasound attenuation and plaque rupture as detected by intravascular ultrasound (IVUS) are associated with the incidence of no-reflow phenomenon after percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI).
Background No-reflow phenomenon is associated with worse long-term outcomes after STEMI. Therefore, reliable and feasible intravascular imaging techniques are needed to identify patient subgroups that would be at high risk for no-reflow phenomenon.
Methods One hundred seventy consecutive patients with STEMI who underwent PCI within 12 h after symptom onset were enrolled. The IVUS interrogation was performed before PCI.
Results No-reflow phenomenon occurred in 30 patients (18%), who had a higher incidence of no ST-segment resolution (50% vs. 9%; p < 0.001), a higher peak creatine kinase level (4,090 IU/l vs. 2,823 IU/l; p < 0.001), and a lower left ventricular ejection fraction in the chronic phase (51% vs. 59%; p < 0.01). Multivariate logistic regression analysis revealed that ultrasound attenuation with a longitudinal length of ≥5 mm, plaque rupture, and reperfusion time correlated with no-reflow phenomenon (all p < 0.05). In patients with both ultrasound attenuation ≥5 mm and plaque rupture, the incidence of no-reflow phenomenon was 88%, and the risk of decreased coronary reflow was higher than that predicted by either factor alone (p = 0.004 for interaction).
Conclusions In patients with STEMI, a longer ultrasound attenuation and plaque rupture on IVUS are associated with an increased incidence of no-reflow phenomenon, suggesting that this subset of patients might be at high risk for distal embolism.
Early and sustained restoration of adequate antegrade reflow in the infarct-related artery has been the primary objective of reperfusion therapy in patients with ST-segment elevation myocardial infarction (STEMI) (1). Percutaneous coronary intervention (PCI) has become an established reperfusion strategy for the treatment of STEMI, because of a higher recanalization rate and less residual stenosis as compared with thrombolysis (2). Nevertheless, microemboli of atherosclerotic plaque debris and thrombus can cause microvascular damage during balloon inflation or stent deployment (3), resulting in a no-reflow phenomenon, characterized by inadequate reflow at the microvascular level despite a reopened epicardial coronary artery (4). Recent studies have reported that angiographic no-reflow phenomena are associated with worse long-term outcomes after STEMI (5,6).
Recent reports suggested that atherosclerotic plaque with ultrasound attenuation might be related to the deterioration of coronary flow (7) and a larger infarct size as well as a higher incidence of fatal arrhythmias after PCI in patients with acute coronary syndrome (8). By contrast, we have previously reported that plaque rupture in the culprit lesion for anterior STEMI is associated with a larger infarct size than the absence of plaque rupture, suggesting that greater plaque embolism might occur after PCI in patients with plaque rupture (9). Therefore, we proposed that ultrasound attenuation and plaque rupture as detected by intravascular ultrasound (IVUS) before PCI might be useful characteristics for the prediction of no-reflow phenomenon after PCI in patients with STEMI. To test this hypothesis, we investigated the association between the morphologic characteristics of culprit lesions on IVUS and angiographic no-reflow phenomenon.
Patients with a first STEMI who underwent IVUS interrogation before PCI were eligible for enrollment. All patients were treated by stent deployment within 12 h after the onset of symptoms. We excluded patients with cardiogenic shock, those with concomitant severe diseases such as malignant disease, those who used any distal protection device or aspiration device, and those with culprit lesions in the left main trunk. We enrolled 170 consecutive patients with STEMI who met all inclusion criteria. A diagnosis of acute myocardial infarction required the presence of continuous chest symptoms for more than 30 min, ST-segment elevation of >0.1 mV in 2 limb leads or >0.2 mV in 2 contiguous precordial leads, and a rise in serum creatine kinase (CK) levels to more than twice the upper limit of normal.
The study protocol was approved by the ethics committee of Yokohama City University Medical Center. Written informed consent was obtained from all participants before initial coronary angiography.
