PLASMAPHERESIS FOR ATHEROSCLEROSIS

Voinov V.A.
First Pavlov State Medical University of St. Petersburg, Russia.

Atherosclerosis is perhaps the most frequent and severe human disease. It is accompanied
by vascular disorders, which are the main causes of lipid metabolism lead to the accumulation of
low-density- and very low-density cholesterol, triglycerides while reducing the content of anti-
atherogenic factors - high-density lipoprotein (HDL). All further consequences deposition of
atherosclerotic plaques in the vessel walls with narrowing of the lumen is quite well known, as
well as their main symptoms: narrowing of the coronary vessels coronary heart disease,
cerebral vascular narrowing with ischemic attacks, peripheral vasoconstriction, leading to
gangrene of the extremities.
Nevertheless, in the pathogenesis of atherosclerosis a certain role plays and autoimmune
factors. This primarily refers to the anticardiolipin antibodies. In addition, identified IgG-
antibodies to vascular endothelium, cardiomyocytes, cardiac conduction system fibers and
smooth muscle [Morozov B.N. et al., 2006].
It is believed that the oxidation of low density lipoprotein (LDL) may change their
antigenic structure, which stimulates the appearance of autoantibodies against these structures
with the formation of immune complexes containing oxidized LDL + autoantibodies. These
complexes facilitate the accumulation of cholesterol esters in macrophages and fibroblasts, with
increased synthesis of cytokines, such as IL1 and TNF-. Excited macrophages (monocytes) are
beginning to adhere to the vascular endothelium and move into the subendothelial space, where
the release of the above cytokines may play a leading role in the interaction of endothelial cells
with mononuclear cells, leading to their direct or indirect damage, as well as proliferation of
smooth muscle cells of the vascular wall [Lopes-Virella MF, Virella G., 1994; Mironova M. et
al., 1997].
Elevated levels of apolipoprotein (a) [Lp (a)] also promotes monocyte chemotactic activity,
forcing them to be introduced through the vascular endothelium in the subendothelial layer,
which is the first step in the atherogenic process [Poon M. et al., 1997].
Possible link between atherosclerosis and immune inflammation. Thus, "intercellular
adhesion molecule", secreted by macrophages, are fixed to the vessel endothelial cells and are
attracted there T-lymphocytes and monocytes, and then promote their migration into the vessel
wall [Watanabe T., Fau J., 1998].
Macrophages engulf low density lipoproteins, are vacuoled ("froth") to the release of some
cytokines (IL-1, IL-2, IL-3, IL-4, IL-6, IL-8, TNF- ), acute phase of inflammation (C-reactive
and stressor" protein), which determine the formation of immune inflammation focus and the
subsequent development of atherosclerotic plaque. Function of C-reactive protein (CRP) is a
"recognition" as well as infectious agents and damaged cells and their decay products. Direct
opsonization CRP and complement activation contribute to the restoration of tissue injury [Van
de Vijver L.P.L. et al., 1996; Watanabe T. et al., 1996; Nagornev V.A., Rabinovich V.S., 1997].
Interesting findings were obtained by morphological study of the vascular intima after
endarterectomy operations. In the composition of atherosclerotic plaques with 75% of cases were
found Chlamidia pneumoniae, in 35% cytomegalovirus and 10% Herpes simplex virus type
1. These data indicate a possible role of these pathogens in the pathogenesis of atherosclerosis
[Chiu B. et al., 1997]. Chlamydia pneumoniae infection is possible in the cells of the
endothelium and smooth muscle of the vascular wall, resulting in local inflammation and fibrosis
with the formation of the typical atherosclerotic plaque. The presence of such infections and
stimulates cytokine output infringing thrombus-resistive endothelial function and enhancing
contractile function of smooth muscle of the vascular wall [Murray LJ et al., 1999].
Bacterial and viral infections are also considered potential triggering factor. Infection has
viscosity increased blood hypercoagulation, affected plasma lipid profile. For infections of gram
negative bacteria endotoxin contribute to the formation of free radicals in the vascular
endothelial cells that can oxidize the lipoproteins. Many pathogens E. coli, Chl. pneumoniae
and cytomegalovirus allocate special "termo-shock proteins", against which antibodies are
formed. However, the antigenic properties of these proteins are close to human autoantibody that
promotes "antigenic mimicry." When the antibodies raised against such pathogens they are as
antibodies against self antigens, in particular vascular endothelial cell antigens. Since these
autoantigens remain in their place throughout life, so the signals for the formation of such
autoantibodies supported indefinitely [Mayr M. et al., 1999]. These data are forced to think about
the need for timely removal of such antibodies against pathogens for during or at the conclusion
of infectious processes that such pathological antigenic mimicry has not had time to consolidate.
Additionally, vascular lesion sites include deposition of immunoglobulins and complement,
including lytic "complex lesion membranes" S5v C9, indicating that complement activation in
atherosclerosis.
