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- William C. Little, MD∗ ( and )
- John Ambrose, MD
- ↵∗University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216
We read with interest the excellent editorial by Narula and Kovacic (1). This letter is to clarify issues in the first paragraph about our serial angiographic studies of culprit lesions before myocardial infarction (MI) (2,3).
We agree that the culprit occlusion causing an MI contains usually substantial atherosclerosis with superimposed thrombus. Furthermore, pathological and cross-sectional intracoronary imaging shows that the culprit usually produces a high-grade stenosis (>90%). However, these observations are not inconsistent with our reports that the culprit frequently did not contain a significant angiographic stenosis when evaluated before MI (2,3). The conclusions of our retrospective studies were recently confirmed in the prospective PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study, in which the mean angiographic stenosis of lesions without intervention that subsequently produced ischemic events was 32% (4). The explanation for the apparent conflict is the difference in how stenoses are measured. Pathological examination and cross-sectional imaging measure the stenosis as the reduction in cross-sectional area (CSA); angiographically, the stenosis is reported as a reduction in lumen diameter. A 75% reduction in CSA is the equivalent of a 50% reduction in diameter (5). Even a 90% reduction in CSA is a <70% reduction in cross-sectional diameter. In addition, positive remodeling increases the reference CSA but not the reference diameter. Thus, a 90% cross-sectional stenosis may be an angiographically insignificant diameter stenosis <50%.
It is clear that the presence of vulnerable plaques and the risk of subsequent occlusion are highest in areas of the coronary tree with high-grade stenoses. Some may occlude silently. However, areas without severe stenosis may also contain vulnerable plaques and are not risk-free, and importantly these nonstenotic areas are much more common and may transform over time to more severe occlusion and acute events. Thus, much of the risk for a subsequent MI is in areas without angiographic stenosis. An angiographically “insignificant” diameter stenosis does not indicate insignificant atherosclerosis or freedom from risk of subsequent events.
These clarifications serve only to strengthen the important conclusion of Narula and Kovacic (1) that advances in imaging beyond coronary angiography have enhanced our understanding of the culprits in MI, but for now our therapeutic focus must be on the entire atherosclerotic process.
- American College of Cardiology Foundation
- Narula J.,
- Kovacic J.C.
- Little W.C.,
- Constantinescu M.,
- Applegate R.J.,
- et al.
- Niccoli G.,
- Stefanini G.G.,
- Capodanno D.,
- Crea F.,
- Ambrose J.A.,
- Berg R.