All patients were given 200 mg of aspirin, an intravenous injection of 4,000 IU heparin, and 2 mg of isosorbide dinitrate immediately after diagnosis of STEMI. In the absence of contraindications cited in the American College of Cardiology/American Heart Association practice guidelines (10), facilitated PCI preceded by early treatment with a half-dose of fibrinolytics was performed before planned PCI. Glycoprotein IIb/IIIa inhibitors were not used because these drugs were not approved in Japan. In the catheterization laboratory, intravenous heparin was given to maintain an activated clotting time of ≥300 s during the procedure, and intracoronary isosorbide dinitrate (2 to 2.5 mg) was administered before angiography and after careful manipulation of the guidewire. Before any balloon inflation or stent implantation, a 40-MHz IVUS catheter (Boston Scientific, Boston, Massachusetts) was advanced distal to the culprit lesion, and IVUS examination was performed with an automated pullback speed of 0.5 mm/s. While pulling back the catheter, we manually infused contrast medium or normal saline suitable for IVUS imaging and carefully observed the lesion. This procedure enabled us to eliminate blood noise and to observe communication between the plaque and the coronary artery lumen.
After pre-interventional IVUS, PCI was performed with a conventional technique. Decision making related to the PCI strategy was left to the discretion of the individual PCI cardiologist.
Coronary angiography was performed with a frame rate of 15/s. Quantitative coronary angiography was performed with an automated edge detection system (MEDIS CMS, Leiden, the Netherlands). Thrombolysis In Myocardial Infarction (TIMI) flow grade was assessed as described previously (11). No-reflow phenomenon was defined as TIMI flow grade 0, 1, or 2 without mechanical obstruction on the angiogram immediately after stent deployment. Corrected Thrombolysis In Myocardial Infarction frame count (CTFC) was also measured immediately after stenting to objectively evaluate coronary reflow, as described by Gibson et al. (12). The number of frames was multiplied by 30 and divided by 15 to report a cine frame count in accordance with standard methods. In patients with TIMI flow grade 0 or 1 after PCI, a CTFC of 100 was used. Collateral flow was graded according to the Rentrop classification (13). Thrombus seen on angiogram was defined as TIMI thrombus grade ≥2 (14).
Electrocardiographic and cardiac enzyme analyses
A 12-lead electrocardiogram was recorded on admission and 1 h after the final angiogram, at a paper speed of 25 mm/s and an amplification of 10 mm/mV. The sum of ST-segment elevation in leads V1 to V6, I, and aVL for anterior infarctions and leads II, III, aVF, and V5 to V6 for nonanterior infarctions on electrocardiograms obtained 1 h after the final angiogram was compared with the value on admission. The ST-segment resolution was categorized as complete (>70%), partial (30% to 70%), or absent (<30%).
Blood samples were obtained on admission, at 3-h intervals during the first 24-h, and at 6-h intervals for the next 2 days after PCI. These samples were analyzed to derive peak CK levels.
We performed left ventriculography during the chronic phase after STEMI (mean 192 ± 31 days). Right anterior oblique views of left ventriculograms were used to measure the left ventricular (LV) ejection fraction. End-diastolic and end-systolic endocardial borders were hand-traced in the frames with maximal and minimal volumes, and end-diastolic and -systolic volumes were calculated by the area-length method.
The arc of backward signal attenuation without dense calcium was measured in degrees with a protractor centered on the lumen. Backward signal attenuation was then classified as 1-quadrant (<90°), 2-quadrant (90° to 179°), 3-quadrant (180° to 269°), or 4-quadrant (270° to 360°) attenuation. Plaque rupture was defined as reported previously (9,15): 1) plaque ulceration with a tear detected in a fibrous cap; or 2) lesions without plaque ulceration but in which the injection of saline or contrast medium confirmed communication between the plaque and the coronary artery lumen (Fig. 1). A lipid pool-like image was defined as a pooling of low-echoic material or echolucent material covered with a high-echoic layer (16). Calcium was brighter than the adventitia with an arc of >90° of acoustic shadowing. The location of calcium was defined as superficial (the leading edge of the acoustic shadowing appears within the shallowest 50% of the plaque plus media [P+M] thickness) or deep (the leading edge of the acoustic shadowing appears within the deepest 50% of the P+M thickness).
