Management of patients with cardiomegaly and heart failure

Cardiomegaly is a considerable enlargement of the heart from its dilatation and/or hypertrophy, accumulation of waste products due to impaired metabolism or development of neoplastic processes.
It is usually manifested by symptoms of heart failure, rhythm and conduction disorders.

COMMON SIGNS OF CARDIOMEGALY
Enlargement of the heart
Rhythm and conduction disturbances
Physical findings: widened borders of the heart, dull sounds, weakened 1st sound over the apex, presystolic gallop, additional 3rd and 4th sounds, murmurs of regurgitation
Signs of the underlying disease which has caused cardiomegaly

MAIN CAUSES OF CARDIOMEGALY
IHD: atherosclerotic cardiosclerosis, post-infarction cardiosclerosis, ischemic cardiomyopathy, cardiac aneurysm
Arterial hypertension
Heart defects (congenital, acquired)
Diffuse myocarditis
Primary and secondary cardiomyopathy
Pericarditis
Cardiac tumours
Athlete’s heart

DIAGNOSIS OF CARDIOMEGALY
Interviewing the patient to find out the main complaints: dyspnoea, fatigability, weakness, less tolerance to physical exertion; feeling of heaviness in the right hypochondrium, peripheral oedemas, pains in the chest (angina or cardialgia), heart palpitations

DIAGNOSIS OF CARDIOMEGALY
History. We should specify: consequence of development of heart failure symptoms (left or right ventricular failure separately or total heart failure at once), episodes of BP elevation, history of acute rheumatic fever, heart murmurs revealed in childhood, history of myocardial infarction, aches in the heart in the past, severe diabetes, connection with past infections, vaccination, alcohol consumption, medications, family history.

DIAGNOSIS OF CARDIOMEGALY
PHYSICAL EXAMINATION:
Inspection: cyanosis, acrocyanosis, paleness, ruddiness of cheeks, swollen veins in the neck, pulsating vessels or precardial area, widened venous network, enlarged abdomen, orthopnoea;
Palpation: assessing the pulse rate (slow, of small amplitude or full, rapid; pulse deficit), chest tremors, apical pulse shifted to the left;
Taking BP: normal, hypertension, high pulse pressure

DIAGNOSIS OF CARDIOMEGALY
PHYSICAL EXAMINATION:
Percussion: wider vascular bundle, wider borders of heart dullness
Auscultation: dull sounds, weakened 1st sound, protodiastolic or presystolic gallop rhythm, extra 3rd and 4th sounds, murmurs of regurgitation, cardiac rhythm disorders;

DIAGNOSIS OF CARDIOMEGALY
LABORATORY FINDINGS:
CDC: diagnosis of anaemia, polycythemia (COPD, cyanotic congenital heart defects), leucocytosis and elevated ESR (infectious endo-, myocarditis, exudative pericarditis)
Blood and urine glucose: diabetes mellitus
Lipid profile: CHD, aortic atherosclerosis
CRP test: endo-, myocarditis, systemic connective tissue diseases (SCTD)
Antinuclear and rheumatoid factors: SCTD
Bacterial blood culture: infectious endocarditis
Т3, Т4, TSH: hypo-, hyperthyroidism
Urea, electrolytes, creatinine: CKD

DIAGNOSIS OF CARDIOMEGALY
INSTRUMENTAL INVESTIGATIONS:
Chest X-ray (shape of the heart, enlargement of certain chambers, vessels): ‘mitral’, ‘aortic’ or spherical shape of the heart;
ECG: the changes are non-specific and manifold (hypertrophy of chambers of the heart, rhythm and conduction disorders, changes due to scarring of the heart)

DIAGNOSIS OF CARDIOMEGALY
INSTRUMENTAL INVESTIGATIONS:
Echocardiography is the most valuable non-invasive methods of diagnosis assesses thoroughly morphological changes in the chambers and valves of the heart, peculiarities of movement of valves, thickened areas and calcinosis, impaired movement of blood in the heart, signs of pulmonary hypertension, elevated LVEDP, width of heart walls, asymmetry due to hypertrophy or symmetry, areas of hypo- or akinesia.

