This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kapadia, S. R. Articles by Tuzcu, E. M. Search for Related Content PubMed PubMed Citation Articles by Kapadia, S. R. Articles by Tuzcu, E. M.

CLINICAL STUDY

Impact of lipid abnormalities in development and progression of transplant coronary disease: a serial intravascular ultrasound study

^a Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

Manuscript received October 7, 1998; revised manuscript received March 7, 2001, accepted March 23, 2001.

Reprint requests and correspondence: Dr. E. Murat Tuzcu, Department of Cardiology, Desk F-25, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195
tuzcue{at}ccf.org

OBJECTIVES

We sought to determine the role of conventional atherosclerosis risk factors in the development and progression of transplant coronary artery disease (CAD) using serial intravascular ultrasound imaging.

BACKGROUND

Transplant artery disease is a combination of allograft vasculopathy and donor atherosclerosis. The clinical determinants for each of these disease processes are not well characterized. Intravascular ultrasound imaging is the most sensitive tool to serially study these processes.

METHODS

Baseline intravascular ultrasound imaging was performed 0.9 ± 0.5 months after transplantation to identify donor atherosclerosis. Follow-up imaging was performed at 1.0 ± 0.07 year to evaluate progression of donor atherosclerosis and development of transplant vasculopathy. Conventional risk factors for CAD included recipient age, gender, smoking history, diabetes mellitus, hypertension and hypercholesterolemia.

RESULTS

Donor-transmitted atherosclerosis was present in 36 patients (39%). At follow-up, progression of donor lesions was seen in 15 patients (42%) and 42 patients (45%) developed transplant vasculopathy, leaving 35 patients (38%) without any disease. There was no difference in any conventional risk factors in patients with and without allograft vasculopathy. However, the severity of allograft vasculopathy was associated with a larger increase in low density lipoprotein (LDL) cholesterol from baseline (p = 0.02). High one-year post-transplant serum triglyceride level and pretransplant body mass index were the only significant predictors (p = 0.03) for progression of donor atherosclerosis.

CONCLUSIONS

Conventional atherosclerosis risk factors do not predict development of allograft vasculopathy, but greater change in serum LDL cholesterol level during the first year after transplant is associated with more severe vasculopathy. Therefore, maintenance of LDL cholesterol as close to pretransplant values as possible may help to limit the rate of progression of acquired allograft vasculopathy.

Abbreviations and Acronyms   BMI = body mass index   CAD = coronary artery disease   CASS = Coronary Artery Surgery Study   EEM = external elastic membrane   HDL = high density lipoprotein   HLA = human leukocyte antigen   IVUS = intravascular ultrasound   LDL = low density lipoprotein

This article has been cited by other articles:

				R.-E. W. Kavey, V. Allada, S. R. Daniels, L. L. Hayman, B. W. McCrindle, J. W. Newburger, R. S. Parekh, and J. Steinberger Cardiovascular Risk Reduction in High-Risk Pediatric Patients: A Scientific Statement From the American Heart Association Expert Panel on Population and Prevention Science; the Councils on Cardiovascular Disease in the Young, Epidemiology and Prevention, Nutrition, Physical Activity and Metabolism, High Blood Pressure Research, Cardiovascular Nursing, and the Kidney in Heart Disease; and the Interdisciplinary Working Group on Quality of Care and Outcomes Research: Endorsed by the American Academy of Pediatrics Circulation, December 12, 2006; 114(24): 2710 - 2738. [Abstract] [Full Text] [PDF]

				J. A. Kobashigawa Cardiac Allograft Vasculopathy in Heart Transplant Patients: Pathologic and Clinical Aspects for Angioplasty/Stenting J. Am. Coll. Cardiol., August 1, 2006; 48(3): 462 - 463. [Full Text] [PDF]

				J. A. Kobashigawa, J. M. Tobis, R. C. Starling, E. M. Tuzcu, A. L. Smith, H. A. Valantine, A. C. Yeung, M. R. Mehra, H. Anzai, B. T. Oeser, et al. Multicenter Intravascular Ultrasound Validation Study Among Heart Transplant Recipients: Outcomes After Five Years J. Am. Coll. Cardiol., May 3, 2005; 45(9): 1532 - 1537. [Abstract] [Full Text] [PDF]

				S. de Denus, A. Al-Jazairi, E. Loh, M. Jessup, E. J Stanek, and S. A Spinler Dyslipidemias and HMG-CoA Reductase Inhibitor Prescription in Heart Transplant Recipients Ann. Pharmacother., July 1, 2004; 38(7): 1136 - 1141. [Abstract] [Full Text] [PDF]

				A. Hognestad, K. Endresen, R. Wergeland, O. Stokke, O. Geiran, T. Holm, S. Simonsen, J. K. Kjekshus, and A. K. Andreassen Plasma C-reactive protein as a marker of cardiac allograft vasculopathy in heart transplant recipients J. Am. Coll. Cardiol., August 6, 2003; 42(3): 477 - 482. [Abstract] [Full Text] [PDF]

				M. H. Yen, G. Pilkington, R. C. Starling, N. B. Ratliff, P. M. McCarthy, J. B. Young, G. M. Chisolm, and M. S. Penn Increased Tissue Factor Expression Predicts Development of Cardiac Allograft Vasculopathy Circulation, September 10, 2002; 106(11): 1379 - 1383. [Abstract] [Full Text] [PDF]

				A. Herskowitz and A. A. Ansari Are we clear about the mechanisms by which biopsy evidence of interstitial fibrosis following cardiac transplantation helps predict late post-transplant coronary artery disease? J. Am. Coll. Cardiol., March 20, 2002; 39(6): 978 - 980. [Full Text] [PDF]