The journal “Rational Pharmacotherapy in Cardiology” has been published since 2005 with the support of the All-Russian Society of Cardiologists and the State Research Center for Preventive Medicine of the Russian Ministry of Health.
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Chief Editor
Oganov Rafael Gegamovich, Doctor of Medical Sciences professor, academician of the Russian Academy of Medical Sciences
Deputy editors-in-chief
Boytsov Sergey Anatolyevich, Doctor of Medical Sciences Professor
Martsevich Sergey Yurievich, Doctor of Medical Sciences Professor
Shalnova Svetlana Anatolyevna, Doctor of Medical Sciences Professor
Executive Secretary
Maslennikova Galina Yakovlevna, Ph.D. Leading Researcher
Deputy Executive Secretary
Kolos Igor Petrovich, Ph.D. Researcher
Commissioning Editor
Lishuta Alexey Sergeevich, Ph.D. assistant
Editorial team:
Alexandrov Andrey Alekseevich, Doctor of Medical Sciences professor (Moscow)
Anichkov Dmitry Alexandrovich, Ph.D. assistant professor
Akhmedzhanov Nadir Migdatovich, Ph.D. Leading Researcher (Moscow)
Burtsev Vladimir Ivanovich, Doctor of Medical Sciences professor (Moscow)
Vasyuk Yuri Aleksandrovich, Doctor of Medical Sciences professor (Moscow)
Gilyarevsky Sergey Rudzherovich, Doctor of Medical Sciences professor (Moscow)
Golikov Alexey Petrovich, Doctor of Medical Sciences professor, academician of the Russian Academy of Medical Sciences (Moscow)
Deev Alexander Dmitrievich, Ph.D. Head of Biostatistics Laboratory (Moscow)
Dovgalevsky Pavel Yakovlevich, Doctor of Medical Sciences professor (Saratov)
Doshchitsin Vladimir Leonidovich, Doctor of Medical Sciences professor (Moscow)
Drapkina Oksana Mikhailovna, Doctor of Medical Sciences professor (Moscow)
Zadionchenko Vladimir Semenovich, Doctor of Medical Sciences professor (Moscow)
Zakirova Alyara Nurmukhamedovna, Doctor of Medical Sciences professor (Ufa)
Kalinina Anna Mikhailovna, Doctor of Medical Sciences professor (Moscow)
Konradi Alexandra Olegovna, Doctor of Medical Sciences professor (St. Petersburg)
Kontsevaya Anna Vasilievna, Doctor of Medical Sciences head of laboratory (Moscow)
Kutishenko Natalya Petrovna, Doctor of Medical Sciences head of laboratory (Moscow)
Kukharchuk Valery Vladimirovich, Doctor of Medical Sciences professor, corresponding member of the Russian Academy of Medical Sciences (Moscow)
Latfullin Ildus Anvarovich, Doctor of Medical Sciences professor (Kazan)
Lopatin Yuri Mikhailovich, Doctor of Medical Sciences professor (Volgograd)
Martynov Anatoly Ivanovich, Doctor of Medical Sciences professor, academician of the Russian Academy of Medical Sciences (Moscow)
Matyushin Gennady Vasilievich, Doctor of Medical Sciences professor (Krasnoyarsk)
Nebieridze David Vasilievich, Doctor of Medical Sciences professor (Moscow)
Nikitin Yuri Petrovich, Doctor of Medical Sciences professor, academician of the Russian Academy of Medical Sciences (Novosibirsk)
Perova Natalya Vladimirovna, Doctor of Medical Sciences professor (Moscow)
Podzolkov Valery Ivanovich, Doctor of Medical Sciences professor (Moscow)
Pozdnyakov Yuri Mikhailovich, Doctor of Medical Sciences professor (Zhukovsky)
Savenkov Mikhail Petrovich, Doctor of Medical Sciences professor (Moscow)
Sulimov Vitaly Andreevich, Doctor of Medical Sciences professor (Moscow)
Tkacheva Olga Nikolaevna, Doctor of Medical Sciences professor (Moscow)
Fishman Boris Borisovich, Doctor of Medical Sciences professor (Veliky Novgorod)
Chazova Irina Evgenievna, Doctor of Medical Sciences professor (Moscow)
Shalaev Sergey Vasilievich, Doctor of Medical Sciences professor (Tyumen)
Shostak Nadezhda Aleksandrovna, Doctor of Medical Sciences professor (Moscow)
Yakusevich Vladimir Valentinovich, Doctor of Medical Sciences professor (Yaroslavl)
Yakushin Sergey Stepanovich, Doctor of Medical Sciences professor (Ryazan)
International Editorial Board:
Adamyan Karlen Grigorievich, Doctor of Medical Sciences Professor, Academician of the Academy of Medical Sciences of the Republic of Armenia (Yerevan, Armenia)
Vardas Panos, professor (Heraklion, Greece)
Vijayraghavan Govindan, professor (Thiruvananthapuram, India)
DeMaria Antonio, professor (San Diego, USA)
Rational pharmacotherapy in cardiology
Rational pharmacotherapy in cardiology
International edition - publications indexed by web of science
News
The 2nd World Congress of Clinical Lipidology will take place in Vienna, Austria from 5-7 December, 2014
This extraordinary event will provide state of the art educational lectures in the field of clinical lipidology, focusing on practical lipid management including difficult to treat hyperlipidemias, genetic dyslipidemias, screening, dietary and nutraceutical approaches and case studies. Major emphasis will be given to new therapeutics, diagnosis and management of high risk patients.
