CLINICAL RESEARCH: ACUTE MYOCARDIAL INFARCTION
Impact of Plaque Rupture on Infarct Size in ST-Segment Elevation Anterior Acute Myocardial Infarction
Ikuyoshi Kusama, MD*,
Kiyoshi Hibi, MD*,*,
Masami Kosuge, MD*,
Naoki Nozawa, MD*,
Hiroyuki Ozaki, MD*,
Hideto Yano, MD*,
Shinnichi Sumita, MD*,
Kengo Tsukahara, MD*,
Jun Okuda, MD*,
Toshiaki Ebina, MD*,
Satoshi Umemura, MD and
Kazuo Kimura, MD*
* Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan
Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Manuscript received February 2, 2007;
revised manuscript received June 6, 2007,
accepted July 3, 2007.
* 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. (Email: hibikiyo{at}urahp.yokohama-cu.ac.jp).
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Abstract
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Objectives: We sought to assess whether coronary plaque rupture at culprit lesions is associated with infarct size in patients with anterior acute myocardial infarction (AMI).
Background: Some patients with AMI have large infarcts despite early reperfusion. Whether culprit plaque morphology impacts infarct size or not remains unknown.
Methods: Patients who had a first anterior AMI with reperfusion within 6 hours after onset were enrolled and divided into 2 groups according to the presence or absence of plaque rupture at the culprit lesion as defined by preintervention intravascular ultrasound (IVUS): patients with rupture (n = 54) and without rupture (n = 37).
Results: Patients with plaque rupture had a higher incidence of no-reflow phenomenon (15% vs. 3%; p = 0.08) and a lower myocardial blush grade (1.5 vs. 2.3; p < 0.05) after percutaneous coronary intervention. The IVUS analysis showed that patients with plaque rupture had a higher incidence of soft plaque and positive remodeling. Peak creatine kinase levels were higher (4,707 vs. 2,309 IU/l; p < 0.0001) and left ventricular ejection fraction in the chronic phase was lower (54% vs. 63%; p < 0.01) in patients with plaque rupture. A multivariate logistic regression analysis revealed that plaque rupture and the proximal lesion site correlated with a left ventricular ejection fraction of <50% in the chronic phase (odds ratios 6.5 and 17.5, respectively; p < 0.05).
Conclusions: Plaque rupture is associated with morphologic characteristics of vulnerable lesions, as well as with larger infarcts and a higher incidence of no-reflow phenomenon, suggesting that plaque embolism contributes to the progression of myocardial damage in patients with anterior AMI.
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Abbreviations and Acronyms
| | AMI = acute myocardial infarction | | AUC = area under the curve | | CK = creatine kinase | | ECG = electrocardiography | | IVUS = intravascular ultrasound | | PCI = percutaneous coronary intervention |
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A number of studies have suggested that plaque rupture with subsequent thrombus formation is the most frequent cause of acute coronary syndromes (1,2). Infarct size in acute myocardial infarction (AMI) is associated with prodromal angina, the duration of coronary occlusion, and collateral flow (3–5). Recent studies have indicated that stent thrombosis causes large myocardial infarctions with a significant decline in left ventricular function, despite immediate reperfusion therapy by emergency percutaneous coronary intervention (PCI) (6). These findings suggest that abrupt coronary occlusion, distal embolism, or both may promote myocardial damage. Similarly, some patients with AMI have large infarcts despite early reperfusion. The relationships among disrupted plaque morphology, infarct size, and clinical presentation remain poorly understood. To determine predictors of infarct size, we investigated the association between infarct size and the morphologic characteristics of culprit lesions by intravascular ultrasound (IVUS).
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Methods
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Study patients.
Patients with a first ST-segment elevation anterior AMI were enrolled. All patients received coronary reperfusion within 6 h after the onset of symptoms, and infarct-related arteries were confirmed by IVUS before any PCI. Patients with malignant disease, infectious disease, or inflammatory diseases, such as collagen disease, were excluded to avoid bias. We also excluded patients with cardiogenic shock, because we performed reperfusion procedures as soon as possible, without preintervention IVUS. We enrolled 91 consecutive patients who met these entry criteria. Acute myocardial infarction was defined as the presence of continuous chest symptoms for more than 30 min, accompanied by ST-segment elevation of >0.2 mV on at least 2 contiguous electrocardiographic (ECG) leads and by a rise in serum creatine kinase (CK) levels to more than twice the upper limit of normal. The protocol for the study was approved by the ethics committee of the Yokohama City University Medical Center. We obtained written informed consent from all participants before initial coronary angiography.
Study protocol.