MANAGEMENT OF PATIENTS WITH CARDIOMEGALY
To confirm cardiomegaly (to determine enlargement of the chambers, dilation or hypertrophy, to estimate the degree of enlargement of the chambers)
To reveal the cause of cardiomegaly
To assess its functional significance
To plan management of the patient

MANAGEMENT OF PATIENTS WITH CARDIOMEGALY
ASSESSMENT OF FUNCTIONAL SIGNIFICANCE OF CARDIOMEGALY:
Symptoms of dyspnoea, weakness, fatigability
Cardiac ventricular function (EF), congestive heart failure
Determination of NYHA functional class of heart failure

MANAGEMENT OF PATIENTS WITH CARDIOMEGALY
PLANNING MANAGEMENT OF THE PATIENT:
Prevention: changing lifestyle, treatment of hypertension, CHD or any other underlying disease
Medical treatment: diuretics, ACE inhibitors (or sartans), beta-blockers, nitrates, antiaggregants, anticoagulants, cardiac glycosides, antiarrhythmic drugs
Surgical treatment

CARDIOMYOPATHIES (CM)
European Society of Cardiology (ESC), 2008
“Cardiomyopathies are structural and functional myocardial diseases in the absence of systemic hypertension, coronary atherosclerosis, valvulopathies, or congenital heart disease”.

CARDIOMYOPATHIES
CM phenotypes
HCM (hypertrophic CM)
DCM (dilated CM)
ARVD (arrhythmogenic right ventricular dysplasia)
RCM (restrictive CM)
Non-classified:
Non compacted myocardium
Stress CM (Takotsubo CM)

ESC RECOMMENDATIONS (2008)
All CM phenotypes are divided into:
Familial (inherited, genetic)
Non-identified genetic disorder
A disease subgroup (including those with known gene mutation, metabolic disorders, glycogen storage disease, impaired fatty acid metabolism, lysosome storage disorders)

Non-familial (acquired, non-genetic)
Idiopathic
A disease subgroup
Toxic CM
Endocrine CM
Alimentary (nutritional) CM (thiamine or selenium deficiency, hypophosphataemia, hypocalcaemia)
Alcohol-induced CM
Tachicardia-induced CM
Peripartum CM
Athlete’s heart
CM in children born to mothers with insulin-independent diabetes
Inflammatory CM

HYPERTROPHIC CARDIOMYOPATHY
Hypertrophic cardiomyopathy is defined by the presence of increased left ventricular (LV) wall thickness that is not solely explained by abnormal loading conditions.
HCMP occurrence is 0.02-0.23% in adults and unknown in children, incidence being equal approximately to 0.3-0.5 per 100000 of population (0.005-0.07%). Most studies note that men develop the disease more often than women; CM prevalence rate in different races is similar.

HYPERTROPHIC CARDIOMYOPATHY
2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy
HCM is prevalently a genetic disease of the muscle of the heart characterised by a set of specific morphological and functional changes and progressing steadily with a high risk of development of severe life-threatening arrhythmia and sudden cardiac death.
HCM synonyms
Idiopathic hypertrophic subaortic stenosis
Muscular subaortic stenosis
Hypertrophic obstructive cardiomayopathy

HYPERTROPHIC CARDIOMYOPATHY
HCM is the main cause of
sudden cardiac death (SCD)
in the young, in sportsmen
in particular
The findings of autopsies of sportsmen who died of SCD show that death may have been caused by non-revealed or clinically silent HCM in 36% of cases.

HYPERTROPHIC CARDIOMYOPATHY
HCM is characterised by considerable (more than 15 mm) hypertrophy of myocardium of the left and/or in rare cases right ventricle, often asymmetric due to thickened IVS, with frequent development of left ventricular outflow tract obstruction (LVOTO) in the absence of known causes (hypertension, heart defects and specific heart diseases).

