CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY
The Relationship Between Coronary Plaque Characteristics and Small Embolic Particles During Coronary Stent Implantation
Takahiro Kawamoto, MD, PhD*,*,
Hiroyuki Okura, MD, PhD*,
Yuji Koyama, MD, PhD*,
Iku Toda, MD, PhD ,
Haruyuki Taguchi, MD, PhD,
Koichi Tamita, MD ,
Atsushi Yamamuro, MD,
Yuki Yoshimura, MD*,
Yoji Neishi, MD, PhD*,
Eiji Toyota, MD, PhD* and
Kiyoshi Yoshida, MD, PhD, FACC*
* Division of Cardiology, Kawasaki Medical School Hospital, Kurashiki, Japan
Division of Cardiology, Bell Land General Hospital, Sakai, Japan
Division of Cardiology, Kobe General Hospital, Kobe, Japan.
Manuscript received February 21, 2007;
revised manuscript received May 16, 2007,
accepted May 21, 2007.
* Reprint requests and correspondence: Dr. Hiroyuki Okura, The Division of Cardiology, Kawasaki Medical School Hospital, 577, Matsushima, Kurashiki, Japan. (Email: hokura{at}fides.dti.ne.jp).
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Abstract
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Objectives: We investigated the relationship between coronary plaque components and small embolic particles during stenting and examined the influence on the coronary microcirculation.
Background: In vivo tissue characterization of atherosclerotic plaques was introduced by the Virtual Histology intravascular ultrasound (VH-IVUS) system (Volcano Therapeutics, Inc., Rancho Cordova, California).
Methods: The study consisted of 44 patients who underwent elective coronary stenting. Plaque characteristics were identified with VH-IVUS, and small embolic particles liberated during stenting were detected as high-intensity transient signals (HITS) with a Doppler guidewire. Coronary flow velocity reserve (CFVR) was also measured before and after stenting.
Results: Patients were divided into the tertiles according to the HITS counts: the lowest, HITS <5 (n = 16); the middle, 5 to 12 (n = 15); and the highest, >12 (n = 13). Dense calcium and necrotic core area identified with VH-IVUS were significantly larger in the highest tertile (lowest vs. middle vs. highest; dense calcium: 0.2 ± 0.3 mm2 vs. 0.3 ± 0.6 mm2 vs. 0.8 ± 0.7 mm2, p = 0.007; necrotic core: 0.5 ± 0.4 mm2 vs. 0.9 ± 0.9 mm2 vs. 1.8 ± 1.0 mm2, p < 0.001, respectively). Multivariate logistic regression analysis revealed only necrotic core area was an independent predictor of high HITS counts (odds ratio 4.41, p = 0.045). Furthermore, there was a significant negative correlation between the HITS count and CFVR after stenting (r = –0.35, p = 0.017).
Conclusions: The necrotic core component identified with VH-IVUS is related to liberation of small embolic particles during coronary stenting, which results in the poorer recovery of CFVR.
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Abbreviations and Acronyms
| | AMI = acute myocardial infarction | | CFVR = coronary flow velocity reserve | | CSA = cross-sectional area | | EEM = external elastic membrane | | HITS = high-intensity transient signals | | IVUS = intravascular ultrasound | | P+M = plaque plus media | | PCI = percutaneous coronary intervention | | VH = Virtual Histology |
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Percutaneous coronary intervention (PCI) causes the mechanical injury and fragmentation of plaque composition, which might lead to the distal embolization of plaque debris or thrombus material. It has already been reported that using distal protection devices, such as an occlusion balloon or a filter device, results in a substantial amount of embolic materials being detected during coronary intervention (1,2). Although liberation of these small embolic particles cannot be visualized angiographically unless a large burden of emboli obstructs a distal coronary artery or results in slow flow and/or no flow because of microvascular dysfunction, these particles could cause some amount of myocardial damage during PCI (3). Indeed, several recent studies have shown that biochemical markers of myocardial injury rise significantly in a substantial proportion of patients undergoing PCI, despite the absence of technical failure, such as prolonged ballooning at the lesion, reduction of flow by a large dissection of the target vessel, or side branch occlusion (4,5). Therefore, distal microembolization has been considered as the most likely cause of myocardial injury, recognized as increase of the cardiac enzyme in cases of angiographically successful coronary interventions (3). Recently, it was reported that these small embolic particles during PCI could be detected with a Doppler guidewire as high-intensity transient signals (HITS) (6,7). However, the specific characteristics of high-risk plaques that tend to release emboli are unknown.
