Increased cerebral CO(2) reactivity after heparin-mediated extracorporal LDL precipitation (HELP) in patients with coronary heart disease and hyperlipidemia

There is experimental and clinical evidence that hypercholesterolemia leads to an impairment of endothelial function in coronary and cerebral arteries. Using transcranial Doppler sonography, we examined CO(2) reactivity as a marker of cerebral vasoreactivity in patients with coronary heart disease and hyperlipidemia before and after drastic lowering of LDL cholesterol, lipoprotein(a) [Lp(a)], and fibrinogen levels by heparin-mediated extracorporal LDL precipitation (HELP). CO(2) reactivity was determined in 13 patients with coronary artery disease and hyperlipidemia undergoing regular HELP therapy. Middle cerebral artery mean blood flow velocity (MFV) was detected by transcranial Doppler. CO(2) reactivity was calculated as the percent change of MFV during hypercapnia, induced by ventilation of carbogene (5% CO(2), 95% O(2)), to normocapnia. Patients with extracranial or intracranial stenoses were excluded. Other parameters such as blood viscosity, heart rate, and blood pressure were measured to control hemorheologic and systemic influences on CO(2) reactivity. A single HELP treatment reduced total cholesterol, LDL cholesterol, Lp(a), triglycerides, and fibrinogen levels by >50% (P