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This year, ICI Meeting 2014 will be taking place on December 14-16, 2014 in Tel Aviv, Israel
ICI Meeting is the premier international conference for Innovations in Cardiovascular Systems: heart, brain, peripheral vessels, high-tech life science industry and emerging Mobile Health solutions. Congress website is: http://2014.icimeeting.com/
International Forum of Cardiology and Internal Medicine
03/25/2013-03/27/2013 Moscow
The main scientific directions of the Forum were:
- Improving the management of cardiac patients
- Emergency and first aid for cardiovascular disease
- Routine clinical examination of cardiac patients
- Prevention of cardiovascular disease at the population and individual
- New medical technologies in the treatment and prevention of cardiac patients
- Interventional cardiology and surgical treatments for cardiovascular disease
- Problems of rehabilitation of cardiac patients
All stages of the Forum’s preparing and its scientific program were available on the Internet on the official site www.cardioprogress.ru.
For quotation: Maksimov M.L. Rational pharmacotherapy of coronary heart disease: b-blockers and calcium antagonists in the treatment of stable angina // Breast Cancer. 2014. No. 2. P. 124
According to official statistics, the first line in the structure of causes of mortality in Russia is invariably occupied by mortality from diseases of the circulatory system, which account for more than 55% of the total number of deaths in the country. Diseases of the circulatory system alone caused the death of 525,431 people in the first half of 2013. Coronary heart disease (CHD) and cerebrovascular diseases are the leading causes of mortality in Russia. They account for 29.1% and 16.9% of deaths from all causes, respectively. The frequency of angina increases sharply with age: in women from 0.1-1% at the age of 45-54 years to 10-15% at the age of 65-74 years; in men from 2-5% at the age of 45-54 years to 10-20% at the age of 65-74 years. In most European countries, the prevalence of angina pectoris is 20-40 thousand per 1 million population. This explains the great interest of practitioners in the issues of proper management of patients with angina pectoris and the choice of optimal treatment methods. The high mortality rate existing in Russia can be reduced with a decisive transition of every doctor from the tactics of symptomatic treatment to the strategy of comprehensive and systematic secondary prevention.
The main pathophysiological mechanism of IHD is the discrepancy between the myocardial oxygen demand and the ability of the coronary blood flow to satisfy them. The development of this discrepancy is facilitated by atherosclerosis and dynamic obstruction of the coronary arteries due to their spasm, disruption of the mechanisms of dilatation of coronary vessels (lack of local vasodilating factors against the background of high myocardial oxygen demand, an unusually large increase in myocardial oxygen demand under the influence of intense physical activity, emotional stress, leading to to the release of catecholamines into the blood, the excess level of which has a cardiotoxic effect).
In the treatment of angina pectoris, two main goals have been identified: to improve the prognosis, prevent the occurrence of myocardial infarction and sudden death and increase life expectancy, as well as reduce the frequency and intensity of angina attacks and improve the patient’s quality of life. To achieve these goals, in addition to non-drug treatment, reducing modifying risk factors, and patient education, it is necessary to prescribe rational daily pharmacotherapy with individual selection and adjustment of drugs according to clinical, instrumental and laboratory data. It is advisable for patients to avoid exercise that causes angina and take nitroglycerin under the tongue to relieve it. It is also important to adequately treat concomitant diseases: arterial hypertension (HTN), diabetes mellitus, hypo- and hyperthyroidism, etc. In patients with coronary artery disease, the blood pressure level must be reduced to the target value of 130/85 mm Hg. Art. In patients with diabetes and/or kidney disease, the target blood pressure level should be less than 130/85 mmHg. Art. Conditions such as anemia and hyperthyroidism require special attention. Lifestyle modifications, medications, and revascularization can help minimize symptoms or completely eliminate angina, although not all of these approaches may be necessary for a particular patient.
1. Medicines that improve the prognosis in patients with angina pectoris
Acetylsalicylic acid (ASA) 75-150 mg/day in all patients in the absence of contraindications (active gastrointestinal bleeding, allergy to ASA or intolerance to it) (A).
Statins in all patients with coronary heart disease (A).
Beta-blockers orally in patients with a history of myocardial infarction or with heart failure (A).
