Autopsy studies have suggested that acute myocardial infarction (AMI) represents a pan-coronary process of vulnerable plaque development. We performed multifocal optical coherence tomographic (OCT) examination to compare coronary lesion instability between AMI and stable angina pectoris (SAP). A total of 42 patients with AMI (n = 26) or SAP (n = 16) who had multivessel disease and underwent multivessel coronary intervention were enrolled in the present study. The OCT examination was performed not only in the infarct-related/target lesions, but also in the noninfarct-related/nontarget lesions. OCT-derived thin-cap fibroatheroma (TCFA) was defined as a lesion with a fibrous cap thickness of <65 μm. In the infarct-related/target lesions, plaque rupture (77% vs 7%, p <0.001) and intracoronary thrombus (100% vs 0%, p <0.001) were observed more frequently in AMI than in SAP. The fibrous cap thickness (57 ± 12 vs 180 ± 65 μm, p <0.001) was significantly thinner in AMI and the frequency of OCT-derived TCFA (85% vs 13%, p <0.001) was significantly greater in AMI than in SAP. In the noninfarct-related/nontarget lesions, the frequency of plaque rupture was not different between the 2 groups. Intracoronary thrombus was observed in 8% of AMI, but it was not found in SAP. The fibrous cap thickness (111 ± 65 vs 181 ± 70 μm, p = 0.002) was significantly thinner in AMI and the frequency of OCT-derived TCFA (38% vs 6%, p = 0.030) was significantly greater in AMI than in SAP. Multiple OCT-derived TCFAs in both the infarct-related/target and the noninfarct-related/nontarget lesions were observed in 38% of patients with AMI but not in patients with SAP (p = 0.007). In conclusion, the present OCT examination demonstrated multiple lesion instability in the presence of AMI.
Coronary plaque rupture and subsequent thrombus formation is the most important mechanism leading to acute myocardial infarction (AMI). Thin cap fibroatheroma (TCFA; fibrous cap thickness of <65 μm) is thought to be a precursor lesion of plaque rupture. In the diffuse nature of coronary atherosclerosis, plaque instability might be expected to develop in a multifocal pattern. One previous study using coronary angiography demonstrated that 40% of patients with AMI had multiple complex lesions and that these patients had a high risk of a recurrent acute coronary event. Recent 3-vessel intravascular ultrasound (IVUS) studies showed that multiple plaque ruptures were more common in AMI compared to stable angina pectoris (SAP). The optical coherence tomographic (OCT) examination is a high-resolution (10 to 15-μm) imaging method for plaque characterization. In vitro studies have demonstrated the potential of OCT studies to identify TCFA. We used OCT scans to compare the frequency of TCFA between patients with AMI and SAP, not only in the infarct-related/target lesions, but also in the noninfarct-related/nontarget lesions.
Methods
A total of 50 patients with AMI or SAP who had untreated multivessel disease and had undergone multivessel coronary intervention were prospectively enrolled in the present study. Patients with (1) chronic total occlusion; (2) a left main coronary artery lesion; (3) a lesion length of >30 mm; (4) a reference vessel diameter of >4 mm; and (5) congestive heart failure with a left ventricular ejection fraction of <40% were excluded because of the potential difficulty in performing and interpreting the OCT findings in such situations. AMI was defined as continuous chest pain that lasted >30 minutes, arrival at our hospital within 12 hours from the onset of chest pain, ST-segment elevation >0.1 mV in ≥2 contiguous leads on the 12-lead electrocardiogram, and abnormal levels of cardiac enzymes (creatine kinase-MB or troponin-T). SAP was defined as chest pain on exertion, positive stress test findings, and no change in the frequency, duration, or intensity of symptoms within 4 weeks before the intervention. The infarct-related lesion in AMI or the target lesion in SAP was identified by the combination of left ventricular wall motion abnormalities, electrocardiographic findings, angiographic lesion morphology, and scintigraphic defects. In the cases with discordant results among those tests, a lesion with more severe diameter stenosis and more complex lesion morphology was selected as the infarct-related/target lesion. The noninfarct-related/nontarget lesion was identified as a lesion with the most severe diameter stenosis (>50%) in the epicardial coronary arteries, not including the infarct-related/target lesion. The demographic and clinical data were prospectively collected. The institutional review board approved the study, and all patients provided informed consent before participation.
