home Auditorium 7 Arterial hypertension and chronic obstructive pulmonary disease—problems in choosing therapy. I. Risk factors

Arterial hypertension and chronic obstructive pulmonary disease—problems in choosing therapy. I. Risk factors

Year of issue: 2009

Genre: Cardiology

Format: PDF

Quality: eBook (originally computer)

Description: We bring to your attention the clinical recommendations (guidelines) “National Clinical Recommendations of the All-Russian Scientific Society of Cardiologists”, developed by groups of experts of the All-Russian Scientific Society of Cardiologists and approved at the Russian National Congresses of Cardiologists. Clinical guidelines are periodic statements that help the practitioner and the patient make the right decisions regarding his health in specific clinical conditions. These recommendations are based on clinical studies and their systematic review and meta-analysis. Clinical recommendations are usually the result of long-term collaboration between specialists, are approved by professional medical societies and are intended for doctors and health care managers, who can use them to select optimal therapy, develop quality indicators and manage the diagnostic and treatment process, create standard equipment sheets, and continuously improve the qualifications of doctors, formation of volumes of medical care within the framework of state guarantees.
Clinical guidelines do not have formal legal force, but are a tool that helps doctors make the optimal therapeutic choice, however, they can be used when deciding on the correctness of treatment, incl. in a court.
Unfortunately, all over the world, Russia is no exception, there is a large gap between existing recommendations and actual clinical practice. There are various reasons for this:
- doctors do not know about their existence, or do not believe them;
- doctors believe that they are overloaded with recommendations;
- doctors rely on personal experience and impressions that the therapeutic approach they choose is the best;
- Doctors' decisions are influenced by economic and social factors.
We hope that the publication of the GFCI recommendations in the form of one monograph will facilitate their use by doctors in practical work and will help improve the quality of care for cardiac patients.

SECTION I
Diagnosis and treatment of arterial hypertension

Committee of Experts
Societies
1. Introduction
2. Definition
3. Classification of hypertension
3.1. Determination of the degree of increase in blood pressure8
3.2. Factors influencing the prognosis; assessment of general (total) cardiovascular risk
3.3. Formulation of diagnosis
4. Diagnostics
4.1. Rules for measuring blood pressure
4.1.1. Methods for measuring blood pressure
4.1.2. Patient position
4.1.3. Conditions for measuring blood pressure
4.1.4. Equipment
4.1.5. Measurement ratio
4.1.6. Measuring technique
4.1.7. Measuring blood pressure at home
4.1.8. 24-hour blood pressure monitoring
4.1.9. Isolated clinical hypertension
4.1.10. Isolated ambulatory hypertension (IAAH)
4.1.11. Central AD
4.2. Examination methods
4.2.1. History taking
4.2.2. Physical examination
4.2.3. Laboratory and instrumental research methods
4.2.4. Study of the condition of target organs
4.2.5. Genetic analysis in patients with hypertension
5. Management tactics for patients with hypertension
5.1. Goals of therapy
5.2. General principles of patient management
5.3. Measures to change the coolant
5.4. Drug therapy
5.4.1. Choice of antihypertensive drug
5.4.2. Combination therapy for hypertension
5.4.3. Concomitant therapy to correct existing risk factors
6. Dynamic observation
7. Features of the treatment of hypertension in certain groups of patients
7.1. Hypertension in the elderly
7.2. AG and MS
7.3. AH and DM
7.4. AG and CVB
7.5. AH and ischemic heart disease
7.6. AH and CHF
7.7. Hypertension with kidney damage
7.8. hypertension in women
7.9. Hypertension in combination with lung pathology
7.10. AH and OSA
7.11. Refractory hypertension
7.12. Malignant hypertension
8. Diagnosis and treatment of secondary forms of hypertension
8.1. Hypertension associated with kidney pathology
8.2. Hypertension with damage to the renal arteries
8.3. Pheochromocytoma
8.4. Primary aldosteronism
8.5. Itsenko-Cushing's syndrome and disease
8.6. Coarctation of the aorta
8.7. Dosage form of hypertension
9. Emergency conditions
9.1. Complicated HA
9.2. Uncomplicated GC
10. Indications for hospitalization
11. Partnerships with patients
12. Conclusion
13. Literature

Working group to prepare the text of the recommendations

SECTION II
Diagnosis and treatment of stable angina
Societies
1. Introduction
2. Classes of recommendations and levels of evidence
3. Definition and causes of angina
4. Epidemiology and risk factors
4.1. Epidemiology
4.2. Natural history and prognosis
4.3. Risk factors (RF)
5. Diagnosis of angina pectoris
5.1. Main clinical signs
5.2. Conditions that provoke and aggravate myocardial ischemia
5.3. Physical examination

5.5. Instrumental diagnostics
5.5.1. ECG at rest
5.5.2. X-ray of the chest organs
5.5.3. ECG tests with FN
5.5.4. Transesophageal atrial electrical stimulation (TEES)
5.5.5. Outpatient ECG monitoring
5.5.6. Echocardiography at rest
5.5.7. Stress EchoCG
5.5.8. Myocardial perfusion scintigraphy with stress
5.5.9. Multislice computed tomography (MSCT) of the heart and coronary vessels
5.6. Invasive methods for studying coronary anatomy
5.6.1. KAG
6. Classification of transient myocardial ischemia
6.1. Stable angina
6.2. Vasospastic (variant) stenocardia
6.3. Painless (silent) myocardial ischemia
7. Differential diagnosis of Roma chest pain syndrome
8. Features of the diagnosis of stable angina in certain groups of patients and with concomitant diseases
8.1. Angina in young people
8.2. Angina pectoris in women RF IHD in women
8.3. Angina in the elderly
8.4. Angina pectoris with hypertension
8.5. Angina pectoris with diabetes
8.6. Cardiac syndrome X
9. Risk stratification
9.1. Risk stratification based on clinical data
9.2. Risk stratification based on stress tests
9.3. Risk stratification based on coronary angiography
10. Treatment
10.1. Treatment goals and tactics
10.2. Main aspects of non-drug treatment of angina pectoris
10.3. Pharmacological treatment
10.3.1. Drugs that improve prognosis in patients with angina pectoris
10.3.2. Drug therapy to relieve symptoms
10.3.3. Criteria for treatment effectiveness
10.3.4. Special situations: syndrome X and vasospastic angina
10.4. Myocardial revascularization
10.4.1. Coronary artery bypass surgery
10.4.2. Percutaneous interventions on the coronary arteries
11. Modern non-drug technologies for the treatment of stable angina
11.1. Enhanced external counterpulsation (EECP)
11.2. Cardiac shock wave therapy (SWT)
11.3. Transmyocardial laser therapy (TMLT)
12. Improving lifestyle and rehabilitation of patients with stable angina pectoris
13. Applications
13.1.Literature
13.2. List of key multicenter studies
13.3. Essential medications for the treatment of stable angina
SECTION III
Kidney function and cardiovascular risk prediction
Working group to prepare the text of the recommendations
Composition of the VNOK expert committee for developing recommendations
Societies
1. Introduction
2. Basic definitions
3. Methods for assessing kidney function
3.1. Serum creatinine
3.2. Glomerular filtration rate and creatinine clearance
3.3. Protein excretion in urine
3.3.1. Methods for determining urinary albumin excretion
3.3.2. Diagnostic criteria for microalbuminuria and proteinuria
4. Diagnostic criteria and classification of chronic kidney disease
5. Screening patients for renal impairment
5.1. Algorithm for determining renal dysfunction
5.2. Diagnosis of kidney damage
6. Management of patients with chronic kidney disease and monitoring of renal function
6.1. Correction of blood pressure and general principles of management of patients with chronic kidney disease
6.2. Detection and correction of dyslipidemia.
6.3. Diagnosis and correction of anemia
7. Kidney function in special situations
7.1. Arterial hypertension
7.2. Metabolic syndrome
7.3. Chronic heart failure
7.4. Acute coronary syndrome and myocardial infarction
8. Conclusion
9. Applications
10. Literature
SECTION IV
Diagnosis and treatment of chronic heart failure
Working group to prepare the text of the recommendations
Composition of the VNOK expert committee for developing recommendations
Societies
I. Introduction
11. Epidemiology of HF in the Russian Federation
III. Terminology used to describe HF