HYPERTROPHIC CARDIOMYOPATHY

HYPERTROPHIC CARDIOMYOPATHY

HYPERTROPHIC CARDIOMYOPATHY

HYPERTROPHIC CARDIOMYOPATHY

HYPERTROPHIC CARDIOMYOPATHY
Pathogenesis of HCM includes 4 interrelated processes:
Left ventricular outflow tract obstruction (LVOTO)
Diastolic dysfunction
Myocardial ischaemia
Mitral regurgitation

HYPERTROPHIC CARDIOMYOPATHY
CLINICAL MANIFESTATION:
Asymptomatic course in 25% cases
Dyspnoea on exertion (90%), orthopnoea;
Angina (70-80%);
Syncope (20%), presyncope (50%)
Greater obstruction in augmentation of cardiac contractility due to exertion;
Cardiac arrhythmias (90%)
Thromboembolic risks of atrial fibrillation
Sudden cardiac death

HYPERTROPHIC CARDIOMYOPATHY
ON EXAMINATION:
intense, raised cardiac impulse shifted slightly to the left
double, triple or even quadruple impulse over the apex of the heart
alternating pulse
An ejection systolic murmur over the apex or in the 3rd-4th intercostal space at the left sternal edge, ‘rhomboid’ character of systolic murmur

HYPERTROPHIC CARDIOMYOPATHY
DIAGNOSIS:
DNA-diagnosis using polymerase chain reaction (PSR)
Genetic testing of relations in the first degree to assess the risk of development of HCM
ECG and daily monitoring of ECG
Chest X-ray, EchoCG, MRI
Cardiac stress tests
Coronary angiography

HYPERTROPHIC CARDIOMYOPATHY

HYPERTROPHIC CARDIOMYOPATHY
Left ventricular wall or IVS thickness >15 mm

HYPERTROPHIC CARDIOMYOPATHY
MEDICAL TREATMENT:
ß-blockers
Increase diastolic filling/relaxation of the LV
Are first choice in obstructive and non-obstructive forms
Decrease myocardial oxygen demand
Have shown no effect on SCD risk
Verapamil (480 mg)
Improve diastolic function of the LV
Relieve symptoms (especially pain behind the breastbone)
Disopyramide
Is used in combination with ß-blockers
Negative inotropic effect
Diuretics
Amiodarone, Sotalol (to treat arrhythmia)

HYPERTROPHIC CARDIOMYOPATHY
Invasive methods of HCM management
Transaortic septal myectomy (Morrow’s procedure)
is a ‘gold’ standard to
decrease left ventricular
outflow tract obstruction
(LVOTO) for both children
and adults.

HYPERTROPHIC CARDIOMYOPATHY
Percutaneous transluminal septal alcohol ablation
May be chosen for highly symptomatic adult patients with LVOTO, resistent to medical treatment and if other methods are undesirable for them

DILATED CARDIOMYOPATHY (DCM)
Is a disease of the cardiac muscle characterised by dilation and impaired contractility of the left ventricle or both ventricles of the heart (WHO).

DILATED CARDIOMYOPATHY
Dilated cardiomyopathy is responsible for 9% of all cases of heart failure. Incidence of dilated cardiomyopathy is 3 to 10 cases per 100 000 people.
It affects men more often, occurring mostly in adults 20 to 50
ESC (2008) DCM diagnosis is confirmed if there is dilation and impaired contractility of the left ventricle in the absence of CHD, valvular pathology or hypertension.

CLINICAL MANIFESTATIONS OF DCM
Symptoms: palpitation, syncopes, weakness, dyspnoea, reduced exercise tolerance and sudden cardiac death.
Most often DCM symptoms occur in adults from 30 to 40
DCM clinical manifestations are connected with:
Progressing CHF
Reduced heart output
Ventricular and supraventricular arrhythmia
Conduction disorders
Thromboembolism, including pulmonary embolism and acute impaired cerebral circulation
Sudden death or death caused by heart failure
Sudden death may occur before Class III HF develops

CLINICAL MANIFESTATIONS OF DCM
Physical changes
Inspection, palpation:
Swollen, pulsating jugular veins
Diffuse apical pulse shifted to the left
Tachypnoea, orthopnoea
Oedemas, anasarca
Percussion: widened borders of the heart to the left, to the right
Auscultation:
The heart – regurgitation murmurs:
– mitral or mitral-tricuspid
Gallop rhythm
(Often) arrhythmia (tachycardia, extrasystolia, atrial fibrillation)
The lungs – rales: moist, stagnant

DIAGNOSIS OF DCM
ECG: no specific changes
- Ventricular arrhythmia
- Atrial fibrillation
- Impaired contractility
- Complete left bundle branch block (LBBB)
- Non-specific ST – T changes
- increase in the amplitude of the R-wave between leads V1-V4