ACE inhibitors or ARBs in the presence of hypertension, heart failure, left ventricular dysfunction, previous myocardial infarction with left ventricular dysfunction, or diabetes mellitus (A).
Class II a
ACE inhibitors or ARBs in all patients with angina and a confirmed diagnosis of coronary heart disease (B).
Clopidogrel as an alternative to ASA in patients with stable angina who cannot take ASA, for example, due to allergies (B).
High-dose statins in the presence of high risk (cardiovascular mortality more than 2% per year) in patients with proven coronary heart disease (B).
Fibrates for low HDL or high triglycerides in patients with diabetes mellitus or metabolic syndrome (B).
2. Drug therapy aimed at relieving symptoms
Short-acting nitroglycerin for angina relief and situational prophylaxis (patients should receive adequate instructions for the use of nitroglycerin) (B).
Assess the effectiveness of the b1-blocker and titrate its dose to the maximum therapeutic dose; assess the feasibility of using a long-acting drug (A).
If the b-blocker is poorly tolerated or has low effectiveness, prescribe monotherapy with BMCC (A) and long-acting nitrate (C).
If monotherapy with a b-blocker is not effective enough, add dihydropyridine BMCC (B).
Class II a
If a beta-blocker is poorly tolerated, prescribe an inhibitor of sinus node If channels - ivabradine (B).
If monotherapy with BMCC or combination therapy with BMCC and a beta-blocker is ineffective, replace BMCC with a long-acting nitrate. Avoid developing nitrate tolerance (C).
⎯Metabolic drugs (trimetazidine MB) can be used in addition to standard drugs or as an alternative to them if they are poorly tolerated (B).
Beta-adrenergic blockers (BABs) are drugs that selectively block β-adrenergic receptors and eliminate the effects of adrenaline on effector organs mediated through β-adrenergic receptors.
BBs are a very heterogeneous group of drugs in their pharmacological effects, the only common property of which is competitive antagonism of β1-adrenergic receptors. Along with blockade of β1-adrenergic receptors, beta-blockers can block β2-adrenergic receptors. In the first case, we talk about non-selective beta blockers, in the second - about β1-selective drugs. BABs also differ in the presence or absence of intrinsic sympathomimetic activity (ISA), vasodilating action, and lipophilicity. Drugs in this group competitively displace adrenaline from its connection with β-adrenergic receptors on the effector organ.
Blockers acting selectively on the heart (selective) are distinguished by a higher affinity for β1-adrenergic receptors of the myocardium than for β2-adrenergic receptors of blood vessels and bronchi (mainly in therapeutic doses). Non-selective beta blockers act on both β1 and β2 adrenergic receptors. BABs have hypotensive, antianginal, antiarrhythmic, negative ino-, chrono-, dromo- and bathmotropic effects. By inhibiting the β-adrenergic receptors of the heart, 75% of which are β1 and 25% are β2 receptors, they reduce the formation of cAMP from ATP stimulated by catecholamines and reduce the intracellular current of calcium ions. This leads to a decrease in heart rate, inhibition of conductivity and decreased myocardial contractility.
The antianginal effect of beta blockers is due to a decrease in myocardial oxygen demand as a result of a decrease in heart rate (diastole lengthens and myocardial perfusion improves) and a decrease in contractility, as well as narrowing of the coronary vessels of non-ischemic areas, which leads to the redistribution of blood to areas of ischemic areas of the myocardium. The mechanism of the hypotensive action of beta blockers is the inhibition of presynaptic β2 receptors, which reduces the release of norepinephrine into the synaptic cleft, and, consequently, the stimulation of α receptors of blood vessels, reducing the activity of the renin-angiotensin-aldosterone system (blockade of β1 receptors of juxtaglomerular cells of the kidneys ), inhibition of the vasomotor center (for drugs that penetrate the central nervous system), restoration of the baroreceptor mechanism (due to a decrease in cardiac output).
The antiarrhythmic effect of beta blockers is determined by the inhibitory effect on factors such as increased activity of the sympathetic nervous system and cAMP, which plays an important role in the occurrence of ventricular fibrillation during myocardial ischemia and increased blood pressure. BABs inhibit impulse conduction in the antegrade and, to a lesser extent, in the retrograde directions through the AV node and along additional pathways. Most selective beta blockers in therapeutic doses do not have a cardiodepressive effect, do not affect glucose metabolism and do not cause sodium ion retention in the body. Selective beta blockers, to a lesser extent than non-selective ones, affect the release of insulin and carbohydrate metabolism, mask the symptoms of hypoglycemia in patients with diabetes, increase the content of triglycerides, reduce the content of free fatty acids and high-density lipoproteins. When used in therapeutic doses, selective beta blockers have a less pronounced effect on the smooth muscles of the bronchi and peripheral arteries and on lipid metabolism than non-selective ones.
