CLINICAL STUDY: MYOCARDIAL INFARCTION
The healing process of infarct-related plaques
Insights from 18 months of serial angioscopic follow-up
Yasunori Ueda, MD, PhDa,*,
Masanori Asakura, MDb,
Osamu Yamaguchi, MDb,
Atsushi Hirayama, MD, PhDa,
Masatsugu Hori, MD, PhD, FACCb and
Kazuhisa Kodama, MD, PhD, FACCa
a Cardiovascular Division, Osaka Police Hospital, OsakaJapan
b Division of Cardiology, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan
Manuscript received February 23, 2001;
revised manuscript received August 3, 2001,
accepted August 24, 2001.
* Reprint requests and correspondence: Dr. Yasunori Ueda, Cardiovascular Division, Osaka Police Hospital, 10-31 Kitayama-cho, Tennoji-ku, Osaka, 543-0035 Japan.
ueda{at}oph.gr.jp
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Abstract
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OBJECTIVES: To clarify the healing process of disrupted culprit plaques of acute myocardial infarction (MI), we serially observed the culprit plaques for 18 months after the onset of acute MI by angioscopy.
BACKGROUND: Although it has been reported that disruption of the yellow plaque and subsequent thrombosis cause acute MI and that the thrombogenicity of the plaque lasts for a month, the healing process of the plaque after disruption has not been clarified.
METHODS: Eighty-five patients with acute MI were prospectively and consecutively enrolled. Angioscopic studies were performed immediately and at 1, 6 and 18 months after successful reperfusion. The prevalence of yellow plaques and thrombus was examined. The color grade of the plaque was determined as 0 (white), 1 (light yellow), 2 (yellow) or 3 (bright yellow).
RESULTS: Although yellow plaque was present at the culprit lesion in most patients throughout follow-up, its color grade was reduced from one to six months (1.9 ± 0.6 vs. 1.1 ± 0.7, p = 0.0003) after reperfusion, especially in the patients without hyperlipidemia (HL). The incidence of thrombus was 92.5% immediately after reperfusion, which was reduced significantly to 63.8%, 4.8% and 11.8% at 1, 6 and 18 months, respectively. The incidence of thrombus (77.8% vs. 45.0%, p = 0.03) at one month was higher in the patients with diabetes mellitus (DM).
CONCLUSIONS: The healing process of yellow plaques at the culprit lesions of MI was detected by angioscopy as reductions of color grade and thrombogenicity at six months and partially at one month after the onset of acute MI. This healing process appears to deteriorate by complicating cases of DM or HL.
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Abbreviations and Acronyms
| | ACS | | acute coronary syndrome | | CABG | | coronary artery bypass graft surgery | | DM | | diabetes mellitus | | HL | | hyperlipidemia | | maxYP | | maximal yellow plaque | | MI | | myocardial infarction | | nYP | | number of yellow plaques | | PTCA | | percutaneous transluminal coronary angioplasty |
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Pathologic and angioscopic studies have revealed that disruption of lipid-rich yellow plaques and subsequent thrombosis play a major role in the development of acute myocardial infarction (MI). It is important to determine how long the thrombogenicity of the culprit plaques lasts, because re-thrombosis may cause re-infarction or post-infarction angina and may worsen the prognosis of the patients. We have previously reported, by angioscopic study (1), that thrombus remains at the culprit lesions in 60% of patients with MI, even at one month after the onset. Van Belle et al. (2) have also suggested that angioscopic characteristics of plaque instability last during one month after the onset of MI. Smalling and Anderson (3) have commented that plaque at culprit lesions frequently remains active for up to 30 days after the onset of MI. However, the healing process of those once-disrupted plaques has not been fully clarified. The healing process is the process of reducing thrombogenicity, which may be achieved by re-covering of the disrupted plaques by neointima, with its functional maturation. To elucidate the healing process of culprit plaques, we angioscopically observed the culprit lesions of MI at 1, 6 and 18 months after the onset.
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Methods
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Patient selection.
Patients with acute MI were prospectively and consecutively enrolled from January 1995 to December 1997. The entry criteria were: 1) acute MI (confirmed by elevation of serum creatine kinase, MB fraction and angiographic demonstration of a culprit lesion) with successful reperfusion; and 2) written, informed consent for the examinations. The exclusion criteria were: 1) left main coronary artery disease; and 2) coronary arteries not suitable for angioscopic examination.