Conventional gray scale intravascular ultrasound (IVUS) is a useful method for characterizing the morphology of atherosclerotic plaques in vivo (8). Recently, in vivo identification of the histopathological characteristics of plaques has been made possible by spectral analysis of radiofrequency ultrasound backscatter signals (9) present in IVUS data. This technology, which is commercially available and named Virtual Histology (VH), offers an opportunity to assess plaque morphological and histopathological characteristics simultaneously in vivo. With this VH-IVUS system (Volcano Therapeutics, Inc., Rancho Cordova, California), 4 different plaque components (fibrous, fibrofatty, dense calcium, and necrotic core) can be identified with approximately 80% to 92% in vitro accuracy (9) and approximately 87.1% to 96.5% in vivo accuracy (10).
The aims of this study were: 1) to identify with VH-IVUS the plaque characteristics that possess a high risk for distal embolization during PCI, and 2) to investigate the influence of small embolic particles on coronary microcirculation.
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Methods
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Study population.
Fifty-one consecutive patients (44 men, 7 women, age 71 ± 8 years) with angina pectoris who were admitted for coronary stenting from November 2005 until January 2007 were included in this study. Patients with cardiogenic shock or unstable hemodynamic status, previous myocardial infarction of the target vessel, previous coronary bypass surgery, restenotic lesion, chronic total occlusion, unsuitable coronary artery anatomy for IVUS examination and/or Doppler velocimetry, angiographically apparent coronary thrombus, severe valvular disease, and atrial fibrillation were excluded. This study was in compliance with the Declaration of Helsinki with regard to investigations in humans, and the study protocol was approved by the Ethics Committee of Kawasaki Medical School Hospital. Written informed consent was obtained from all patients before cardiac catheterization.
Coronary flow velocimetry and IVUS examination.
After intravenous administration of 5,000 U of heparin, diagnostic coronary angiography was performed via the femoral or radial artery with the Judkins technique. Before PCI, an additional 2,000 U of heparin was administered and a 0.014-inch Doppler guide wire (FloWire, Volcano Therapeutics) was advanced beyond the stenosis. Doppler velocimetry was performed at rest and during hyperemia induced by an intravenous injection of 0.15 mg/kg/min adenosine 5’-triphosphate, and coronary flow velocity reserve (CFVR), which was defined as hyperemic averaged peak velocity divided by resting averaged peak velocity, was obtained. The IVUS images were acquired with a commercially available IVUS console (IVUS3 system, Volcano Therapeutics) and 2.9-F, 20-MHz, phased-array IVUS catheters (Eagle Eye Gold, Volcano Therapeutics). The IVUS examination was performed before intervention with the console’s automated pullback system (0.5 mm/s). During stent implantation, a waveform of coronary flow velocity signal was monitored continuously and recorded on an S-VHS videotape to detect HITS from the start of balloon inflation to 30 s after balloon deflation. More than 10 min after the completion of PCI, CFVR measurement was repeated.
VH-IVUS analysis.
Serial IVUS images were digitized and stored in the hard disk of the IVUS console. Morphometric parameters of external elastic membrane (EEM) cross-sectional area (CSA) and lumen CSA were measured as previously reported (11–13). 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 x 100 (8,13).
In each lesion, an IVUS cross sectional image containing the smallest lumen CSA (= target lesion) was selected for analysis. If the lumen CSA was found to be the same in several cross sectional images, the image with the largest plaque burden was selected.
After tracing of the EEM and lumen CSA, each plaque segment was classified following 4 types of characteristics (fibrous, fibrofatty, dense calcium, and necrotic core) according to the radiofrequency signal processing of VH-IVUS technology (9). They were color-coded and displayed on the IVUS console: fibrous as green, fibrofatty as light green, dense calcium as white, and necrotic core as red.
HITS analysis.
The HITS were determined by the following definitions (7): 1) visual high-intensity signals, and 2) unidirectional signals within the advancing velocity spectrum apart from baseline. We analyzed the coronary blood flow velocity spectrum recorded on an S-VHS videotape, and the occurrences of HITS were counted for 30 s after balloon deflation for stent implantation.
Statistics.