BBs are first-line drugs (A) in patients with angina attacks, who have had myocardial infarction, or when diagnosing episodes of myocardial ischemia in patients using instrumental methods. By reducing adrenergic activation of the heart, beta blockers increase exercise tolerance and reduce the frequency and intensity of angina attacks, thereby providing improvement in symptoms, and reduce myocardial oxygen demand. In addition, they increase the delivery of oxygen to the myocardium (by increasing collateral blood flow and redistributing it in favor of the ischemic layers of the myocardium - the subendocardium). The choice of drug for angina depends on the clinical situation and the individual reaction of the patient.
In the pharmacotherapy of patients with coronary artery disease, preference should be given to selective long-acting beta blockers, without ICA. These drugs are much less likely than non-selective beta blockers to cause side effects of therapy and therefore can be used in patients with coronary artery disease with a tendency to bronchospasm, patients with COPD, metabolic syndrome, diabetes mellitus and peripheral circulatory disorders. Their effectiveness has been proven in large clinical studies. Such data were obtained with the use of sustained-release metoprolol, bisoprolol, nebivolol and carvedilol. Therefore, these beta blockers are recommended to be prescribed to patients who have suffered AMI. When prescribing alprenolol, atenolol, oxprenolol, no positive results were obtained. A meta-analysis of 82 randomized studies showed that long-term use of beta blockers leads to an additional reduction in the risk of death and the development of recurrent myocardial infarction in patients who had a history of myocardial infarction and were taking ASA, fibrinolytics, and ACE inhibitors.
Data from large prospective studies indicate that long-term use of beta blockers increases the survival of patients after myocardial infarction by 25% due to a significant reduction in the number of deaths from cardiovascular diseases, including sudden death and recurrent AMI. In patients with coronary artery disease, the most pronounced cardioprotective effect is exerted by lipophilic drugs (they reduce mortality by an average of 30%) - betaxolol, carvedilol, metoprolol, propranolol, timolol, etc. and beta-blockers without BCA (by an average of 28%): metoprolol, propranolol and timolol. At the same time, neither beta blockers with BCA (alprenolol, oxprenolol and pindolol), nor hydrophilic drugs (atenolol and sotalol) with long-term use prevent death in this category of patients. Bisoprolol is a highly selective β1-blocker, without BCA, which successfully combines the advantages of lipo- and hydrophilic blockers, a long half-life and a small number of side effects.
Bisoprolol has a dual elimination route - metabolism in the liver and filtration in the kidneys (balanced clearance), which makes it possible to use it in cases of impaired liver or kidney function. However, in case of severe renal/liver failure, it is recommended to reduce the dose by 2 times. 30% binds to blood plasma proteins, so interaction with other drugs at the level of protein binding is excluded. Metabolized by 40-60%. The main metabolic pathway is the oxidation of CYP2D6, which is characterized by genetic polymorphism. However, unlike propranolol, metoprolol, carvedilol, nebivolol, the pharmacokinetics of bisoprolol do not depend on the genetic polymorphism of CYP2D6, thus, its pharmacokinetics do not depend on the genetic characteristics of the patient. Bisoprolol can be used in patients with COPD subject to concomitant adequate bronchodilator therapy under careful monitoring of the clinical condition of patients and parameters of external respiratory function.
As evidenced by real clinical practice, drugs with different trade names, based on the same active substance, can differ significantly in therapeutic effectiveness. The study “Comparison of the clinical effectiveness of the original drug bisoprolol and its generic in patients with stable angina pectoris in combination with chronic obstructive pulmonary disease” showed that only when prescribing the original drug bisoprolol (Concor, Takeda Pharmaceuticals LLC) the target heart rate range and improvement of endothelial function are achieved, which makes it possible to realize long-term cardiovascular effects and talk about its greater clinical effectiveness. The generic drug had no effect on endothelial function: there were no significant changes in EDV, as well as in serum concentrations of nitric oxide metabolites. It was noted that in patients with coronary artery disease with concomitant COPD, only the original bisoprolol is able to improve the functional state of the endothelium. Initially, all patients in the study N.Yu. Grigorieva et al. there were bronchial obstructions. After 12 weeks in patients taking the original drug, the respiratory function parameters did not change, which is due to the proven high cardioselectivity (1:75) of bisoprolol. In those examined who took the generic drug, after 4 weeks. treatment, there were no significant changes in respiratory function indicators, however, after 12 weeks. a statistically significant decrease in respiratory function indicators was registered. The deterioration of bronchial obstruction when taking generic bisoprolol is most likely due to the quality of its main molecule and the excipients contained in it, which could affect bronchial obstruction. Thus, in order to prevent the development of bronchial obstruction, patients with coronary artery disease who have concomitant COPD should be prescribed original bisoprolol.