IV. Definition of CHF
1. Principles of diagnosis of CHF
1.1. The role of symptoms and objective signs in the diagnosis of CHF
1.2. Electrocardiography
1.3. Hematological and biochemical blood tests and general urine analysis
1.4. Echocardiography
1.5. Magnetic resonance imaging
1.6. Radioisotope methods
1.7. Pulmonary function assessment
1.8. Load tests
1.9. X-ray of the chest organs
1.10. Determination of the level of sodium-uretic peptides
1.11. Assessment of the severity of CHF/Classification of CHF
1.12. Algorithm for diagnosing CHF
2. Treatment of CHF
2.1. Goals in the treatment of CHF
2.2. Prevention of CHF
3. Non-drug treatment of CHF
3.1. Diet of patients with CHF
3.2. Alcohol
3.3. Physical activity mode
3.4. Methods of physical activity in the form of walking
3.5. Mode. General recommendations
3.6. Psychological rehabilitation and creation of outpatient observation schools for patients with CHF
3.7. Medical and social work
4. Drug treatment of CHF. General principles
5. Basic drugs for drug treatment of CHF
5.1. ACE inhibitors
5.1.1 Side effects (requiring treatment interruption) complicate the use of ACE inhibitors quite rarely
5.1.2. Practical issues of using ACE inhibitors for CHF (doses, treatment tactics, precautions)
5.2. β-adrenergic receptor blockers
5.3. Aldosterone antagonists
5.4 Diuretics (diuretics) in the treatment of CHF
5.4.1. General issues of dehydration therapy for CHF
5.5. Cardiac glycosides
5.6. Angiotensin II receptor antagonists
6. Additional agents in the treatment of CHF
6.1. Statins
6.2. Antithrombotic agents in the treatment of CHF (indirect anticoagulants)
7. Auxiliary agents in the treatment of CHF
7.1. Peripheral vasodilators
7.2. Slow calcium channel blockers
7.3. Antiarrhythmic drugs in the treatment of CHF
7.4. Antiplatelet agents (in particular, aspirin) in the treatment of CHF
7.5. Non-glycoside inotropic agents in the treatment of CHF
7.6. Metabolically active drugs (cytoprotectors) in the treatment of CHF
7.7 Drugs not recommended for use in CHF
8. Drug therapy for patients with CHF and preserved LV systolic function or diastolic CHF
9. Surgical and electrophysiological methods of treating CHF
9.1. Electrophysiological methods of treating CHF
9.2. Surgical and mechanical methods of treating CHF
V. Appendix
Appendix 1. Classification of CHF OSSN 2002 (with comments and appendices)
Appendix 2.
List of studies
VI. Literature
SECTION V
Diagnosis and treatment of patients with acute myocardial infarction with ST segment elevation ECG
Working group to prepare the text of the recommendations
Composition of the VNOK expert committee for developing recommendations
Society
1. Introduction
2. Terminology OKOiST and OKiST
3. Some links in the pathogenesis of OKdST (MICT)
4. Clinical picture
4.1. Pre-infarction period. Unstable angina
4.2. Classic (typical) variant of STEMI
4.3. Atypical forms of STEMI
5. Diagnosis of MI^T

5.1. Anamnesis
5.2. Physical examination
5.3. Cellular composition of blood and ESR
5.4. Increased body temperature
5.5. ECG
5.6. Biochemical markers of myocardial necrosis
5.7. X-ray of the chest organs
5.8. Ultrasound
5.9. Radionuclide methods
5.10. Differential diagnosis
5.11. Assessment of the size of the lesion
5.12. Necessary and sufficient signs for diagnosing MI Criteria for AMI
6. General principles of organizing medical care for patients with myocardial infarction
6.1. NIR for coronary patients
6.1.1. Location and layout of the BIC
6.1.2. NIR equipment
6.1.3. BIK staff
6.1.4. Some issues of organizing the work of the BIC
6.1.5. Length of stay in BIC
7. Assessment of the severity of the patient’s condition (prognosis) in the initial period of the disease
8. Treatment in the initial period of the disease
8.1. Anesthesia. Sedative therapy
8.2. Oxygen therapy
8.3. Organic nitrates
8.4. ASK
8.5. Clopidogrel
8.6. UFH and LMWH
8.7. Other antithrombotic drugs
8.8. β-adrenergic receptor blockers
8.9. RAAS inhibitors
8.10. Prevention of VF
8.11. Metabolic therapy and blood glucose control
8.12. Magnesium salts
8.13. Calcium channel blockers
8.14. Physical activity
8.15. Diet
8.16. Regulation of physiological functions
9. Restoration of coronary perfusion
9.1. General concept
9.2. The value of the time factor
9.3. TLT. Indications, contraindications
9.4. Thrombolytic drugs. Treatment regimens
9.5. Concomitant therapy
9.6. Complications of TLT
9.7. Diagnosis and assessment of restoration of myocardial perfusion
9.8. Reperfusion syndrome. The "by-reflow" phenomenon
9.9. TBA
9.10. Choosing a reperfusion therapy method
9.11. Surgical myocardial revascularization
10. Complications of MI
10.1. Acute heart failure
10.1.1. Shock
10.1.2. Stagnation of blood in the pulmonary circulation. Pulmonary edema
10.1.3. Monitoring central hemodynamic parameters
10.2. Treatment of acute heart failure
10.2.1. Treatment of shock
10.2.2. Treatment of pulmonary edema
10.3. Heart breaks
10.3.1. IVS rupture
10.3.2. Papillary muscle infarction; papillary muscle rupture
10.3.3. Rupture of the outer wall of the left ventricle (external cardiac rupture)
10.4. Acute LV aneurysm
10.5. Arterial TE
10.6. TELA
10.7. Pericarditis
10.8. Repeated myocardial ischemia. Early post-infarction angina. Repeated MI
10.9. Rhythm and conduction disorders
10.9.1. Supraventricular arrhythmias
10.9.2. Ventricular arrhythmias
10.9.3. Bradyarrhythmias
10.10. RV MI
11. Treatment in regular wards of the cardiology department
11.1. Antiplatelet agents
11.2. Anticoagulants
11.3. β-adrenergic receptor blockers
11.4. Organic nitrates
11.5. ACEI
11.6. Angiotensin II receptor blockers
11.7. Aldosterone receptor blockers
11.8. Statins
11.9. Length of hospital stay
12. Assessment of the patient’s condition before discharge from the hospital
12.1. Determination of LV function. Identification and assessment of viable myocardium
12.2. KAG
12.3. Assessment and prediction of rhythm and conduction disorders Ventricular arrhythmias and SCD
13. Treatment of patients after discharge from hospital
13.1. Blood pressure control
13.2. Physical activity
13.3. Smoking
13.4. Diet
13.5. Weight control
13.6. Effect on lipid profile
13.7. Antiplatelet agents ASA
13.8. Anticoagulants
13.9. β-adrenergic receptor blockers
13.10. RAAS inhibitors
13.11. Treatment of cardiac arrhythmias and prevention of SCD
13.12. Treatment of diabetes
13.13. Other drug treatments
14. Applications
Appendix 1. Clinical classification of types of MI
Appendix 2. Diseases and conditions that complicate ECG diagnosis of STEMI
Appendix 3. Reasons for increased levels of cardiac troponins in the blood in the absence of obvious manifestations of coronary artery disease
Appendix 4. Criteria for myocardial infarction
Appendix 5. Treatment of uncomplicated STEMI at the prehospital stage
Appendix 6. Formulas for calculating creatinine clearance and glomerular filtration rate
Appendix 7. Assessment of the prognosis of a patient with STEMI in the early stages of the disease
Appendix 8. Classification of bleeding severity
Appendix 9. Degree of coronary blood flow according to TIMI criteria
Appendix 10. Drug treatment of STEMI
Appendix 11. Rules for the transition from direct anticoagulants to indirect anticoagulants
Appendix 12. Initial energy of the electrical discharge when eliminating arrhythmias not associated with circulatory arrest
Appendix 13. Secondary prevention of MI
SECTION VI
4.2.4. Fibric acid derivatives (fibrates)
4.2.5. A nicotinic acid
4.2.6. sh-Z PUFA
4.2.7. Combination therapy
4.2.8. Extracorporeal treatments
4.3. Features of correction of lipid metabolism disorders in certain groups of patients
5. Conclusion
6. Summary of Russian recommendations “Diagnostics and correction of lipid metabolism disorders for the purpose of prevention and treatment of atherosclerosis.” (Brief recommendations)
Sequence of diagnosis and correction of lipid metabolism disorders
10-year risk of death from CVD in populations at high CVD risk

Working group to prepare the text of the recommendations
Composition of the VNOK expert committee for the development of recommendations
Societies
SECTION VII
Diagnosis and treatment of metabolic syndrome
1. Introduction
2. Factors influencing the development of MS
3. Definition of MS
4. Diagnosis of MS
4.1. Diagnostic criteria for MS
4.2. Additional criteria
4.3. Formulating a diagnosis for MS
Diagnosis and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis

Composition of the VNOK expert committee for developing recommendations
Societies
1. Introduction
2. Main disorders of lipid metabolism and lipid risk factors
2.1. Lipid risk factors for the development of CVD and optimal values of lipid parameters
3. Non-lipid risk factors for the development of CVD of atherosclerotic origin
3.1. Risk categories
3.2. Assessment of individual risk of death from CVD. SCORE table
3.3. Screening for DLP
4. Correction of RF and therapy of DLP
4.1. Non-drug measures to prevent atherosclerosis
4.1.1. Diet
4.1.2. Weight correction
4.1.3. F
4.1.4. Stop smoking
4.1.5. Alcohol consumption
4.2. Drug therapy for lipid metabolism disorders
4.2.1. HMG-CoA reductase inhibitors (statins)
4.2.2. Inhibitor of cholesterol absorption in the intestine (ezetimibe)
4.2.3. Bile acid sequestrants (ion exchange resins)
4.4. Examples of diagnostic reports
4.5. Diagnosis of MS at the primary health care level (in urban and district clinics)
4.6. Diagnosis of MS in hospitals and specialized clinics
4.7. Methods for diagnosing MS
4.8. Differential diagnosis of MS
5. Treatment of MS
5.1. Basic principles of MS treatment
5.2. Non-drug treatment of obesity
5.3. Treatment of patients with obesity and breathing disorders during sleep
6. Drug treatment of obesity
6.1. Drugs affecting IR
6.2. Lipid-lowering therapy for MS
6.3. Antihypertensive therapy
7. Combined antihypertensive therapy in patients with MS
8. Treatment algorithm for patients with MS
9. Conclusion
10. Literature
SECTION VIII
Diagnosis and treatment of pulmonary hypertension
Working group to prepare the text of the recommendations
Societies
1. Introduction
2. Definition
3. Clinical classification of PH
3.1. Classification of congenital systemic-pulmonary shunts
4. Pathogenesis of PH
5. Diagnostics
5.1. Stages of diagnosing PH
6. Treatment of PH
6.1. General recommendations
6.2. Drug treatment
6.3. Combination therapy
6.4. Surgery
7. Treatment algorithm for patients with PH
8. Appendix 1
9. Appendix 2
Dyspnoea rating scale according to Borg G 1982
TITLE IX
Treatment of acute coronary syndrome without persistent ST segment elevation on ECG
Preparation of the text of recommendations
Composition of the VNOK expert committee for developing recommendations
Society
1. Introduction
1.1. Some definitions
1.1.1. Correlation between the concepts of NS and IBMP BT. NS with elevated CTr levels
2. Diagnosis
2.1. Clinical symptoms
2.2. Physical examination
2.3. ECG
2.4. Biochemical markers of myocardial damage
2.5. Risk assessment
2.5.1. FR
3. Treatment methods
3.1. Anti-ischemic drugs
3.1.1. BAB
3.1.2. Nitrates
3.1.3. AK
3.2. Antithrombotic drugs. Antithrombins
3.2.1. Heparins (UFH and LMWH)
3.2.2. Direct thrombin inhibitors
3.2.3. Treatment of hemorrhagic complications associated with antithrombin therapy
3.3. Antithrombotic drugs. Antiplatelet agents
3.3.1. Aspirin (acetylsalicylic acid)
3.3.2. ADP receptor antagonists: thienopyridines
3.3.3. GP blockers Ilb/IIIa platelet receptors
3.4. Indirect anticoagulants for ACS
3.5. Fibrinolytic (thrombolytic) treatment
3.6. Coronary revascularization
3.6.1. KAG
3.6.2. 4KB. Stents
3.6.3. KS
3.6.4. Indications for 4KB and surgical interventions
3.6.5. Comparison of the effectiveness of invasive and drug treatment methods
4. Treatment strategy for patients with ACS
4.1. Initial assessment of the patient
4.2. Patients with signs of acute occlusion of a large coronary artery
4.3. Patients with suspected BT-ACSBP
4.3.1. Use of heparin
4.3.2. Patients with a high immediate risk of death or MI based on initial observation (8-12 hours)
4.3.3. Patients at low risk of dying or developing MI in the near future
4.4. Management of patients after stabilization
5. Approximate sequence of actions for the management of patients with ST-ACS
5.1. First contact with a doctor (local doctor, clinic cardiologist)
5.2. Emergency doctor
5.3. Hospital waiting room
5.3.1. Hospitals without a cardiac ICU or with the ability to provide emergency treatment to patients in the emergency room
5.3.2. Hospitals with cardiac ICU
5.4. BIT (in its absence, the department in which treatment is carried out)
5.4.1. Institutions with surgical service or capacity to perform 4KB
5.5. Cardiology department after transfer from BIT
6. Application
7. Literature
SECTION X
Diagnosis and treatment of acute heart failure
Working group to prepare the text of the recommendations
Composition of the VNOK expert committee for developing recommendations
1. Introduction
2. Epidemiology and etiology of AHF
3. Definition and clinical classification of AHF
3.1. Clinical variants of AHF (Table 2)
3.2. Clinical syndromes in AHF and main methods of treatment
4. Pathophysiology of AHF
5. Diagnosis of AHF
5.1. Clinical assessment
5.2. ECG
5.3. Chest X-ray
5.4. Laboratory research
5.5. EchoCG
5.6. Other diagnostic methods
6. Treatment goals for AHF
6.1. Organization of treatment of AHF
7. Monitoring the condition of a patient with AHF
7.1. Non-invasive monitoring
7.2. Invasive monitoring
7.2.1. Arterial catheterization
7.2.2. Central vein catheterization
7.2.3. KLA
8. Treatment of AHF
8.1. General approaches
8.2. Oxygen therapy and respiratory support
8.2.1. Oxygen therapy
8.2.2. Breathing support without endotracheal intubation (non-invasive ventilation)
8.2.3. Respiratory support with endotracheal intubation
9. Drug treatment
9.1. Morphine
9.2. Vasodilators
9.2.1. Nitrates
9.2.2. Sodium nitroprusside
9.2.3. Neziritnd
9.2.4. AK
9.3. ACEI
9.4. Diuretics
9.5. BAB
9.6. Inotropic agents
9.6.1. Dopamine
9.6.2. Dobutamine
9.6.3. IFDE
9.6.4. Levosimendan
9.6.5. Vasopressors
9.6.6. Cardiac glycosides
9.7. Anticoagulants
9.8. Surgery
9.9. Mechanical methods of supporting blood circulation
9.9.1. VACP
9.9.2. Ventricular Support Devices
9.10. Heart transplant
10. Features of treatment of AHF depending on the cause of decompensation
10.1. IHD
10.2. Pathology of the heart valve apparatus
10.3. Thrombosis of artificial heart valve
10.4. Dissecting aortic aneurysm
10.5. Cardiac tamponade
10.6. AG
10.7. Kidney failure
10.8. Lung diseases and bronchial obstruction
10.9. Heart rhythm disturbances
10.9.1. Bradyarrhythmias
10.9.2. Supraventricular tachyarrhythmias
10.9.3. Ventricular arrhythmias
11. Tactics for managing a patient with AHF: final recommendations
SECTION XI
Diagnosis and treatment of atrial fibrillation
Working group to prepare the text of the recommendations
Composition of the VNOK expert committee for developing recommendations
Societies
1. Introduction
2. Definition
3. Epidemiology and prognosis
3.2. Morbidity
3.3. Forecast
4. Classification
5. Pathophysiological mechanisms of AF
5.1. Atrial pathology in patients with AF
5.2. Mechanisms of AF development
5.3. Electrical remodeling of the atria
5.4. AV conduction
5.5. Hemodynamic consequences of AF
5.6. Thromboembolism
6. Associated conditions and clinical manifestations
6.1. Acute causes of AF
6.2. AF without organic heart pathology
6.3. AF associated with organic myocardial disease
6.4. Neurogenic AF
6.5. Clinical symptoms
7. Principles of diagnosing AF
8. Treatment
8.1. Cardioversion
8.1.1. Pharmacological cardioversion
8.1.2. Electrical cardioversion
8.1.3. Recommendations for pharmacological or electrical cardioversion of AF
8.2. Maintaining sinus rhythm
8.2.1. Predictors of relapses of AF and pharmacotherapy for their prevention
8.2.2. General approach to antiarrhythmic therapy
8.2.3. The choice of antiarrhythmic drugs in patients with certain CVDs, syndromes and their complications
8.2.4. Recommendations for pharmacological therapy to maintain sinus rhythm
8.3. Non-pharmacological treatments for AF
8.4. Control of 4JS in AF
8.4.1. Recommendations for monitoring 4VS in patients with AF
9. Prevention of thromboembolic complications
9.1. ACT or AAT strategy for the prevention of IS and thromboembolism
9.1.1. Recommendations for performing ACT or AAT in patients with AF
9.2. Restoration of sinus rhythm
9.2.1. Recommendations for ACT and AAT for the prevention of IS and thromboembolism in patients with AF undergoing cardioversion
10. Selected diseases
10.1. Postoperative AF
10.1.1. Recommendations for the prevention and treatment of postoperative AF
10.2. AMI
10.2.1. Recommendations for the treatment of patients with AF and AMI
10.3.WPW syndrome
10.3.1. Recommendations for the treatment of AF and ventricular preexcitation syndrome
10.4. Hyperthyroidism
10.4.1. Recommendations for the treatment of AF in patients with hyperthyroidism
10.5. Pregnancy
10.5.1. Recommendations for the treatment of AF during pregnancy
10.6. HCM
10.6.1. Recommendations for the treatment of AF in patients with HCM
10.7. Lung diseases
10.7.1. Recommendations for the treatment of AF in patients with lung diseases
11. Suggested treatment strategies - review of AF treatment algorithms
11.1. Newly diagnosed AF (Figure 4)
11.2. Recurrent paroxysmal AF (Figure 5, 6)
11.3. Recurrent persistent AF (Figure 6.7)
11.4. Persistent form of AF (Figure 7)

Under the term " arterial hypertension", "arterial hypertension" refers to the syndrome of increased blood pressure (BP) in hypertension and symptomatic arterial hypertension.