DIAGNOSIS OF DCM
Cardiomegaly (cardiothoracic ratio > 50%)
Pulmonary congestion

DIAGNOSIS OF DCM
Dilation of heart cavities
EF < 40%
Sings of pulmonary hypertension
Hypokinesis of walls
No findings to support IHD, defects and other cardiac problems
Sings of dyssynchrony of myocardium

DIAGNOSIS OF DCM
Radionuclide methods
Can be used to assess the size of heart chambers, contractility of the left and right ventricles, dyssynchrony, focal changes. Differential diagnosis with IHD. Allow to make an early diagnosis of impaired areas and take a biopsy from these areas
MRI and MSCT
1. Differential diagnosis with other cardiomyopathies: ARVD, endocardial fibroelastosis (EFE), amyloidosis, sarcoidosis, myocarditis, between infiltrative and inflammatory CM.
2. Identifying patients with a high risk of sudden cardiac death (with vast areas of fibrosis).
Coronary ventriculography
To reveal intact arteries. Invasive measurement of parameters
Endomyocardial biopsy

EXCLUSION CRITERIA FOR DCM
Systemic arterial hypertension (> 160/100 mm Hg)
Ischaemic heart diseases (50% coronary stenosisin one or several vessels on coronary ventriculography)
Alcohol abuse (> 40 g/day for females ,> 80 g/day for males)
Systemic diseases of the connective tissue
Specific diseases of pericardium
Congenital heart defects
Acquired heart defects
Pulmonary heart disease

MANAGEMENT OF DCM
To exclude factors which may worsen dysfunction of myocardium
Medical treatment:
Management of heart failure
Treatment and prevention of arrhythmias/ sudden cardiac death
Prevention of thromboembolism
Surgical treatment

MYOCARDITIS
Inflammatory impairment of the heart muscle due to influence (direct or indirect through immune mechanisms) of a number of factors; associated with damage to mechanical and electric functions of the heart.
The true incidence of myocarditis in population is unknown.
A cause of sudden death.
Clinical symptoms vary from subclinical disease to sudden death in newly developed atrial or ventricular arrhythmia, complete heart block or acute symptoms resembling myocardial infarction.
Most researches mention prevalence of the disease in males.

ETIOLOGY OF MYOCARDITIS
Bacteria
Rickettsiae and Spirochaete
Viruses
Protozoa
Fungi
Parasitic diseases
Deficiencies (hypophosphataemia, hypomagnesemia, hypocalcaemia, carnitine or selenium deficiency)
Allergic and toxic reactions
Action of some medications and cardiotoxic factors
Autoimmune diseases
Sequelae of burns, corrosions and frostbite
Post-transplantation conditions

VIRAL INFECTION IN MYOCARDITIS
Coxsackie of A and B groups, ЕСНО, A and B flu, herpes (herpes virus type 6), cytomegalovirus, Epstein-Barr virus , parvovirus В 19, coronavirus, arbovirus, hepatitis В, С, D viruses, HIV, epidemic parotitis, polio.
The most common viral genome identified in biopsy of myocardium in European population is parvovirus В 19 and human herpes virus type 6.
Among pathogenic bacteria, intracellular pathogens (of Chlamidia genus) have been the most significant recently.

MYOCARDITIS
THE COURSE OF THE DISEASE
Mild: mostly focal, without cavity dilation, systolic dysfunction, potentially dangerous arrhythmias, heart failure stages 0-1.
Moderate: focal or diffuse with initial dilation, moderate impairment of LV contractility, without malignant arrhythmia
Severe: diffuse myocarditis with cardiomegaly, systolic dysfunction, life-threatening rhythm and conduction disorders

DIAGNOSIS OF MYOCARDITIS
1 CRITERIA OF INFLAMMATION, INFECTION:
Fatigue, hyperthermia, accelerated ESR, leucocytosis, elevation of C-reactive protein
Routine microbiologic and serologic reactions (positive neutralisation reaction, complement-binding reaction, haemagglutination) are of significance to make a diagnosis of non-viral myocarditis only
Immune, histochemical study of biopsy material, PCR-guided diagnosis to confirm viral myocarditis