The OCT examinations were performed before any intervention in patients with AMI with a Thrombolysis In Myocardial Infarction flow grade 3 or patients with SAP. In patients with AMI with a Thrombolysis In Myocardial Infarction flow grade of 0 to 2, the infarct-related lesions were evaluated by OCT imaging after thrombectomy using a thrombus aspiration catheter (Export catheter, Medtronic Japan, Tokyo, Japan). The OCT images were obtained with a M2CV OCT system (LightLab Imaging, Westford, Massachusetts). The OCT imaging procedure started with advancing the tip of a 0.014-in. coronary guidewire into the distal coronary artery. The occlusion catheter was then advanced over the wire until the balloon was positioned proximally to the lesion. After the guidewire and OCT image wire were exchanged, lactated Ringer’s solution was continuously flushed through the central lumen of the occlusion catheter by a power injector (0.5 ml/s), and the balloon was inflated gradually using a custom inflation device until blood flow was fully occluded. If the lesion was located near the ostium of the coronary arteries, we used a nonocclusive, continuous-flushing technique for OCT imaging. To flush the coronary artery without occlusion, dextran-40 and lactated Ringer’s solution (Low Molecular Dextran L Injection, Otsuka Pharmaceutical Factory, Tokushima, Japan) was infused through the guiding catheter using a power injector (2.5 to 4.5 ml/s). Motorized pullback OCT imaging was performed at a rate of 1.0 mm/s for a length of 30 mm. The images were acquired at 15 frames/s and were digitally archived in the OCT system console for off-line analysis.
All OCT images were analyzed by 2 independent investigators (HK and TT) who were unaware of the clinical presentation. When discordance was present between the observers, a consensus reading was obtained. The presence of plaque rupture, intracoronary thrombus, or OCT-derived TCFA was noted. Plaque rupture was identified by the presence of fibrous cap discontinuity and a cavity formation in the plaque. Intracoronary thrombus was defined as a mass protruding into the vessel lumen from the surface of the vessel wall. A fibrous cap was identified as a signal-rich homogenous region overlying a lipid core, which was characterized by a signal-poor region on the OCT image. The thinnest part of the fibrous cap was measured 3 times, and the average value was calculated. The lesion with a fibrous cap of <65 μm was diagnosed as OCT-derived TCFA. Representative OCT images are shown in Figure 1 .
Quantitative coronary angiography was conducted using the Cardiovascular Measurement System (CMSMEDIS Medical Imaging System, Leiden, The Netherlands). The percent diameter stenosis of the lesion was calculated by an independent operator.
Statistical analysis was performed using StatView, version 5.0.1 (SAS Institute, Cary, North Carolina). Categorical variables were presented as frequencies, with comparison using chi-square statistics or Fisher’s exact test (if the expected cell value was <5). Continuous variables are presented as the mean ± SD and were compared using unpaired Student’s t tests. A p value <0.05 was considered statistically significant.
Results
Of the 50 patients with AMI or SAP who had multivessel disease, 8 patients were released from the study according to the exclusion criteria. The remaining 42 patients, including 26 patients with AMI ( Table 1 ) and 16 with SAP ( Table 2 ), were included in the present study. The infarct-related/target and noninfarct-related/nontarget lesions were successfully evaluated by OCT imaging in all patients without any serious procedural complications. Only 4 lesions near the coronary ostium were observed with a nonocclusive technique for OCT imaging. The mean evaluation length on the OCT scans was 27 ± 3 mm. No significant differences were found in terms of age, gender, or classic coronary risk factors between the 2 groups.