All data are expressed as the mean value ± SD. All statistical analyses were done with StatView (SAS Institute, Cary, North Carolina). Continuous variables were compared among tertiles by use of 1-way analysis of variance and confirmed by the Fisher protected least significant difference test as post hoc comparisons. Categorical variables were compared by use of the chi-square test. Linear regression analysis was applied to investigate the relationship between each parameter that displayed significant difference among tertiles. The correlations were verified by nonparametric analysis of the Spearman rank correlation test. Multivariate logistic regression analysis was conducted to identify independent predictors for high HITS counts. The model included the parameters that correlated significantly in the univariate analysis. A p value <0.05 was considered to be significant.
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Results
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A Doppler guidewire was positioned beyond the target lesions in all 51 enrolled cases, but IVUS catheter could not be advanced beyond the stenosis in 2 cases, and coronary waveform after the balloon deflation was not clear enough for HITS analysis in 5 cases. Finally, 44 cases (37 men, 7 women, age 71 ± 8 years) were included in the analysis. During PCI, angiographic slow flow and/or no flow were not observed and coronary stenting were successfully completed in all cases.
The number of detected HITS was 9.3 ± 7.8 (range 0 to 28). We divided the study patients into tertiles according to HITS count as follows: HITS number <5 for the lowest tertile (n = 16), 5 to 12 for the middle tertile (n = 15), and higher than 12 for the highest tertile (n = 13). There was no statistically significant difference in the baseline patient characteristics (Table 1). Morphometric IVUS parameters and plaque characteristics by VH-IVUS are shown in Table 2. The EEM CSA and P+M CSA were larger in the middle and the highest tertiles. Although fibrous area did not differ significantly among the tertiles, fibrofatty area tended to be higher in the middle tertile but not significantly, and dense calcium and necrotic core area were significantly larger in the highest tertile.
The linear regression analysis revealed that there were weak but significant correlations between the HITS count and EEM CSA (r = 0.30, p = 0.04) (Fig. 1), P+M CSA (r = 0.29, p = 0.05) (Fig. 1), dense calcium area (r = 0.44, p < 0.01) (Fig. 2), and necrotic core area (r = 0.53, p < 0.001) (Fig. 2). The correlations were also confirmed by nonparametric analysis of the Spearman rank correlation test (p = 0.01 for EEM CSA, p = 0.02 for P+M CSA, p < 0.01 for dense calcium area, and p < 0.01 for necrotic core area). Multivariate logistic regression analysis to identify independent predictors of the highest HITS count tertile was conducted, including these 4 parameters: EEM CSA, P+M CSA, dense calcium area, and necrotic core area. Among these parameters, only necrotic core area was found to be an independent predictor (Table 3).
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Figure 1 The Correlation Between HITS Number and IVUS Parameters
Scatterplots demonstrating significant correlation between the number of high-intensity transient signals (HITS) and external elastic membrane (EEM) cross-sectional area (CSA) or plaque plus media (P+M) CSA. IVUS = intravascular ultrasound.
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Figure 2 The Correlation Between HITS Number and VH Parameters
Scatterplots demonstrating significant correlation between the number of high-intensity transient signals (HITS) and dense calcium (DC) or necrotic core (NC) area. VH = Virtual Histology.
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As for CFVR data, although there was no significant difference in baseline CFVR among the tertiles, CFVR after PCI was significantly higher in the lowest tertile (Table 4). Furthermore, linear regression analysis revealed that there was a weak but significant negative correlation between the HITS count and CFVR after PCI (r = –0.32, p = 0.03).
Figure 3
shows VH-IVUS color-coded images and coronary waveforms immediately after balloon deflation from 2 representative cases.
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Figure 3 Representative Cases
Representative cases with images of gray scale IVUS, color-coded Virtual Histology IVUS, and coronary blood flow spectrum. Many HITS were detected in the lower case but not in the upper case. DC = dense calcium (white); FF = fibrofatty (light green); FI = fibrous (green); NC = necrotic core (red); other abbreviations as in Figure 1.
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Discussion
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The results of the present study demonstrated that: 1) small embolic particles, which could not be detected angiographically, were liberated and were documented as HITS during stenting; 2) the HITS count, representing the amount of emboli, was related to baseline plaque morphology and composition, such as EEM CSA, P+M CSA, dense calcium area, and necrotic core area as identified by VH-IVUS; and 3) the number of HITS was related to restricted CFVR after PCI. This is the first report to clarify the relationship between plaque components and small embolic particles and to further examine the influence of these embolic particles on coronary microcirculation.
