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non-rheumatic carditis

Non-rheumatic carditis - disease is characterized mainly by inflammatory


lesions of the myocardium with different etiology that develops against the
backdrop of the body's immunological failure.
Etiology
Carditis may be a manifestation of any infectious disease. However, the most
common cause are viruses, especially in children in the first years of life, and in a
third of cases of carditis develop against superinfection. The leading role in the
emergence of non-rheumatic carditis belongs enterovirus Coxsackie A and B in
children, ECHO, is much smaller - flu, paramyxovirus. Cytomegalovirus, herpes
simplex virus, adenovirus, rubella virus and toxoplasmosis pathogen usually
associated with congenital heart disease.
Possible bacterial carditis in children, who often are the manifestation of any
severe bacterial infection. Acute and chronic tonsillitis in children older than three
years of often complicated by non-rheumatic carditis. At the age of 5-6 years, the
most common cause of carditis in children is a streptococcal infection.
Furthermore, carditis etiology are fungal, allergic genesis (dosage, serum,
post-vaccination), toxic (in diphtheria) and also due to exposure to a variety of
other factors. idiopathic isolated carditis, etiology which hitherto unclear, but
probably due to viruses. Quite often a manifestation carditis mixed infection: viral
and viral, bacterial, viral, etc.
Pathogenesis
Given the diversity of the causes of carditis, clearly explain the pathogenesis
of carditis unlikely. However, most authors leading role attributed to the
persistence of the virus in the body, particularly in cardiomyocytes and cells of the
immune system. Its activation under the influence of adverse factors, resulting in
the destruction of myofibrils and immunological reactions of immediate type, is
further enhanced by the destruction of cardiomyocytes inducing autoimmune
processes and the formation of immune complexes.
Immune inflammation is credited with a leading role in the development of
bacterial carditis.
Biologically active substances in the freed immune inflammation in
myocardial contractility are potent activators homeostasis system, followed
microthrombogenesis and impaired microcirculation of the heart muscle and other
organs.
Carditis accompany the development of genetically determined metabolic
disorders and immune system (the cases of family carditis).
St. George V. (1999) identified three main groups of pathogenic processes
that have the greatest importance in the development of carditis:
- direct impact on cardiomyocytes pathogen, which mainly occurs in viral
infections;
- vascular lesions of the myocardium, which can be caused both
endotheliotropic pathogen or infectious lesions immunocomplex and infectious
nature;
- myocardial damage associated with the damaging effect of antibodies and
activated lymphocytes, cross-react with heart tissue (most often seen after a
streptococcal infection).
Morphological carditis pattern depends on the period of its occurrence, and
flow manifested varying degree of destructive combining, infiltrative inflammatory
and sclerotic changes in all three layers of the heart and its vessels, with a rare
lesion valves and the conduction system. Usually there is an increase in heart size,
myocardial hypertrophy of both ventricles, most of the left, the increase or
decrease of its cavity. In early congenital carditis expressed significant thickening
of the endocardium due to the elastic (fibroelastosis) or fibrous (elastofibroz)
tissue. At late congenital and acquired Cardito always have inflammatory cell
infiltrates with areas of necrosis and sclerosis.
Clinic
Clinic of the disease depends on the patient's age, the nature of the course
and the period of occurrence of carditis.
Single universally accepted classification of carditis does not exist.
However, depending on the period of exposure to pathogenic causes, carditis
divided into congenital and acquired (Table 1).

Table 1
The period of the Congenital (antenatal) - early and late;
disease Acquired.
causative factor Viral, bacterial, viral, bacterial, parasitic, fungal,
Yersinia, allergy (drug, serum, post-vaccination),
idiopathic.
Form (for preferential Carditis;
localization process) The defeat of the cardiac conduction system.
Flow: Acute up to 3 months;
Subacute to 18 months;
Chronic - more than 18 months (relapsing, primary
chronic); congestive, hypertrophic, restrictive
options.
The form and degree Left ventricular I, IIA, IIB, III degree
of heart failure Right ventricular I, IIA, IIB, III degree
Total.
Outcomes and Cardio, myocardial hypertrophy, rhythm and
complications conduction disturbances, pulmonary hypertension,
failure of the valve apparatus, constrictive
myopericarditis, thromboembolism.

