WO2012070972A1 - Method for treating cardiovascular disease patients - Google Patents

Abstract

The invention can be used in medicine and veterinary science in conjunction with traditional cardiovascular disease treatment methods in order to enhance treatment efficacy. The method for treating cardiovascular disease patients is characterized in that an antiviral drug is used as a complement to a conventional therapy before the start of said conventional therapy and in parallel therewith, wherein the antiviral drug may be aciclovir, valaciclovir, alpha interferon, specific antiviral immunoglobulin or a combination of the aforesaid agents, which are suitable for inclusion in conventional treatment regimens for cardiovascular disease patients. The proposed method makes it possible to significantly increase the effectiveness of treatment of patients with diseases of the cardiovascular system, reduce the number of relapses, improve the patient's quality of life and significantly extend the patient's life. Since the proposed drugs are permitted for use, there are no technical difficulties in including same in the treatment regimens of patients with diseases of the cardiovascular system.

Description

 A method for the treatment of patients with cardiovascular disease

Technical field

 The invention relates to medicine, namely to cardiology and is intended to increase the effectiveness of the treatment of human cardiovascular pathologies.

State of the art

Cardiovascular diseases (including atherosclerosis and its complications) are the main cause of death in developed countries [']. For Ukraine, this problem is even more relevant: according to the WHO, in Ukraine in 2005 cardiovascular diseases (CVD) caused about 60% of all deaths, which significantly exceeds the same indicator in developed countries in Europe - 38% [ ² ]. Therefore, any new information on the mechanisms of development of atherosclerosis, as well as the development of new, more effective methods of its treatment, are of great social importance.

In accordance with modern concepts of medical science, atherosclerosis is a chronic inflammatory disease of the walls of large arteries [ ³ , ⁴ , ⁵ ]. With atherosclerosis, lipids, fibrous elements and calcium salts accumulate in the arteries, which leads to a decrease in the lumen of the arteries and a decrease in their elasticity. In principle, this process begins almost from birth and accompanies the inevitable process of aging of the body [6, 7, 8]. The development of atherosclerosis begins with damage to the endothelium of blood vessels and a violation of its functions. The damaged vessel wall, in addition to the local compensatory reaction, initiates a powerful systemic response in the form of a cascade of molecular reactions and cellular processes, such as the isolation of adhesion molecules and chemotaxis factors, pro-inflammatory cytokines, growth factors, leukocyte involvement, bone marrow precursor cells and their vascular uptake wall to repair damage, etc. [ ⁹ ]. Normally, this process leads to the restoration of endothelial function and homeostasis; however, in some cases, with an unfavorable combination of risk factors, the process can become pathological, leading to a destructive systemic inflammatory reaction.

Several risk factors are known, both genetically determined and external, causing endothelial damage and activating atherogenesis: elevated cholesterol (in particular low-density lipoprotein - LDL), elevated homocysteine, hypertension, diabetes, smoking, genetic predisposition, age (aging). Process of atherogenesis It is long and difficult; several detailed review articles [ ¹⁰ ] are devoted to this topic. The following stages can be distinguished in the development of atherosclerosis.

 Stage I - fatty streaks - accumulation of LDL particles in the subendothelial layer (intima) of the vessel. LDL undergoes oxidation (the process is stimulated by free radicals) and in this form, lipoprotein penetrates more actively into intima. LDL plays a key role in this process: the higher its level, the faster atherogenesis occurs. Subsequently, with the active participation of inflammatory mediators (interleukin-1, tumor necrosis factor — TNF-a, growth factors, adhesion molecules), active migration of monocytes and T-lymphocytes to the site of microdamage of the endothelium occurs, their penetration into the intima, transformation of monocytes into macrophages and capture of oxidized macrophages LDL - this is how foam cells are formed. Plots of mass accumulation of foam cells at this stage can already be visualized as fatty streaks.

 Stage II - formation of a necrotic nucleus Over time, foam cells die off, and their lipoprotein-containing residues accumulate in the intima and subsequently form the necrotic nucleus of an atherosclerotic lesion. Cells of unstriated muscle tissue (HMT cells, SMC cells) migrating from the medial layer of the vessel are sometimes embedded in fatty veins.

 Stage III - extracellular accumulation of lipoprotein Oxidized LDL continues to accumulate in the intima, atherosclerotic plaque increases in size.

