Nonrheumatic carditis in children презентация

Classification
4. Clinical presentation of carditis
5. Treatment
6. The differential diagnosis of cardiomyopathy

that aren’t caused by b-hemolytic Streptococcus of group A and diffuse connective tissue diseases
NC is polyetiologic disease

and is 9,4%.
Severe forms are more frequent in children especially in infants.
In children died from sudden death mortality due to NC is 17 %.
NC morbidity increased during viral disease epidemia.

by antibodies and activated lymphocytes

Vascular damages by viruses with microvasculature impairment

Miocardium edema with IC storage

Necrosis and inflammatory changes in myocardium (cell infiltrates)

Collagen tissue development
Myocardium fibrotic changes

of gestation; inflammatory reactions are absent but tissue prolifiration is present)
Fibroelastosis
Elastofibrosis

Late
(appear withing last 3 mo of gestation; inflammatory reaction is developed)
Fibrosis is absent

contractile dysfunction and heart dilation
Main symptom is cardiomegaly and congestive heart disease, dyspnea, cough
Sometimes congestive heart disease manifest itself after viral diseases
Body weight gaining retardation, paleness, flaccidity, sweat, naso-labial cyanosis, weak suckling

2-3 years old.
Neonates has normal body weight but than retard weight and height gaining due to progressed congestive heart disease.
Children have frequent common cold and respiratory diseases
Skin is pale with perioral cyanosis.
Flaccidity, weakness especially during feeding, attacks of agitation, convulsions, acrocyanosis
Constant tachycardia, dyspnea during rest and crying.
Stable rhythm and conductivity disturbances

up, apex beat is wide, early formation of “cor hibus” that is quite visible at 5-6 mo old.
Auscultation : muffled 1 sound at apex ans accentuated II sound at lung artery. If congestive heart disease progresses gallop rhythm appear. Systolic murmur can appear due to relative mitral valve insufficiancy.
Congestive heart disease in fibroelastosis is –resistant to treatment that differ it from acute or subacute carditis.

waves voltage, interval Q-T elongation,T wave inversion, deviation of axe
X-Ray: lung pattern amplification due to vein congestion. Heart size is increased. Shape of heart is round or trapeziform with smoothed waist especially for inborn carditis.
Echo CG: endocardium consolidation, left ventricular and atrium dilation, hypokinesia of ventricular septum, dislocation of mitral wave to posterior wall, decreasing of ejection fraction (less than 60% for infants and 55% for adolescents)
in 40 % of patients there are thrombi in apex of LV.

ECG and EchoCG
2. Cardiosclerosis, including endocardium thickening (Echo CG signs –contractile capacity decreasing, constant ECG changes like intraventricular and AV- blockages, extrasystols)
3. Pulmonary hypertension that indicative for severity and poor prognosis : crimson discoloration of face, acrocyanosis, II sound accentuation in lung artery, right ventricular hypertension
4. Insuficiency of AV-valves (comparative or organic)
5. Constrictive pericarditis
6. Thrombus-embolic syndrome( neurologic symptoms –convulsions, paresis, abdominal pains, urine tests changes, hypertension)

sucking in infants), fast exhausting after usual loadings ( games, studying etc.)
On the ground of ARD symptoms resolution clinical signs of cardiac damage progress: greyish-pale skin, naso-labial cyanosis, acrocyanosis, dyspnea with wheesing and rales
Obsessive cough, reinforced after changing position
In patients with thymomegaly voice become low
In 20% attacks of cyanosis, excitability, loss of conscience, convulsions, vomiting can occur.
Fever recur 2-3 weeks later
Hepatomegaly appear as a sign of heart failure
Sometimes very intensive abdomen pains can be as an initial symptom and children turn to surgeon
Arrhythmias.
Diuresis decreasing, edema.