Congenital carditis.The diagnosis is sometimes placed in the antenatal


period, but more often in the first weeks and months of life in connection with the
development of acute heart failure (AHF) against any disease. Cardites come early
(there are up to 7 th month of pregnancy) and late(After the 7th month of fetal
development). It draws the attention of low birth weight in children with early
congenital carditis, while later it may be normal; inexplicable failure to thrive in
the future, paleness, weakness, fatigue and increasing cyanosis during feeding,
unreasonable general anxiety attacks, sometimes aphonia, etc. The most constant
feature vrozhdennyhkarditovschitaetsyanedostatochnost blood circulation, which
in most patients is detected in the first six months of life, often in the background
intekurrentnyh diseases. Usually it is total. The history of children with congenital
carditis is almost always the mother during pregnancy were observed acute and
chronic infectious diseases; may be an indication of shortness of breath, existing
from birth, OCH against various diseases, vaccinations. In most cases, there is a
significant expansion of the relative dullness of the heart. When later carditis
usually radiographic finding. Muted tones and voiceless mandatory symptom of
early congenital carditis, as well as tachycardia, resistant to treatment.
When later Cardito tones loud enough. There can be various arrhythmias
usually cease upon the appointment of cardiac therapy. Half of the patients are
heard noises usually systolic relative or organic mitral valve insufficiency, rarely
mezodiastolichesky over the top of the heart at the same time rough systolic - a
relative or an organic stenosis of the left atrioventricular opening. Half of the
patients there is no noise.
In some patients, perhaps a combination of congenital carditis with
congenital heart disease (stenosis or atresia of the aorta, aortic kaorktatsiya etc.).
Typically inconsistency between clinical signs of defect (small intensity noise, no
symptoms of hypertension, and others.) And a significant increase in heart size,
heart failure refractory. On fibroelastosis ECG - sinus tachycardia, a rhythm the
rigid, high-voltage QRS complexes, left ventricular hypertrophy, myocardial
ischemia signs his suendokardialnyh departments; when elastofibroze -
intraventricular conduction disorders, hypertrophy of both ventricles.
For early congenital carditis characterized by rigid rhythm with the positive
dynamics in the process of treatment of elastofibroze in which in addition, may be
conduction abnormalities. Often, especially when combined with malformations
observed signs of congestion and hypertrophy of the right heart. When X-ray
thorax visible spherical, ovoid, or heart trapezoidal shade, there is a sharp decrease
in left ventricular pulsation amplitude, especially at fibroelastosis.
Late congenital carditis difficult diagnosed, children are born with a normal
weight, in the future prevail extracardiac symptoms mentioned above. Heart border
moderately dilated, often are heard loud tones, noise is usually absent. Develop
bronchitis, pneumonia, heart failure is less pronounced, typical of various
arrhythmias (tachy, bradyarrhythmia, blockade). ECG rhythm disturbances except
there are signs of left ventricular overload and atrial positive (more) teeth T. In the
X-ray shadow of the heart increased, but less than in the early carditis.
The diagnosis of congenital carditis can be confirmed morphologically in the
study of biopsies of the heart muscle and endocardial obtained during cardiac
catheterization. Clinical and instrumental symptoms of congenital carditis graphics
are similar to a severe form of chronic non-rheumatic carditis, with a questionable
prognosis in early carditis and a clear positive trend against the background of the
treatment in patients with advanced Cardito.
acquired cardites depending on the nature of the flow is divided into acute,
subacute and chronic (Table 1).
Acute rheumatic carditisIt occurs at the height of the clinical manifestations
of SARS or 1-2 weeks after it at any age, but severe forms typical of children
during the first 3 years of life and are caused by diffuse myocardial damage. In
older children carditis often occurs with damage to the vascular system and is
characterized by moderate and mild.
In the history of the children there are indications of frequent acute
respiratory viral infection, allergic exudative-catarrhal or limfatiko-hypoplastic
diathesis. Against the background of the clinical manifestations of SARS or a
fading condition of the patient worsens progressively reduced appetite, increases
general lethargy, fatigue, anxiety, especially at night. Nausea, vomiting, abdominal
pain, simulate appendicitis, may be unmotivated temperature climbs to 38-390C.
In some patients, one of the first non-cardiac symptoms are sudden-onset episodes
of cyanosis, agitation, brief loss of consciousness, clinical and tonic convulsions, is
not associated with a rise in temperature and usually pass on their own. Older
children may complain of persistent pain in the heart.
Rapidly growing phenomenon of heart failure, which is usually left
ventricle, but in young children it is soon to become total. It draws attention to the
growing shortness of breath, especially at night, often with noisy wheezing breath,
wheezing in the lungs (obstructive component) and a variety of arrhythmias:
tachycardia, tachyarrhythmia, bradycardia. The boundaries of the heart often
moderately dilated, but may be normal. Notes muted tones and deafness, especially
if cardiomegaly, gallop rhythm. Auscultated gentle systolic sound over the top, but
it may be absent, as it is not characteristic of acute carditis. Sometimes systolic
murmur has a rough tone in patients with a significant increase of the heart,
In individual patients can be auscultated pericardial friction over the heart or
on any one portion (the noise is listened in systole and diastole is not associated
with heart tones).
Pericarditis further worsens the condition of the patient. Decreased urine
output, increased liver, spleen, appears pastoznost tissues. Tachycardia can be
caused extrasystoles, atrial flutter, ectopic chronic tachycardia, paroxysmal
tachycardia and may be either transient or persistent. In children with a primary
lesion of the conduction system of the heart border, sonorous tones remain normal,
as with bradycardia caused by atrioventricular block, especially with complete
atrioventricular block I tone at the top to get clap minimal manifestations of heart
failure, but with full atrioventricular block may be attacks of Morgagni-Adams
Stokes. Characterized by significant changes in the ECG, especially in the first 2-3
weeks of disease, reduced voltage complexes QRS, T wave, ST segment shift
below isolines elongation electrical systole and systolic index increase, the HOMO
and heterotopic frequency and heart rate, conduction disturbances may be up to
complete atrioventricular block and blockade predserdnozheludochkovogo beam,
features overload hypertrophy and increasing both the left and right divisions heart.
Some patients found infarktopodobnye ECG waveforms, reflecting predominant
vascular disease.
The X-ray indicated increased pulmonary pattern due to the overflow of the
venous bed, increasing the size of the heart - from moderate to an advantageous
extension of the boundaries of the left until total cardiomegaly; sluggish ripple.
Heart shadow of configuration varies from normal to the spherical, aortic, mitral.