On admission, all patients received 200 mg aspirin, an intravenous bolus injection of 5,000 IU heparin, and isosorbide dinitrate. In the absence of contraindications according to American College of Cardiology/American Heart Association practice guidelines (7), most patients (84%) received intravenous thrombolytic therapy. In the catheterization laboratory, coronary angiography was performed via the femoral approach. Periprocedural intravenous heparin was given to maintain an activated clotting time  250 s. Intracoronary isosorbide dinitrate (2.0 to 2.5 mg) was administered before angiography to prevent coronary artery spasm. After careful manipulation of the guidewire and additional intracoronary isosorbide dinitrate (2.0 to 2.5 mg), the IVUS catheter was advanced distal to the culprit lesion. After examination by IVUS, thrombus aspiration was performed in patients with obvious thrombus formation on angiography, IVUS, or both.
All IVUS studies were performed with a commercially available system (Scimed; Boston Scientific, Boston, Massachusetts) before any balloon inflation or stent implantation. A 40-MHz IVUS catheter was advanced distal to the culprit lesion, and imaging was performed in a retrograde fashion to the aorto-ostial junction at an automatic pullback speed of 0.5 mm/s, facilitating observation of the lesion. While pulling back the catheter, we manually infused contrast medium or normal saline suitable for IVUS imaging while carefully observing the lesion. This procedure enabled us to eliminate blood noise and to observe communication between the plaque and the coronary artery lumen. The IVUS images were recorded on S-VHS videotape for off-line analysis.
Cardiac enzyme measurements.
Blood samples were obtained on admission, at 3-h intervals during the first 24 h, at 6-h intervals for the next 2 days, and then daily until discharge. Peak levels of CK and CK-MB and the areas under the curves (AUCs) for CK and CK-MB as calculated by the linear-trapezoidal method (8) were derived.
Electrocardiographic analysis.
A 12-lead ECG was recorded on admission at a paper speed of 25 mm/s and an amplification of 10 mm/mV.
Angiographic analysis.
Coronary angiograms were reviewed separately by 2 independent observers who were unaware of the IVUS findings. Coronary artery segments were identified and categorized according to the reporting system of the American Heart Association. Perfusion degree was evaluated according to the TIMI (Thrombolysis In Myocardial Infarction) criteria (9). No reflow after reperfusion was defined as postprocedural TIMI flow grade 0, 1, or 2 in the absence of mechanical obstruction on final postprocedural angiograms (10). Myocardial blush grade was graded as follows: 0, no myocardial blush or contrast density; 1, minimal myocardial blush or contrast density; 2, moderate myocardial blush or contrast density, but less than that obtained during angiography of a contralateral or ipsilateral noninfarct-related coronary artery; and 3, normal myocardial blush or contrast density, comparable to that obtained during angiography of a contralateral or ipsilateral noninfarct-related coronary artery. When myocardial blush persisted, this finding was graded as 0 (11).
Left ventriculogram.
Right anterior oblique views of left ventriculograms obtained at the chronic phase after AMI (mean 155 ± 15 days) were used to assess global and regional left ventricular function. End-diastolic and end-systolic endocardial borders were hand-traced in the frames with maximal and minimal volume, respectively. Left ventricular end-diastolic and -systolic volumes were calculated by the area-length method described by Sandler and Dodge (12) and were corrected for body surface area to determine volume index. Regional wall motion in the territory of the infarcted area was assessed by the centerline method, using 100 chords, and expressed as SD/chord. The number of contiguous chords showing >2 SD below normal wall motion by the centerline method (percent abnormally contracting segment) was used as an index of infarct size.
Analysis of IVUS images.
Morphologic features on IVUS images were independently interpreted by 2 experienced observers blinded to the angiographic and clinical data. Images for which the 2 observers agreed on the diagnosis were included in subsequent analysis. Evaluation of lesion morphology and other measurements during IVUS was done according to the American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement, and Reporting of Intravascular Ultrasound Studies (13). We defined lesions with plaque rupture on IVUS as follows: 1) lesions with fissure/dissection; or 2) lesions without fissure/dissection, but in which the injection of saline or contrast medium confirmed communication between the plaque and the coronary artery lumen (Fig. 1) (14). We defined the other lesions as nonruptured plaque. Plaque composition was assessed visually and classified as echolucent when >75% of the plaque area was less bright than the adventitia; otherwise, plaque composition was classified as fibrous.
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Figure 1 Typical IVUS Images of Plaque Rupture and Nonruptured Plaque
Typical intravascular ultrasound images of plaque rupture (A, B) and nonruptured plaque (C, D). (B) Plaque ulceration with a fissure (arrowheads) and a communication (arrow) between the cavity of the rupture (R) and the lumen (L). (D) Lumen surface with preserved continuity. IVUS = intravascular ultrasound.
