Time-Sequencing Morphometric Changes of Target Vessel Immediately after Percutaneous Coronary Balloon Angioplasty.
10.4070/kcj.1998.28.2.222
- Author:
Dongsoo KIM
;
Yangsoo JANG
;
Hyuckmoon KWON
;
Bum Kee HONG
;
Hyun Seung KIM
- Publication Type:Original Article
- Keywords:
Percutaneous coronary balloon angioplasty;
Intravascular ultrasound balloon catheter;
Plaque morphology
- MeSH:
Angioplasty;
Angioplasty, Balloon;
Angioplasty, Balloon, Coronary*;
Catheters;
Coronary Angiography;
Humans;
Male;
Membranes;
Phenobarbital;
Ultrasonography
- From:Korean Circulation Journal
1998;28(2):222-229
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Plaque compression (and/or redistribution) and vessel expansion are important mechanisms of percutaneous coroanry balloon angioplasty. We investigated the mechanisms of balloon angioplasty according to plaque characteristics by intravascular ultrasound and assessed the time-sequencing morphometric changes of target vessel after balloon dilation without catheter change using intravascular ultrasound balloon catheter. METHOD: We studied balloon angioplasty in 10 patients (eight male, average age of 55.3 years). Quantitative coronary angiography and intravascular ultrasound images were attained at baseline and at timed intervals of 0sec, 60sec and 180sec post-balloon angioplasty. The following categories were attained : reference diameter, minimal lumen diameter, cross sectional area (CSA) of lumen (L), external elastic membrane (EEM), and plaque + media (P+M). We also assessed the plaque morphology of target lesion and classified them into two groups according to intravascular ultrasound imaging : a soft plaque group versus a group characterized by fibrous and/or mildly calcified plaque. RESULTS: The proportions of plaque compression in the total luminal gain were 80% in the soft plaque group and 70% in the other ; the absolute amount of plaque compression was 26.9% in soft plaque and 24.0% in the other group. The time sequencing changes of target lesion EEM CSA of both group were 14.4+/-2.9mm2, 14.3+/-3.8mm2 (baseline) 15.1+/-2.5mm2, 15.4+/-3.7mm2 (immediate) 15.0+/-2.8mm2, 14.5+/-3.9mm2 (180sec), those of P+M CSA (target lesion) were 10.4+/-3.3mm2, 10.7+/-2.4mm2 (baseline) 7.6+/-2.7mm2, 8.1+/-2.4mm2 (immediate) 7.9+/-2.9mm2, 8.5+/-3.4mm2 (180sec). Target lesion lumen CSA were 4.0+/-1.1mm2, 3.6+/-2.0mm2 (baseline) 7.5+/-1.1mm2, 7.3+/-3.2mm2 (immediate) 7.1+/-1.3mm2, 6.0+/-1.7mm2 (180sec) respectively. CONCLUSION: Plaque compression (and/or redistribution) is the predominant mechanism of luminal gain in both groups. The absolute amounts of P+M CSA changes and time sequencing increment of target lesion were similar in both groups. In the non-soft group, the immediate increment and time sequencing reduction of EEM CSA in target lesion were greater than those of the soft plaque group.