Connection with
intercurrent infection

index is increasing (>0,55)
Echo-CG: left ventricular dilatation, decreased contractile myocardium capacity (<60-55%)
ECG:
Decreased voltage during 2-3 week of disease, than it become high, especially QRS and then again decrease.
Sinus tachycardia or signs of different arrhythmias.
ST-segment and T wave changes ( repolarization process abnormality).
Lab data: elevated ESR and α, γ-globulins, CRP(+), neutrophyl leucocytosis.
Creatinephosphokinase (CPK) and lactatedehydrogenase (LDG) ensymes level is elevated
Right ventricular biopsy is a diagnostic standard (!)

of CVS.
Diet № 10. Restriction of water intake, diet is enriched by potassium containing products: raisin, dried apricots, nuts, dried plums etc. Medication corrector of Mg and K drugs are asparcam, magnerot, panangin

on causative factor)
- antiviral drugs

anti-inflammatory drugs (NSAID)-are contraindicated in acute phase of disease because they enhance cell damage ( diclophenac, naproxen, ibuprofen)

of chronic infection focuses)
Semisynthetic penicyllines: Augmentin, Amoxycilline 10-14 days long.
Macrolides:
Roxytromycine – 7,5mg/ kg BID;
Azythromycine – 10 mg/kg once per day;
If suspicion of infective endocarditis under suspicion parenterally: Ampicilline 100-150 mg/kg, Amicacine 2 mg/kg, Vancomicine 10-15 mg/kg
Treatment duration is dependent on etiology: Streptococcal -4 weeks, Staphylococcus – 6 weeks, Gr”-” bacteria – 4 weeks
Glucocorticoids in severe course (shock, allergy), congestive heart disease, rhythm abnormalities: Prednisolon 0,8-1,5 mg/kg/day. In viral etiology in acute phase of AVD are contraindicated as they can enhance damage of cardiomyocytes.
Nonsteroid drugs in subacute and acute course of moderate severity
In chronic and subacute courses – aminochinoline drugs minimum for 6 mo long.
Antiviral therapy – IV immuneglobulins in high dosages..

4 mg/kg/day
Indopamide (arifon) 1,25-2,5 mg /day.
Metalazone 2,5-5 mg/day bid.
Furosemide 1-3 mg/kg/day.
Angiotensin converting enzyme inhibitors (ACEI):
Captopryl (capoten) 0,3-1,5 mg/kg/day
Lisinopryl 2,5-20 mg/day
Enalapryl (renitec, enap) 0,1-0,4 mg/kg/day

– 6,25 mg/day, can be increased to 25-50 mg/day bid.
Methaprolol– 5-10 mg/day bid.
Sotalol– 2 mg/kg/day to 6 mg/kg/day bid.
Propranolol 0,5-4 mg/kg/day per os tid 0,01-0,02 mg/kg slowly IV.
Ca-channels blockers:
Verapamil (isoptin) 1-4 mg/kg /day per os; and 0,1-0,15 mg/kg IV slowly.
Diltiazem 2-3 mg/kg/day tid.

diluted in 5% glucose
Ritmilen (dizopyramid) 5-10mg/kg/day; adolescents 400 mg/day tid.
Anticoagulants
- dipiridamol, varfarin
Metabolic antiaggrigate activity medications
– actovegin, vitamax, vitamins (В12, В15), carnitin,

( frequently inherited ones) clinically presented by mechanical or/and electrical myocardium dysfunction with disproportional hypertrophy or dilatation.

Myocardium affection can be primary or secondary and terminate by heart failure or sudden death

– is myocardium affection in systemic or polyorganic disease

(inherited,genetic)
2.1.2. acquired
2.1.3. mixed
2.2 Secondary
2.2.1 infiltrative
2.2.2. toxic
2.2.3 storage
2.2.4 endomyocardial
2.2.5 inflammatory (granulamatous)
2.2.6 endocrine
2.2.7 heart affectionin neuro-muscular diseases
2.2.8 alimentary
2.2.9 connective tissue diseases

hemodynamic outflow obstruction and nonspecific clinical presentation: syncope, stenocardia, life threatening arrhythmia

gradient < 30 mmHg
Latent outflow pressure gradient raises more than 30 mm Hg only after loading test

different directions
High risk rate of sudden death
Disease progression with dyspnoe, chest pains and syncope
Congestive heart disease with LV remodelling
Atrium flutter with thromboembolia

