High-grade culprit lesions are a common cause of ST-segment elevation myocardial infarction
Michael Liang1, Takashi Kajiya1, Mark Y Chan1
1National University Heart Centre Singapore, Singapore.
Insights
Contrary to belief, most ST-segment elevation myocardial infarction (STEMI) cases involve culprit lesions with over 50% arterial stenosis. This study challenges the conventional view on atherosclerotic plaque rupture severity in STEMI patients undergoing primary percutaneous coronary intervention.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Pathology of Atherosclerosis
Background:
- Conventional understanding suggests moderate stenoses (<50% diameter loss) cause most ST-segment elevation myocardial infarction (STEMI).
- This paradigm is based on assumptions about the nature of ruptured atherosclerotic plaques.
- The actual severity of culprit lesions in STEMI patients requires further investigation.
Purpose of the Study:
- To analyze the characteristics of culprit lesions in patients presenting with STEMI.
- To determine the degree of stenosis in lesions causing STEMI and undergoing primary percutaneous coronary intervention (PPCI).
- To challenge or confirm the existing knowledge regarding lesion severity in STEMI.
Main Methods:
- A retrospective analysis of patients who underwent PPCI between June 2008 and August 2010.
- Quantitative coronary angiography was performed on culprit lesions post-intervention.
- Measurements included minimal luminal diameter, reference vessel diameter, diameter stenosis, and lesion length.
Main Results:
- Out of 1,021 patients, 80.2% had culprit lesions with >50% diameter stenosis.
- Mean diameter stenosis was 61 ± 16%, with a mean minimal luminal diameter of 1.1 ± 0.5 mm.
- High-grade stenoses (>50%) were more common in male patients and persisted even after balloon angioplasty in many cases.
Conclusions:
- The findings contradict the conventional view that STEMI is primarily caused by lesions with <50% stenosis.
- A significant majority of STEMI culprit lesions in this cohort exhibited high-grade stenosis (>50%).
- This suggests a need to re-evaluate the understanding of plaque rupture mechanisms in STEMI.
Introduction:
Conventional knowledge holds that the majority of ruptured atherosclerotic plaques causing ST-segment elevation myocardial infarction (STEMI) are found in moderate stenoses that produce < 50% loss of arterial diameter. This study aimed to analyse the culprit lesions in patients who presented with STEMI and underwent primary percutaneous coronary intervention (PPCI) at our institution.
Methods:
Patients who underwent PPCI between June 2008 and August 2010 at our institution were included in the analysis. Quantitative coronary angiography was performed for the culprit lesions immediately after antegrade flow was restored by thrombectomy, low-profile balloon predilatation or guidewire crossing.
Results:
A total of 1,021 patients were included in the study. The mean age was 57 ± 12 years and 85.2% were male. Lesion measurement was done after coronary flow was restored by thrombectomy (73.1%), balloon dilatation (24.1%) and following guidewire passage across the lesion (2.8%). Mean minimal luminal diameter was 1.1 ± 0.5 mm, mean reference vessel diameter was 2.8 ± 0.6 mm, mean diameter stenosis was 61 ± 16% and mean lesion length was 16 ± 6 mm. Most (80.2%) of the culprit lesions had diameter stenoses > 50% (p < 0.01). Although balloon angioplasty was performed in 24.1% of the patients, the majority (64.2%) still had diameter stenoses > 50%. High-grade stenoses (> 50%) were more frequently observed in male patients (p = 0.04).
Conclusion:
Contrary to the existing paradigm, we found that most of the patients with STEMI in our institution had culprit lesions with diameter stenosis > 50%.
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