DIAGNOSIS OF MYOCARDITIS
2 CRITERIA OF MYOCARDIAL INVOLVEMENT:
Clinical: cardialgia, heart palpitations, irregular heart work, HF symptoms associated with infection, allergy or other underlying disease, weakened I(II) sound, systolic murmur at the apex, widened borders of the heart
ECG: tachycardia, bradicardia, arrhythmias, blockades, decreased voltage, repolarisiation disorders, long QT
EchoCG: cavity dilation,< EF, hypokinesis of myocardium, thicker walls, fluid accumulation in a pericardial cavity, valve regurgitation, blood clots in the cavities
Biochemical: elevated cardiac troponin levels, CPK-MB, LDH, level of antimyocardial antibodies (to sarcolemmal and microfibrillar proteins of cardiomyocytes)

DIAGNOSIS OF MYOCARDITIS
New York Heart Association (NYHA)
History of infection confirmed clinically and biochemically or another cause (allergy, toxins, medications, burns, etc.)
Sinus tachycardia
Weakened S1
Gallop rhythm
Enlarged heart
Congestive heart failure
Pathological changes on an ECG
Elevated serum enzyme or isoenzyme activity

MANAGEMENT OF MYOCARDITIS
1 Etiotropic treatment
Antibacterial, antiviral, antiparasitic drugs
2 Pathogenic treatment
Non-steroidal anti-inflammatory drugs (NSAIDs)
Glucocorticoids (GCs) (if severe)
Immunosuppressive drugs (second-line therapy)
3 Symptomatic treatment
Management of HF
Treatment of rhythm and conduction disorders
Prevention and treatment of thromboembolism

HF is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.
HEART FAILURE (HF)

A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body
It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent
HEART FAILURE (HF)

HF – is an imprecise term used to describe the pathological state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of an elevated filling pressure.
In practice,HF may be diagnosed whenever a patient with significant heart disease develops the signs or symptoms of a low cardiac output,pulmonary congestion or systemic venous congestion.
HEART FAILURE (HF)

CLASSIFICATION
Heart failure can be classified in several ways 1 - Acute and chronic HF 2 – Left , right and biventricular HF 3 - Systolic and diastolic dysfunction 4 - Forward and backward HF 5 - High-output HF 6 - Functional classes (NYHA)

ACCF/AHA stages of HF
Stage A: At high risk for HF but without structural heart disease or symtoms of HF
Stage B: Structural heart disease but without signs or symptoms of HF
Stage C: Structural heart disease with prior or current symptoms of HF
Stage D: Refractory HF Requiring specialized interventions
ACCF/AHA guidelines, 2001

ESC Guidelines for diagnostic and treatment of acute and chronic HF (2016)
Definition of heart failure with: preserved (HFpEF), mid-range (HFmrEF) and reduced ejection fraction (HFrEF)
1) LVEF < 40% with reduced EF
2) LVEF – 40-49% with mid-range EF
3) LVEF > 50 % with preserved EF

NEW YORK НЕАRT ASSOCIATION (NYHA) FUNCTIONAL CLASSIFICATION OF CHF
I class. Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnoea or anginal pain.
II class. Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dysponea, or anginal pain.
III class. Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dysponea or anginal pain.
IV class. Patients with cardiac disease resulting in inability to сап on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.

MANAGEMENT OF
HEART FAILURE (HF)
The main purposes:
To reduce mortality !!!
To relieve HF symptoms
To slow down HF progress
To improve the quality of life (QOL)
To reduce duration of hospital treatment
To improve prognosis

THE MAIN PRINCIPLES OF
HF MANAGEMENT
To reveal and exclude triggering factors
To normalise cardiac output
To eliminate fluid retention in the body
To reduce peripheral tension
To reduce sympathoadrenal effects
To improve blood supply and metabolism of myocardium

METHODS OF HF MANAGEMENT
Non-medical (changing lifestyle)
Pharmacotherapy (ACE inhibitors or ARBs, beta-blockers, aldosterone antagonists, diuretics, cardiac glycosides, ivabradine, anticoagulants, antiarrhythmic drugs, statins, cardiometabolic drugs)
Mechanical (thoracocentesis, paracentesis, dialysis, ultrafiltration)
Surgical (pace-makers, ICD (implantable cardioverter defibrillator), coronary revascularisation, heart transplantation)