Study protocol
Angioscopic studies of the infarct-related coronary arteries were performed immediately and at 1, 6 and 18 months after successful reperfusion. Reperfusion therapy was performed with balloon angioplasty with or without thrombolysis and stenting. Because only a few patients underwent stenting, those patients were excluded. Intravenous heparin (100 U/kg) was administered at the beginning of catheterization, and the same amount was added before angioplasty. Heparinization (8,000 to 10,000 U/day) was continued for a week. Oral aspirin (81 to 162 mg/day) was started as soon as possible in case there was no contraindication. New antiplatelet agent glycoprotein IIb/IIIa blockers were not used in any of the study patients, because they have not been approved for clinical use in Japan. Patients who received a repeat intervention of the culprit lesion during follow-up were excluded from analysis thereafter. Data on the patients’ characteristics were collected within a few weeks after hospital admission. Hyperlipidemic patients in this study were defined as: 1) patients with serum total cholesterol >220 mg/dl (according to the guidelines of the Japan Atherosclerosis Society); or 2) patients already taking lipid-lowering drugs. Obesity was defined as a body mass index of >26.4 kg/m2. The study protocol was approved by the Ethical Committee of the Osaka Police Hospital.
Angioscopic procedures and evaluations
Catheterization was performed by the femoral approach, using an 8F sheath and catheter. The coronary angiogram was recorded by the Advantx medical system (General Electric). The angioscope MC-800E (Nihon Kohden) and the optic fiber AS-003 (Nihon Kohden) were used. Angioscopic studies were made while the blood was cleared away from view, by injection of 3% dextran-40, as previously reported (1). The angioscopic images were recorded by a S-VHS videotape recorder. The existence of yellow plaques and thrombus at the culprit lesions and in the rest of the coronary segments was evaluated. The color of the culprit plaques was graded as 0 (white), 1 (light yellow), 2 (yellow) or 3 (bright yellow), according to the sample colors presented in Figure 1. The number of yellow plaques (nYP) in a coronary artery, excluding culprit lesions, was counted, and the maximal color grade among those yellow plaques (maxYP) was determined. The atherosclerosis index was calculated as nYP x maxYP. Angioscopic studies were performed by two angioscopic specialists who had no knowledge of the background data of the patients, and in case of disagreement, a third reviewer determined the evaluation.
Major adverse events and angioscopic findings
Data on major adverse events (death, acute MI, unstable angina, coronary artery bypass graft surgery [CABG] or percutaneous transluminal coronary angioplasty [PTCA]) that occurred after the onset of acute MI, by the end of May 2001, were collected from the clinical records. Angioscopically determined variables of atherosclerosis (nYP, maxYP and atherosclerosis index) immediately after reperfusion were compared between patients who had an acute coronary syndrome (ACS: acute MI or unstable angina) and those who did not. The follow-up interval was 4.6 ± 1.5 years.
Statistics
Continuous data are presented as the mean value ± SD. Changes in the prevalence of yellow plaques and thrombus were analyzed by the Steel test, and changes in the color grade of the plaques were analyzed by two-way, repeated-measures analysis of variance (ANOVA). Differences in the patient characteristics between subgroups or the effects of patient characteristics on thrombus or yellow plaques were analyzed by ANOVA or the chi-square test. A p value <0.05 was regarded as statistically significant.
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Results
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Patient characteristics.
Eighty-five patients were enrolled in this study. As the reperfusion therapy, thrombolysis or primary/rescue/delayed PTCA, or both, were performed. Rescue PTCA was performed at  30 min after the administration of the thrombolytic agent (tissue plasminogen activator). Delayed PTCA was performed at 1.8 ± 1.7 months. Four patients who underwent stenting were excluded. Follow-up catheterization was not performed in 9, 16 and 34 patients at 1, 6 and 18 months, respectively, because informed consent was not obtained. Due to a repeat intervention of the culprit lesion before follow-up catheterization, 9, 16 and 34 patients were excluded from analysis at 1, 6 and 18 months, respectively. Angioscopic studies were not performed immediately and at 1, 6 and 18 months after reperfusion in 26, 22, 36 and 14 patients, respectively, because the angioscopic specialist was not available at the time of examination. A clear angioscopic image was not acquired in two patients, immediately after reperfusion and at one month. Therefore, angioscopic observations were successfully performed immediately and at 1, 6 and 18 months after reperfusion in 53, 47, 21 and 17 patients, respectively. The characteristics of the study patients at each time point are presented in Table 1. The angiographic characteristics and method of reperfusion are presented in Table 2. Patients with hyperlipidemia (HL) had significantly higher serum total cholesterol levels (237 ± 38 vs. 180 ± 24 mg/dl, p < 0.0001) and triglycerides (153 ± 90 vs. 104 ± 43 mg/dl, p = 0.01) than those without HL. The characteristics of the study patients with or without HL and diabetes mellitus (DM) at each time point are presented in Tables 3 and 4, respectively. There was no significant difference in patient characteristics for any subgroup at any time point (Tables 1–4).