Systolic heart function as a rule is normal
Chest pain like in stenocardia as a rule develops due to outflow obstruction and decreasing of coronary circulation. Syncope as a rule appear suddenly after emotional or physical strain due to decreased outflow. Later syncope can appear at rest
Disease can manifest by arrhythmias ( atrium, ventricular fluttering or fibrillation). Every arrhythmia episode can be fatal for patient

to subsiding of myocardial tissue by connective tissue and decreased pump function of heart and form substrate for life threatening arrhythmias
Outflow obstruction develops due to disproportional ventricular septum hypertrophy predispose to leaflets contact with septum and produce increased gradient during systole.
Prolonged hypertrophy predispose for disorder of myocardium relaxation and development of ventricular walls rigidity. Diastolic dysfunction develops and later lead to systolyc heart dysfunction.

dislocated to left. Ps is accelerated, dicrotic.
Auscultation- systolic murmur at apex and in 4 left intercostal space near sternum. Murmur is very variable. It can be louder during physical exertion, in vertical position, during tachycardia or after nitrate or diuretic intake

in II, III, aVF leads
Arrythmia and conductivity disorders ( atrium fibrillation, different blockages
Cholter monitoring is helpful to reveal threatening to life signs like unstable ventricular tachycardia, atrium fibrillation, signs of myocardium ischemia

ventricular septum and left ventricular wall. Hypertrophy can be symmetric and assymmetric (predominant septum hypertrophy).
Outflow obstruction with gradient more than 30 mmHg ( tests with physical strain)
Dilation of left atrium, mitral regurgitation and in terminal stages left ventricular dilation

decrease outflow obstruction at rest
Verapamil decrease dyastolic dysfunction, can be drug of choice in patients with bronchial asthma
Anticoagulants ( varfarin, heparin, dipiridamol etc)
Surgical treatment ( myoectomy by Morrow or alcohol septum ablation) is necessary in refractory medical treatment, progressive considerable hypertrophy, gradient more than 50 mm Hg
NB!
Nitrates, ACEI medications, digoxin, nifedepin are prohibited in obstructive cardiomyopathy

( inheritance, chronic viral myocarditis, immune response disorders etc) and is characterised by heart chambers dilation with left and right ventricular systolic function disorder and later diastolic dysfunction

simple DCMP with locuses 1q32,2p31, 9q13, 10q21-q23; mitochondrial DCMP are more frequent, connected with X-chromosome)
Secondary CMP
Inflammatory (9%)
Ischemic (8%)
Due to hypertension
Due to amiloidosis
in AIDS patients
Chronic alcoholism

disease. Disease progression manifested by
Dyspnea, asthmatic attacks
Fatigability, muscle weakness
Ventricular arrhythmia accompanied by syncope
Atrium fibrillation, thromboembolia, systolic heart dysfunction
Right ventricular failure signs: edema of legs, hepatomegaly, ascitis

congestive moist rales in lungs apex I sound is muffled, sometimes gallop rhythm or additional III sound, systolic murmur of relative mitral or tricuspid insufficiency, arrhythmia
Chest palpation: enhanced, wide dislocated to left and down apex beat
Percussion: heart borders are dislocated to left and right side

in lungs or alveolar edema
ECG –nonspecific changes of ST segment and T-wave, voltage decrease, QRS deformation, sinus tachycardia, rhythm and conductivity disorders
Echo- CG: dilation of chambers, systolic dysfunction decreasing of LV output less than 55%, relative mitral and tricuspid regurgitation
Endomyocardial biopsy in suspicion of inflammatory CMP to evaluate myocardiocytes distruction and inflammatory cells infiltration

etiology;
in cases of life threatening arrhythmias;
progressive congestive heart disease:
in acute conditions like heart asthma, lung edema;
complications like pneumonia, systemic embolia, arrhythmia, syncope

( they increase LV output, improve physical loading tolerance, improve surviving of patients)
Beta-adrenoblockers (atenolol, propranolol, carvedilol, betacsolol etc)- they improve hemodynamics, protect cardiomyocytes, decrease tachycardia, prevent arrhythmias
Treatment of different arrhythmia forms (amiadoron, sotalol, antiarrhythmic medications class IA, cardioversion)
Surgical treatment heart transplantation

of main clinical variants
Additional (instrumental) methods of invastigations
Medical check-up
Prevention of complications of NC.
Classification of heart failure
Principles of treatment of heart failure