Circulation, Vol 87, 1123-1129, Copyright © 1993 by American Heart Association
CM Gibson, RE Kuntz, M Nobuyoshi, B Rosner and DS Baim
BACKGROUND. Since many restenosis trials include patients in whom more than
one lesion is treated, analysis of the angiographic data on a "per lesion"
basis might be confounded by potential correlations of restenosis among
multiple treated lesions within each patient. The goals of this study were:
1) to determine whether there was any correlation in the rate of restenosis
among multiple lesions that underwent conventional angioplasty, stenting,
or directional atherectomy within the same patient and 2) to determine
whether lesions treated in a multilesion intervention experience a
different magnitude of restenosis than lesions undergoing single-lesion
procedures. METHODS AND RESULTS. Of 441 patients treated by Palmaz-Schatz
stenting (n = 114), directional atherectomy (n = 100), or conventional
balloon angioplasty (n = 227), 67 underwent multilesion procedures
involving treatment of 146 lesions. A general linear model with intraclass
correlation (GLIMIC) was used to calculate the coefficient of correlation
(rho) of the change in the measured minimum luminal diameter (late loss)
from the time of the initial procedure to 6-month angiogram among the
multiple lesions within the same patient for all 441 patients. This showed
no correlation among multiple lesions within the same patient for the late
loss in minimum luminal diameter (rho = - 0.12 [95% CI: -0.40, 0.12]),
among lesions in the same vessel (rho = 0.14 [95% CI: -0.34, 0.62]), or
among different vessels (rho = -0.18 [95% CI: -0.52, 0.16]), suggesting
that the magnitude of late loss is independent among multiple lesions
within the same patient. There was no difference (p = 0.96) between the
observed incidence of zero-, one-, and two-vessel restenosis (> or = 50%
diameter stenosis at follow-up) for patients with multiple-lesion treatment
and that predicted assuming lesion-to-lesion independence. Similarly, there
was no difference in late loss or in the overall binary restenosis rate
when single-lesion procedures were compared with multilesion procedures.
Multivariable analysis of the late loss in lumen diameter (which adjusted
for the effects of the acute result and the device used) demonstrated no
independent effect (p = 0.20) of single-lesion versus multilesion status.
CONCLUSIONS. Luminal encroachment appears to occur at independent rates
among multiple lesions treated in a single patient. The observed incidence
of restenosis for patients with multiple treated lesions is accurately
predicted assuming independent probabilities of restenosis. Lesion-based
analysis, even when including multiple treated lesions within the same
patient, is thus valid for evaluating conventional angioplasty, stenting,
or directional atherectomy.
ARTICLES
Lesion-to-lesion independence of restenosis after treatment by conventional angioplasty, stenting, or directional atherectomy. Validation of lesion-based restenosis analysis
Charles A. Dana Research Institute, Harvard Medical School, Boston, MA.
This article has been cited by other articles:
![]() |
R A Byrne, S Eberle, A Kastrati, A Dibra, G Ndrepepa, R Iijima, J Mehilli, and A Schomig Distribution of angiographic measures of restenosis after drug-eluting stent implantation Heart, October 1, 2009; 95(19): 1572 - 1578. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. T. Willerson Myocardial Revascularization with Cardiologic Interventional Devices Card. Surg. Adult, January 1, 2003; 2(2003): 561 - 580. [Full Text] |
||||
![]() |
T.-l. Yue, J. Chen, W. Bao, P. K. Narayanan, A. Bril, W. Jiang, P. G. Lysko, J.-L. Gu, R. Boyce, D. M. Zimmerman, et al. In Vivo Myocardial Protection From Ischemia/Reperfusion Injury by the Peroxisome Proliferator-Activated Receptor-{gamma} Agonist Rosiglitazone Circulation, November 20, 2001; 104(21): 2588 - 2594. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Takagi, T. Akasaka, A. Yamamuro, Y. Honda, T. Hozumi, S. Morioka, and K. Yoshida Troglitazone reduces neointimal tissue proliferation after coronary stent implantation in patients with non-insulin dependent diabetes mellitus: A serial intravascular ultrasound study J. Am. Coll. Cardiol., November 1, 2000; 36(5): 1529 - 1535. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Takagi, K. Yoshida, T. Akasaka, S. Kaji, T. Kawamoto, Y. Honda, A. Yamamuro, T. Hozumi, and S. Morioka Hyperinsulinemia during oral glucose tolerance test is associated with increased neointimal tissue proliferation after coronary stent implantation in nondiabetic patients: A serial intravascular ultrasound study J. Am. Coll. Cardiol., September 1, 2000; 36(3): 731 - 738. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Escaned, J. Goicolea, F. Alfonso, M. J. Perez-Vizcayno, R. Hernandez, A. Fernandez-Ortiz, C. Banuelos, and C. Macaya Propensity and mechanisms of restenosis in different coronary stent designs: Complementary value of the analysis of the luminal gain-loss relationship J. Am. Coll. Cardiol., November 1, 1999; 34(5): 1490 - 1497. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Magdy, M. Al-Abbady, A. Ghoga, K. Heib, and C. Ozbek Restenosis After Angioplasty in Patients with Left Ventricular Dysfunction Asian Cardiovasc Thorac Ann, September 1, 1999; 7(3): 209 - 213. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Kastrati, A. Schomig, S. Elezi, H. Schuhlen, M. Wilhelm, and J. Dirschinger Interlesion Dependence of the Risk for Restenosis in Patients With Coronary Stent Placement in Multiple Lesions Circulation, June 23, 1998; 97(24): 2396 - 2401. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Schomig, A. Kastrati, S. Elezi, H. Schuhlen, J. Dirschinger, F. Dannegger, M. Wilhelm, and K. Ulm Bimodal Distribution of Angiographic Measures of Restenosis Six Months After Coronary Stent Placement Circulation, December 2, 1997; 96(11): 3880 - 3887. [Abstract] [Full Text] |
||||
![]() |
W. Casscells Growth Factor Therapies for Vascular Injury and Ischemia Circulation, June 1, 1995; 91(11): 2699 - 2702. [Full Text] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1993 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |