Differences in the morphology of unstable and stable coronary lesions and their impact on the mechanisms of angioplasty. An in vivo study with intravascular ultrasound.

The aim of this study was to compare the morphology of stable and unstable coronary lesions using intravascular ultrasound in patients undergoing coronary balloon angioplasty and to determine whether lesion morphology had any influence on the mechanism of balloon angioplasty. Thirty three (15 stable and 18 unstable) patients undergoing single lesion percutaneous transluminal coronary angioplasty were studied with intravascular ultrasound before and after intervention. All examinations, recorded on S-VHS video tape, were studied off-line and matched sites from the point of minimum lumen area after the procedure and the corresponding site prior to intervention were compared. The morphology of lesions before intervention was noted and the mechanisms of angioplasty (vessel stretch, lesion remodelling and lesion tears) were determined by comparing pre- and post-interventional morphology and dimensions. The only significant morphological difference between stable and unstable lesions was the presence of a demarcated inner layer in unstable lesions, delimited by a fine circumferential line. This pattern was noted in 77% (14/18) of unstable lesions and in 7% (1/15) of stable lesions (P < 0.01). Unstable lesions tended to have more echolucent zones than stable lesions (72% (13/18) vs 46% (7/15), P = 0.13). The mechanisms of angioplasty were also found to differ. Whereas lesion remodelling (or 'compression') was seen in 77% (14/18) of unstable lesions, it occurred in only 13% (2/15) of stable lesions and mean lesion cross-sectional area reduction was greater in unstable lesions, - 14.8 +/- 8.3% (2.1 +/- 1.3 mm2) compared to stable lesions, - 4.1 +/- 8.4% (0.42 +/- 0.9 mm2), P < 0.01. In contrast, vessel stretch was seen more frequently in stable lesions (73%, 11/15) compared to unstable lesions (22%, 4/18) P < 0.01 and the mean increase in vessel cross-sectional area was + 13.5 +/- 6.8 (1.6 +/- 0.9 mm2) in stable lesions compared to + 5.5 +/- 5.6% (0.8 +/- 0.9 mm2) in unstable lesions, P < 0.01. Lesion tear was present to a similar degree in both groups of patients. In this observational study we found a set of echographic markers that distinguished unstable lesions. The mechanisms of angioplasty differed between stable and unstable angina, with greater lesion remodelling seen in unstable lesions and vessel stretch in stable lesions. Taken together, these findings suggest that the markers we describe may be echographic indicators of mural thrombus.