Comprehensive analysis of intravascular ultrasound and angiographic morphology of culprit lesions between ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome.

Background: Some plaques lead to ST-segment elevation myocardial infarction (STEMI), whereas others cause non-ST-segment elevation acute coronary syndrome (NSTEACS). We used angiography and intravascular ultrasound (IVUS) to investigate the difference of culprit lesion morphologies in ACS.

Methods: Consecutive 158 ACS patients whose culprit lesions were imaged by preintervention IVUS were enrolled (STEMI=81; NSTEACS=77). IVUS and angiographic findings of the culprit lesions, and clinical characteristics were compared between the groups.

Results: There were no significant differences in patients' characteristics except for lower rate of statin use in patients with STEMI (20% vs 44%, p=0.001). Although angiographic complex culprit morphology (Ambrose classification) and thrombus were more common in STEMI than in NSTEACS (84% vs 62%, p=0.002; 51% vs 5%, p<0.0001, respectively), SYNTAX score was lower in STEMI (8.6 ± 5.4 vs 11.5 ± 7.1, p=0.01). In patients with STEMI, culprit echogenicity was more hypoechoic (64% vs 40%, p=0.01), and the incidence of plaque rupture, attenuation and "microcalcification" were significantly higher (56% vs 17%, p<0.0001; 85% vs 69%, p=0.01; 77% vs 61%, p=0.04, respectively). Furthermore, the maximum area of ruptured cavity, echolucent zone and arc of microcalcification were significantly greater in STEMI compared with NSTEACS (1.80 ± 0.99 mm(2) vs 1.13 ± 0.86 mm(2), p=0.006; 1.52 ± 0.74 mm(2) vs 1.21 ± 0.81 mm(2), p=0.004; 99.9 ± 54.6° vs 77.4 ± 51.2°, p=0.01, respectively). Quantitative IVUS analysis showed that vessel and plaque area were significantly larger at minimum lumen area site (16.6 ± 5.4 mm(2) vs 14.2 ± 5.5 mm(2), p=0.003; 13.9 ± 5.1 mm(2) vs 11.6 ± 5.2 mm(2), p=0.003, respectively).

Conclusion: Morphological feature (outward vessel remodeling, plaque buildup and IVUS vulnerability of culprit lesions) might relate to clinical presentation in patients with ACS.