 Stage IV - formation of the lipid core. The accumulation of HMT cells continues; Calcification is included in the process of lipoprotein accumulation in the intima, which occurs initially inside the BDC cells, and after their death, between the muscle wall of the vessel and the outer part of the atherosclerotic plaque.

Stage V - the formation of atheroma. Between fatty deposits and intima, a protective layer is formed, consisting mainly of fibrin and collagen fibers. This encapsulated body fat is called atheroma. For some time, atheroma grows into the vascular wall, causing compensatory expansion of the vessel, but after reaching a critical size, it begins to protrude into the lumen of the vessel, reducing its diameter and affecting blood flow; stenosis develops. It should be noted that before this stage (and in many cases later) the development of atherosclerosis is asymptomatic and practically without clinical manifestations, and only stenosis of more than 77% is considered in cardiology as the limit after which a clinically expressed disease begins Stage VI - rupture of atheroma and thrombosis. In case of a violation of the integrity of the fibrous capsule covering the atheroma, platelets and tissue factors are released, which trigger a cascade of biochemical blood coagulation reactions. This forms a blood clot. If the duration of the previous stages of the development of atherosclerosis is from several weeks to tens of years, then thrombosis can occur in a matter of minutes, leading to blockage of the vessel and often causing catastrophic consequences in the form of a heart attack or stroke. According to clinical studies, only about 14% of the expressed clinical manifestations occurs with narrowing of the lumen of blood vessels to 77% or more; most life-threatening manifestations and deaths result from plaque destruction and subsequent thrombosis [''].

Infectious component in the etiology of atherosclerosis. Despite the fact that the risk factors for atherosclerosis are currently well known, even their combination cannot explain more than half of the clinical cases of atherosclerosis [ ¹² ]. Therefore, infectious diseases are also adding to the list of risk factors with increasing confidence. An infectious etiology has been confirmed for a number of chronic diseases, such as gastric ulcer (Helicobacter pylori), cervical cancer (various papillomaviruses), cirrhosis and liver cancer (hepatitis B and C viruses). More and more data indicate the involvement of infections in the etiology of diabetes mellitus, Alzheimer's disease, various neurological and CVD [ ¹³ ]. The assumption of the infectious nature of atherosclerosis first appeared in the middle of the XIX century. in the works of R. Virchow [ ¹⁴ ], and later, in 1889, Gilbert, Lion. The association of atherosclerosis with viral infection was experimentally substantiated in the 70s of the last century by the works of C. G. Fabricant et al., In which atherosclerosis-like changes in blood vessels developed in chickens infected with Marek's virus, an avian version of the herpes virus [ ¹⁵ ]. Many viruses have been proposed for the role of possible pathogens of atherogenesis: cytomegalovirus (CMV) [ ¹⁶ , ¹⁷ , ¹⁸ , ¹⁹ , ²⁰ , ²¹ , ²² ], herpes simplex (HSV) [ ²³ , ²⁴ ] and Epstein-Barr [ ²⁵ , ²⁶ ] and many others. The largest number of experimental studies on the association of infection and atherosclerosis is devoted to Ch. pneumoniae and cytomegalovirus. Both of these microorganisms are very likely to be found in vessels affected by atherosclerosis and atherosclerotic plaques, and their seropositivity correlates well with atherosclerosis and the severity of CVD [ ²⁷ , 12, ²⁸ ].

Although the association of two infectious agents is Ch. pneumoniae and cytomegalovirus - with cardiovascular disease can be considered proven, this does not mean the presence of a causal relationship. At the same time, Koch's classical postulates are not feasible in the case of such a multifactorial disease as atherosclerosis [1, 31]. Most likely, infections are neither a necessary nor sufficient reason for the development of atherosclerosis, but these are risk factors that increase the likelihood of developing a pathology. In order to prove the participation of infections in atherogenesis, in addition to histopathological data, a clear idea of the mechanism (s) of pathogenesis, experimentally confirmed in vitro and in vivo, and subsequently, on treatment methods whose effectiveness has been shown in experiment and in clinical conditions, is necessary. A number of mechanisms are known for the pathogenic action of infectious agents on the cardiovascular system [ ²⁹ ]:

 • increased proliferation of GM cells and increased migration (human cytomegalovirus);

 • protection of endothelial cells from apoptosis, which leads to their excessive accumulation and increase in the size of atherosclerotic plaques (cytomegalovirus, Ch. Pneumoniae);

 • accelerated accumulation of lipids (cytomegalovirus, Ch. Pneumoniae);

