Coronary Angiographic Predictors of MI
Abstract & commentary
Synopsis: Quantitative analysis of coronary artery lesion morphology on angiography may provide better predictors of subsequent MI than visual inspection.
Source: Ledru F, et al. J Am Coll Cardiol 1999; 33:1353-1361.
The severity of coronary artery stenoses is known to be correlated with an increased incidence of ischemic events, but predicting which artery will cause the next myocardial infarction (MI) is challenging. Thus, Ledru and colleagues evaluated the prior coronary angiograms of 84 patients with acute MI in order to determine if any lesion characteristics could predict the subsequent culprit vessel as determined by angiography within four weeks after MI. Quantitative coronary angiography analysis was used to determine luminal diameters, plaque symmetry, and plaque angles. The results showed that culprit lesions were more symmetrical, had steeper outflow angles, smaller luminal diameters, and had larger lesions than control plaques. Stenosis severity only predicted MI within one year of angiography, whereas the symmetry index and outflow angles predicted MI at the three-year follow-up. Minimal luminal diameter and inflow plaque angles were unrelated to culprit lesion frequencies. The time between angiography and subsequent MI was related to percent stenoses and outflow angle of the lesion, whereas lesion symmetry was not related to time. Ledru et al conclude that quantitative analysis of coronary artery lesion morphology on angiography may provide better predictors of subsequent MI than visual inspection. These observations may help us understand the pathophysiologic mechanisms of plaque rupture and ultimately may help us make better decisions with regard to prophylactic angioplasty.
Comment by Michael H. Crawford, MD
A decade ago, Dr. William Little and associates surprised the medical community by debunking the myth that the tightest lesion angiographically measured by percent stenosis was the culprit lesion for the next MI. Although the data were solid and replicated by others, cardiologists still spent the last decade practicing as if they could identify plaque characteristics that do predict future events. Interestingly, good old percent stenoses did predict future culprit vessels within one year in this study, but not longer. Longer term events were better predicted by stenosis symmetry and outflow angles. Also, future culprit lesions were generally 40-70% stenoses. Lesions less than 40% were less often future culprits. What was actually predicted by these characteristics was a lack of future MI events, since the positive predictive accuracy was 50% vs. a negative predictive accuracy of 87%.
This study is also somewhat iconoclastic since the irregular ugly-looking lesions were less likely to be culprits and the smooth, symmetric ones were culprits. Although the paper provides no scientific explanation for this observation, recent atherosclerosis biology studies offer some possible explanations. It may be that irregular plaques are like extinct volcanoes and more symmetric plaques are loaded with lipid gruel and have a thin fibrous cap that allows the flow of blood to push the lipid core downstream, creating an acute outflow angle. This may also explain the observation in this study that aspirin had little effect on such future culprits.
There were limitations to this study. It was retrospective in design and had the bias of including patients with a prior catheterization done for a variety of reasons that could have affected outcomes. Also, the post-MI catheterization was done for various different reasons. In addition, only those patients presenting with ECG ST elevation who had a second catheterization were included. We do not know what plaque morphology predicts non-Q presentations. Finally, intravascular ultrasound, 3D reconstruction, and other newer techniques were not used to corroborate the quantitative angiographic findings.
The real issue is whether interventional cardiologists will be impressed enough by these results to modify their practice. This would require performing angioplasty post-MI only on symmetric 40-70% lesions with acute outflow angles and leaving others alone, especially if imaging tests failed to identify the other lesions as causing ischemia. My guess, based upon a survey of our institution’s interventional cardiologists, is that they will wait and see.
Angiographic features that predict future culprit lesions include which of the following?
a. Percent stenosis
b. Plaque symmetry
c. Plaque outflow angle
d. All of the above
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