Key result
STEMI culprit lesions demonstrated similar anatomical severity to stable, ischemia-inducing lesions (percentage area stenosis 91.6% vs 90.1%; P=0.11).
Why the study?
Are STEMI culprit lesions anatomically severe after thrombus aspiration compared to stable ischaemia-inducing lesions?
Observational (n=386)
Are STEMI culprit lesions anatomically severe after thrombus aspiration compared to stable ischaemia-inducing lesions?
Absolute Event Rate: 91.6% vs 90.1%
p-value: p=0.11
STEMI culprit lesions, when assessed after thrombus aspiration, are angiographically severe and comparable to stable, ischemia-inducing lesions, challenging the historical notion that STEMI primarily arises from mildly stenotic plaques.
Questions mild-stenosis predominance in STEMI post-aspiration; leaves open prospective validation of severity as rupture predictor.
BACKGROUND: Historical data report fatal myocardial infarction occurring when mildly-stenotic coronary plaques rupture; however, recent data suggest haemodynamically-significant coronary stenoses with fractional flow reserve (FFR) ≤ 0.8 and vessels with high plaque burden and minimum luminal area (MLA) < 4 mm(2) by intravascular ultrasound (IVUS) may be prognostically important. Therefore, we sought to re-evaluate culprit stenosis severity in patients presenting with ST-segment elevation myocardial infarction (STEMI). METHODS: Patients undergoing primary percutaneous coronary intervention (PPCI) for STEMI with adjunctive thrombectomy between October 2008 and February 2010 (n = 336/572; 59%) underwent quantitative coronary angiography (QCA) after thrombus aspiration to determine vessel reference area (RA), MLA and percentage area stenosis (AS). To validate findings, QCA and FFR were measured in 50 patients with stable angina and an angiographically-intermediate lesion. RESULTS: STEMI patients had anatomically-severe underlying culprit disease similar to that of the stable cohort (AS: 91.6 ± 9.5% versus 90.1 ± 8.1%; P = 0.11). Additionally, anatomically-severe lesions defined by QCA were more likely to be functionally-significant by FFR and vice-versa (P = 0.02 and 0.002 respectively). CONCLUSION: These contemporary data suggest that STEMI culprit lesions, defined by luminal stenosis after thrombus aspiration, are angiographically significant, with similar stenosis severity to stable, ischaemia-inducing lesions.
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Hoole et al. (2012) conducted an observational in ST-segment elevation myocardial infarction (STEMI) (n=386). STEMI culprit lesions vs. Stable angina lesions was evaluated on Percentage area stenosis (AS) (p=0.11). STEMI culprit lesions demonstrated similar anatomical severity to stable, ischemia-inducing lesions (percentage area stenosis 91.6% vs 90.1%; P=0.11).
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