 • increased procoagulant activity of endothelial cells (cytomegalovirus, herpes simplex virus);

 • increased expression of cytokines, chemokines and adhesion molecules, the appearance of acute phase proteins (C-reactive protein, serum amyloid C and others), which leads to a vicious cycle of a hyperergic inflammatory reaction and, as a result, to damage to the endothelium (almost all pathogenic microorganisms from the number of “suspects”);

 • an increase in the level of reactive oxygen species (oxygen ions, free radicals, peroxides) that cause enhanced oxidation of HDL (cytomegalovirus);

• autoimmune reactions; some proteins produced by pathogens are homologous to the proteins of the human body, which can cause an autoimmune reaction, in particular, a high degree of homologous ™ is observed for heat shock proteins (Heat Shock Protein, HSP) of various bacteria and humans (HSP60).

Numerous data obtained in an animal experiment confirm the results of histopathology and in vitro studies. According to CG Fabricant et al. [15], the Marek virus caused atherosclerosis in chickens, and the immunization of healthy animals prevented the development of pathology regardless of the amount of cholesterol in the food taken. The effects of immunostimulating therapy on the development of atherosclerosis in rabbits experimentally infected with the herpes simplex virus: a significant inhibition of the development of atherosclerosis was noted [16]. A significant amount of data obtained as a result of histopathological analysis, as well as in vitro, in vivo in the experiment, confirms the hypothesis of an infectious component in the etiology of atherosclerosis.

The next step in developing the concept of an infectious component in the etiology of atherogenesis was clinical trials using antibiotics. Since the largest amount of experimental data indicates the involvement of Ch. pneumoniae to atherogenesis, most of the tests were aimed at its elimination. Most effective against Ch. pneumoniae are considered antibiotics of the macrolide group, in particular azithromycin, because of their ability to penetrate into the cell and affect intracellular parasites [ ³⁰ , ³¹ ]. From 1997 to 2005, a number of clinical trials were conducted in the world using azithromycin (or other macrolides - roxithromycin and clarithromycin) as one of the agents in the complex treatment of CVD (coronary heart disease, myocardial infarction and unstable angina) [ ³² , ³³ , ³⁴ , ³⁵ ]. Of more than 100 studies, 1 1 were promising, randomized, placebo-controlled. They evaluated the effect of antibiotic therapy on the incidence of myocardial infarction and stroke, their re-development and overall mortality due to CVD [33]. Comparing the results of the tests is a difficult task due to the difference in the criteria for inclusion of patients, the design of the tests themselves and the duration of follow-up after treatment. Nevertheless, according to the results of the analysis of the tests, it can be concluded: despite the fact that after the first pilot studies, encouraging results were obtained, larger-scale clinical trials did not show any advantage of antibiotic therapy in the treatment of CVD.

Atherosclerosis is a widespread chronic disease with a multifactorial and not fully understood etiology, prolonged and latent pathogenesis. The evolution of understanding of the causes and mechanisms of the occurrence of this disease by modern science is rapidly developing, although it lags behind the needs of the time. In the 90s of the XX century. they hoped that cardiovascular diseases could be eliminated by the end of the century by controlling cholesterol and blood pressure; 10 years later, it became obvious that such an optimistic forecast must be reviewed [10]. So there was a paradigm shift, as a result of which atherosclerosis ceased to be a simple violation of cholesterol metabolism and was recognized as an inflammatory disease [, 10]. Traditional and promising methods of treating atherosclerosis with drugs are aimed at various parts of the pathogenetic chain, such as lipid metabolism (statins, fibrates, cholesterol absorption inhibitors), blockade of the renin-angiotensin system (angiotensin converting enzyme inhibitors - ACE inhibitors), blockade (3-adrenergic receptors, excessive accumulation calcium (antagonists of calcium ions), oxidative stress (analogues of tocopherols - vitamin E, probucol, AGI-1067), excessive proliferation of GM cells (inhibitors of the growth of GM cells), aggregation thrombocytes (platelet activation inhibitors), inflammatory processes in vessels (acetylsalicylic acid, AGI-1067), thrombosis (antithrombotic drugs, heparin, thrombin antagonists) .Most promising are drugs with pleiotropic effect, i.e., acting simultaneously on different mechanisms of pathogenesis such as statins (lipid metabolism, anti-atherosclerotic, anti-inflammatory and anti-thrombotic effects) and a new class of therapeutic agents - vascular protectants that have antioxidant and anti-inflammatory properties, as well as reducing postangioplastic restenosis [ ³⁷ ].

