OBJECTIVE: The purpose of this study was to evaluate plaque characteristics of culprit and non-culprit lesions in ST-elevation myocardial infarction (STEMI) patients at the index procedure and 10 months later using iMap intravascular ultrasound (IVUS). BACKGROUND: The exact site of the plaque rupture or erosion in coronary arteries with subsequent thrombosis cannot be precisely defined. Our hypothesis is that in STEMI patients angiographically guided stenting could fail to identify necrotic tissue and thus may leave an uncovered significant amount of vulnerable plaque. METHODS: In 63 consecutive STEMI patients the culprit artery was analyzed with iMap IVUS at the time of the index procedure and 10 months later. The most stenotic culprit segment was compared to the segment proximal to the culprit lesion. RESULTS: A high percentage of necrotic tissue was observed in the culprit lesion and a comparatively lower percentage of necrotic tissue was observed in the non-culprit lesions proximal to the culprit at the index procedure by iMap IVUS (31.9%±10.0% vs 27.8%±11.8%, p=0.012). The proportion of necrotic tissue in the segment proximal to the culprit lesion was unchanged at 10-month follow-up (27.1%±11.9% vs 25.5%±12.8%, p=0.147). The percentage of lipidic tissue in the proximal segment decreased at 10-month follow-up (9.8%±2.9% vs 8.8±3.0%, p=0.009). CONCLUSIONS: In STEMI patients, culprit lesion segments and non-culprit segments contain high proportions of necrotic tissue. However, a comparatively higher proportion of necrotic tissue was found in the culprit lesions according to iMap IVUS. The percentage of necrotic tissue remained high at 10-month follow-up in both culprit and non-culprit segments.
OBJECTIVE: The purpose of this study was to evaluate plaque characteristics of culprit and non-culprit lesions in ST-elevation myocardial infarction (STEMI) patients at the index procedure and 10 months later using iMap intravascular ultrasound (IVUS). BACKGROUND: The exact site of the plaque rupture or erosion in coronary arteries with subsequent thrombosis cannot be precisely defined. Our hypothesis is that in STEMI patients angiographically guided stenting could fail to identify necrotic tissue and thus may leave an uncovered significant amount of vulnerable plaque. METHODS: In 63 consecutive STEMI patients the culprit artery was analyzed with iMap IVUS at the time of the index procedure and 10 months later. The most stenotic culprit segment was compared to the segment proximal to the culprit lesion. RESULTS: A high percentage of necrotic tissue was observed in the culprit lesion and a comparatively lower percentage of necrotic tissue was observed in the non-culprit lesions proximal to the culprit at the index procedure by iMap IVUS (31.9%±10.0% vs 27.8%±11.8%, p=0.012). The proportion of necrotic tissue in the segment proximal to the culprit lesion was unchanged at 10-month follow-up (27.1%±11.9% vs 25.5%±12.8%, p=0.147). The percentage of lipidic tissue in the proximal segment decreased at 10-month follow-up (9.8%±2.9% vs 8.8±3.0%, p=0.009). CONCLUSIONS: In STEMI patients, culprit lesion segments and non-culprit segments contain high proportions of necrotic tissue. However, a comparatively higher proportion of necrotic tissue was found in the culprit lesions according to iMap IVUS. The percentage of necrotic tissue remained high at 10-month follow-up in both culprit and non-culprit segments.