Abstract
High concentrations of lipoprotein(a) (Lp(a)) represent an important independent and causal risk factor associated with adverse outcome in atherosclerotic cardiovascular disease (CVD). Effective Lp(a) lowering drug treatment is not available. Lipoprotein apheresis (LA) has been proven to prevent cardiovascular events in patients with Lp(a)-hyperlipoproteinemia (Lp(a)-HLP) and progressive CVD. Here we present the course of a male patient with established peripheral arterial occlusive disease (PAOD) at the early age of 41 and coronary artery disease (CAD), who during follow-up developed over 2 years a progressive syndrome of cerebellar and spinal cord deficits against the background of multifactorial cardiovascular risk including positive family history of CVD. Spastic tetraplegia and dependency on wheel chair and nursing care represented the nadir of neurological deficits. All conventional risk factors including LDL-cholesterol had already been treated and after exclusion of other causes, genetically determined Lp(a)-HLP was considered as the major underlying etiologic factor of ischemic vascular disease in this patient including spinal cord ischemia with vascular myelopathy. Treatment with an intensive regimen of chronic LA over 4.5 years now was successful to stabilize PAOD and CAD and led to very impressive neurologic and overall physical rehabilitation and improvement of quality of life.Measurement of Lp(a) concentration must be recommended to assess individual cardiovascular risk. Extracorporeal clearance of Lp(a) by LA should be considered as treatment option for select patients with progressive Lp(a)-associated ischemic syndromes.
Highlights
Lipoprotein(a) (Lp(a)) was first described in 1963, it lasted until 2010 to become fully clear that high Lp(a) concentrations represent an important independent and causal risk factor associated with adverse outcome in atherosclerotic cardiovascular disease (CVD) [1, 2]
We describe the case of a male patient beginning at the early age of 41 with presentation of established peripheral arterial occlusive disease (PAOD), who developed a multilocular ischemic syndrome with coronary artery disease (CAD), cerebellar ischemia and chronic spinal cord ischemia resulting in vascular myelopathy
We present a male patient with an extraordinary history of multilocular vascular complications beginning at the early age of 41 with PAOD, followed by CAD, and neurological deficits of the central nervous system (CNS) in cerebellum and cervical spinal cord
Summary
Lipoprotein(a) (Lp(a)) was first described in 1963, it lasted until 2010 to become fully clear that high Lp(a) concentrations represent an important independent and causal risk factor associated with adverse outcome in atherosclerotic cardiovascular disease (CVD) [1, 2]. E., difficulties to concentrate and loss of memory, vertigo with nausea and vomiting, diplopia and partial vision field loss in the left eye According to this complex neurologic syndrome with exclusion of demyelinating, inflammatory, or neoplastic disorders, ischemic vascular disease was hypothesized mainly localized in cerebellum and cervical spinal cord affecting territories of cerebellar arteries downstream of A. basilaris and spinal cord arteries downstream of both Aa. vertebrales, especially A. spinalis ant., A. spinalis post., as well as supply regions of both carotid arteries. 4.5 years with regular LA showed an almost fully rehabilitated patient regarding neurological symptoms including visual function and completely restored neurocognitive and physical abilities His migraine attacks had disappeared completely already few weeks after LA initiation and have not recurred so far. No further progression of atherosclerotic lesions was observed in coronary, peripheral, or CNS vascular beds clinically (e. g. no angina during treadmill exercise test up to 150 watts, unlimited walking distance without claudication), and by ultrasound and MRI imaging
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