Data from studies have shown that the use of bisoprolol not only reduces the severity of clinical symptoms, but also significantly improves the prognosis. In patients with stable angina, the number and duration of transient episodes of ischemia can be significantly reduced, there is a decrease in mortality, the incidence of coronary artery disease and an improvement in the general condition of patients. Bisoprolol increases exercise tolerance to a greater extent than atenolol and metoprolol; it causes a significant increase in physical activity and a dose-dependent effect on its tolerance. It has been shown that bisoprolol, to a much greater extent than atenolol and metoprolol, improves the quality of life of patients and reduces anxiety and fatigue. It is very important that bisoprolol reduces cardiovascular mortality and the risk of fatal MI in high-risk patients undergoing cardiac surgery.
Thus, in a double-blind study by L. van de Ven et al. demonstrated that in stable angina pectoris, the effectiveness of bisoprolol at a dose of 10 mg 1 time/day is significantly higher than that of isosorbide dinitrate at a dose of 20 mg 3 times/day.
The multicenter controlled study TIBBS (Total Ischemic Burden Bisoprolol Study) compared the effects of bisoprolol (Concor) and long-acting nifedipine on transient myocardial ischemia in patients with stable angina. This study included 330 patients who had suffered at least 3 episodes of myocardial ischemia within 48 hours before randomization according to Holter electrocardiogram monitoring. 161 patients received bisoprolol (Concor) therapy, 169 received sustained-release nifedipine. All patients received placebo for 10 days, then for 4 weeks. - bisoprolol at a dose of 10 mg/day or retarded nifedipine at a dose of 20 mg 2 times/day. In the next 4 weeks. patients received double doses of the same drugs. At the end of the study, the average number of episodes of myocardial ischemia was statistically significantly lower in the Concor group. In addition, the number of ischemic episodes in the early morning hours was significantly reduced in this group. Bisoprolol was more effective than extended-release nifedipine regarding the duration of ischemic episodes (bisoprolol - 68%, versus nifedipine - 28%), the severity of ischemic attacks (-70% on bisoprolol and -40% on nifedipine), the number of ischemic episodes (-60% on bisoprolol versus 29% on nifedipine). It is also important that the TIBBS study noted a direct correlation of the number and duration of myocardial ischemia episodes with the incidence of deaths, fatal cardiovascular events and myocardial revascularization operations. Thus, Concor, by eliminating episodes of myocardial ischemia, also has a beneficial effect on the prognosis for stable angina.
Another important class of drugs used in the complex pharmacotherapy of IHD is today certainly recognized as slow calcium channel blockers (SCBCs) or (according to the terminology of other sources) calcium antagonists. The ability of BMCC to relax the smooth muscles of the walls of muscular arteries, arterioles and, thus, reduce total peripheral vascular resistance (TPVR) served as the basis for the widespread use of these drugs in hypertension and coronary artery disease. Blockers of slow calcium channels have a vasodilating effect, and the most powerful vasodilators are drugs from the dihydropyridine group. In case of vasospastic angina (variant angina, Prinzmetal's angina), BMCC - dihydropyridine derivatives - are used to prevent attacks. Dihydropyridines, to a greater extent than other BMCCs, eliminate spasm of the coronary arteries and are therefore the drugs of choice for vasospastic angina. The mechanism of antianginal and hypotensive action is due to their ability to cause dilation of peripheral and coronary arteries, therefore, these drugs can be considered as a supplement, and sometimes as an alternative to nitrates, which also have a vasodilating effect.
The use of short-acting dihydropyridine derivatives should be avoided, as they can worsen the symptoms and prognosis of life in patients with coronary artery disease. The powerful vasodilation caused by nifedipine leads to stimulation of the sympathoadrenal system with the development of hypercatecholaminemia, causing tachycardia, facial flushing, and an arrhythmogenic effect. In addition, coronary dilatation can cause steal syndrome. According to modern recommendations, patients with coronary artery disease should be prescribed only long-acting dihydropyridine BMCCs of the second and third generation, used once a day, especially when coronary artery disease and hypertension are combined. Amlodipine, which has a sufficient evidence base in multicenter clinical trials, should be considered the first choice drug. Amlodipine causes dilation of large-caliber coronary arteries, as well as coronary arterioles, both intact and ischemic areas of the myocardium. This ensures the supply of oxygen to myocardial cells during spasms of the coronary arteries. In addition, by dilating peripheral arterioles, amlodipine reduces peripheral vascular resistance; reflex tachycardia, as a rule, does not develop. The effectiveness of amlodipine in patients with angina pectoris is higher than that of diltiazem.