Significant role in the pathogenesis of circulatory disturbances play hemo-rheology
violations. Increasing the viscosity of the blood and plasma depends on improving the
concentration of fibrinogen and lipid fractions total cholesterol, LDL and triglycerides. Are
significant and increasing aggregation blood cells while reducing of erythrocytes deformation
ability. All together, it predisposes to poor blood flow, especially in the presence of local
narrowing of blood vessels at the level of plaques also [Walzl M. et al., 1998]. In the presence of
antiphospholipid antibodies, such as anti-2-glycoprotein I, increases platelet aggregation,
contributing hypercoagulable state which is especially dangerous in the presence of
vasoconstrictions [Kandiah D.A. et al., 1998]. Procoagulant status, manifested in increased levels
of D-dimers on the background of lipid transport disorders contributes to repeated coronary
thrombosis in patients with myocardial infarction [Moss A.J. et al., 1999].
Long been known for the negative role of smoking in the genesis of vascular lesions. At the
same time, many of the pathogenetic mechanisms play a role also the suppression of release of
tissue activator of fibrinolysis. Last stimulates rapid release of tissue plasminogen activator from
the vascular endothelium. Otherwise, there are increased the possibility of thrombosis of arteries
[Newby D.E. et al., 1999].
Potential risk factor for atherosclerosis is an increase in homocysteine levels occurring
during the metabolism of methionine. Activation of this process may contribute to both genetic
mutations and lack of folic acid and vitamins B6 and B12. There is possible role of lack of
coenzyme re-converting chomocysteine to methionine or cystathionine also [Greenlund K.J. et
al., 1999].
Lipid deposition in the vessel walls may begin as early as adolescence, as evidenced by the
yellowish color of the vascular intima. By the age of 30 there are about half the surface of the
aortic intima covered by these fatty deposits in the form of yellowish stripes. These changes will
not narrow the lumen of blood vessels and do not manifest clinically. In the future, these fatty
layers may disappear, but in their place there are appeared fibrous plaques that can already
produce symptoms of circulatory disorders. Occlusion developed in necrosis, calcification and
fibrous plaques in their places of thrombosis formation [Gerrity R.G., Antonov A.S., 1997].
In all these cases the leading mechanism for the development of the disease is the
accumulation of atherogenic and other biologically active factors in which drug therapy is
virtually powerless. Known effect is achieved with statins, but we must remember that in such
cases, the risk of developing breast cancer increases 12 times. In addition, the lipid-lowering
effect of statin treatment leads to complications such as increased activity of liver transaminases
several times and rhabdomyolysis with increase creatinine phosphokinase (CPK) [Lepaev Y.V.,
Efremova T.I., 2008]. It should also be noted that the drug treatment of patients with elevated
levels of Lp (a) is ineffective at all, and for patients with liver diseases and allergies are even
dangerous [Konovalov G.A. et al, 2009]. Therefore, most often treatment is limited to
symptomatic therapy, aimed at expanding the narrowed vessels. There are the same dedicated
and surgical methods of treatment with atherosclerotic occlusive vascular disease.
However, only the efferent therapy, mainly plasmapheresis, seems truly pathogenic. Given
sufficiently slow rate of reproduction and accumulation of atherogenic products and, especially,
the presence of autoimmune mechanisms of the pathogenesis of atherosclerosis, periodic courses
of such therapy allow you to maintain an acceptable level of pathological products and more
stable remission, especially in cases where there were not yet irreversible organic circulatory
disorders [ Konovalov G.A. et al, 1998; Gavrilov O.K. et al., 1999; Chebyshev A.N. et al., 2004].
In these cases justified preventive courses of plasmapheresis in conjunction with UFO blood up
to two times per year.
In cases of toxic hepatopathy on background statin therapy use plasmapheresis courses
with Reamberin as plasma substitute led to a significant reduction in transaminase levels to
nearly baseline with normalization of health and clinical parameters [Lepaev Y.V., Efremova T.I.,
2008].
Hyperlipidemic patients with coronary artery disease provides substantial assistance for
periodic sessions of plasmapheresis followed plasma-immunosorption using special columns
"LDL Lipopak" [Konovalov G.A. et al., 2008, 2009]. Promising results were obtained using
columns "Sferotsell LP- M" [Sokolov A.A. et al., 2002]. Good results have been achieved by the
removal of LDL with the use of special columns based on dextran sulfate, which is passed
through the plasma obtained by plasmapheresis [Bambauer R. at al., 2000; Kamimura M. et al.,
2002]. At elevated levels of lipoprotein (a ) [Lp (a )] with normal LDL is more expedient to use
special columns "Lp (a) Lipopak " (POKARD, Russia), which leads to a decrease in Lp (a)
averaged 80% [Afanasyeva O.I. et al., 2002]. After a single session lipoprotein apheresis in 24
hours observed reduction of Lp (a) by 51.1%, LDL by 54.6%, HDL 17%, apolipoprotein B
39.2%, ejection fraction increased from 64.89% to 67.07%. After 96 hours, these parameters
were restored, but still did not reach the initial level [Bohl S. et al., 2009].