However, even with an integrated approach and the use of the latest pleiotropic drugs, the treatment of atherosclerosis still remains pathogenetic. Perhaps the next turning point in the evolution of the treatment of atherosclerosis and CVD will be a revision of the concept of therapy and the transition from pathogenetic treatment to etiotropic and pathogenetic, as well as preventive (in the early stages before the onset of clinical manifestations) in order to prevent the development of severe forms of atherosclerosis. One of the types of such therapy could be the treatment of infections that are a risk factor for the development of atherosclerosis (Ch. Pneumoniae, herpes simplex virus and cytomegalovirus). Interferon and its inducers were effective in the treatment of viral myocarditis of various etiologies caused by entero- and adenoviruses, as well as herpetic viruses [ ³⁸ ]. In vitro studies are encouraging, but large-scale clinical trials are needed to introduce atherosclerosis therapy using interferons, as well as identifying groups of patients and disease stages for which such therapy would be most effective.

The results of numerous studies indicate that infectious diseases significantly affect the etiology and pathogenesis of atherosclerosis, but data on the alleged pathogens are contradictory. Due to the fact that atherosclerosis is a multifactorial disease, Koch's postulates in this case are not applicable and most likely the only infection that is a trigger of atherogenesis will not be detected. The most likely risk factor is the “burden of infection” factor. Data from many studies indicate a direct correlation between the number of infections detected in one patient and the severity of cardiovascular disease, as well as mortality from CVD.

 Clinical trials using antibiotics did not reduce the likelihood of heart attack and mortality from CVD. There can be many reasons, but the main one, most likely, is that the action of antibiotics was directed only to one infection, while the herpesvirus infections play the main role in the development of atherosclerosis. The use of the most affordable tabletted antiherpetic drug valaciclovir and its injection analogue in the complex treatment of diseases caused by atherosclerosis can significantly improve the prognosis of the disease, prolong the duration of remissions and prevent relapse of heart attacks and brain strokes.

 A known method for the diagnosis, prevention and treatment of restenosis / atherosclerosis, which consists in a combination of the diagnosis of cytomegalovirus in the patient's body with subsequent therapeutic vaccination of patients against cytomegalovirus infection [39]. The diagnostic method also applies genotyping of the histocompatibility complex. The disadvantage of this method is that it does not take into account the role of other herpes viruses in the development of atherosclerosis - herpes viruses of types 1 and 2, Epstein-Barr virus, herpes of type 6. Also, the developers did not offer an effective treatment regimen for atherosclerosis, and vaccination of the body in the presence of a large number of cytomegalovirus antigens is ineffective, and specific immunity is unstable. Thus, the effect of the proposed scheme for the prevention of atherosclerosis will be unstable. In addition, the developers proposed a complex vaccination schedule not only for cytomegalovirus antigens, but also for the cellular protein p53, which can lead to the development of autoimmune reactions to their own tissues.

Disclosure of invention

The objective of the invention was to increase the effectiveness of the method of treatment of cardiovascular diseases, taking into account the participation of herpes viruses in the etiology and pathogenesis of the above diseases. The problem is solved by including antiviral drugs in standard treatment regimens for cardiovascular diseases. Use drugs of acyclovir (injectable and tablet acyclovir and valacyclovir), other antiviral agents (specific antiviral immunoglobulins and alpha-interferon) before, after and in conjunction with the standards for the treatment of cardiovascular diseases (surgical and chemotherapeutic). Valacyclovir is used 3-7 courses from 7 to 20 days, 1-2 g 3-4 times a day. Acyclovir intravenous is used 0.5-1.0 g 3-4 times a day also from 7 to 20 days 3-7 courses. This combination leads to the rehabilitation of the immune system, expands the range of standard treatment methods, significantly increases the effectiveness of treatment for patients, prevents relapse in patients with unstable angina, normalizes blood lipids and cholesterol levels, and provides long-term stable remission in case of cardiovascular diseases. Examples of carrying out the invention