Summarizing the above, we can note the relevance of the appearance on the Russian pharmaceutical market of a combination of the most widely used calcium antagonist (amlodipine) with the most widely used β-blocker (bisoprolol) in one tablet prescribed 1 time per day - Concor AM (Takeda Pharmaceuticals LLC ). This combination is rational hypotensive and anti-ischemic. Complementary effects due to different mechanisms of action: amlodipine reduces central aortic pressure and peripheral vascular resistance, and bisoprolol reduces left ventricular stroke volume and renin secretion, which prevents vasoconstriction. The drugs weaken the reflex reactions associated with taking another component of the combination: bisoprolol prevents the negative effect of reflex activation of the SNS caused by taking amlodipine, and amlodipine prevents reflex vasoconstriction caused by the action of bisoprolol.
It is also worth noting the similar pharmacokinetic parameters of the two drugs: long half-life, action for 24 hours. Thus, in a study by R. Rana et al. in 801 patients with newly diagnosed essential hypertension stage 2 for 4 weeks. treatment with Concor AM (5 mg bisoprolol + 5 mg amlodipine) target blood pressure values (<140 и <90 мм рт. ст. для САД и ДАД соответственно) были достигнуты у 82,5% пациентов. Помимо предсказуемой гипотензивной эффективности комбинации было показано отчетливое снижение ЧСС на 10,4%. За 4 нед. терапии средняя ЧСС снизилась с исходного среднего 83,3 уд./ мин. до 74,6 уд./мин. При этом отмечена хорошая переносимость комбинации, низкая частота нежелательных лекарственных реакций. Исследователи отметили отличную или хорошую эффективность препарата у 91,4% пациентов, а 90,6% больных - отличную или хорошую его переносимость . Это важно, поскольку повышенная ЧСС является одним из значимых факторов риска сердечно-сосудистого заболевания. Обоснованием применимости комбинации бисопролола и амлодипина в лечении пациентов с ИБС можно считать: высокую эффективность и безопасность обоих препаратов, особенно при сочетании ИБС и АГ .
Thus, β-blockers in world and Russian medical practice today are widely used in the treatment and prevention of cardiovascular diseases and their complications. They are recognized as first-line drugs in most international and national recommendations for the treatment of coronary artery disease and hypertension. Bisoprolol and other highly selective beta blockers without ICA are recommended as the primary therapy for all forms of coronary artery disease, including patients with acute coronary syndrome and post-AMI. Drugs in this group are the first choice for the treatment of patients with angina pectoris, especially patients who have had an MI, since they lead to a proven reduction in mortality and the incidence of recurrent MI. If monotherapy with beta blockers is insufficient, then nitrates or calcium antagonists from the dihydropyridine group are added to the treatment.
The combination of bisoprolol in combination with amlodipine (Concor AM) is a rational antihypertensive combination, which, taking into account the reduction in heart rate and myocardial load, can be successfully used in the treatment of coronary artery disease, stable angina, especially in combination with hypertension. The presence of 4 different-dose options for the composition of the drug Concor AM (bisoprolol/amlodipine 5 mg/5 mg, 5 mg/10 mg, 10 mg/5 mg, 10 mg/10 mg) determines the convenience for the doctor and patient in selecting an adequate dose of the combined drug. Bisoprolol in combination with amlodipine (Concor AM) can be considered an indispensable drug in the treatment of coronary artery disease, especially if nitrates are poorly tolerated.
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Scientific and practical peer-reviewed journal for cardiologists and therapists "Rational Pharmacotherapy in Cardiology" has been published since 2005 with the support of the Russian Society of Cardiology and the State Research Center for Preventive Medicine. It is a nationwide publication with a frequency of 6 issues per year. Included in the List of publications of the Higher Attestation Commission for publishing the results of dissertations of candidates and doctors of sciences. Distributed by subscription and free of charge at specialized events.
The Editorial Board includes leading Russian scientists in the field of cardiology, preventive cardiology, internal medicine, clinical pharmacology and preventive pharmacotherapy, including 38 doctors of science, including 6 academicians of the Russian Academy of Sciences. The International Editorial Council includes well-known foreign cardiologists.
The main content of the journal is represented by original scientific articles, scientific reviews, lectures, and the results of analysis of clinical practice. The journal covers the problems of early diagnosis, primary and secondary prevention of cardiovascular diseases and comorbidities, the effective use of drug therapy, and current issues of experimental and clinical pharmacology.
All materials are posted free of charge and undergo a thorough scientific examination: double-blind review, plagiarism check, multi-stage editing. Authors are required to provide a disclosure of conflicts of interest related to publication. Reviewers are experts in the subject matter of the materials being reviewed. In each issue, the best original articles are translated and published in Russian and English.
The journal has a website in Russian (www.rpcardio.ru) and English (www.rpcardio.com) in which the full texts of published materials for all years are publicly available. The journal is also presented in open access on the website of the Scientific Electronic Library (SEL) and is included in the Russian Science Citation Index (RSCI). In May 2016, the two-year impact factor of the RSCI for 2015 was 1.051. Full-text electronic versions of all published materials are also available on the websites of the Russian Scientific Electronic Library CyberLeninka and the international open access website DOAJ. Published materials are presented in the electronic databases Web of Science, SCOPUS, EMBASE, Index Copernicus, Ulrich’s Periodicals Directory.