Quantitative analysis was performed according to the American College of Cardiology clinical expert consensus document on IVUS (15). External elastic membrane (EEM) cross-sectional area (CSA), P+M CSA, and lumen CSA at the reference and lesion sites were analyzed with planimetry software (TapeMeasure, Indec Systems, Capitola, California). If EEM circumference could not be identified because of attenuation, we interpolated the EEM area (7). Remodeling was positive when the lesion EEM CSA was greater than both the proximal and distal reference EEM CSA (17). The length (in millimeters) of ultrasound attenuation was measured from the number of seconds of videotape in which ultrasound attenuation was identified (millimeters = seconds of videotape × 0.5 mm/s). Total plaque volume was calculated as the sum of P+M CSA at 1-mm axial intervals for the IVUS images from a lesion segment of 20 mm, centered on the smallest pre-intervention lumen CSA.
Statistical analysis was performed with StatView version 5.0 software (SAS Institute, Cary, North Carolina). Results of continuous variables are reported as mean ± SD. Qualitative data are presented as n (%). Continuous variables were compared by means of Student t test, and categorical data were compared by the chi-square test or Fisher exact test. Intraobserver and interobserver agreements were measured by calculating Cohen's kappa value. A kappa value of 0.61 to 0.80 indicates good agreement, and a value of 0.81 to 1.0 indicates excellent agreement. Pearson's correlation analysis was performed to evaluate the relation between length of ultrasound attenuation and CTFC after PCI. To determine the optimal threshold of the length of ultrasound attenuation for the prediction of no-reflow phenomenon, receiver-operating characteristics curve analysis was applied. The cutoff point was defined as the greatest sum of the sensitivity and specificity estimates. Associations between the occurrence of no-reflow phenomenon and clinical variables were assessed by multivariate logistic regression analysis. Only significant variables on the univariate analysis were included in the multivariate analysis, except for EEM CSA at the lesion and reference sites, which were excluded because they strongly correlated with total plaque volume. An F test was used to test for the presence of interactions between IVUS morphological findings on CTFC after PCI. For all analyses, values of p < 0.05 were considered to indicate statistical significance.
Reproducibility of data
We assessed reproducibility of the angiographic and IVUS findings in a random sample of 30 patients. Coronary angiograms were reviewed separately by 2 independent observers blinded to the clinical and IVUS findings. Intraobserver variability was 0.16 ± 0.27 mm for reference vessel diameter and 2.4 ± 1.5 frames for CTFC. Interobserver variability was 0.19 ± 0.25 mm for reference vessel diameter and 2.1 ± 1.7 frames for CTFC. The kappa values for intraobserver and interobserver agreements of TIMI flow grade were 0.91 and 0.86, respectively. The diagnosis of morphological features on IVUS images required an independent review and agreement by 2 experienced observers who were blinded to the clinical and angiographic information. On assessment of intraobserver agreement, the kappa value was 0.93 for ultrasound attenuation and 0.87 for plaque rupture. On assessment of interobserver agreement, the kappa value was 0.92 for ultrasound attenuation and 0.86 for plaque rupture.
Patient characteristics and angiographic findings
No-reflow phenomenon immediately after stent deployment was observed in 30 of 170 patients (18%), including 14 patients in whom TIMI flow grade 3 was achieved after intracoronary administration of nicorandil and the use of intra-aortic balloon pumping. Patients were classified according to coronary reflow after PCI: 30 patients had TIMI flow grade 0, 1, or 2 (no-reflow group); and 140 patients had TIMI flow grade 3 (reflow group). Baseline clinical characteristics and angiographic findings are summarized in Table 1. There were no differences between the groups in age, sex, incidence of coronary risk factors, Killip class ≥2, facilitated PCI with fibrinolytics, or pre-infarction angina. Reperfusion time (4.0 ± 2.3 h vs. 3.1 ± 1.9 h; p = 0.02) was longer in the no-reflow group than in the reflow group. Angiographic findings and PCI procedural data were similar in the groups.
Comparison of ST-segment resolution after PCI, infarct size, and LV function in the chronic phase between no-reflow and reflow groups
The ST-segment resolution after PCI, peak CK levels, and left ventriculographic findings in the chronic phase were compared between the no-reflow and the reflow groups (Table 2). The ST-segment resolution was absent in 15 of the 30 patients (50%) in the no-reflow group and 13 of the 140 (9%) in the reflow group (p < 0.001). The peak CK level was higher (4,090 ± 2,354 IU/l vs. 2,823 ± 1,692 IU/l; p < 0.001), the LV ejection fraction at follow-up was lower (51 ± 13% vs. 59 ± 10%; p < 0.01), and the LV end-systolic volume index at follow-up was greater (38 ± 23 ml/m2 vs. 27 ± 12 ml/m2; p < 0.01) in the no-reflow group than in the reflow group.