Example 1. Patient L., 52 years old, was admitted to the hospital with a diagnosis of IHD. Angina pectoris, III functional class. Postinfarction cardiosclerosis (myocardial infarction in 1981). Atherosclerosis of the coronary arteries. NK II A Art. Cerebral atherosclerosis. HCHSN. Symptomatic hypertension. Upon admission, he complained of constricting pains in the region of the heart radiating to the left scapula, which occur at rest and during physical activity (up to 4-5 times a day) and were relieved by taking nitroglycerin (up to 8 times a day), as well as shortness of breath when walking dizziness, recurrent headaches, tinnitus, irritability, and insomnia. The patient was prescribed treatment: antianginal drugs (nitrosorbide 30 mg / add, Corinfar 30 mg / day) also has a hypotensive effect), valacyclovir 2 tablets. (1.0 g) 3 times a day. As a result of treatment, a decrease in blood serum levels of total cholesterol from 6.71 mmol / L to 3.26 mmol / L, triglycerides from 3.4 mmol / L to 1.04 mmol / L, b-lipoproteins from 770 mind was found. od. up to 310 mind. od., cholesterol \ low-density liporoteids (cholesterol / LDL) from 3.99 mmol / l to 3.68 mmol / l, cholesterol \ LDL from 1.55 mmol / l to 0.47 mmol / l. The atherogenic index from 4.74 to 3.38, as well as an increase in high-density cholesterol / lipoproteins (cholesterol / HDL) from 1.17 mmol / L to 1.20 mmol / L. In the course of treatment, inhibition of free radical lipid oxidation was observed; the content of malondialdehyde in blood serum decreased from 0.50 μmol / ml to 0.31 μmol / ml, diene conjugates from 1.32 μmol / ml to 0.70 μmol / ml, triene conjugates from 0.23 μmol / ml to 0.14 μmol / ml, the content of a-tocopherol was restored from 2.69 μmol / ml to 4.32 μmol / ml, glutathione reductase activity from 12.4 μmol / l h to 22.0 μmol / l h. On the electrocardiogram, there was a decrease in the T-index from 35.0 to 0, SST to 11.0 to 0, NST from 10.0 to 0. Hemodynamic parameters also improved; the total peripheral resistance of blood vessels decreased from 2917.9 dyne sec-cm ^"5 to 2673.6 dyne-sec-cm ^{" 5} , and the specific peripheral resistance - from 74.53 dm. od. up to 65.97 mind. od., energy consumption - from 15.96 conv. units up to 10.37 conv. units, the volumetric ejection rate increased from 126.5 ml / s to 169.71 ml / s and the power of the left ventricle from 2.02 watts to 2.29 watts. After 7 weeks of treatment, the patient's condition improved significantly. Angina pains and shortness of breath do not bother; they do not use nitroglycerin tablets. Dizziness and headaches decreased.

JVs2 example. Patient M., 60 years old. Diagnosis: CHD: Post-infarction cardiosclerosis (1999r). Hypertension 3 stages. NK -1 tbsp. Treatment: metoprolol (corvitol) 50 mg 2 r / d, enalapril (renitec) 10 mg 2 r / d, aspirin 80 mg / day, simvastatin (zocor) 10 mg in the evening. After 6 months of using simvastatin at a dose of 10 mg per day, the following indicators of the lipid and liver complex were obtained: total cholesterol 4.9 mmol / L (target value 5.0 mmol / L), triglycerides 1.55 mmol / L, ACT 110 IU / l (norm 10-39 mU / l), ALT 100 mU / l (norm 10-35 mU / l). After using valaciclovir, 2 tablets. (1.0 g) 3 times a day, 3 courses of 7 days, the following indicators were obtained: total cholesterol 4.7 mmol / L (target value 5.0 mmol / L), triglycerides 1.3 mmol / L, ACT 22 IU / l (norm 10-39 mU / l), ALT 32 mU / l (norm 10-35 mU / l).

Example JV "3. Patient H, 40 years old. Diagnosis: coronary heart disease: post-infarction cardiosclerosis (1998). NK 1 tbsp. Treatment: metoprolol (corvitol) 25 mg 2p / d, aspirin 80 mg / day, simvastatin (zocor) 10 mg in the evening. After 5 months of using simvastatin at a dose of 10 mg per day, the following indicators of lipid and liver complexes were obtained: total cholesterol 5.6 mmol / L (target value 5.0 mmol / L), triglycerides 2.55 mmol / L, ACT 89 E / l (norm 10-39 mU / l), ALT 96 mU / l (norm 10-35 mU / l). After applying valaciclovir according to the 1 g regimen 3 times a day with 5 courses of 7 days at 7-day intervals, the following indicators were obtained: total cholesterol 4.9 mmol / L, triglycerides 1.95 mmol / L, ACT 38 IU / L (normal 10-39 mU / l), ALT 30 mU / l (normal 10-35 mU / l). As shown by the examples provided, the combination a standard treatment regimen with valaciclovir with an increase in transaminases while taking statins can increase the effectiveness of the treatment of atherosclerosis and dyslipidemia.