It should be emphasized that the semantic difference in the terms " hypertension" And " hypertension"practically none. As follows from the etymology, hyper - from the Greek above, over - a prefix indicating excess of the norm; tensio - from Latin - tension; tonos - from Greek - tension. Thus, the terms "hypertension" and " "hypertension" essentially mean the same thing - "hypertension".

Historically (since the time of G.F. Lang) it has developed so that in Russia the term “hypertensive disease” and, accordingly, “arterial hypertension” are used; in foreign literature the term “ arterial hypertension".

Hypertension (HTN) is usually understood as a chronic disease, the main manifestation of which is arterial hypertension syndrome, not associated with the presence of pathological processes in which an increase in blood pressure (BP) is caused by known, in many cases remediable causes (“symptomatic arterial hypertension”) (WOK Recommendations, 2004).

Classification of arterial hypertension

I. Stages of hypertension:

Hypertension (HD) stage I assumes the absence of changes in “target organs”.
Hypertension (HD) stage II is established in the presence of changes on the part of one or more “target organs”.
Hypertension (HD) stage III established in the presence of associated clinical conditions.

II. Degrees of arterial hypertension:

The degrees of arterial hypertension (Blood Pressure (BP) levels) are presented in Table No. 1. If the values of systolic Blood Pressure (BP) and diastolic Blood Pressure (BP) fall into different categories, then a higher degree of arterial hypertension (AH) is established. The most accurate degree of Arterial Hypertension (AH) can be determined in the case of newly diagnosed Arterial Hypertension (AH) and in patients not taking antihypertensive drugs.

Table No. 1. Determination and classification of blood pressure (BP) levels (mm Hg)

The classification is presented before 2017 and after 2017 (in brackets)

Blood pressure (BP) categories	Systolic blood pressure (BP)	Diastolic blood pressure (BP)
Optimal blood pressure	< 120	< 80
Normal blood pressure	120-129 (< 120* )	80-84 (< 80* )
High normal blood pressure	130-139 (120-129* )	85-89 (< 80* )
1st degree hypertension (mild)	140-159 (130-139* )	90-99 (80-89* )
2nd degree hypertension (moderate)	160-179 (140-159* )	100-109 (90-99* )
AH of the 3rd degree of severity (severe)	>= 180 (>= 160* )	>= 110 (>= 100* )
Isolated systolic hypertension	>= 140

* - new classification of the degree of hypertension from 2017 (ACC/AHA Hypertension Guidelines).

III. Risk stratification criteria for patients with hypertension:

I. Risk factors:

a) Basic:
- men > 55 years old - women > 65 years old
- smoking.

b) Dyslipidemia
TC > 6.5 mmol/l (250 mg/dl)
LDL-C > 4.0 mmol/L (> 155 mg/dL)
HDL-C

c) (for women

G) Abdominal obesity: waist circumference > 102 cm for men or > 88 cm for women

d) C-reactive protein:
> 1 mg/dl)

e) :

- Sedentary lifestyle
- Increased fibrinogen

and) Diabetes:
- Fasting blood glucose > 7 mmol/L (126 mg/dL)
- Blood glucose after a meal or 2 hours after taking 75 g of glucose > 11 mmol/L (198 mg/dL)

II. Target organ damage (stage 2 hypertension):

a) Left ventricular hypertrophy:
ECG: Sokolov-Lyon sign > 38 mm;
Cornell product > 2440 mm x ms;
EchoCG: LVMI > 125 g/m2 for men and > 110 g/m2 for women
Rg-graphy of the chest - cardio-thoracic index>50%

b) (thickness of the intima-media layer of the carotid artery >

G) Microalbuminuria: 30-300 mg/day; urine albumin/creatinine ratio > 22 mg/g (2.5 mg/mmol) for men and >

III. Associated (concomitant) clinical conditions (stage 3 hypertension)

A) Basic:
- men > 55 years old - women > 65 years old
- smoking

b) Dyslipidemia:
TC > 6.5 mmol/l (> 250 mg/dl)
or LDL-C > 4.0 mmol/L (> 155 mg/dL)
or HDL-C

V) Family history of early cardiovascular disease(among women

G) Abdominal obesity: waist circumference > 102 cm for men or > 88 cm for women

d) C-reactive protein:
> 1 mg/dl)

e) Additional risk factors that negatively affect the prognosis of a patient with arterial hypertension (AH):
- Impaired glucose tolerance
- Sedentary lifestyle
- Increased fibrinogen

and) Left ventricular hypertrophy
ECG: Sokolov-Lyon sign > 38 mm;
Cornell product > 2440 mm x ms;
EchoCG: LVMI > 125 g/m2 for men and > 110 g/m2 for women
Rg-graphy of the chest - cardio-thoracic index>50%

h) Ultrasound signs of thickening of the artery wall(carotid artery intima-media thickness >0.9 mm) or atherosclerotic plaques

And) Slight increase in serum creatinine 115-133 µmol/l (1.3-1.5 mg/dl) for men or 107-124 µmol/l (1.2-1.4 mg/dl) for women

To) Microalbuminuria: 30-300 mg/day; urine albumin/creatinine ratio > 22 mg/g (2.5 mg/mmol) for men and > 31 mg/g (3.5 mg/mmol) for women

l) Cerebrovascular disease:
Ischemic stroke
Hemorrhagic stroke
Transient cerebrovascular accident

m) Heart disease:
Myocardial infarction
Angina pectoris
Coronary revascularization
Congestive heart failure

m) Kidney disease:
Diabetic nephropathy
Renal failure (serum creatinine > 133 µmol/L (> 5 mg/dL) for men or > 124 µmol/L (> 1.4 mg/dL) for women
Proteinuria (>300 mg/day)

O) Peripheral artery disease:
Dissecting aortic aneurysm
Symptomatic peripheral artery disease

P) Hypertensive retinopathy:
Hemorrhages or exudates
Papilledema

Table No. 3. Risk stratification of patients with arterial hypertension (AH)

Abbreviations in the table below:
HP - low risk,
UR - moderate risk,
VS - high risk.

Abbreviations in the table above:
HP - low risk of arterial hypertension,
UR - moderate risk of arterial hypertension,
VS - high risk of arterial hypertension.

National clinical guidelines of the GFCS Diagnosis and treatment of chronic heart failure, third revision (adopted and published) Diagnosis and treatment of cardiovascular diseases during pregnancy (adopted and published) Diagnosis and treatment of arterial hypertension, fourth revision (accepted and recommended for publication) Prevention of cardiovascular diseases vascular diseases (accepted, recommended for publication)

Drugs for the treatment of CHF BASIC Their effect on the clinic, quality of life and prognosis has been proven and is beyond doubt 1. ACEI 2. BAB 3. Ant. Aldoster. 4. Diuretics. 5. Digoxin 6. ARA ADDITIONAL Efficacy and safety have been studied, but require clarification AUXILIARY The effect on the prognosis is unknown, the use is dictated by the clinic 1. Statins 2. Anticoagulants 1.PVD 2.BMCC 3. Amiodarone 4. Aspirin 5. Neglycoside. inotropic A B C

Adrenergic blockers for CHF Bisoprolol Metoprolol succinate Carvedilol Nebivolol* In normal clinical situations only “on top”, with severe tachycardia, exception for bisoprolol (B) The use of atenolol and metoprolol tartrate (!) for CHF is contraindicated

CYTOPROTECTERS IN THE TREATMENT OF CHF NO SOLID EVIDENCE RESEARCH IS ONGOING Trimetazidine can be prescribed Trimetazidine CAN ONLY BE PRESCRIBED IN ADDITION TO THE BASIC TREATMENT OF CHF! THE USE OF TAURINE, CARNITINE, COENZYME Q 10, MILDRONATE IN THE TREATMENT OF CHF IS NOT INDICATED! VNOK, 2010

Target blood pressure level

Hypertension is one of the most common pathologies of the cardiovascular system and is widespread throughout the world, especially in civilized countries. It is most susceptible to active people whose lives are full of actions and emotions. According to the classification, there are various forms, degrees and stages of hypertension.

According to statistics, from 10 to 20% of adults in the world are sick. It is believed that half do not know about their disease: hypertension can occur without any symptoms. Half of the patients diagnosed with this condition are not treated, and of those who are treated, only 50% do it correctly. The disease develops equally often in both men and women, and occurs even in teenage children. Most people get sick after 40 years of age. Half of all older people have been diagnosed with this condition. Hypertension often leads to stroke and heart attack and is a common cause of death, including in people of working age.

The disease manifests itself as high blood pressure, which is scientifically called arterial hypertension. The last term refers to any increase in blood pressure, regardless of the cause. As for hypertension, which is also called primary or essential hypertension, it is an independent disease of unknown etiology. It should be distinguished from secondary, or symptomatic, arterial hypertension, which develops as a sign of various diseases: heart, kidney, endocrine and others.