The incidence of no-reflow phenomenon and the arc of backward signal attenuation on IVUS
The incidences of no-reflow phenomenon in patients with 1-, 2-, 3-, and 4-quadrant attenuation were 10%, 10%, 33%, and 33%, respectively. The incidence of no-reflow phenomenon was significantly higher in the patients with 3- and 4-quadrant attenuation than in the other groups but was similar in patients with 1-quadrant attenuation and those with 2-quadrant attenuation. Therefore, ultrasound attenuation was defined as IVUS images with backward signal attenuation of ≥180° behind plaque without dense calcium (Table 3,Fig. 2).
Pre-intervention IVUS findings
The morphological and quantitative IVUS findings are summarized in Table 3. Culprit lesions in the no-reflow group had significantly higher prevalence of plaque rupture (87% vs. 51%, p < 0.001) and ultrasound attenuation (≥180° backward signal attenuation) (63% vs. 27%, p < 0.001) compared with those in the reflow group. The incidence of lipid pool-like image and calcium was similar in the groups. The EEM CSA at the proximal reference site (17.7 ± 4.8 mm2 vs. 15.0 ± 4.3 mm2; p < 0.01) and EEM CSA at the lesion site (17.4 ± 4.6 mm2 vs. 14.6 ± 3.9 mm2; p < 0.001) were larger, and total plaque volume (200 ± 59 mm3 vs. 167 ± 51 mm3; p < 0.01) was greater in the no-reflow group than in the reflow group.
IVUS measurements of atherosclerotic plaque with ultrasound attenuation
Among the 170 patients, 57 (34%) had ultrasound attenuation in their culprit lesions. Atherosclerotic plaque with ultrasound attenuation had a larger EEM CSA at the lesion site (15.9 ± 4.3 mm2 vs. 14.7 ± 4.1 mm2; p = 0.07), a smaller lumen CSA (2.1 ± 0.6 mm2 vs. 2.5 ± 1.0 mm2; p < 0.01), a greater total plaque volume (187 ± 54 mm3 vs. 166 ± 53 mm3; p = 0.02), and a higher remodeling index (1.13 ± 0.24 vs. 1.04 ± 0.22; p = 0.01) than atherosclerotic plaque without ultrasound attenuation. The incidence of angiographic thrombus, plaque rupture, and lipid pool-like images was similar in patients with and those without ultrasound attenuation (data not shown).
Impact of ultrasound attenuation on the incidence of no-reflow phenomenon
Patients with ultrasound attenuation had a higher incidence of no-reflow phenomenon than those without ultrasound attenuation (33% vs. 10%; p < 0.001). Among the 57 patients with ultrasound attenuation, the length of ultrasound attenuation strongly correlated with CTFC after PCI (r = 0.61, p < 0.0001) (Fig. 3). The receiver-operating characteristics curve showed that 5 mm was the optimal threshold of the length of ultrasound attenuation to predict no-reflow phenomenon. The use of this value yielded a sensitivity of 79% and a specificity of 84% (Fig. 4). According to this threshold, we divided the patients with ultrasound attenuation into 2 groups: those with ultrasound attenuation ≥5 mm (n = 21) and those with ultrasound attenuation <5 mm (n = 36). The incidence of no-reflow phenomenon was higher in patients with ultrasound attenuation ≥5 mm than in those either with ultrasound attenuation <5 mm (71% vs. 11%; p < 0.001) or without ultrasound attenuation (71% vs. 10%; p < 0.001). The incidence of no-reflow phenomenon was similar in patients with ultrasound attenuation <5 mm and in those without ultrasound attenuation.
Determinants of no-reflow phenomenon
Independent predictors related to the occurrence of no-reflow phenomenon were determined by multiple logistic regression analysis, in which ultrasound attenuation with a longitudinal length of ≥5 mm, plaque rupture, total plaque volume, and reperfusion time were entered. Multivariate analysis confirmed ultrasound attenuation with a longitudinal length of ≥5 mm (odds ratio [OR]: 20.1, 95% confidence interval [CI]: 5.87 to 69.0; p < 0.001), plaque rupture (OR: 5.94, 95% CI: 1.64 to 21.5; p < 0.01), and reperfusion time (per hour) (OR: 1.26, 95% CI: 1.00 to 1.58; p = 0.047) as independent predictors of no-reflow phenomenon.
