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Yaroustovsky et al. Vessel Plus 2019;3:9 I http://dx.doi.org/10.20517/2574-1209.2019.02 Page 5 of 11

Table 2. Clinical characteristics of patients before lipid-filtration therapy
The disorders of lpid The manifestations
Patients metabolism of atherosclerosis Revascularization Drug therapy Comorbidity
(with drug therapy) (vessels) procedure
No.1 Hypercholesterolemia Coronary Coronary artery bypass Statin (rosuvastatin 20), Ezetrol Hypertensive
(LDL > 4.5 mmol/L, Brachiocephalic graft (n = 3), Mitral valve antiplatelet agents (clopidogrel, disease
atherogenic index Femoral repair with Carpentier acetylsalicylic acid) Hyperuricemia
> 4.5) techniques ACE inhibitors
hypefibrinogenemia β-blockers
(> 4 g/L) Calcium antagonists
hyperLp(a)emia
(> 150 mg/dL)
No.2 Hypercholesterolemia Coronary No Statin (rosuvastatin 40), Left ventricular
(LDL > 6.5 mmol/L, Brachiocephalic Ezetrol antiplatelet agents aneurysm
atherogenic index > 7) (acetylsalicylic acid) Hyperuricemia
hypefibrinogenemia β-blockers
(> 4 g/L)
hyperLp(a)emia
(> 60 mg/dL)
No.3 Hypercholesterolemia Brachiocephalic No Statin (rosuvastatin 40) Iron deficiency
(LDL > 4 mmol/L, antiplatelet agents anemia
atherogenic index > 3) (acetylsalicylic acid) Vascular
hypefibrinogenemia calcification
(> 4 g/L)
hyperLp(a)emia
(> 300 mg/dL)
LDL: low density lipoprotein; ACE: angiotensin converting enzyme

didn’t occur, but in one case. The patient with high Lp(a) (more than 180 mg/dL) had dyspnea on exertion
(fast walking) and needed coronarography. Subtotal stenosis of the right coronary artery was found out, and
was exposed to stenting. In our opinion, it was caused by the extensive posttraumatic bruising of the lower
limb in the context of inflammation. During this period according to the laboratory data the patient had
high fibrinogenemia (6.5-7.4 g/L), high level of C-reactive protein 3.4-12.6 mg/dL, erythrocyte sedimentation
rate (ESR) - 25-32 mm/min, Lp(a) 185-171 mg/dL, LDL - 2.5-2.7 mmol/L, atherogenic index - 1.9-2. The high
level of CRP is responsible for atherosclerotic process progression and development of acute complications
(even in the presence of normal levels of LDL).

As anticoagulation we used the heparin (15-30 U/kg/h). The level of circuit anticoagulation was estimated
according to the activated clotting time, which was maintained within 180-200 s. The heparin supply was
stopped before the last 10-15 min of the session.

We noted statistically significant dynamics of almost the studied indications after the procedures
[Tables 3-6]. The patients of the 1st group had twofold decrease of total cholesterol and threefold decrease
of LDL. The patients of the 2nd group had similar changes: threefold decrease of the total cholesterol and
68% decrease of LDL. Both types of lipid apheresis treatment proved to be effective for Lp(a)emia. We noted
significant decrease (more than 65%) of this atherogenic indication following these therapies [Tables 3 and 4].
Hematological parameters, ESR, hemoglobin concentration, fibrinogen, coagulation factors and activity of
antithrombin had statistical significance immediately after the procedures [Tables 5 and 6].

After H.E.L.P.-apheresis HDL decreased by 29%, and after cascade lipid-filtration - by 22%. It was confirmed
by the dynamics of apoprotein index ApoB100/apoA before and after the therapy (decrease by 33% and
almost by 60% while H.E.L.P.-apheresis and cascade lipid-filtration, respectively) and by the atherogenic
index (38% and 53%, respectively) [Tables 3 and 4]. Significant changes were also found in the decrease of
total protein and albumin levels following both the techniques. The total level of protein decreased by 24%
and albumin - by 22% during H.E.L.P.-apheresis, and by 22% and 14%, respectively, during cascade lipid-