In the case of acute pancreatitis induced hyper-triglyceridemia plasmapheresis allowed to
reduce the concentration from 5430 mg/dl to 403 mg/dl [Nakagawa M. et al., 2008].
In cases where the use of fibrinolytic therapy (streptokinase) on 4-6th day there is the
development of hypercoagulability, which can be stopped after 2-3 sessions of plasmapheresis.
This significantly decreases the level of fibrinogen and fibrin monomer complexes [Hoffmann
E., 2003]. Intensive plasmapheresis can be applied as a separate treatment of thrombus, including
thrombosis in the acute stage, and the conditions of the thrombolytic therapy also.
Perhaps the use of adsorption columns of dextran-sulfate cellulose [Yokoyama S. et al.,
1985; Kojima S., 2001].
The most effective in improving the rheology and microcirculation is cascade plasma
filtration when received by one of the methods of plasma passed through custom micropore
filter which passes only low molecular weight proteins (albumin) and detain macromolecular,
including atherogenic, lipoproteins [Klingel R. et al., 2003; Konovalov G.A., 2009; Bosh T.,
Wendler T., 2004]. Cascade plasmapheresis reduces the concentration of total cholesterol by
67%, LDL by 72%, Lp (a) 70%, triglycerides 54% and HDL by only 30% [ Konovalov G.A.
et al., 2009]. V.M.Kreynes et al. (2009) show that using a cascade plasmapheresis possible rapid
and substantial reduce the severity of hyperlipidemia, and continuing through 3 weeks after the
procedure atherogenic ratio decreased by 28% due to lower LDL cholesterol by 37.3% while
increasing HDL cholesterol by 10.4%. Application termo-filtration with increasing temperature
up to 38oC separates the plasma further increases the removal of LDL and HDL reduces losses
[Klingel R. et al., 2004; Krebs A. et al., 2004].
However, given a sufficiently large variety of accumulating pathological products
lipoproteins, apoproteins, cholesterol, triglycerides, lipid peroxidation products, medium weight
oligopeptides, kinins, circulating immune complexes, and also possibly some autoantibodies,
enough full therapeutic effect can be expected from even conventional plasmapheresis when
from plasma removed by 100% all those in it products. In the patient's blood cholesterol level is
reduced by 25%, triglycerides 10% of fibrinogen 18% with a significant improvement of
clinical parameters [Kazakov F.I. et al., 2008]. It should be emphasized that the authors have
used techniques plasma exchange with cryo-sorption of autoplasma note that the real increase in
the efficiency of removal of cholesterol and atherogenic lipoproteins compared to conventional
non-selective plasmapheresis was not as pronounced as it was previously thought [Sokolov A.A.
et al. 2007].
One of the additional indications for plasmapheresis in patients with dyslipidemia is the
development of rhabdomyolysis with statins manifested myalgia, myopathy, muscle weakness, a
tenfold increase in creatinine phosphokinase activity, increased levels of creatinine and
myoglobin [Konovalov G.A. et al., 2009].
Plasmapheresis is more indicated in patients with atherosclerosis and diabetes mellitus.
Significantly improved peripheral blood flow in the lower extremities also, especially in patients
with diabetic angiopathy. Aneurysm of the abdominal aorta and multifocal atherosclerotic
lesions of major vessels plasmapheresis has helped reduce the prothrombin and thrombin time,
spontaneous platelet aggregation and fibrinolysis, as well as blood viscosity [Mukhamadeyev
I.S., 2005].
Positive results in lesions of the peripheral vessels also reached laser (HeNe or infrared)
irradiation of blood [Logvinov N.L., Samoilova E.V., 1999; Sokolov E.I. et al., 1999; Shano V.N.
et al., 1999]. Found a pronounced therapeutic effect of intravascular (as intravenous and intra-
arterial) laser irradiation of blood in patients with obliterative processes in the vessels of the
lower limbs, allowing 2-3 times to increase the distance that can elapse before the patient is pain
in the muscles. After laser irradiation improves collateral circulation with the onset of warming
feeling in the distal extremities. It was able to achieve healing of local necrotic ulcers on the toes
or achieve faster demarcation departments with irreversible damage to a leaner amputation
[Galinzyanov F.I., 1996; Losev R.Z., Tsarev O.A., 1998; Yaitsky N.A. et al., 2006]. It is noted
that laser irradiation of blood prevents deterioration of capillary blood flow during the upcoming
discrete plasmapheresis [Marchenko A.V. et al., 2003]. In addition, after the photo-hemotherapy
significantly improved some functional parameters such as erythrocyte deformability and
aggregation properties of the normalization of the aggregation state of their membranes [Efimov
A.S. et al., 2004].
Positive effect in the treatment of obliterating atherosclerosis of the lower extremities is
provided during hemosorption also [Perepelitsa V.N., 2007]. Performing of regular sessions with
LDL-apheresis every 2 weeks in parallel with the simvastin was much more effective than using
only the drug. This prevented the progression as well as coronary and peripheral stenoses of
lower limb arteries [Kroon A.A. et al., 1996].

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