Hypertension is characterized by a chronic course, a persistent and prolonged increase in pressure, not associated with pathologies of any organs or systems. This is a disruption of the heart and the regulation of vascular tone.

Classifications of hypertension

Over the entire period of studying the disease, more than one classification of hypertension has been developed: according to the appearance of the patient, the reasons for the increase in pressure, etiology, the level of pressure and its stability, the degree of organ damage, and the nature of the course. Some of them have lost their relevance, while others continue to be used by doctors today, most often this is a classification by degree and stage.

In recent years, the upper limits of normal blood pressure have changed. If recently the value was 160/90 mm Hg. column was considered normal for an elderly person, today this figure has changed. According to WHO, for all ages, the upper limit of normal is considered to be 139/89 mm Hg. pillar Blood pressure equal to 140/90 mm Hg. column, is the initial stage of hypertension.

The classification of pressure by level is of practical importance:

The optimal is 120/80 mmHg. pillar
Normal ranges from 120/80–129/84.
Border – 130/85–139/89.
Stage 1 hypertension – 140/90–159/99.
Stage 2 hypertension – 160/100–179/109.
Stage 3 hypertension – from 180/110 and above.

Classification of hypertension is very important for correct diagnosis and choice of treatment depending on the form and stage.

According to the very first classification, which was adopted at the beginning of the 20th century, hypertension was divided into pale and red. The form of pathology was determined by the type of patient. With the pale variety, the patient had an appropriate complexion and cold extremities due to spasms of small vessels. Red hypertension was characterized by dilation of blood vessels at the time of increased hypertension, as a result of which the patient’s face turned red and became covered with spots.

In the 1930s, two more types of the disease were identified, which differed in the nature of their course:

The benign form is a slowly progressive disease, in which three stages were distinguished according to the degree of stability of pressure changes and the severity of pathological processes in the organs.
Malignant arterial hypertension progresses rapidly and often begins to develop at a young age. As a rule, it is secondary and has an endocrine origin. The course is usually severe: the pressure is constantly at high levels, and symptoms of encephalopathy are present.

Classification by origin is very important. It is necessary to distinguish primary (idiopathic) hypertension, which is called hypertension, from the secondary (symptomatic) form. If the first occurs for no apparent reason, then the second is a sign of other diseases and accounts for about 10% of all hypertension. Most often, there is an increase in blood pressure due to renal, cardiac, endocrine, neurological pathologies, as well as as a result of constant use of a number of medications.

Modern classification of hypertension

There is no uniform systematization, but most often doctors use the classification that was recommended by WHO and the International Society of Hypertension (ISHA) in 1999. According to WHO, hypertension is classified primarily by the degree of increase in blood pressure, of which there are three:

The first degree - mild (borderline hypertension) - is characterized by pressure from 140/90 to 159/99 mm Hg. pillar
In the second degree of hypertension - moderate - hypertension ranges from 160/100 to 179/109 mm Hg. pillar
In the third degree - severe - the pressure is 180/110 mm Hg. pillar and above.

You can find classifiers that distinguish 4 degrees of hypertension. In this case, the third form is characterized by pressure from 180/110 to 209/119 mm Hg. column, and the fourth is very heavy - from 210/110 mm Hg. pillar and above. The degree (mild, moderate, severe) indicates solely the level of pressure, but not the severity of the course and condition of the patient.

In addition, doctors distinguish three stages of hypertension, which characterize the degree of organ damage. Classification by stages:

Stage I. The increase in pressure is insignificant and inconsistent, the functioning of the cardiovascular system is not impaired. Patients usually have no complaints.
Stage II. Blood pressure is high. There is an enlargement of the left ventricle. Usually there are no other changes, but local or generalized narrowing of the retinal vessels may be noted.
Stage III. There are signs of organ damage:
- heart failure, myocardial infarction, angina pectoris;
- chronic renal failure;
- stroke, hypertensive encephalopathy, transient cerebral circulatory disorders;
- from the fundus of the eye: hemorrhages, exudates, swelling of the optic nerve;
- lesions of peripheral arteries, aortic aneurysm.

When classifying hypertension, variants of increased pressure are also taken into account. The following forms are distinguished:

systolic – only the upper pressure is increased, the lower – less than 90 mm Hg. pillar;
diastolic – lower pressure is increased, upper – from 140 mm Hg. pillar and below;
systolic-diastolic;
labile – blood pressure rises for a short time and normalizes on its own, without medications.

Certain types of hypertension

Some varieties and stages of the disease are not reflected in the classification and stand apart.

Hypertensive crises

This is the most severe manifestation of arterial hypertension, in which the pressure rises to critical levels. As a result, cerebral circulation is disrupted, intracranial pressure rises, and brain hyperemia occurs. The patient experiences severe headaches and dizziness, accompanied by nausea or vomiting.
Hypertensive crises, in turn, are divided according to the mechanism of pressure increase. In the hyperkinetic form, the systolic pressure rises, in the hypokinetic form, the diastolic pressure rises; in the eukinetic crisis, both the upper and lower levels increase.

Refractory hypertension

In this case, we are talking about arterial hypertension, which cannot be treated with medications, that is, the pressure does not decrease even when using three or more drugs. This form of hypertension is easily confused with those cases where treatment is ineffective due to an incorrect diagnosis and incorrect choice of medications, as well as due to the patient’s non-compliance with doctor’s prescriptions.

White coat hypertension

This term in medicine means a condition in which an increase in pressure occurs only in a medical facility during blood pressure measurement. This seemingly harmless phenomenon should not be ignored. According to doctors, a more dangerous stage of the disease may occur.

Hypertension 1st degree

Features of stage 2 hypertension

Blood circulation can be disrupted anywhere in the human body. Blood circulating through arterial vessels may encounter an obstacle on its way in every organ if the walls of the arteries and arterioles have changed as a result of pathological processes. Ischemia can occur in the intestines, kidneys, and spinal cord. Although the latter tolerates heart attacks and hemorrhages better than the brain, a spinal stroke can put a person in a wheelchair for a long time, if not forever, immobilizing him, and lead to complete or partial loss of ability to work.

In the path of arterial blood moving under pressure, there may be an aneurysm that withstood a long load, and then ruptured... Severe hemorrhage, often giving no chance of life. An aneurysm can find a place and form in any arterial vessel.

In varicose veins, behind the blood carrying metabolic products, the venous valves may simply not close, preventing reverse flow. In this case, the blood can only return back to stagnate in the organs and limbs.

Varicose veins are characteristic not only of the vessels of the lower extremities; all pelvic organs, the spinal cord, and upper extremities are well susceptible to it (although they are located above the heart). There are “purely female” varicose veins, when the pathology affects the venous vessels of the reproductive organs (uterus, vagina, ovaries, etc.), and there are also “purely male” ones - varicocele, for example. And there are those that equally cause trouble for both the male and female populations of the planet. Varicose veins of the rectum, or simply hemorrhoids, have plagued our sedentary generation from a young age.

Disruption of the venous valves, dilation of veins, and the formation of blood clots leads to venous insufficiency (VI), which is very dangerous due to its complications. Chronic VL, characteristic of superficial veins, represents good conditions for the development of thrombophlebitis and trophic ulcers. An acute form of venous insufficiency can create a life-threatening situation when it is complicated by deep vein thrombosis, which, in turn, will result in post-thrombotic syndrome. And it all started with venous insufficiency...

A complication of acute venous thrombosis of deep and superficial veins is pulmonary embolism - the culprit of high mortality, which in its symptoms is even ahead of venous thrombosis, that is, thrombosis is the cause, but has not yet manifested itself, and PE has already taken the initiative. Any operation, injury or childbirth can be complicated by pulmonary embolism and lead to death, since the fulminant form ends in death within 10 minutes, the acute form - within 24 hours, and only the subacute form gives a person a certain chance, developing gradually and manifesting itself as a pulmonary infarction.

Arterial diseases of the extremities

Leriche syndrome

As a result of atherosclerosis of the lower extremities, a chronic ischemic focus is formed, characteristic of Leriche syndrome. The clinical manifestations of these diseases are almost completely the same, with the only difference being that intermittent claudication in atherosclerosis stops in a low position (on the calf muscles) and does not spread upward.

Diagnostic methods are typical for Leriche syndrome, where ultrasound is a priority.

Surgical treatment for indications such as ischemia of IIB, III, IV degrees (bypass surgery in the femoral-popliteal-tabial segment using various prostheses or the great saphenous femoral vein of the patient himself). In special cases, the operation is performed by percutaneous arterial dilatation and endarterectomy.

Conservative treatment of atherosclerosis of the lower extremities does not differ from that for Leriche syndrome.

Buerger's disease

Buerger's disease (thromboangiitis obliterans, endarteritis obliterans) is a very serious inflammatory disease that occurs with severe ischemia and frequent damage to the venous node due to thrombosis.

The reasons cannot be said in the affirmative, but the provocateurs have been reliably identified. These are hypothermia and smoking.

