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Hypercholesterolemia impairs endothelial function and subsequently decreases coronary vasodilatatory capacity. We examined the quantitative effects of one single LDL apheresis on vasodilatatory capacity. Using N-13 ammonia as a tracer for dynamic quantitative positron emission tomography (PET), mean myocardial perfusion measurements were carried out before and 20 h later after LDL apheresis, both under resting conditions and after pharmacological vasodilatation with dipyridamole. LDL apheresis was carried out using the heparin induced extracorporeal LDL precipitation (H.E.L.P.) procedure. We examined 47 patients (12 women and 35 men), with angiographically-proven coronary artery disease. All of them suffered from hypercholesterolemia. Of the patients, 35 received a chronic weekly H.E.L.P. procedure (group A), while H.E.L.P. procedure treatment was started for the first time in 12 patients, who were subsequently enrolled in a chronic apheresis program (group B). H.E.L.P. apheresis was combined with cholesterol lowering drugs in all patients. Both groups underwent positron emission tomography twice (prior to LDL apheresis and 20 h later). In group A, LDL cholesterol levels decreased from 175 +/- 50 mg/dL to 60 +/- 21 mg/dL immediately after H.E.L.P. (77 +/- 25 mg/dL before the second PET). Corresponding values for fibrinogen levels were 287 +/- 75 mg/dL to 102 +/- 29 mg/dL (155 +/- 52 mg/dL), minimal coronary resistance dropped from 0.56 +/- 0.20 to 0.44 +/- 0.17 mm Hg x 100 g x min/mL (P < 0.0001). Plasma viscosity decreased by 7.8%. In group B, LDL cholesterol decreased from 187 +/- 45 mg/dL to 75 +/- 27 mg/dL (85 +/- 29 mg/dL) and fibrinogen from 348 +/- 65 mg/dL to 126 +/- 38 mg/dL (168 +/- 45 mg/dL). Minimal coronary resistance was reduced from 0.61 +/- 0.23 to 0.53 +/- 0.19 mm Hg x 100 g x min/mL (P < 0.01). Plasma viscosity was observed to decrease by 7.6%. The strong LDL drop in patients under chronic H.E.L.P. treatment has a significant impact on coronary vasodilatatory capacity within 20 h leading to an improved overall cardiac perfusion. Nearly the same effect can be seen in patients after their first H.E.L.P. treatment.

In children with familial hypercholesterolemia, coronary heart disease requires both medical theraphy and LDL apheresis. We report a case of verified occlusion of the anterior descending branch of the left coronary artery in a 10-year-old patient. The pathological findings revealed by ergometry established the diagnosis. The goal was to achieve the greatest possible reduction of lipid parameters and fibrinogen by lowering plasma viscosity employing LDL apheresis. It is astonishing that this treatment is also well tolerated by children. The basic vascular approaches suffice and shunt operations are not absolutely necessary. The efficacy of this method became vividly apparent by the changes in the skin lesions. Additional angiographic follow-up and further clinical course wil provide information on the usefulness of this treatment strategy with maximum lipid theraphy and the expected improvement in prognosis.

Due to endothelial dysfunction (ED), coronary vasodilation capacity is reduced in patients with hypercholesterolemia. Cholesterol lowering may largely restore endothelial function. Currently, it is supposed that the onset of this therapeutic effect takes weeks or even months. However, by means of LDL apheresis, a significant LDL reduction may be achieved within hours. Dynamic quantitative positron emission tomography (PET) performed before and after LDL apheresis showed that mean global myocardial perfusion can be measured at rest and after pharmacological vasodilation with dipyridamole using N13 ammonia as tracer.A total of 35 patients (11 women and 24 men) with documented coronary heart disease and hypercholesterolemia underwent PET immediately prior to LDL apheresis and 18-20 hours thereafter. In addition to the decrease in LDL cholesterol (from 175+/-50 to 77+/-25 mg/dl) and fibrinogen (from 287+/-75 to 155+/-52 mg/dl), a significant improvement of myocardial blood flow under dipyridamole (177+/-59 vs 217+/-82 ml/min 100 g, p<0.0001), of coronary flow reserve (2.10+/-0.82 vs 2.62+/-1.02, p<0.0001) and of minimal coronary resistance (0.56+/-0.20 vs 0.44+/-0.17 mmHg 100 g min/ml, p<0.0001) were achieved. Plasma viscosity decreased only by 7.8%. Within 20 hours after single LDL apheresis a 20% improvement of coronary vasodilation capacity was noninvasively demonstrated and quantified.