 Thus, in the course of treatment, the patient taking Valaciclovir normalized lipid profile, lipid peroxidation, electrocardiotography and tetrapolar rheography. In this case, no side effects of valaciclovir were observed.

 The use in the scheme of less than 3 courses of 7 days less than 1.0 g 3 times a day for valaciclovir for oral use and acyclovir in a dose of less than 0.5 g 2 times a day with injection does not give a long-term remission of the disease and a significant positive stabilization of the patient's condition. The use of an antiviral drug for a longer period is impractical, since the patient begins a period of remission and the drug becomes ineffective.

 Example JY ° 4. Patient L., 48 years old. Diagnosis: CHD: Post-infarction cardiosclerosis (2006). Hypertension 3 stages. H -1 tbsp. Treatment: Corvitol 50 mg 2p / d, Renec 10 mg 2p / d, Aspirin 80 mg / day, Zocor 20 mg in the evening. After 6 months of consuming Zocor at a dose of 20 mg per day, the following indicators of the lipid and liver complex were obtained: total cholesterol 3.9 mmol / L (target value 4.0 mmol / L), triglycerides 1.40 mmol / L, ACT 67 IU / l (norm 10-39 mU / l), ALT 88 mU / l (norm 10-35 mU / l). As a result of an immunofluorescence study of blood immunocytes, antigens of the Epstein-Barr virus, cytomegalovirus and type 1 herpes virus were detected.

 The patient was used a combination of antiviral drugs: immunoglobulin against Epstein-Barr virus at a dose of 13 ml of a 10% solution immediately (7 ml in one syringe) intramuscularly once a week 3 times, valaciclovir 2 tablets. (1.0 g) 3 times a day 3 courses of 7 days, Laferobion 3 million ME 1 time per day daily for 7 consecutive days, the following indicators were obtained: total cholesterol 1.5 mmol / l, triglycerides 1.3 mmol / L, ACT 20 IU / L (norm 10-39 IU / L), ALT 35 IU / L (norm 10-35 IU / L). Repeated examination by immunofluorescence after 2 months in the immunocytes did not reveal antigens of any of the previously detected viruses.

Industrial applicability

The invention relates to medicine, namely cardiology and can be used in cardiology departments of hospitals and for the treatment of ambulatory patients for inclusion in a comprehensive treatment in order to increase the effectiveness of treatment, all of the proposed components are manufactured by the pharmaceutical industry and are available for use.

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 39 US Patent N 6183752 Restenosis / atherosclerosis diagnosis, prophylaxis and therapy

Claims

Claim:  1. A method of treating patients with cardiovascular diseases, including standard therapy, characterized in that prior to the start of standard therapy and in parallel with it, an antiviral drug is used as an additional component of standard therapy. 2. A method for the treatment of patients with cardiovascular disease according to claim 1 characterized in that valaciclovir is used as an antiviral drug 3. A method for the treatment of patients with cardiovascular disease according to claim 2 characterized in that the antiviral drug is used in 3-7 courses for 7-20 days starting treatment 1-5 days before the start of conservative therapy and in parallel with it in doses of 1-2 g 3-4 times a day with breaks between courses of 7 -20 days. 4. A method for the treatment of patients with cardiovascular disease according to claim 1 characterized in that an injectable intravenous form of acyclovir is used as an antiviral drug 5. A method for the treatment of patients with cardiovascular disease according to claim 4 characterized in that acyclovir is used in 3-7 courses of 7-20 days starting treatment 1-5 days before the start of conservative therapy and in parallel with it in doses of 0.5-1 g 1-4 times a day with breaks between courses of 7-20 days. 6. A method for the treatment of patients with cardiovascular diseases according to claim 1, characterized in that the injection form of alpha interferon is used as an antiviral drug 7. A method for the treatment of patients with cardiovascular diseases according to claim 1, characterized in that the injection form of a specific antiviral immunoglobulin is used as an antiviral drug 8. A method of treating patients with cardiovascular disease according to claim 1, characterized in that a combination of drugs according to claim 2-7 is used as an antiviral drug