Unfortunately, young people are not immune to this disease and it occurs mainly in males aged 18-35 years. The pathological process usually does not spread beyond the lower extremities, however, it does not affect one leg at a time, but occurs in parallel in both. The characteristic clinical picture manifests itself in three variants, but pain in the foot and fingers is almost always present:

Option 1 is distinguished by the severity and malignancy of the process and affects mainly young people;
2nd is characterized by a calmer wave-like course (subacute) with exacerbations and remissions of varying duration;
Option 3 can last for years (chronically), progresses slowly and has long-term remissions.

The most striking symptom of Buerger's disease is considered to be untreatable ulcers on the toes that are prone to infection. This indicates damage to the arteries of the foot and leg and the prospect of the pathological process spreading to the popliteal and femoral arteries.

Effective diagnostic methods are:

Measurement of finger and ankle blood pressure;
Determination of the spectrum on the arteries of the foot and pressure on the arteries at various levels;
Transcutaneous determination of oxygen tension on the foot and lower leg in vertical and horizontal positions;
Doppler ultrasound, duplex scanning;
Seldinger angiography in case of planning reconstructive surgery.

Treatment of obliterating endarteritis is a complex task and not always solvable. Buerger's disease is treated only in a hospital setting, where rheopolyglucin infusions are prescribed, which are supplemented with hormones, anticoagulants, disaggregants, and vasodilators.

Surgical treatment is reconstruction of the arteries, the outcome of which is determined by the severity of ischemic lesions.

Obstruction of the arteries of the extremities (occlusion)

Acute obstruction of the arteries of the limb, resulting from thrombosis in young people who already have thromboangiitis or the elderly with atherosclerosis, and embolism of the main arteries in people with “embologenic” diseases, is formed under the influence of several factors:

Hypercoagulation;
The impact of an inflammatory or atherosclerotic process on the arterial wall;
Hemodynamic disturbances (central and regional).

Typically, acute arterial obstruction is accompanied by arterial spasm in both limbs, even if the second is considered healthy. The clinical picture of the disease is expressed by acute ischemia syndrome:

Sharp pain;
Cold limb;
Sunken veins;
Impaired sensitivity and motor activity;
Abrupt stop of pulse.

Compared with embolism, the course of thrombosis is less acute. This is explained by a long-term stenotic process in the arteries and the formation of collaterals.

Treatment depends on the patient’s condition and the severity of the disease, which is determined by the degree and location of the ischemic focus. In the acute period, as a rule, infusions of rheopolyglucin and sodium bicarbonate are prescribed, then vasodilators, hemodez and anticoagulants are used.

Surgery is performed according to indications in accordance with the general condition of the patient and the location of ischemia.

Arteriovenous fistulas

Congenital arteriovenous fistulas (malformations) are most common in the lower extremities, although the upper extremities are no exception. In addition, this pathology can easily be localized in internal organs: liver, kidneys, lungs.

Pathological changes occur as a result of venous hypertension and hypoxia of the distal sections, the cause of which is the bypass of the arterial segment with arterial blood, which is discharged directly into the venous bed. The disease is congenital and manifests itself literally from the first days of a child’s life.

Diagnostic methods to help establish a diagnosis:

Occlusion plethysmography is able to capture the moment of a sudden increase in volumetric blood flow in the affected area;
Duplex scanning - compares the increased volumetric blood flow with the norm, detects the increased size of the vessel itself;
Angiography, which is indicated when determining the localization of the pathological focus in the arterial bed.

An increase in peripheral circulatory disorders leads to a decrease in the functional abilities of the limb, which is an indication for surgical treatment, which is carried out in several stages.

Neurovascular syndromes of the upper limbs

A group of diseases associated with extravasal compression of the subclavian arteries and brachial plexus is called “thoracic outlet compression syndrome.”

The clinical picture of the disease is manifested by various vascular-neurological disorders of a local nature:

Pain in the hands;
The onset of rapid fatigue of the fingers, which makes it difficult to perform certain types of work (writing, sewing).

The disease has several typical syndromes that serve as the basis for diagnosis.

Treatment is conservative, symptomatic or surgical.

Raynaud's disease

Raynaud's disease occurs from spasm of the small arteries of the extremities, tongue or tip of the nose and is considered “female”. Why it appears and where it originates is still unknown to science.

The symptoms of Raynaud's disease cause a lot of trouble, because at first, patients do not feel very sick, but they do not consider themselves absolutely healthy. Pain in the fingers (usually on the hands) and chilliness at first are the only manifestations of the disease, which are eventually joined by impaired tissue trophism, swelling and cyanosis, and small areas of necrosis on the nail phalanges.

The diagnosis is based on capillaroscopy of the nail bed and a cold test (assessing the condition of the hand after immersing it in cold water for a couple of minutes).

Treatment is carried out with peripheral vasodilators, antiplatelet agents, and vitamins. Barotherapy, plasmapheresis, physical therapy, and in some cases transcutaneous nerve stimulation are used. Surgical treatment is carried out in exceptional cases.

Vein diseases

Varicose veins

Varicose veins of the lower extremities are so widespread, thoroughly studied and familiar to almost every inhabitant of our planet (not me, but my neighbor), that it seems there is nothing to add to the accumulated information.

Varicose veins can be primary (hereditary incompetence of venous valves, congenital weakness of connective tissue) and secondary, when it is formed as a consequence of past diseases.

Clinical manifestations are clearly visible on the legs in the summer, which also causes pain, heaviness, pigmentation, and can be complicated by thrombophlebitis.

Ultrasound methods serve as the basis for diagnosis. Treatment is distinguished by a variety of types and techniques: compression hosiery, hirudotherapy, venotonics, diet, regimen, physical education, folk remedies, sclerotherapy, surgery.

Thrombosis and phlebitis

Acute venous thrombosis is caused by:

The formation of a blood clot, which occurs during hypercoagulation;
Changes in the vessel wall as a result of traumatic effects or an inflammatory process;
Impaired blood flow through the veins when the effect of the muscle pump is weakened (the speed of blood flow decreases).

Thrombosis spares neither deep veins, often resulting from myocardial infarction or stroke, nor superficial ones, complicated by thrombophlebitis with the possible development of pulmonary embolism.

Typically, thrombosis has little effect on the general condition of the patient. Pain, swelling, hyperemia at the site of the lesion - these are, perhaps, the main symptoms. True, in severe cases, a sharp arterial spasm (blue phlegmasia) occurs, then cyanosis will become another symptom.

Diagnosis of thrombosis is typical for all vascular diseases.

Treatment with anticoagulants, antiplatelet agents, non-steroidal anti-inflammatory drugs with mandatory bandaging of the affected limb. Thrombolytic therapy is prescribed no later than the 5th day from the onset of the disease, in specialized medical institutions and taking into account all indications and contraindications for this type of treatment.

For thrombosis of the superficial venous system, the background is usually varicose veins, to which an infection joins, forming an inflammatory focus. It promotes strong fixation of the thrombus, which, of course, reduces the risk of pulmonary embolism to some extent, but thrombosis can spread to the trunk of the common femoral vein (through the mouth of the great saphenous vein), then separation of the tail part of the thrombus is possible, and the danger of pulmonary embolism arises again.

Ascending thrombophlebitis is characterized by pain in the limb, hyperemia, and infiltration along the affected vessel, so diagnosis usually does not cause difficulties, but duplex scanning in such cases will not be superfluous.

Treatment is local application of heparin or troxevasin ointment, anti-inflammatory therapy, elastic bandaging. Surgical treatment is indicated for ascending thrombosis to the level of the middle third of the thigh.

Having an unclear etiology and occurring mainly in young men, acute subclavian vein thrombosis is called Paget-Schroetter syndrome and is characterized by severe pain in the arm, swelling, dilatation of the saphenous veins, cyanosis of the limb, and even sometimes sensory disturbance.

Superior vena cava syndrome

The cause of superior vena cava syndrome can be thrombosis of the trunk of the superior vena cava or a tumor compressing it. Lung cancer, aneurysm of the ascending aortic arch, Hodgkin's disease, if any, will only contribute to thrombosis and worsen the situation.

The clinical picture of superior vena cava syndrome is represented not only by venous congestion in the upper extremities, but also by the manifestation of general cerebral symptoms (venous congestion in the brain). External manifestations of the pathology are also tense and dilated veins in the patient’s chest and abdomen.

Budd-Chiari syndrome

Budd-Chiari syndrome is the name given to obliterating phlebitis of the hepatic veins, which generally enters the vessel of their surrounding tissues. In a third of patients, the disease is accompanied by venous insufficiency of the lower extremities. This is caused by narrowing or complete obliteration (coarctation) of the trunk of the inferior vena cava where it passes through the diaphragm.

Symptoms characteristic of the acute form in the form of abdominal pain, enlargement of the liver and spleen, ascites, hematemesis and jaundice, ending in hepatic coma and death, develop slowly in the chronic course, but threaten an equally serious complication when thrombosis moves to the inferior vena cava. In this case, pulmonary embolism is also possible.

Venous hypoplasia

Congenital aplasia or hypoplasia of the venous system of the extremities begins to manifest itself from the first years of a baby’s life and gives the following symptoms:

Increased volume of limbs;
Phlebeurysm;
Preservation of the lateral embryonic vein;
Hemangiomas (capillary, cavernous, branched), which are a frequent but not obligatory companion to the pathology.