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Figure 3 Prevalence of thrombus (A) and mean (±SD) color grade (B) in patients with HL (solid bars) and patients without HL (hatched bars). The prevalence of thrombus and the mean color grade immediately after reperfusion and at one month were not different between the patients with HL and those without HL. The mean color grade at six months was significantly higher in the patients with HL. 0 M = immediately after reperfusion; M = months after reperfusion. *p < 0.05 vs. patients without HL.
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Figure 4 Prevalence of thrombus (A) and mean (±SD) color grade (B) in patients with DM (solid bars) and patients without DM (hatched bars). The prevalence of thrombus and the mean color grade immediately after reperfusion were not different between the patients with HL and those without HL. The prevalence of thrombus was significantly higher and the mean color grade tended (p = 0.08) to be higher in the patients with DM at one month. The mean color grade at six months was not different between the patients with DM and those without DM. 0 M = immediately after reperfusion; M = months after reperfusion. *p < 0.05 vs. patients without DM.
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Yellow plaques
Yellow plaques (Fig. 2A) remained at the culprit lesions immediately and at 1, 6 and 18 months after reperfusion in 94.3%, 100%, 85.7% and 82.4% of patients , respectively. A mild but significant reduction in the prevalence was detected at six months. The mean color grade of culprit yellow plaques (Fig. 2B) was reduced significantly from one to six months (1.9 ± 0.6 vs. 1.1 ± 0.7, p = 0.0003) after reperfusion.
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Figure 2 Prevalence of yellow plaque at the culprit lesions (A), mean (±SD) color grade of the culprit plaque (B) and prevalence of thrombus at the culprit plaques (C). Yellow plaques remained for as long as 18 months at the culprit lesions of acute MI, although the color grade was reduced significantly and the prevalence was reduced mildly but significantly from one to six months after reperfusion. The prevalence of thrombus was decreased significantly from immediately to one month after reperfusion, and further from one to six months. 0M = immediately after reperfusion; M = month(s) after reperfusion. A: *p < 0.05 vs. 1 M. B: *p < 0.005 vs. 1 M. C: *p < 0.005 vs. 0 M.  p < 0.005 vs. 1 M.
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Although the color grade of the culprit plaques immediately after reperfusion and at one month was not significantly influenced by any of the patient characteristics listed in Table 1 or 2, the color grade at six months was significantly higher in the patients with HL (1.4 ± 0.6 vs. 0.7 ± 0.5, p = 0.03) (Fig. 3). In other words, the color grade was reduced more in patients without HL (–1.3 ± 0.8 vs. –0.5 ± 0.7, p = 0.04). Other characteristics listed in Table 1 or 2 had no significant influence on the reduction of color grade. Although not statistically significant, the color grade of the plaque at one month tended to be higher (2.1 ± 0.7 vs. 1.8 ± 0.6, p = 0.08) (Fig. 4) in patients with DM, in accordance with the higher prevalence of thrombus on the plaque.
Thrombus on the culprit plaques
Thrombus (Fig. 2C) was detected on the culprit plaques in 92.5% of patients immediately after reperfusion, whereas it was decreased significantly to 63.8% at 1 month and further to 4.8% and 11.8% at 6 and 18 months, respectively.
At one month, thrombus was detected more frequently in patients with DM (77.8% vs. 45.0%, p = 0.02) (Fig. 4). Other characteristics listed in Table 1 or 2 had no influence on the prevalence of thrombus. Plaques with thrombus had a higher color grade (2.0 ± 0.7 vs. 1.3 ± 0.7, p < 0.0001) than those without thrombus, when analyzed by including the data of all plaques at all time points.
Major adverse events and angioscopic findings
Observed major adverse events were three deaths (1 suicide and 2 for unknown reasons), seven acute MIs (4 at original culprit lesion and 3 at new lesion), two cases of unstable angina (1 at original culprit lesion and 1 at new lesion) and 36 nonurgent coronary interventions (34 PTCA and 2 CABG). Angioscopic data had no significant association with the incidence of all major adverse events. However, angioscopically determined variables of atherosclerosis—nYP (3.5 ± 1.9 vs. 2.1 ± 1.5, p = 0.08), maxYP (2.5 ± 0.6 vs. 1.7 ± 0.9, p = 0.09) and atherosclerosis index (9.5 ± 6.8 vs. 4.4 ± 4.0, p = 0.02)—were larger in patients with ACS than in those without it. The prevalence of thrombus at one month was not associated with ACS events.
