[Mechanism of acute coronary syndrome studied with coronary arteriograms]
1Second Department of Internal Medicine, Gifu University School of Medicine.
Insights
Acute coronary syndrome (ACS) mechanisms involve plaque rupture. Our study shows coronary artery stenosis rapidly worsens before ACS events, highlighting the need for further research into lesion progression.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Pathophysiology
Background:
- Acute coronary syndrome (ACS) mechanisms have been studied using coronary arteriograms (CAG) since 1980.
- Previous research indicates total occlusion at acute myocardial infarction (AMI) onset, with milder stenosis in unstable angina.
- Angiographic findings classify culprit lesions in ACS, often linked to plaque rupture and thrombus.
Purpose of the Study:
- To investigate the progression of coronary artery stenosis leading to acute coronary syndrome (ACS).
- To understand the abrupt changes in coronary lesions preceding ACS events.
- To identify challenges in predicting future AMI based on prior CAG findings.
Main Methods:
- Review of existing literature on coronary arteriograms (CAG) and acute coronary syndrome (ACS).
- Analysis of studies reporting on lesion morphology and occlusion rates in relation to ACS onset.
- Comparison of stenosis severity in unstable angina versus non-Q wave AMI.
Main Results:
- Coronary artery stenosis can deteriorate abruptly, reaching severe levels shortly before ACS.
- Predicting future AMI based on CAG findings 1-2 years prior is difficult due to mild to moderate pre-existing stenosis.
- Lesion morphology, such as eccentric or irregular types, is more prevalent in ACS, suggesting plaque rupture.
Conclusions:
- The progression of coronary lesions leading to ACS is complex and requires further investigation.
- Sudden deterioration of stenosis is a key factor in the acute phase of ACS.
- Current methods for predicting AMI from CAG findings are limited.
Abstract:
Numbers of studies using the coronary arteriograms (CAG) have been reported on the mechanism of the acute coronary syndrome (ACS) since 1980. DeWood et al. have shown that the rate of total occlusion in the culprit lesions gradually decreases as the interval from attack to CAG increases, suggesting that the occlusion is total or subtotal at the onset of acute myocardial infarction (AMI). Additionally, the stenosis is significantly mild in unstable angina compared with non-Q AMI. Ambrose et al. classified the morphology of the culprit lesions on CAG and revealed that their type II eccentric lesion or multiple irregularities, which are considered to be related to plaque rupture with or without thrombus, are more common in ACS than the other morphologies. The concept of ACS by Fuster et al. is substantially based on these angiographical findings. Little et al. reported that the pre-existing stenosis 1-2 years before the onset of AMI is mostly mild to moderate, indicating that the prediction of future AMI by CAG findings is of difficulty. Our study suggested the stenosis deteriorates abruptly and reached severe level in some cases just before the attack of ACS. Therefore, the continuous effort is needed to clarify the mechanism of the progression of coronary lesions which result in ACS.
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