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External elastic membrane (EEM) cross-sectional area (CSA) and lumen CSA (in mm2) at the lesion site and at the proximal and distal reference sites were analyzed using planimetry software (TapeMeasure, Indec Systems, Capitola, California). The reference segments were the most normal-looking CSA within 5 mm proximal and distal to the lesion but before any side branch. Remodeling was considered positive when the lesion EEM CSA was greater than both the proximal and distal reference EEM CSA, negative when the lesion EEM CSA was less than both the proximal and distal reference EEM CSA, and intermediate when the lesion EEM CSA was intermediate between the proximal and distal reference EEM CSA (15).
Statistical analysis.
Statistical analysis was performed with StatView 5.0 software (SAS Institute, Cary, North Carolina). Results are expressed as mean ± SD for continuous variables. Qualitative data are presented as number (%). Continuous variables were compared by means of Student t test, and categoric data were compared by the chi-square test or Fisher exact test between groups. The Cochran-Mantel-Haenszel test was used for comparison of ordinal categoric variables between groups. Univariate and logistic regression analyses were used to identify predictors of left ventricular ejection fraction <50% at discharge. Covariables examined included clinical characteristics (age, gender, presence of preinfarction angina, elapsed time from symptom onset to reperfusion, and coronary risk factors), angiographic characteristics (distribution of culprit lesions, myocardial blush grade, and no-reflow phenomenon), and qualitative IVUS factors (plaque morphology and presence of plaque rupture). Univariate cariables with a value of p < 0.2 were entered into the multivariate models. For all analyses, values of p < 0.05 were considered to indicate statistical significance.
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Results
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Patient characteristics.
Patients were classified according to the presence or absence of plaque rupture as determined by preintervention IVUS; 54 patients had plaque rupture (rupture group), and 37 did not have plaque rupture (nonrupture group). Patient characteristics are summarized in Table 1. The proportions of men (89% vs. 68%; p < 0.05) and current smokers (74% vs. 44%; p < 0.01) were higher and the incidence of preinfarction angina was lower (31% vs. 54%; p < 0.05) in the rupture group than in the nonrupture group. Patients older than 75 years (n = 5), patients who entered another clinical trial that prohibited thrombolysis before PCI (n = 4), and patients who had a history of ischemic stroke (n = 4) or active peptic ulcer (n = 2) did not receive thrombolytic therapy.
Angiographic findings.
The angiographic findings are shown in Table 2. There were no differences between the groups in the incidence of multivessel disease or proximal lesions of the left anterior descending artery. Seventy-five patients (82%) were treated with stenting, and 10 (11%) received balloon angioplasty only. In patients (n = 6) who achieved a TIMI flow grade of 3 at initial angiography with intermediate severity of culprit lesion, PCI was not performed. Thrombus aspiration was attempted after IVUS interrogation and before balloon inflation in 2 patients. No distal protection device was used in this study. The incidence of no-reflow phenomenon was slightly but not significantly higher, and that of myocardial blush grade was lower in the rupture group than in the nonrupture group.
Left ventricular function in chronic phase.
Sixty-five patients (71%) underwent left ventriculogram in the chronic phase. Twenty-six patients were excluded from this examination for the following reasons: 10 patients were lost to follow-up or transfered to other hospitals, 7 had renal dysfunction, 2 had allergy to contrast medium, 2 had bronchial asthma, and 5 did not give informed consent for repeat catheterization in the chronic phase. There were no differences in the number of Q waves on admission ECG, peak CK levels, or the AUC of CK levels between patients with left ventriculograms and those without left ventriculograms (data not shown). Left ventriculographic findings in the chronic phase are summarized in Table 2. Left ventricular ejection fraction and regional wall motion were lower, and left ventricular end-systolic volume and infarct size as assessed on the basis of percent abnormally contracting segment were greater in the rupture group than in the nonrupture group.
IVUS results.
Coronary artery lesions were successfully observed in all patients on IVUS, without serious procedural complications. The preintervention IVUS findings are summarized in Table 3. Culprit lesions in the rupture group involved a larger vessel area and showed positive remodeling with soft plaque morphology.
Electrocardiographic findings.
The number of Q waves on the admission ECG was greater in the rupture group than in the nonrupture group (2.3 ± 1.6 vs. 1.1 ± 1.2; p < 0.05) among patients with a reperfusion time of <120 min (n = 39) but did not differ between the groups (2.5 ± 1.6 vs. 2.4 ± 1.5, respectively; p = 0.785) among patients with a reperfusion time of 120 min (n = 52).