Pharmacotherapy for HF
1 DRUGS PROVED TO BE ABLE TO REDUCE MORBIDITY AND MORTALITY RATES IN CASE OF CHF EXACTLY
used for all patients (ACE inhibitors or ARBs, beta-blockers, aldosterone antagonists);
used under certain clinical conditions (diuretics, cardiac glycosides, ivabradine, anticoagulants);
2 DRUGS NOT INFLUENCING PROGNOSIS FOR CHF BUT RELIEVING SYMPTOMS IN CERTAIN CLINICAL SITUATIONS
(antiarrhythmic drugs, statins, calcium channel blockers (CCB), antiaggregants, cytoprotectants, vasodilators)

ACE inhibitors recommended
by Russian Cardiology Society
Enalapril 2,5×2 - 20×2
Captopril 6,25×3 - 50×3
Fosinopril 5×1 - 20×1
Perindopril 2×1 - 8×1
Lisinopril 2,5×1 - 20×1
Ramipril 2,5×2 - 5×2
Spirapril 3×1 - 6×1
Trandolapril 1×1 - 4×1
Chinapryl 5×1 - 40×1
Zofenopril 7,5×1 - 30×1

RULES FOR ADMINISTRATION OF ACE INHIBITORS
To discontinue active diuretic therapy or to reduce the dosage of diuretics within 24 h.
To discontinue or to reduce the dosage of systemic vasodilators.
Not to start treatment if BP is < 90 mm Hg, plasma К > 5.0 mmol/L, creatinine > 220 mcmol/L.
To monitor BP, plasma K, creatinine after each dose titration, then once in three months.
If GFR is 15-30% reduced the dose may remain the same; in 30-50% the dose should be decreased by two times, in >50% the drug should be discontinued

ESC recommendations.
ARBs II with proved influence on prognosis
Candesartan from 4-8 mg daily to 32 mg daily
Valsartan from 20-40 mg twice a day to 160 mg twice a day
Losartan from 50 mg daily to 150 mg daily

ESC recommendations.
β-blockers with proved influence on prognosis
Bisoprolol
from 1.25 mg daily to 10 mg daily
Carvedilol
from 3.125 mg twice a day to 25-50 mg twice a day
Metoprolol succinate
from 12.5 mg daily to 200 mg daily
Nebivolol
from 1.25 mg daily to 10 mg daily

Peculiarities of taking ß-blockers
To all patients with manifestations of CHF due to IHD or DCM, if the level of EF <45%.
If the level of EF <25%, carvedilol is preferable.
Treatment should start after correction of hypervolemia.
Individual titration, aiming at reaching target doses.

ESC recommendations.
Aldosterone antagonists
Eplerenone
from 25 mg daily to 50 mg daily
Spironolactone
from 25 mg daily to 25-50 mg daily

ESC recommendations.
Aldosterone antagonists
Contraindicated:
K level >5.0 mmol/L, creatinine >220 mcmol/L,
While taking other sparing diuretics, concomitant use of ACE inhibitors and ARBs II.
Treatment only monitoring potassium and creatinine levels
Initial dosage is 12.5-25 mg (50 mg for patients not taking ACE inhibitors or ARBs).
Therapeutic dosage is 25-75 mg (100-150 mg for patients not taking ACE inhibitors or ARBs).

IVABRADIN, a standard medication for CHF management
Reviewing European recommendations on HF (2012):
Ivabradin should be included into medical treatment for CHF of every patient with CHF Class II-IV and LVEF <35%, heart rate ≥70 bpm, sinus rhythm.
Heart rate has been recognised as a routine parameter determining the further management
Heart rate <70 bpm is included into the algorithm of management of patients with CHF
Ivabradin improves outcomes in patients with CHF

Indications for administration of diuretics:
To eliminate clinical symptoms of fluid retention. They contribute to better exercise tolerance.
Preventive consumption for haemodynamically stable patients disposed to hypervolemia.

Doses of diuretics during active stage of HF treatment
Furosemide from 20–40 mg to 40-240 mg
Torasemide from 5–10 mg to 10–100 mg
Hydrochlorothiazide
from 12.5-25 mg to 25-100 mg
Indapamide from 2.5 mg to 2.5 - 5 mg
Spironaloctone from 12.5-25 mg in combination with ACE inhibitors or ARBs II to 25-75 mg in combination with ACE inhibitors or ARBs II
from 50 mg without ACE inhibitors or ARBs II to 100-150 mg without ACE inhibitors or ARBs II