ABSENCE OF FOCAL COMPENSATORY ENLARGEMENT OR CONSTRICTION IN DISEASEDHUMAN CORONARY SAPHENOUS-VEIN BYPASS GRAFTS - AN INTRAVASCULAR ULTRASOUND STUDY

Citation
T. Nishioka et al., ABSENCE OF FOCAL COMPENSATORY ENLARGEMENT OR CONSTRICTION IN DISEASEDHUMAN CORONARY SAPHENOUS-VEIN BYPASS GRAFTS - AN INTRAVASCULAR ULTRASOUND STUDY, Circulation, 93(4), 1996, pp. 683-690
Citations number
24
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
93
Issue
4
Year of publication
1996
Pages
683 - 690
Database
ISI
SICI code
0009-7322(1996)93:4<683:AOFCEO>2.0.ZU;2-Z
Abstract
Background No in vivo data are available on the occurrence of compensa tory enlargement or vessel constriction in diseased human coronary sap henous vein bypass grafts (SVBGs). The aim of this intravascular ultra sound (IVUS) study was to examine to what extent lumen reduction is ac companied by (1) vessel wall thickening and (2) arterial wall constric tion in SVBGs. Methods and Results We used IVUS to examine 43 SVBGs fr om 42 patients (32 men, 10 women; mean age, 72+/-5 years) 8 to 23 (11/-4) years after SVBG. IVUS images were obtained with a 3.5F monorail ultrasound catheter with a 30-MHz frequency and were analyzed at the l esion site, the reference site, and an intermediate site. The lumen ar ea was significantly (P<.01) decreased; the vessel wall area (SVBG cro ss-sectional area minus lumen area) and the plaque area (area within t he external elastic lamina minus lumen area) were significantly (P<.01 ) increased from the reference site through the lesion site. However. SVBG cross-sectional area was the same at these three sites (24.0+/-8. 1 versus 24.4+/-8.6 versus 24.5+/-8.6 mm(2), P=NS), and the external e lastic lamina area was also quite constant in each vessel (17.8+/-6.0 versus 17.7+/-6.4 versus 17.6+/-6.2 mm(2), P=NS). Conclusions These in vivo IVUS data from human coronary SVBGs demonstrate that (1) no foca l compensatory enlarge ment or vessel constriction occurred in stenoti c segments compared with the reference segments and that (2) the absen ce of focal compensatory enlargement appears to be a potentially impor tant factor in the progression of stenoses in coronary SVBGs.