We analyzed the data by stratifying patients according to age, reperfusion time, infarct-related artery, TIMI flow grade at initial angiography, thrombus seen on angiogram, reference vessel diameter, high-pressure stenting, and facilitated PCI with fibrinolytics (Table 4). In all subgroups, the frequencies of no-reflow phenomenon were still significantly higher in patients with ultrasound attenuation ≥5 mm than in those with ultrasound attenuation <5 mm or without ultrasound attenuation.
Effect of interaction between ultrasound attenuation and plaque rupture on coronary reflow after PCI
Potential interactions between ultrasound attenuation ≥5 mm and plaque rupture were assessed with respect to their effect on coronary reflow after PCI. There was a statistically significant interaction between ultrasound attenuation ≥5 mm and plaque rupture as related to CTFC after PCI (p = 0.004 for interaction). Thus, patients with both ultrasound attenuation ≥5 mm and plaque rupture had higher CTFC after PCI (66.1 ± 29.4) than that expected from the sum of the individual effects of these factors. In this subset of 16 patients, the frequency of no-reflow phenomenon was 88%, which was higher than that of any other subset of patients (Fig. 5).
The principal finding of the present IVUS study was that longer ultrasound attenuation without dense calcification and plaque rupture at culprit lesions were strongly associated with no-reflow phenomenon in patients with STEMI. In addition, a significant interaction was observed between longer ultrasound attenuation and plaque rupture, which was associated with diminished coronary reflow as assessed by CTFC after PCI, suggesting that lesions with both longer ultrasound attenuation and plaque rupture had the highest risk of no-reflow phenomenon.
Previous studies have shown that abnormalities at the level of the microvasculature cause no-reflow phenomenon (18,19). Various factors have been proposed as determinants of microvascular damage, including the generation of oxygen free radicals, tissue edema, endothelial dysfunction, neutrophil plugging of microvessels, vasoconstriction, and distal embolism (20). Regardless of the underlying causes, no-reflow phenomenon is related to long-term mortality in patients with STEMI (5,6). In the present study, no-reflow phenomenon was associated with the absence of ST-segment resolution after PCI, larger infarct size, and lower LV ejection fraction in the chronic phase, consistent with the results of previous studies (5,6,16).
No-reflow phenomenon is a process that starts during the ischemic period and then increases during reperfusion. Prolonged ischemia and delayed reperfusion can cause changes in endothelial cells and lead to extensive microvascular dysfunction (21). In the present study, reperfusion time was an independent predictor of no-reflow phenomenon. Reperfusion-related injury can also disrupt the coronary microcirculation, resulting in expansion of the no-reflow phenomenon. In addition, distal atherothrombotic embolization contributes to microvascular injury to some extent, particularly during PCI. In the present study, 7 patients with no-reflow phenomenon had normal coronary flow (TIMI flow grade 3) at baseline that deteriorated immediately after stent deployment. In these patients, distal embolism during PCI probably increased microvascular damage, subsequently leading to diminished coronary flow after PCI. In patients with STEMI, a high atherothrombotic burden and a decrease in plaque volume as assessed by IVUS during PCI have a negative impact on coronary reflow after PCI (22,23). Recent IVUS studies showed that atherosclerotic plaque with ultrasound attenuation might be related to the deterioration of coronary flow in patients with acute coronary syndrome (7,8). These studies suggested that 1 of the mechanisms of no-reflow phenomenon was microvascular dysfunction resulting from distal embolism of plaque contents induced by PCI.
Recently, several studies have investigated the pathology of ultrasound attenuation without dense calcification in coronary plaque. In a study of autopsy specimens of human coronary arteries, Hara et al. (24) showed that ultrasound attenuation was associated with fibrofatty tissue containing scattered cholesterol clefts and Von Kossa-positive granules corresponding to microcalcification, which caused ultrasound wave reflection and dispersion. Histopathological examination of coronary plaque obtained by directional atherectomy demonstrated that hyalinized fibrous plaque and expansive remodeling were related to images with backward ultrasound attenuation (25). Another histological study of human cadaveric coronary arteries revealed that fibrofatty plaque and a necrotic core were more frequently found in attenuated plaque (26). In addition, Johnstone et al. (27) reported that white thrombi produced by blood from rabbits might cause backscattered energy attenuation, suggesting that thrombus has a role in ultrasound attenuation. In the present study, we demonstrated that vessel size and plaque thickness were related to the formation of ultrasound attenuation. Taken together, available evidence suggests that tissue characteristics, including cholesterol clefts and microcalcification, and white thrombus as well as plaque burden play important roles in producing ultrasound attenuation in the setting of STEMI.