| Pt. No. | Age (years)/Gender | Risk Factors | Infarct-Related Lesion | Noninfarct-Related Lesion | ||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Plaque Rupture | Thrombus | Fibrous Cap Thickness (μm) | TCFA | Plaque Rupture | Thrombus | Fibrous Cap Thickness (μm) | TCFA | |||
| 1 | 49/Male | HT, DM, HC, SM | Yes | Yes | 50 | Yes | No | No | 50 | Yes |
| 2 | 52/Male | HT, HC | Yes | Yes | 60 | Yes | No | No | 57 | Yes |
| 3 | 57/Male | HT | Yes | Yes | 40 | Yes | Yes | No | 40 | Yes |
| 4 | 57/Male | HC | Yes | Yes | 60 | Yes | No | No | 73 | No |
| 5 | 57/Male | HT, HC, SM | No | Yes | 77 | No | No | No | 163 | No |
| 6 | 58/Male | HT, SM | Yes | Yes | 60 | Yes | No | No | 60 | Yes |
| 7 | 58/Male | HT, DM, HC | No | Yes | 60 | Yes | No | No | 157 | No |
| 8 | 60/Male | HT, DM, HC | Yes | Yes | 50 | Yes | No | No | 70 | No |
| 9 | 61/Male | HT, HC | No | Yes | 57 | Yes | No | No | 60 | Yes |
| 10 | 62/Male | HC | Yes | Yes | 50 | Yes | No | No | 103 | No |
| 11 | 62/Male | HT, DM | Yes | Yes | 63 | Yes | No | No | 217 | No |
| 12 | 64/Female | DM, HC | Yes | Yes | 60 | Yes | No | No | 60 | Yes |
| 13 | 65/Male | HT | No | Yes | 90 | No | No | No | 193 | No |
| 14 | 66/Male | HT, HC | Yes | Yes | 50 | Yes | No | No | 103 | No |
| 15 | 67/Male | HT | Yes | Yes | 53 | Yes | No | No | 100 | No |
| 16 | 67/Male | HT | Yes | Yes | 70 | No | No | No | 137 | No |
| 17 | 67/Female | HT, HC | No | Yes | 73 | No | No | No | 210 | No |
| 18 | 68/Female | DM, HC | Yes | Yes | 40 | Yes | Yes | Yes | 47 | Yes |
| 19 | 72/Female | HC | Yes | Yes | 57 | Yes | No | No | 110 | No |
| 20 | 72/Male | HT, DM | Yes | Yes | 57 | Yes | No | No | 103 | No |
| 21 | 72/Female | HT, DM, HC | No | Yes | 63 | Yes | No | No | 267 | No |
| 22 | 74/Male | DM, HC, SM | Yes | Yes | 43 | Yes | No | No | 60 | Yes |
| 23 | 75/Male | HT, SM | Yes | Yes | 60 | Yes | No | No | 170 | No |
| 24 | 76/Male | HC | Yes | Yes | 40 | Yes | Yes | Yes | 57 | Yes |
| 25 | 77/Male | HT, SM | Yes | Yes | 40 | Yes | No | No | 187 | No |
| 26 | 82/Female | HT, DM, SM | Yes | Yes | 50 | Yes | No | No | 40 | Yes |
| Pt. No. | Age (years)/Gender | Risk Factors | Target Lesion | Nontarget Lesion | ||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Plaque Rupture | Thrombus | Fibrous Cap Thickness (μm) | TCFA | Plaque Rupture | Thrombus | Fibrous Cap Thickness (μm) | TCFA | |||
| 1 | 55/Male | HT, SM | No | No | 193 | No | No | No | 230 | No |
| 2 | 58/Male | DM | No | No | 230 | No | No | No | 190 | No |
| 3 | 59/Female | HT, HC, SM | No | No | 223 | No | No | No | 257 | No |
| 4 | 62/Female | DM | Yes | No | 60 | Yes | No | No | 97 | No |
| 5 | 62/Female | HC, SM | No | No | 173 | No | No | No | 287 | No |
| 6 | 64/Male | HT, SM | No | No | 193 | No | No | No | 247 | No |
| 7 | 66/Male | HT, HC | No | No | 133 | No | No | No | 207 | No |
| 8 | 66/Male | HT | No | No | 170 | No | No | No | 193 | No |
| 9 | 67/Male | HC | No | No | 63 | Yes | No | No | 143 | No |
| 10 | 67/Female | HC | No | No | 220 | No | No | No | 180 | No |
| 11 | 69/Female | HT, HC, SM | No | No | 107 | No | Yes | No | 60 | Yes |
| 12 | 69/Male | HT, DM, HC | No | No | 283 | No | No | No | 213 | No |
| 13 | 72/Male | HT, SM | No | No | 177 | No | No | No | 80 | No |
| 14 | 72/Male | HT | No | No | 240 | No | No | No | 177 | No |
| 15 | 77/Male | HT, HC | No | No | 257 | No | No | No | 237 | No |
| 16 | 78/Male | HT, DM | No | No | 160 | No | No | No | 80 | No |
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