Coronary lesion morphology in acute myocardial infarction: demonstration of early remodeling after streptokinase treatment

Cardiac Department, London Chest Hospital, England.

Coronary lesion morphology was analyzed in 72 patients 1 to 8 days after streptokinase treatment for acute myocardial infarction and compared with lesion morphology in a control group of 24 patients with stable angina. In the streptokinase group the infarct-related artery was patent in 55 patients (76%). Compared with stenoses in the stable angina group, there were no differences in the stenosis length, severity, calcification or in the proportion located at an acute bend or at a branch point. However, lesions in the streptokinase group were more often irregular (p less than 0.005) and eccentric (p less than 0.01), had a shoulder (p less than 0.0001), globular filling defects (p less than 0.01), linear filling defects (p less than 0.00005) and contrast staining (p less than 0.05). Plaque ulceration index was higher in the streptokinase than in the stable angina group (6.2 +/- 7.9 versus 3.5 +/- 3.4, p less than 0.001). Of the 72 streptokinase-treated patients, 35 were maintained on heparin infusion until angioplasty 2 to 10 days later. At repeat angiography before angioplasty, globular lesion filling defects seen in eight patients had disappeared, whereas linear filling defects persisted in 7 of 14 cases. Fewer lesions were irregular (p less than 0.0001) and the ulceration index decreased from 7.4 +/- 10.4 to 3.0 +/- 1.6 (p less than 0.001). These data show that the lesion in the infarct-related artery after streptokinase treatment is irregular and often associated with filling defects, perhaps corresponding to plaque fissuring and intraluminal thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				S. H. Rezkalla and D. R. Holmes Jr Lipid-rich plaque masquerading as a coronary thrombus. Clin. Med. Res., June 1, 2006; 4(2): 119 - 122. [Abstract] [Full Text] [PDF]

				P Avanzas, R Arroyo-Espliguero, J Cosin-Sales, G Aldama, C Pizzi, J Quiles, and J C Kaski Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes Heart, August 1, 2004; 90(8): 847 - 852. [Abstract] [Full Text] [PDF]

				L. Badimon, G. Vilahur, S. Sanchez, and X. Duran Atheromatous plaque formation and thrombogenesis: formation, risk factors and therapeutic approaches Eur. Heart J. Suppl., August 1, 2001; 3(suppl_I): I16 - I22. [Abstract] [PDF]

				S. M. Zaacks, P. R. Liebson, J. E. Calvin, J. E. Parrillo, and L. W. Klein Unstable angina and non-Q wave myocardial infarction: does the clinical diagnosis have therapeutic implications? J. Am. Coll. Cardiol., January 1, 1999; 33(1): 107 - 118. [Abstract] [Full Text] [PDF]

				E. Van Belle, J.-M. Lablanche, C. Bauters, N. Renaud, E. P. McFadden, and M. E. Bertrand Coronary Angioscopic Findings in the Infarct-Related Vessel Within 1 Month of Acute Myocardial Infarction : Natural History and the Effect of Thrombolysis Circulation, January 13, 1998; 97(1): 26 - 33. [Abstract] [Full Text] [PDF]

				M. D. Guazzi, M. Bussotti, L. Grancini, N. De Cesare, M. Guazzi, I. L. Pera, and A. Loaldi Evidence of Multifocal Activity of Coronary Disease in Patients With Acute Myocardial Infarction Circulation, August 19, 1997; 96(4): 1145 - 1151. [Abstract] [Full Text]