[Qualitative and quantitative descriptions of the mechanisms of action of the angioplasty balloon on coronary stenosis. An endovascular ultrasonic study].
The barotrauma induced by inflation of the balloon on an obstructive atherosclerotic plaque induces several distinct, complex effects. The object of this study was to describe these mechanisms based on endovascular echographic sections of coronary stenoses before and after balloon angioplasty. The 32 lesions analysed were richly cellular (81.2%) and associated with calcifications in 31% of cases. The remodelling index before angioplasty was used to individualize a majority of lesions with chronic arterial constriction (56.2%). The modelling of the plaque (dilatation or constriction) had no effect on the final luminal result. Global analysis of the endoluminal gain (4.38 +/- 2.28 mm2) showed that it was mainly due to reduction of plaque surface (78.2% of gain) without prejudging the mechanism, and less due to expansion of the global arterial surface (21.8% of the gain). The type of remodelling affected the mechanisms of action of balloon angioplasty. Dissection was present in 53.1% of cases. Fragmentation of the plaque with embolisation is a common phenomenon (28% of cases). The authors conclude that there are four mechanisms which coexist: 1) Reduction of plaque thickness cannot physically correspond to simple compression of tissue. The plaque is redistributed longitudinally. 2) Arterial expansion only plays a minor part in endoluminal gain. 3) Plaque rupture is directly related to the acute increase in wall stress often exceeding the thresholds of rupture of its components. Finally, 4) embolisation by parietal fragmentation, a mechanism often unknown or ignored which plays an essential part in the potentially deleterious effects.
Finet
G
G
Service d'hémodynamique, hôpital cardiovasculaire et pneumologique, hospices civils de Lyon, Lyon.
Abrysch
F
F
Rioufol
G
G
Ohayon
J
J
Lagache
M
M
D000800:Angioplasty, Balloon / Q000009:adverse effects* / Q000295:instrumentation*; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000503:physiopathology / Q000628:therapy*; D003327:Coronary Disease / Q000000981:diagnostic imaging* / Q000503:physiopathology / Q000628:therapy*; D017548:Echocardiography, Transesophageal; D006801:Humans; D014661:Vasoconstriction; D014664:Vasodilation