Valuation of infarct size.
Peak CK (4,707 ± 3,017 IU/l vs. 2,309 ± 1,496 IU/l; p < 0.0001) and CK-MB levels (383 ± 257 IU/l vs. 209 ± 135 IU/l; p < 0.01) as well as AUCs for CK (110,827 ± 69,297 IU/l·h vs. 58,041 ± 32,814 IU/l·h; p < 0.0001) and CK-MB levels (8,128 ± 4,709 IU/l·h vs. 4,889 ± 2,667 IU/l·h; p < 0.001) were all higher in the rupture group than in the nonrupture group (Fig. 2). We evaluated infarct size, as represented by peak CK levels and AUC of CK, according to age, gender, established coronary risk factors, and reperfusion time (Table 4). In all subgroups, peak CK levels and AUC of CK were significantly higher in the plaque rupture group than in the nonrupture group.
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Figure 2 Comparison of Infarct Size Between the Rupture and Nonrupture Groups
Comparison of peak creatine kinase (CK) (A), peak CK-MB (B), area under the curve (AUC) of CK (C), and AUC of CK-MB (D) levels between the rupture and nonrupture groups.
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Determinants of left ventricular dysfunction in chronic phase.
A multivariate logistic regression analysis revealed that the presence of plaque rupture and the proximal lesion site were independent predictors of a left ventricular ejection fraction of <50% in the chronic phases (Table 5).
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Discussion
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To our knowledge, this is the first clinical study to demonstrate that plaque rupture at culprit lesions is associated with morphologic characteristics of vulnerable lesions as well as with larger infarcts and a higher incidence of no-reflow phenomenon in patients with anterior AMI. Independent predictors of left ventricular dysfunction were plaque rupture and proximal lesion site.
Plaque rupture with subsequent thrombus formation is the most frequent cause of acute coronary syndromes (1,2). Several postmortem studies have demonstrated that about 60% of all cases of AMI are caused by plaque rupture and the other 40% by plaque erosion (16,17). In the present study, the rate of plaque rupture on IVUS was 59.3%, similar to the rates reported by Sano et al. (56%) (14) and Hong et al. (66%) (18). It is unclear whether the nonrupture plaques identified by IVUS are erosive lesions, because IVUS has a limited capability to assess the lumen surface of culprit plaque. Plaque erosions can be confirmed only by angioscopy in vivo. In a previous study by Hayashi et al. (19), culprit lesions in patients with AMI were evaluated by means of both IVUS and angioscopy. The evaluation of plaque morphology differed in only 1 (1.4%) case between the 2 modalities (19), indicating that lesions without plaque rupture on IVUS are roughly equivalent to erosive lesions.
The present study showed that proportions of men and current smokers were higher among patients with plaque rupture than among those without plaque rupture, consistent with earlier postmortem studies. Farb et al. (17) demonstrated that eroded lesions were more common in younger individuals and women. Burke et al. (20) reported that cigarette smoking was associated with coronary thrombosis in men and plaque erosion in women. Kojima et al. (21) reported that the presence of plaque rupture in patients with AMI is associated with current smoking. More severe damage of the endothelial cell lining and increased sympathetic discharge in smokers may heighten atherosclerotic plaque vulnerability, leading to sudden plaque rupture.
In a retrospective pathologic study, Kojima et al. (21) showed that patients with plaque rupture had a higher incidence of infarction of sudden onset than those with plaque erosion. In addition, new-onset rest angina occurred in 76% of patients with plaque rupture compared with only 24% of those with plaque erosion. Similarly, in the present study the incidence of preinfarction angina was lower in patients with plaque rupture. Although the mechanism underlying the relation between preinfarction angina and plaque morphology remains unclear, the present findings suggest that rupture of soft plaque with positive remodeling may cause abrupt coronary occlusion after sudden thrombus formation, without prodromal angina.
In patients with AMI, Tanaka et al. (10) showed that large vessels with lipid pool-like images were associated with a high risk of no reflow after primary intervention. Several studies have suggested that plaque content, rather than thrombus, may be the major determinant of microcirculatory damage (10,22). Our findings confirm and further extend these previous findings and provide evidence that ruptured plaque with echolucent plaque morphology as well as positive remodeling may cause microvascular dysfunction and no-reflow phenomenon. High thrombogenicity caused by exposure to the components of lipid-rich plaque at the rupture site may thus lead to acute coronary occlusion with large amounts of nondissolvable thrombus.