Members of the editorial board:
Editor-in-Chief - Boytsov S.A.
Deputy editors-in-chief:
Drapkina O.M., Martsevich S.Yu., Oganov R.G., Shalnova S.A.
Lishuta A.S. (Commissioning Editor)
Butina E.K. (executive Secretary)
Editorial board:
Anichkov D.A., Akhmedzhanov N.M., Burtsev V.I. , Vasyuk Yu.A., Gilyarevsky S.R., Gorbunov V.M., Deev D.A., Doshchicin V.L., Zadionchenko V.S. , Kalinina A.M., Kontsevaya A.V., Kutishenko N.P., Kukharchuk V.V., Lukyanov M.M., Martynov A.I., Napalkov D.A., Nebieridze D.V., Podzolkov V.I., Pozdnyakov Yu.M., Savenkov M.P. , Smirnova M.I., Tkacheva O.N., Chazova I.E. , Shostak N.A., Yakusevich V.V., Yakushin S.S.
Editorial Council:
Adamyan K. G. (Yerevan, Armenia), Vardas P. (Heraklion, Greece), Vijeiraghavan G.
(Thiruvananthapuram, India), Golikov A.P. (Moscow, Russia), DeMaria A. (San Diego, USA),
Dovgalevsky P.Ya. (Samara, Russia), Dzhusipov A.K. (Almaty, Kazakhstan), Zakirova A.N. (Ufa,
Russia), Kenda M.F. (Ljubljana, Slovenia), Kovalenko V.N. (Kyiv, Ukraine), Conradi A.O.
(St. Petersburg, Russia), Kurbanov R. D. (Tashkent, Uzbekistan), Latfullin I. A. (Kazan, Russia),
Lopatin Yu.M. (Volgograd, Russia), Matyushin G.V., (Krasnoyarsk, Russia), Mrochek A.G. (Minsk,
Belarus), Nikitin Yu.P., (Novosibirsk, Russia), Oleynikov V.E. (Penza, Russia), Perova N.V.
(Moscow, Russia), Popovich M. I. (Chisinau, Moldova), Pushka P. (Helsinki, Finland),
Stachenko S. (Edmonton, Canada), Fishman B.B. (Veliky Novgorod, Russia),
Tsinamdzgvrishvili B.V. (Tbilisi, Georgia), Shalaev S.V. (Tyumen, Russia).
Year of issue: 2005
Genre: Cardiology
Format: PDF
Quality: eBook (originally computer)
Description: The practical guide “Rational pharmacotherapy of cardiovascular diseases” provides the classification and clinical pharmacology of drugs used for cardiovascular diseases. Typical clinical manifestations, diagnostic criteria, basic principles and treatment regimens for cardiovascular diseases with levels of evidence are described. The features of managing different groups of patients are covered, and treatment algorithms for individual nosological forms are given. The guide provides extensive background information to facilitate rational, individualized selection of a drug and treatment regimen.
The practical guide “Rational pharmacotherapy of cardiovascular diseases” is intended for practicing physicians, students of higher medical educational institutions and students of advanced training courses.
Clinical pharmacology of drugs for the treatment of cardiovascular diseases
Beta blockers
Calcium antagonists (calcium channel blockers)
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Centrally acting antihypertensives
Central α2 receptor agonists
Imidazoline 1 receptor agonists
Direct acting vasodilators (myotropic)
Alpha blockers
Ganglioblockers
Diuretics
Loop (potent) diuretics
Thiazide and thiazide-like diuretics
Carbonic anhydrase inhibitors
Potassium sparing diuretics
Aldosterone receptor antagonists
Nitrates
Cardiac glycosides
Adrenergic agonists
Antiarrhythmic drugs
Drugs affecting blood clotting and platelet function
Direct anticoagulants
Unfractionated (standard) heparin
Low molecular weight (fractionated) heparins
Fondaparinux sodium
Direct acting thrombin inhibitors
Indirect anticoagulants
Antiplatelet agents
Acetylsalicylic acid
Thienopyridine derivatives
Blockers of glycoprotein IIb/IIIa platelet receptors
Fibrinolytics
Lipid-lowering drugs
HMG-CoA reductase inhibitors (statins)
Fibric acid derivatives (fibrates)
Nicotinic acid and its derivatives
Bile acid sequestrants
Nonsteroidal anti-inflammatory drugs
Narcotic analgesics
Phlebotonics
Clinical guidelines
Chronic ischemic heart disease
Unstable angina
Myocardial infarction
Atherosclerosis. Lipid disorders
Arterial hypertension. Hypertonic disease