Several IVUS studies have shown that plaque burden was related to the subsequent creatine kinase-MB isoenzyme elevation after PCI (4,5,14–16). In addition to the impact of plaque burden, specific plaque characteristics, such as lipid pool-like image, intracoronary mural thrombus, or ultrasonic attenuation, that were assessed by gray scale IVUS, have been shown to be related to no reflow phenomenon during PCI in patients with acute coronary syndrome (17–20). These reports indicated that small embolic particles were possibly liberated from such plaques and subsequently induced myocardial damage. In another study, it was reported that lesion-associated coronary artery calcium increased with extent and severity of atherosclerosis and correlated with volume of the atherosclerotic plaque (21). However, the relationship between specific plaque components and the liberation of emboli has not been fully investigated and discussed. In the present study, we clearly showed the necrotic core component of the plaque as assessed by VH-IVUS was independently related to the liberation of embolic particles during coronary stenting, suggesting that not only the total amount of the plaque but also its components should be considered and that a necrotic core component should be especially recognized as a possible precursor of distal embolization during PCI procedures. The necrotic core component contains fragile tissues, such as lipid deposition with foam cells, intramural bleeding, and/or cholesterol crystals, and these tissues are often separated from the vessel lumen by only a thin fibrous cap, so they are thought to be easily liberated as small emboli during coronary stenting.
A previous publication has shown that patients with acute coronary syndrome have larger necrotic core area according to VH analysis (10), but we did not find a difference in any plaque components between the patients with unstable angina and stable angina in the present study (data not shown). This discrepancy could be because we excluded patients with acute myocardial infarction (AMI) and angiographically apparent coronary thrombus, who should possess large necrotic lesions.
Coronary flow velocity spectrum after reperfusion, as assessed by Doppler guidewire, has been shown to predict prognosis and functional recovery in patients with AMI (22–24). In addition, previous reports have shown that a low postprocedural CFVR was associated with a poorer outcome, such as acute thrombosis, repeat myocardial infarction, target vessel revascularization, and restenosis (25–28). Such restricted postprocedural CFVR could be explained by the influence of small emboli that could not be detected angiographically. Here we showed the relationship between HITS counts and restricted CFVR after stenting, and this result indicates that micro-embolic particles during PCI could damage coronary microcirculation even without angiographically evident slow flow and/or no flow. The randomized multicenter EMERALD (Enhanced Myocardial Efficacy and Removal by Aspiration of Liberalized Debris) trial failed to show the usefulness of distal protection devices in patients with AMI (29). Although our present study did not include AMI patients, it might be possible that these embolic particles only induce subclinical myocardial damage. But we believe selective use of distal protection devices on the basis of VH-IVUS findings will prevent rare but critical microvascular injury during PCI.
Clinical implications.
By using VH-IVUS, high-risk plaque, which tends to release micro-emboli, was identified before PCI. With the assistance of VH-IVUS findings, the operators can be more aware of the possibilities of distal embolization after stenting, allowing them to prevent slow flow or no flow by using a distal protection device and therefore preserve coronary microcirculation function. We clearly showed that these small embolic particles damage coronary microcirculation immediately after stenting, but the long-term influence has not been elucidated. Further investigation is needed to clarify whether the restricted CFVR will affect long-term clinical outcomes, such as mortality, left ventricular function, AMI, and congestive heart failure and whether the restricted CFVR will recover or not.
Study limitations.
First, VH-IVUS does not identify thrombus because of a lack of histological validation. A substantial degree of thrombus should take part in the plaque components in patients with AMI. As already discussed, thrombus has been reported as another important predictor of distal embolization during PCI in patients with AMI. Therefore, patients with AMI who have a higher chance of intracoronary or mural thrombus were not included in this study. Those who had shown angiographically apparent lesion-associated coronary thrombus were also excluded from this study. However, a small amount of mural thrombus might influence the results of this study. In the future, we believe new technology will make it possible to distinguish thrombus from other components of coronary plaque and to assess the relationship between thrombus and small embolic particles.
Second, although HITS is a useful and sensitive method to detect small embolic particles, it does not reveal the true amount of emboli.
Third, although CFVR immediately after PCI was restricted in patients with high HITS counts, its clinical implication in our study population is uncertain. Long-term clinical follow-up is necessary to clarify the impact of small embolic particle and restricted CFVR on cardiac function and prognosis.
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Conclusions
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Liberation of small embolic particles during coronary intervention was related to not only the baseline plaque morphology but also plaque components, especially the necrotic core component as identified by VH-IVUS. Furthermore, liberation of those embolic particles, which were not recognized angiographically, resulted in poorer recovery of CFVR even after successful restoration of epicardial coronary artery stenosis.
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Abstract
Methods