Using angioscopy, Mizote et al. (23) demonstrated that microcirculatory damage and left ventricular dysfunction after PCI are more frequent among patients with ruptured plaque than among those without ruptured plaque. Their findings suggested that plaque morphology with fibrous cap disruption as assessed by angioscopy might be a predictor of greater distal embolism. Distal protection devices were therefore suggested to be clinically useful for preventing no-reflow phenomenon and improving left ventricular function in patients with ruptured plaque. Angioscopy is a useful tool for examining the inner surface as well as intraluminal structures of coronary arteries and may have several advantages over IVUS for assessing thrombus formation. However, angioscopic procedures are troublesome and time consuming compared with IVUS procedures, because the former require low-pressure inflation of a proximal occlusive cuff or continuous flushing of normal saline solution through the irrigation channel of the angioscope. Moreover, because of its large size, advancement of an angioscopic catheter across severe coronary lesions may itself induce mechanical embolization. Therefore, in patients with AMI, IVUS procedures may be better suited for the assessment of culprit lesions, because they require less time and use smaller devices than angioscopy.
Recently, several randomized trials (24–26) assessing the value of embolic protection devices during primary PCI in patients with AMI failed to demonstrate any positive effect of "routine" embolic protection on either myocardial reperfusion or clinical outcomes. These negative results may be attributed to several factors: 1) The several extra minutes required for additional balloon occlusion may have increased infarct size and worsened clinical outcomes, offsetting the potential benefits of removing emboli; 2) embolization may have been caused by passing the device over the lesion; and 3) there may have been little chance for myocardial recovery to begin with. On the other hand, several studies have suggested that distal protection may be clinically beneficial in certain subsets of patients who have specific plaque morphology associated with an increased risk of atheroembolism (27–29). Although aspiration of atherothrombotic emboli may not improve outcomes in all patients with AMI, reliable and feasible intravascular imaging techniques are needed to identify patient subgroups that would maximally benefit from embolic protection during the "super-acute phase" of AMI. We believe that IVUS might provide important information that would facilitate the identification of patients at greatest risk.
Consistent with our findings, Hayashi et al. (19) suggested that patients with ruptured plaque on angioscopy had larger infarctions than those with eroded plaque. However, they studied not only patients with anterior AMI but also those with inferior and posterior AMI. Furthermore, they included patients treated within 24 h after the onset of AMI. Reperfusion >6 h after symptom onset has a less beneficial effect on myocardial salvage than earlier establishment of an open infarct-related artery (30). To reduce effects of confounding factors, we limited our subjects to patients who had had a first anterior AMI with reperfusion within 6 h after symptom onset, making the present study design more robust. We believe that we confirmed the association between the incidence of plaque rupture and myocardial infarct size more clearly than earlier studies.
The number of leads with abnormal Q waves on admission is an index of myocardial damage before reperfusion (31) and is not affected by myocardial damage during PCI. A greater number of Q waves implies broader transmural damage. Among patients who received reperfusion therapy within 2 h, the presence of plaque rupture was associated with a greater number of leads with abnormal Q waves on the admission ECG than was the absence of plaque rupture. Although successful reperfusion within 2 h after symptom onset can lead to myocardial salvage, the present results suggest that plaque rupture already rapidly caused myocardial damage before reperfusion, followed by greater distal embolism during reperfusion procedures.
Study limitations.
The present study had several limitations. It was a single-center retrospective study with a relatively small number of patients. Individual patient characteristics were assessed on the basis of clinical histories obtained by staff physicians, but ischemic episodes are not necessarily symptomatic. We enrolled only patients with anterior AMI, because infarct size, arterial length, and branching patterns differ among the left anterior descending, left circumflex, and right coronary arteries. Therefore, our results cannot be extrapolated to inferior or posterior infarction.
We excluded patients with cardiogenic shock, because we did not perform preintervention IVUS, thereby shortening the time to reperfusion. Obviously, patients with cardiogenic shock may represent those with the largest infarcts. Not all cases of plaque rupture present with fissure/dissection or with plaques with communications to the lumen on preintervention IVUS. Although we carefully examined lesions by flushing the surrounding region with saline or contrast medium, lesions with small ruptured plaques may be misread as nonruptured plaques. Although we used serum cardiac enzyme levels and left ventricular function in the chronic phase to assess infarct size, left ventriculograms may not accurately represent the infarct size at the time of admission. Finally, it should be emphasized that a type I error cannot be excluded, owing to the number of variables examined and the multiple comparisons performed on a fairly limited patient group.
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Conclusions
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Plaque rupture at culprit lesions is associated with morphologic characteristics of vulnerable lesions and with larger infarcts in patients with anterior AMI, suggesting that plaque embolism contributes to the progression of myocardial damage. Further investigations are needed to determine whether distal protection can benefit this subset of patients.
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