REGRESSION OF TRANSPLANT CORONARY-ARTERY DISEASE DURING CHRONIC LOW-DENSITY LIPOPROTEIN-APHERESIS

Background: The pathogenesis of transplant coronary artery disease (Tx CAD) is probably multifactorial. Immune mechanisms may be the primary and triggering stimuli, whereas risk factors such as hyperlipoproteine mia or lipoprotein(a) elevation may accelerate the progression of the disease. With the heparin-induced-low-density lipoprotein-precipitatio n (HELP), low-density lipoprotein (LDL), fibrinogen, and lipoprotein(a ) can be reduced about 55%, 50%, and 60%, respectively. Methods: We tr eated eight heart transplant recipients (52.6 +/- 8.1 years old; all m en) with weekly LDL-apheresis (HELP-system). At the beginning of the H ELP treatment, all patients had survived at least 2 years after surger y, had LDL levels higher than 150 mg/dl in spite of 10 mg pravastatin per day and diet, and had development of significant coronary artery d isease as shown by annual coronary angiography. We analyzed three angi ograms in each patient taken 16.2 +/- 6.5 months before, at the beginn ing of (-0.5 +/- 6 months), and after 21.8 +/- 7.4 months of HELP ther apy. Two hundred seventy-three coronary artery segments (34 +/- 6 per patient; 6 to 65 single measurements per segment) were analyzed by qua ntitative coronary angiography. Statistical significances of differenc es between the angiograms taken at the three time points were evaluate d by the paired t test. Results: Measurements of all coronary artery s egments showed a significant decrease of mean luminal diameter during the last 1 to 2.5 years before the HELP treatment from 3.61 +/- 1.1 mm to 3.15 +/- 1 mm (p < 0.0001). During the following 1 to 2.5 years of HELP therapy, the mean luminal diameter increased to 3.4 +/- 1.15 mm (p < 0.0001). Conclusions: In long-term heart transplantation survivor s with hyperlipidemia, who have development of a rapid progressive cor onary artery disease, LDL-apheresis can lead to disease regression. Fu rther studies will be needed to determine whether immunologic factors and growth factors involved in the TxCAD pathogenesis are also elimina ted by the HELP therapy and whether HELP is also effective in patients with TxCAD without severe hypercholesterolemia.