The severity of the pathological process is determined by the degree of narrowing and extent of aplasia of the deep venous system. The disease is fraught with trophic tissue disorders, which is a reason for surgical intervention. Conservative treatment is limited to elastic bandaging and the use of drugs such as troxevasin.

The disease is diagnosed using duplex ultrasound scanning (visualization of veins, determination of the speed and volume of blood flow) and serial venography.

Damage to the celiac trunk, abdominal aorta, mesenteric, renal and iliac arteries

Atherosclerotic changes, aneurysms, inflammatory foci and other factors that negatively affect the vascular wall can alter normal blood flow and lead to circulatory disorders in the internal organs, upper and lower extremities.

Visceral circulation disorders

Ischemia is characteristic not only of the cerebral and coronary arteries; disturbance of visceral circulation, although to a lesser extent, nevertheless occurs in the liver and intestines. The reasons for this are usually:

Atherosclerotic process in the celiac trunk, in the superior and inferior mesenteric arteries;
Nonspecific arteritis (Takayasu disease);
Narrowing of the celiac trunk;
Narrowing of the falciform ligament of the diaphragm;
Anomalies of the origin of the celiac trunk.

Symptoms of chronic visceral circulatory disorders include:

Abdominal pain that occurs after eating a large and fatty meal, which lasts from 2 to 3 hours (the pain is especially intense when the celiac trunk and superior mesenteric artery are affected);
Severe intestinal dysfunction, alternating diarrhea and constipation, rapid weight loss (impaired blood supply to the mesenteric arteries).

Methods for diagnosing pathology:

Auscultation (systolic murmur in the epigastrium);
X-ray, gastro, colonoscopy (no gross organic changes);
Kaprogram (mucus, neutral fat, undigested muscle fibers);
Biochemical blood test (decreased albumin, increased globulin fraction);
Duplex scanning;
Angiography of the abdominal aorta and its branches in two projections (according to strict indications, if there is suspicion of damage to the visceral and renal arteries).

The patient is indicated for symptomatic treatment with the use of antispasmodics and enzymes, as well as mandatory diet. Surgery is performed if there are reliable signs of stenosis of the main artery.

A complication of impaired visceral circulation can be acute thrombosis with the development of acute mesenteric obstruction leading to intestinal gangrene. This circumstance makes the prognosis for this disease unfavorable.

Abdominal aortic aneurysm

Abdominal aortic aneurysm is more common in men. The causes of the disease can be:

Atherosclerosis;
Takayasu's disease (to a lesser extent);
Syphilis;
Mycoses (rare);
Closed abdominal injuries.

Most often, aneurysms form below the opening of the renal arteries.

Symptoms of an aneurysm:

Pain throughout the abdomen, in the lumbosacral region and in the back;
The presence of a pulsating formation of dense consistency (during palpation);
Systolic murmur over the aneurysm during auscultation.

Reasons to suspect a ruptured aneurysm would be severe pain in the abdomen and lower back, a sharp drop in blood pressure, and a rapid deterioration in the patient’s condition. The previously pulsating formation becomes softer and decreases in size.

Diagnostic measures include:

Survey radiography in two projections;
B-scan (ultrasound) is a reliable diagnostic method that allows you to determine the exact characteristics of the aneurysm;
Angiography requires strict indications (the presence of signs of damage to the visceral and renal arteries).

Treatment is surgical if an aneurysm is detected: emergency if there is a threat of rupture and the development of pain, planned if there are no obvious clinical manifestations and the presence of an aneurysm more than 4 cm in diameter. The prognosis without surgical treatment is unfavorable; patients usually live no more than two years.

Vasorenal hypertension (VRH)

A third of patients with persistent uncontrolled arterial hypertension also have cerebral hypertension, which is considered predominantly a congenital disease; the acquired form is extremely rare and is caused mainly by atherosclerosis and nonspecific arteritis.

Symptoms are expressed by persistent systolic and diastolic blood pressure, which cannot be corrected with antihypertensive drugs.

The absence of previous or existing kidney diseases, but the presence of signs of damage to the branches of the aortic arch, arteries of the lower extremities and coronary arteries gives reason to assume stenosis of the renal arteries.

Diagnostics:

Urography;
Duplex scanning reveals impaired blood flow in the renal artery due to stenosis;
Angiography (establishing or refuting the diagnosis).

Treatment is transaortic endarterectomy, percutaneous dilatation of the renal artery reduces blood pressure in 70-80% of patients, but they still need supportive treatment and careful monitoring of blood pressure.

Occlusive diseases of the abdominal aorta (Leriche syndrome)

The pathological process (occlusion or stenosis) localized in the terminal abdominal aorta and iliac arteries is usually combined with that in the femoropopliteal segment. The presence of several such foci in the arterial bed is fraught with severe manifestations of ischemia of the lower extremities (intermittent claudication) and the development of end-stage gangrene of the foot and fingers.

In the list of causes of the disease, atherosclerosis occupies a leading position. Nonspecific arteritis and post-embolic occlusions are significantly inferior to it, since they cause this pathology relatively rarely. And an exceptional case is congenital pathology in this area of the aorta.

Clinical picture of the disease:

Feeling of fatigue in the lower extremities when walking short distances;
Pain in the calf muscles, thigh and buttocks, which over time leads to lack of sleep due to night pain and the development of gangrenous changes in the legs;
The appearance of a triad of symptoms indicating damage to the aorta and iliac arteries: intermittent claudication, impotence, absence or weakening of the pulse in the femoral arteries (Leriche syndrome).

Diagnostics:

Doppler ultrasound;
Duplex scanning;
Aortoangiography if indicated (intermittent claudication less than 200 m).

If indicated, surgical treatment is performed: bifurcation aortofemoral bypass with implantation of a synthetic prosthesis or percutaneous dilatation (in case of iliac artery stenosis).

Conservative treatment is reduced to the use of angioprotectors, vasodilators, antiplatelet agents and drugs that improve microcirculation. The patient is recommended to completely quit smoking.

