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Regression of Transplant Coronary Artery Disease During Chronic H.E.L.P.-Apheresis

Regression of Transplant Coronary Artery Disease During Chronic H.E.L.P.-Apheresis: A Case Report

Jai-Wun Park, M.D.

Despite the lack of understanding of the pathogenesis of transplant coronary artery disease, immune mechanisms may be primary and triggering stimuli in the early post-transplant phase [Hosenpud et al., 1992]. In the long-term phase, however, classical risk factors like hyperlipidemia and obesity may accelerate the progression of the disease [Winters et al., 1990].

This report concerns a heart-transplant patient with familial hypercholesterotemia who showed rapid development of a severe transplant coronary artery disease and in whom a significant regression occurred during chronic H.E.L.P.-apheresis.

The first coronary angiogram was performed six months after operation [1991]. Three serial angiograms followed on a yearly basis. To obtain reproducible QCA (Quantitative Coronary Anglography)- data, all angiograms were performed following exactly the same procedural protocol. The assessment of the 1992 and 1993 angiograms revealed so dramatic a progression of the transplant coronary artery disease that an additional treatment with H.E.L.P. on a weekly basis was given.

The lipid profile before introduction of chronic H.E.L.P.-apheresis was as follows: Cholesterol 258-397 mg/dl, LDL 174-286 mg/dl, HDL 45-59 mg/dl, Triglycerides 124-198 mg/dl, Lp(a) 138 mg/dl. The hpid lowering therapy consisted of an intensified diet and 10 mg pravastatine per day. During 12 months H.E.L.P.-therapy the mean LDL interval value (LDL before and following therapy divided by two) was 137 mg/dl, the mean Lp(a) interval value 53 mg/dl, and the mean fibrinogen interval value 192 mg/dl.

The QCA analyses of four serial angiograms (Fig.1) clearly demonstrated that in the first 2.5 years following surgery there was a rapid simultaneous progression in both the transplant coronary artery disease,involving the entire coronary system, and the development of the segmental stenotic lesion. Drastic reduction of the serum LDL, Lp(a),and fibrinogen levels by means of a year's treatment of weekly H.E.L.P.-apheresis halted further progression in the decrease of coronary diameter throughout the whole of the coronary system and brought about the marked regression of segmental obstructive lesions.

Thus, in transplant coronary artery disease patients with familial hypercholesterolemia, chronic H.E.L.P. apheresis can prevent further progression of luminal narrowing within the whole coronary system and bring about marked regression in the stenotic lesions, even in advanced cases.

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