We previously reported that plaque rupture was related to larger infarcts, a higher incidence of no-reflow phenomenon, and long-term decreased LV function in patients with anterior STEMI (9). In the current study, we demonstrated that the frequency of no-reflow phenomenon in patients with both ultrasound attenuation ≥5 mm and plaque rupture was 88%. With angioscopy, Mizote et al. (3) showed that microcirculatory damage after PCI was more frequent among patients with ruptured plaque than among those without ruptured plaque. It is plausible that components of atherosclerotic plaque with ultrasound attenuation are easily released into the coronary circulation during PCI through the “rupture hole” in patients with plaque rupture.
Conventional 40-MHz gray-scale IVUS has been used throughout the world as an intravascular imaging technique during PCI. Therefore, prediction of no-reflow phenomenon with 40-MHz gray-scale IVUS might have a substantial impact on decision making in the catheterization laboratory. Although several trials have been conducted with a variety of embolic protection devices, conflicting results have cast doubt on whether the routine use of embolic protection devices is warranted (28). Therefore, the selective use of embolic protection devices for the patients at high risk for distal embolization during PCI might be an attractive option.
The findings of the present study have to be interpreted in the context of the following limitations. First, this was a retrospective observational analysis from a single center. Further prospective studies are warranted to investigate the interaction between IVUS parameters and coronary flow to elucidate the mechanisms of no-reflow phenomenon. Second, because IVUS findings were obtained with a 40-MHz IVUS transducer, our results must be interpreted with caution, especially when extrapolating our findings to other IVUS systems. Third, the true incidence of plaque rupture might have been underestimated, because thrombi overlying plaque-rupture sites obscure fissures, dissections, or communications between the plaque and the coronary artery lumen on pre-interventional IVUS. Nevertheless, our results would be strengthened further if ruptured plaque with increased thrombus burden was misinterpreted to be nonruptured plaque. Fourth, because we included patients with STEMI who were treated by PCI within 12 h after symptom onset, our findings are not applicable to patients with STEMI treated more than 12 h after symptom onset or to patients with angina pectoris. Fifth, Doppler measurements of coronary flow velocity patterns and coronary flow reserve might be more useful for the assessment of coronary reflow and microvascular function than TIMI flow grade and CTFC (29). Sixth, the use of fibrinolytics might have affected our results. Although the subgroup analysis demonstrated that the frequencies of no-reflow phenomenon in the presence of long ultrasound attenuation were significantly higher than those in the absence of long ultrasound attenuation, irrespective of the use of fibrinolytics, our observations need to be confirmed in patients who receive primary PCI alone. Seventh, glycoprotein IIb/IIIa inhibitors were not approved in Japan at the time of this study, excluding potential effects of these drugs on the incidence of no-reflow phenomenon. Finally, multivariate modeling with a relatively small number of events is subject to overfitting, although an attempt was made to limit the number of variables entered for adjustment. Thus, our results should be considered hypothesis-generating.
In the setting of STEMI, the presence of longer ultrasound attenuation and plaque rupture as assessed by pre-interventional IVUS is associated with a higher incidence of no-reflow phenomenon after PCI. Further studies are required to clarify whether pharmacologic or mechanical intervention can reduce no-reflow phenomenon in this subset of patients at high risk.
- Abbreviations and Acronyms
- confidence interval
- creatine kinase
- cross-sectional area
- corrected Thrombolysis In Myocardial Infarction frame count
- external elastic membrane
- intravascular ultrasound
- left ventricular
- odds ratio
- percutaneous coronary intervention
- plaque plus media
- ST-segment elevation myocardial infarction
- Thrombolysis In Myocardial Infarction
- Received September 22, 2009.
- Revision received December 22, 2009.
- Accepted January 8, 2010.
- American College of Cardiology Foundation
- The Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO IIb) Angioplasty Substudy Investigators
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