Secondary (symptomatic) arterial hypertension
Hypertension due to kidney disease
Hypertension in glomerulonephritis and pyelonephritis
Hypertension in diabetic nephropathy
Vasorenal hypertension
Hypertension caused by diseases of the cardiovascular system
Hypertension in coarctation of the aorta
AH in nonspecific aortoarteritis
Hypertension caused by diseases of the endocrine system
Hypertension with hypersecretion of mineralocorticoids
Hypertension with hypersecretion of glucocorticoids (Itsenko-Cushing syndrome and disease)
AH in pheochromocytoma
Hypertension in hypothyroidism
Metabolic syndrome
Pulmonary hypertension
Heart rhythm disturbances
Changes in the automaticity of the sinoatrial node
Sinus arrhythmia
Sinus bradycardia
Sinus tachycardia
Sick sinus syndrome
Ectopic contractions and rhythms
Passive (substituting or slipping) complexes and rhythms
Active ectopic impulses (complexes) and rhythms. Extrasystole Supraventricular tachycardia
Automatic atrial tachycardia
Reciprocal tachycardias
Reciprocal AV nodal tachycardia
Atrial flutter
Atrial fibrillation (atrial fibrillation)
Ventricular tachycardia
Ventricular flutter and fibrillation
WPW syndrome
Thromboembolic complications in patients with atrial fibrillation
Heart failure
Cardiomyopathies
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Myocarditis
Pericardial diseases
Pericarditis
Cardiac tamponade
Constrictive pericarditis
Infective endocarditis
Acute rheumatic fever and rheumatic heart disease
Systemic vasculitis
Polyarteritis nodosa
Microscopic polyangiitis
Wegener's granulomatosis
Churg-Strauss syndrome (allergic angiitis and granulomatosis)
Hemorrhagic vasculitis (Henoch-Schönlein purpura)
Giant cell arteritis and polymyalgia rheumatica
Takayasu arteritis (nonspecific aortoarteritis)
Essential cryoglobulinemic vasculitis
Deep vein thrombosis and pulmonary embolism
Chronic venous insufficiency of the lower extremities
Descriptions of medicines
Aymalin
Acridilol
Acripamide
Aksetin
Actovegin
Amiodarone
Amlodipine
Amphetamine
Aponil
Aspirin cardio
Atenolol
Atorvastatin
Acenocoumarol
Acetazolamide
Bezafibrate
Bendazole
Betak
Betaxolol
Bisogamma
Bisoprolol
Bretylium tosylate
Bumecaine
Warfarin Nycomed
Verapamil
Veroshpiron
Vincamine
Gallopamil
Gemfibrozil
Heparin sodium
Heparinoid
Hydralazine
Hydrochlorothiazide
Glucobay
Glucophage
Dalteparin sodium
Detralex
Diazem
Diakarb
Digitoxin
Digoxin
Diltiazem
Dipyridamole
Diroton
Doxazosin
Isoprenaline
Isosorbide dinitrate
Isosorbide mononitrate
Invoril
Indapamide
Indapamide
Indobufen
Ionic
Irbesartan
Iruzid
Irumed
Candesartan
Kapoten
Captopril
Carvedilol
Cardiomagnyl
Clexane
Clerimed
Clonidine
Klopamide
Concor
Concor Cor
Xanthinol nicotinate
Lanatoside C
Lappaconitine hydrobromide
Lacidipine
Lisinopril
Lovastatin
Losartan
Medakson
Honeyclave
Medostatin
Melox
Methyldopa
Metocard
Metoprolol
Mildronate
Minoxidil
Moxonidine
Molsidomin
Moexipril
Nadolol
Nadroparin calcium
Nebivolol
Nebilet
Nicardipine
A nicotinic acid
Nimodipine
Nitrendipine
Nitroglycerine
Nitrocor spray
Nifedipine
Nifecard HL
Nicergoline
Normodipine
Oxprenolol
Omelar Cardio
Osmo-Adalat
Perindopril
Pindolol
Pravastatin
Prazosin
Primalia bitartrate
Preductal MV
Prestarium
Procainamide
Propaphenone
Propranolol
Proroksan
Purolaza
Ramipril
Renipril
Renipril GT
Rilmenidine
Riodipine
Selemicin
Simvastatin
symbol
SotaHEXAL
Spirapril
Talinolol
Telmisartan
Terazosin
Ticlopidine
Tinzaparin sodium
Trandolapril
Triamterene
Trimetazidine
Trinitrolong
Ouabain
Urapidil
Urokinase
Felodipin
Fenyndion
Phenytoin
Fenofibrate
Phentolamine
Fluvastatin
Flunarizine
Fosinopril
Quinapril
Quinidine
Chlorthalidone
Celiprolol
Cilazapril
Cinnarizine
Ciprofibrate
Ednit
Enalapril
EnalaprilHEXAL
Enalaprilat
Enam
Enarenal
Enoxaparin sodium
Eprosartan
Eptifibatide
Esmolol
Ethyl biscoumacetate
LITERATURE