The pathophysiology of plaque disruption and healing in nonculprit segments has not been clarified. Therefore, we investigated the frequency of plaque disruptions in nonculprit segments and whether those plaques are stabilized during follow-ups in patients with acute myocardial infarction (AMI) by serial angioscopic observations. Analyzed were 13 consecutive patients with AMI in whom infarct-related arteries were serially observed by angioscopy immediately after reperfusion and at 1- and 6-month follow-ups. Color of plaques was graded as 0 (white), 1 (slight yellow), 2 (yellow), or 3 (intensive yellow). Plaques with thrombus were defined as disrupted. Although number of nonculprit yellow plaques did not change from immediately after reperfusion to 6 months, the maximum color grade of those plaques and incidence of disrupted plaques in nonculprit segments (immediate vs 1 month vs 6 months 31% vs 8% vs 0%) decreased significantly by 6 months. Plaque stabilization as shown by disappearance of thrombus was significantly associated with plaque regression as shown by a decrease of maximum yellow color grade in nonculprit segments. In conclusion, patients with AMI frequently had disrupted and actively thrombogenic yellow plaques in nonculprit segments of the culprit vessel, and those plaques healed with decreases of yellow color grade and thrombogenicity during 6-months follow-up. Plaque disruption and healing occur not only at the culprit lesion but may be a pan-coronary process in patients with AMI.
We investigated by serial angioscopic examinations the frequency of disrupted plaques with active thrombogenesis in nonculprit segments to elucidate the healing process of those plaques during follow-ups in patients with acute myocardial infarction (AMI).
Methods
Study patients were patients with AMI enrolled prospectively and consecutively from January 1995 through December 1997 for a previous study to clarify the healing process of disrupted culprit plaques of AMI. Briefly, included patients were those with AMI and successful reperfusion without left main coronary artery disease. Angioscopic examinations of infarct-related coronary arteries were performed immediately and at 1 month and 6 months after reperfusion with percutaneous coronary intervention (PCI). Patients who received repeat PCI were excluded thereafter. Angioscopic observations were successful in 53, 47, and 21 patients at each time point, respectively. In the present study, we analyzed 13 patients who had successful observation at all 3 time points. Intravenous heparin (100 U/kg) was administered at the beginning of catheterization, and the same amount was added before PCI. Heparinization (8,000 to 10,000 U/day) was continued for 1 week after reperfusion. Oral aspirin (81 to 162 mg/day) was started as soon as possible. Antiplatelet glycoprotein IIb/IIIa blockers were not used for any study patient because these were not approved for clinical use in Japan. Hypercholesterolemic patients were those with serum total cholesterol >220 mg/dl or those already taking lipid-lowering drug. Obesity was defined as a body mass index >26.4 kg/m 2 . Written informed consent was acquired from all patients. The protocol was approved by the Osaka Police Hospital ethical committee. Details of study patients and the protocol were described previously. A representative case is presented in Figure 1 .
As described in a previous report, catheterization was performed from a femoral approach using an 8Fr sheath and catheters; coronary angiogram was recorded by an Advantx medical system (GE Yokogawa, Tokyo, Japan) and an angioscope (MC-800E, Nihon Kohden) and optic fiber (AS-003, Nihon Kohden, Tokyo, Japan) were used. Angioscopic observations were made while blood was cleared away from view by injection of 3% dextran-40 as previously reported.
In the present study, yellow plaques and thrombus in nonculprit segments of the infarct-related artery were evaluated by reviewing the recorded angioscopic images. Plaques with thrombus were defined as disrupted so that we could include only fresh and unhealed disrupted (ruptured or eroded) plaques because intravascular ultrasound (IVUS) cannot exclude old/healed plaque ruptures (cavity) without active thrombogenesis or cannot include fresh/unhealed plaque erosion without a cavity. All yellow plaques angioscopically separated by a white area from the culprit plaque were defined as nonculprit yellow plaques. Yellow plaque was defined as a yellow area on the luminal surface, which could have a smooth or irregular surface with or without protrusion into the lumen. Color of plaques was graded as 0 (white), 1 (light yellow), 2 (yellow), or 3 (intensive yellow) according to standard colors as previously reported. Thrombus was defined as white or red material that had a cottonlike or ragged appearance or that presented fragmentation that could protrude into the lumen or adhere to the luminal surface. Number of yellow plaques in nonculprit segments was counted, and the maximum color grade of those yellow plaques was recorded. Presence or absence of disrupted plaques in nonculprit segments was evaluated. Angioscopic evaluations were performed by 2 specialists in angioscopy who were blinded to background data of patients; and in case of disagreement a third reviewer determined the evaluation. Inter- and intraobserver reproducibilities for interpretation of angioscopic images were 96% and 100% for plaque color and 94% and 91% for thrombus, respectively. Changes in number of yellow plaques, maximum yellow color grade, and incidence of disrupted plaques during follow-ups were analyzed.
Continuous data were presented as mean ± SD. Changes in number of yellow plaques, maximum color grade, and incidence of thrombus were analyzed by repeated measurement analysis of variance with Newman–Keuls test. Associations between categorical data were tested by chi-square test. A p value <0.05 was regarded as statistically significant.
Results
Patients’ characteristics and angioscopic findings are presented in Table 1 . In 13 study patients, 20 nonculprit yellow plaques were detected immediately after reperfusion and the number of plaques per patient was 1.5 ± 1.0 (range 0 to 3).
| Patient Number | Patient Characteristics | Angioscopic Findings | |||
|---|---|---|---|---|---|
| Age (years)/Sex | Risk Factors | Medications | Maximum Yellow Grade | Disrupted Plaque | |
| Hypertension/Hypercholesterolemia/Diabetes Mellitus/Current smoking/Obesity/Diseased Vessel | Beta Blocker/Angiotensin-Converting Enzyme Inhibitor/Nitrate/Calcium Channel Blocker/Aspirin/Statin | Immediately/6 Months | Immediately/6 Months | ||
| 1 | 46/M | +/+/+/+/−/2 | −/+/+/+/+/+ | 2/1 | absent/absent |
| 2 | 49/M | −/−/−/+/−/1 | −/+/−/−/+/− | 2/1 | absent/absent |
| 3 | 50/M | +/+/+/−/+/1 | −/+/+/+/+/+ | 1/0 | absent/absent |
| 4 | 54/M | +/+/+/−/−/1 | −/+/+/+/+/− | 2/2 | absent/absent |
| 5 | 59/M | −/+/−/−/−/2 | +/−/+/+/+/+ | 2/2 | absent/absent |
| 6 | 61/M | −/+/+/−/−/1 | −/−/+/+/+/− | 0/0 | absent/absent |
| 7 | 62/M | −/−/+/−/−/1 | +/−/+/+/+/− | 3/1 | present/absent |
| 8 | 62/F | −/+/+/−/−/1 | −/+/+/+/+/− | 1/1 | absent/absent |
| 9 | 62/M | +/−/−/−/−/3 | −/−/+/+/+/− | 2/1 | present/absent |
| 10 | 67/F | +/+/+/+/−/1 | −/−/+/+/+/− | 3/2 | present/absent |
| 11 | 67/M | −/+/−/−/−/2 | −/+/+/+/+/− | 2/1 | present/absent |
| 12 | 71/F | +/−/−/−/−/1 | −/−/+/+/+/− | 0/1 | absent/absent |
| 13 | 79/M | −/−/+/−/−/1 | −/+/+/−/+/− | 1/1 | absent/absent |
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