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Discussion
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Stabilization of the culprit plaques in the healing process after MI.
The once-disrupted yellow plaques at the culprit lesions of acute MI were accompanied by thrombus, suggesting high thrombogenicity, in 64% of patients, even at one month after the onset, as previously reported (1). However, in the present study, those plaques were demonstrated to lose thrombogenicity in the majority of patients at six months after the onset of MI, when thrombus was detected in only 4.8% of the patients. In accordance with the stabilization (reduction in thrombogenicity) of the plaques, the color grade of the plaques was significantly reduced at six months, when plaques even lost their yellow color completely and became white in 14% of patients. The disappearance of thrombus and yellow plaque at six months after PTCA has been reported (4), with a small number of patients with unstable angina. In the present study, we have revealed the disappearance of thrombus and the regression of yellow plaque in patients with acute MI by serial examinations. Furthermore, we have revealed that the stabilization of plaques are deteriorated in patients with DM or HL. Because from one to six months after PTCA is the period of active intimal proliferation after vascular injury, it is likely that the neointima formed over the disrupted plaques has stabilized the thrombogenic potential of the plaques and reduced their color grade by separating the lipid core from the blood flow.
Yellow color of the plaque and its instability
The relationship between the yellow color of the plaque and its thrombogenicity or unstable clinical syndrome has been established by angioscopic and pathologic studies (1,5,6), and the yellow color of the plaque has been demonstrated to be predictive of early adverse coronary events after PTCA (7) in patients with ACS and of ACS (8) in patients with stable effort angina. It has also been reported previously (8) that the glistening yellow plaques cause ACS more frequently than the nonglistening ones. The results of the present study have suggested that yellow plaques of higher color grades have a higher incidence of causing thrombus formation. These results support the idea that the instability of plaques are related with their yellow color, not only in the process of plaque disruption, but also in the healing process after disruption. The grading of yellow color may increase the predictive value of the angioscopic examinations for adverse coronary events.
Influence of DM and HL on the healing process
Although the prevalence of yellow plaques and thrombus in the culprit arteries of patients with unstable angina has been reported (9) to be higher in those with DM, the present study has revealed, for the first time, to the best of our knowledge, that the prevalence of thrombus at the culprit plaques of MI one month after the onset is higher in patients with DM than in those without it, suggesting that the thrombogenicity of the plaque is originally higher or the healing process of the disrupted plaque is delayed in patients with DM (Fig. 4). Because the color grade of the plaque at one month tended to be higher in patients with DM, although it was not different immediately after reperfusion, the neointimal re-covering and thickening over the yellow plaque may be delayed in those patients. In contrast, HL delayed the reduction of color grade at six months, although it had no significant effect on the prevalence of thrombus or color grade immediately after reperfusion or at one month (Fig. 3). The prevalence of thrombus at six months was too low to reveal the difference between the patients with HL and those without HL. The data on the non-HL subgroup at 18 months might be biased because of the small sample size (n = 3).
Major adverse events and angioscopic findings
Although the association between the presence of intracoronary thrombus and an increased incidence of an adverse outcome after PTCA and the association between the presence of intracoronary thrombus and post-infarction angina have been previously reported (10,11), we could not detect the association between the presence of thrombus and major adverse events in this study. One of the explanations for this difference might be that the major adverse events in this study happened rather remote from the onset of the original MI and might have a different nature from that of post-infarction angina or abrupt occlusion after PTCA, as described in previous reports. However, we have revealed that patients with ACS had more advanced yellow plaque formation, and we believe that angioscopic examination of yellow plaque formation may be able to evaluate the risk of future ACS.
Study limitations
This study has two major limitations: 1) the study group was small, and thus the number of patients followed up at 18 months became small; and 2) the evaluation of plaque color was rather subjective, although this kind of often-used grading system is easy and practical. Although the prevalence of thrombus or plaque color at the culprit lesions may possibly differ after different reperfusion therapies (especially when a stent is implanted), study group was too small to evaluate this effect. Although an unusually high rate of patients had DM complications, no obvious cause for this result was identified.
Conclusions
Disrupted yellow plaques at the culprit lesions of acute MI were accompanied by thrombus in 93% of the patients immediately after reperfusion; however, the incidence of thrombus detected at the plaque decreased to 64% at one month and to 5% at six months. According to the reduction of thrombogenicity, the color grade of the plaques was reduced. The higher color grade of the plaques was associated with a higher incidence of thrombus. The healing process of the culprit plaques of MI was angioscopically demonstrated as reductions in both the color grade and incidence of thrombus of the plaques, which appeared to be deteriorated in patients with HL or DM.
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References
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Abstract
Methods