CORRESPONDENCE
Can angiography predict the vulnerable lesion that progresses to myocardial infarction?
Dimitris Tousoulis, MD, PhD, FACCa,
Graham Davies, MD, FRCPa,
Christodoulos Stefanadis, MD, FACCb and
Pavlos Toutouzas, MD, FACCb
a Hammersmith Hospital, Du Cane Road, London W12, United Kingdom
b Athens University, Vasillisis Sofias 114, Athens, Greece
Ledru et al. (1), in their interesting study, attempted to identify the most powerful angiographic predictors of a future acute myocardial infarction with known coronary anatomy. They showed that the symmetry index and the outflow angles were the two independent predictors of infarction at three-year follow-up. Stenosis severity predicted only those infarctions occurring within one year of angiography.
The identification of predictive markers for acute myocardial infarction remains a challenge. Many attempts have been made, and different markers have been proposed. Biochemical markers have been found—for example, serum C-reactive protein level, which is higher in those patients with unstable angina who subsequently develop acute myocardial infarction (2). Other investigators have proposed different angiographic markers. Ambrose et al. (3,4) found that on the initial angiogram the lesion responsible for the infarction had <50% stenosis in one-half of cases and <70% stenosis in more than two-thirds. They showed that the morphologic characteristics of the plaque may also be useful predictive markers for an acute coronary syndrome. Stenoses with an eccentric outline and a narrow neck and those with overhanging edges, scalloped borders or multiple irregularities often progressed to acute myocardial infarction. Little et al. (5) also reported that the artery that subsequently occluded had only mild stenosis (<50%) on the first angiogram in two-thirds of patients and <70% stenosis in the vast majority of patients. They also showed that the stenoses that progressed to acute myocardial infarction usually were of complex morphology. By contrast, Taeymans et al. (6) showed that stenoses that progressed to total occlusion were the more severe, and the inflow and outflow angles were steeper than those of lesions that did not occlude. Similarly, Ledru et al. (1) showed that culprit lesions had steeper outflow angles and were longer than control nonculprit lesions. However, it is difficult to properly evaluate steepness of the outflow angle and symmetry index from only one projection, because they are both inextricably dependent on the angle of projection.
A recent study from our group (7) also showed that the development of myocardial infarction cannot be predicted from the severity of preexisting stenosis, but is related to lesion morphology. A preexisting irregular, eccentric morphology is significantly more common in infarct-related than in non–infarct-related stenoses. For acute myocardial infarction, therefore, stenosis morphology seems to be more predictive than stenosis severity. We have also analyzed the morphologic characteristics of stenoses using a computerized angiographic analysis system (CASS system, Pie Medical Data), and we found that stenoses with a symmetrical, smooth diameter function shadow are likely to remain stable (Fig. 1A), whereas stenoses with an asymmetrical, irregular diameter function shadow (Fig. 1B) often progressed to acute myocardial infarction. Thus, computerized analysis may allow for the identification of vulnerable lesions.
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Figure 1 Two patterns of computerized diameter function in two non severe lesions. (A) the stenosis diameter borders are smooth and symmetrical; (B) the stenosis diameter borders are irregular and asymmetrical.
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Although complex lesions appear to increase the risk of future myocardial infarction (8,9), the majority of complex lesions remain stable for years (10). Therefore, new noninvasive and invasive (e.g., ultrasound, thermographic catheter) diagnostic modalities and new biochemical markers will be necessary in the future to enable early identification of vulnerable atherosclerotic plaques and to prevent acute myocardial infarction.
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References
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- Ledru F, Theroux P, Lespérance J, et al. Geometric features of coronary artery lesions favoring acute occlusion and myocardial infarction: a quantitative angiographic study. J Am Coll Cardiol. 1999;33:1353–1361[Abstract/Free Full Text]
- Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med. 1994;331:417–424[Abstract/Free Full Text]
- Ambrose JA, Winters SL, Arora RR, et al. Coronary angiographic morphology in myocardial infarction: a link between the pathogenesis of unstable angina and myocardial infarction. J Am Coll Cardiol. 1985;6:1233–1238[Abstract]
- Ambrose JA, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol. 1988;12:56–62[Abstract]
- Little WC, Constantinescu M, Applegate RJ, et al. Can coronary angiography predict the site of subsequent myocardial infarction in patients with mild to moderate coronary artery disease? Circulation. 1988;78:1157–1166[Abstract/Free Full Text]
- Taeymans Y, Theroux P, Lesperance J, Waters D. Quantitative angiographic morphology of the coronary artery lesions at risk of thrombotic occlusion. Circulation. 1992;85:78–85[Abstract/Free Full Text]
- Tousoulis D, Davies G, Crake T, Lefroy D, Rosen S, Maseri A. Angiographic characteristics of the infarct- and non–infarct-related stenoses in patients with stable angina progressed to acute myocardial infarction. Am Heart J. 1998;136:382–388[CrossRef][Medline]
- Kaski JC, Chen L, Chester MR. Rapid angiographic progression of coronary artery disease in patients with angina pectoris. Circulation. 1995;92:2058–2065[Abstract/Free Full Text]
- Chen L, Chester MK, Crook R, Kaski JC. Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris. J Am Coll Cardiol. 1996;28:597–603[Abstract]
- Kaski JC, Tousoulis D, Pereira WI, Crea F, Maseri A. Progression of complex coronary artery stenosis in patients with angina pectoris: its relation to clinical events. Coron Artery Dis. 1992;3:305–312
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