Arterial hypertension (AH), being one of the main independent risk factors for the development of stroke and coronary heart disease (CHD), as well as cardiovascular complications - myocardial infarction (MI) and heart failure, is an extremely important health problem in most countries of the world. Successful control of such a common and dangerous disease requires a well-designed and organized detection and treatment program. Recommendations on hypertension, which are regularly revised as new data become available, have certainly become such a program. Since the release in 2008 of the third version of the Russian recommendations for the prevention, diagnosis and treatment of hypertension, new data have been obtained that require a revision of this document. In this regard, on the initiative of the Russian Medical Society for Hypertension (RMSHA) and the All-Russian Scientific Society of Cardiology (VNOK), a new, fourth version of this important document was recently developed, which was discussed in detail and presented at the annual Congress of VNOK in September 2010.
This document is based on the recommendations for the treatment of hypertension of the European Society of Arterial Hypertension (ESH) and the European Society of Cardiology (ESC) 2007 and 2009. and the results of major Russian studies on the problem of hypertension. As in previous versions of the recommendations, blood pressure is considered as one of the elements of the system for stratifying general (total) cardiovascular risk. When assessing overall cardiovascular risk, a large number of variables are taken into account, but the value of blood pressure is decisive due to its high prognostic significance. At the same time, blood pressure level is the most regulated variable in the stratification system. Experience shows that the effectiveness of a doctor’s actions in treating each individual patient and the achievement of success in controlling blood pressure among the country’s population as a whole largely depend on the coordination of actions of both therapists and cardiologists, which is ensured by a unified diagnostic and treatment approach. It was this task that was considered as the main one when preparing recommendations.
Target blood pressure level
The intensity of treatment for a patient with hypertension is largely determined by the goal set in terms of reducing and achieving a certain level of blood pressure. When treating patients with hypertension, blood pressure should be less than 140/90 mm Hg, which is its target level. If the prescribed therapy is well tolerated, it is advisable to reduce blood pressure to lower values. In patients with a high and very high risk of cardiovascular complications, it is necessary to reduce blood pressure to 140/90 mmHg. or less within 4 weeks. In the future, subject to good tolerance, it is recommended to reduce blood pressure to 130-139/80-89 mm Hg. When carrying out antihypertensive therapy, it should be borne in mind that it can be difficult to achieve a systolic blood pressure level of less than 140 mmHg. in patients with diabetes mellitus, target organ damage, in elderly patients and those already having cardiovascular complications. Achieving a lower target blood pressure level is possible only if it is well tolerated and may take longer than reducing it to less than 140/90 mmHg. If lowering blood pressure is poorly tolerated, it is recommended to lower it in several stages. At each stage, blood pressure decreases by 10-15% from the initial level in 2-4 weeks. followed by a break to allow the patient to adapt to lower blood pressure values. The next stage of lowering blood pressure and, accordingly, increasing antihypertensive therapy in the form of increasing doses or the number of drugs taken is possible only if the already achieved blood pressure values are well tolerated. If moving to the next stage causes the patient's condition to worsen, it is advisable to return to the previous level for some more time. Thus, a decrease in blood pressure to the target level occurs in several stages, the number of which is individual and depends on both the initial blood pressure level and the tolerability of antihypertensive therapy. The use of a step-by-step scheme for lowering blood pressure, taking into account individual tolerance, especially in patients with a high and very high risk of complications, allows one to achieve the target blood pressure level and avoid episodes of hypotension, which are associated with an increased risk of developing myocardial infarction and stroke. When reaching the target blood pressure level, it is necessary to take into account the lower limit of reducing systolic blood pressure to 110-115 mm Hg. and diastolic blood pressure up to 70-75 mm Hg, and also ensure that during treatment there is no increase in pulse blood pressure in elderly patients, which occurs mainly due to a decrease in diastolic blood pressure.
Experts divided all classes of antihypertensive drugs into primary and additional (Table 1). The recommendations note that all major classes of antihypertensive drugs (ACE inhibitors, angiotensin receptor blockers, diuretics, calcium channel blockers, b-blockers) reduce blood pressure equally; each drug has proven effects and its own contraindications in certain clinical situations; in most patients with hypertension, effective blood pressure control can be achieved only with combination therapy, and in 15-20% of patients, blood pressure control cannot be achieved with a two-component combination; Fixed combinations of antihypertensive drugs are preferable.
Deficiencies in the management of hypertension are usually associated with undertreatment due to inappropriate drug or dose selection, lack of synergism when using drug combinations, and problems associated with treatment adherence. It has been shown that combinations of drugs always have advantages over monotherapy in lowering blood pressure.
Prescribing combinations of antihypertensive drugs can solve all these problems, and therefore their use is recommended by authoritative experts in terms of optimizing the treatment of hypertension. Recently, it has been shown that certain combinations of drugs not only have benefits in controlling blood pressure, but also improve the prognosis in individuals with established hypertension, whether associated with other diseases or not. Since the doctor has a huge choice of various antihypertensive combinations (Table 2), the main problem is to choose the best combination with the greatest evidence for the optimal treatment of patients with hypertension.
The section “Drug therapy” emphasizes that in all patients with hypertension it is necessary to achieve a gradual reduction in blood pressure to target levels. Particular care should be taken to reduce blood pressure in the elderly and in patients who have had myocardial infarction and stroke. The number of drugs prescribed depends on the initial blood pressure level and concomitant diseases. For example, with grade 1 hypertension and the absence of a high risk of complications, it is possible to achieve target blood pressure with monotherapy in approximately 50% of patients. For grade 2 and 3 hypertension and the presence of high-risk factors, in most cases a combination of two or three drugs may be required. Currently, it is possible to use two strategies for initial treatment of hypertension: monotherapy and low-dose combination therapy, followed by increasing the amount and/or doses of the drug if necessary (Scheme 1). Monotherapy at the start of treatment may be chosen for patients with low or intermediate risk. A low-dose combination of two drugs should be preferred in patients at high or very high risk of complications. Monotherapy is based on finding the optimal drug for the patient; switching to combination therapy is advisable only if the latter has no effect. Low-dose combination therapy at the start of treatment involves the selection of an effective combination of drugs with different mechanisms of action.
Each of these approaches has its own advantages and disadvantages. The advantage of low-dose monotherapy is that if the drug is successfully selected, the patient will not have to take another drug. However, the monotherapy strategy requires the doctor to painstakingly search for the optimal antihypertensive drug for the patient with frequent changes in medications and their dosages, which deprives the doctor and the patient of confidence in success and ultimately leads to a decrease in patient adherence to treatment. This is especially true for patients with stage 1 and 2 hypertension, most of whom do not experience discomfort from increased blood pressure and are not motivated to treatment.
In combination therapy, in most cases, the prescription of drugs with different mechanisms of action allows, on the one hand, to achieve target blood pressure, and on the other, to minimize the number of side effects. Combination therapy also makes it possible to suppress counterregulatory mechanisms of increased blood pressure. The use of fixed combinations of antihypertensive drugs in one tablet increases patient adherence to treatment. In patients with blood pressure ≥ 160/100 mmHg, who are at high and very high risk, full-dose combination therapy can be prescribed at the start of treatment. In 15-20% of patients, blood pressure control cannot be achieved when using two drugs. In this case, a combination of three or more drugs is used.
As noted earlier, along with monotherapy, combinations of two, three or more antihypertensive drugs are used to control blood pressure. Combination therapy has many advantages: enhancing the antihypertensive effect due to the multidirectional effect of drugs on the pathogenetic mechanisms of the development of hypertension, which increases the number of patients with a stable decrease in blood pressure; reducing the incidence of side effects, both due to lower doses of combined antihypertensive drugs, and due to the mutual neutralization of these effects; ensuring the most effective organ protection and reducing the risk and number of cardiovascular complications. However, it must be remembered that combination therapy is taking at least two medications, the frequency of administration of which may be different. Therefore, the use of drugs in the form of combination therapy must meet the following conditions: the drugs must have a complementary effect; an improvement in the result should be achieved when they are used together; drugs must have similar pharmacodynamic and pharmacokinetic parameters, which is especially important for fixed combinations.
Priority of rational combinations of antihypertensive drugs
RMOAG experts suggest dividing combinations of two antihypertensive drugs into rational (effective), possible and irrational. American experts, who presented a new algorithm for combination antihypertensive therapy in 2010 (Table 3), take almost the same positions on this issue. This position fully coincides with the opinion of European hypertension experts expressed in November 2009 on the issues of combination therapy and presented in Figure 1.
The Russian recommendations emphasize that the full benefits of combination therapy are inherent only in rational combinations of antihypertensive drugs (Table 2). Among the many rational combinations, some deserve special attention, having advantages not only from the theoretical standpoint of the main mechanism of action, but also practically proven high antihypertensive effectiveness. First of all, this is a combination of an ACE inhibitor with a diuretic, which enhances the advantages and eliminates the disadvantages. This combination is the most popular in the treatment of hypertension due to its high antihypertensive effectiveness, protection of target organs, good safety and tolerability. The published recommendations of the American Society of Hypertension (ASH) for combination therapy of hypertension (Table 3) also give priority (more preferable) to combinations of drugs that block the activity of the renin-angiotensin system (angiotensin receptor blockers or ACE inhibitors) with diuretics or calcium antagonists.
The drugs potentiate each other’s action due to their complementary effect on the main links in blood pressure regulation and blockade of counter-regulatory mechanisms. A decrease in the volume of circulating fluid due to the saluretic effect of diuretics leads to stimulation of the renin:2:(s:4:"TEXT";s:65522:"-angiotensin system (RAS), which is counteracted by an ACE inhibitor. In patients with low plasma renin activity, ACE inhibitors are usually not effective enough, and the addition of a diuretic, leading to an increase in RAS activity, allows the ACE inhibitor to realize its effect. This expands the range of patients responding to therapy, and target blood pressure levels are achieved in more than 80% of patients. ACE inhibitors prevent hypokalemia and reduce the negative impact diuretics on carbohydrate, lipid and purine metabolism.
ACE inhibitors are widely used in the treatment of patients with hypertension, acute forms of coronary artery disease, and chronic heart failure. One of the representatives of a large group of ACE inhibitors is lisinopril. The drug has been studied in detail in several large-scale clinical studies. Lisinopril has demonstrated preventive and therapeutic efficacy in heart failure, including after acute MI, and in concomitant diabetes mellitus (GISSI 3, ATLAS, CALM, IMPRESS studies). In the largest clinical study on the treatment of hypertension with various classes of drugs, ALLHAT, among those taking lisinopril, the incidence of type 2 diabetes significantly decreased.
The Russian pharmacoepidemiological study PYTHAGOR III studied the preferences of practicing physicians in the choice of antihypertensive therapy. The results were compared with the previous phase of the PYTHAGORUS I study in 2002. According to this survey of doctors, the structure of antihypertensive drugs that are prescribed to patients with hypertension in real practice is represented by five main classes: ACE inhibitors (25%), β -adrenergic blockers (23%), diuretics (22%), calcium antagonists (18%) and angiotensin receptor blockers. In comparison with the results of the PYTHAGOR I study, there is a decrease in the proportion of ACE inhibitors by 22% and β-blockers by 16%, an increase in the proportion of calcium antagonists by 20% and an almost 5-fold increase in the proportion of angiotensin II receptor blockers.
In the structure of drugs of the class of ACE inhibitors, the largest shares are enalapril (21%), lisinopril (19%), perindopril (17%), fosinopril (15%) and ramipril (10%). However, in recent years there has been a tendency to increase the importance and frequency of use of combination antihypertensive therapy to achieve the target level in patients with hypertension. According to the PYTHAGORUS III study, in comparison with 2002, the vast majority (about 70%) of doctors prefer to use combination therapy in the form of free (69%), fixed (43%) and low-dose combinations (29%) and only 28% continue to use the tactic monotherapy. Among combinations of antihypertensive drugs, 90% of doctors prefer prescribing ACE inhibitors with a diuretic, 52% - β-blockers with a diuretic, 50% of doctors prescribe combinations that do not contain diuretics (calcium antagonists with ACE inhibitors or