On PCG often detected amplitude reduction and expansion I tone, muscle


noise, additional tones. Myocardial hypertrophy on echocardiogram, reduction or
expansion of the left ventricle, reducing dysfunction and relaxation.

In the process of the active anti-inflammatory therapy and cardiac clinical


symptoms of acute carditis in patients quite fast (up to 3 months.) Diminish and
disappear. The changes identified in the survey tool is stored for a longer time to
12-18 months.
Half the patients (N.A.Belokon, M.B.Kuberger, 1987) acute or subacute
carditis takes a chronic course.
subacute carditisare more common in older children, are characterized by a
prolonged course and more torpid to therapy. They can be primary subacute when
4-6 months. SARS after a previously healthy child gradually growing signs of
heart failure and outcome of acute carditis.
For typical subacute carditis all manifestations of acute, but may be formed
cardiac hump (process limitation characteristic), usually loud tones, sometimes
auscultated systolic murmur of mitral valve insufficiency, of the pulmonary artery
accent II tone, heart failure poorly treatable.
The ECG can be rigid rhythm of his other disorders, which are marked
resistance. Typical of subacute carditis persistent atrial overload signs often with
positive teeth T. The latter two features distinguish from acute carditis subacute
(N.A.Belokon, M.B.Kuberger, 1987). These other instrumental methods of
inspection are adequate to those observed during acute course of disease, but more
resistant.
chronic carditis- the lot of older children. They can be primary chronic,
which are identified either by random inspection or when the signs of heart failure
or outcome of acute and subacute carditis.
There are two variants of chronic carditis: with an increase in the left
ventricular cavity and minor hypertrophy of its myocardial expressed
cardiosclerosis (stagnant or dilatation embodiment - HKI) and with a normal or
somewhat reduced cavity of the left ventricle due to the pronounced myocardial
hypertrophy (gipertrofichesy and sharply reduced the cavity of the left ventricle to
myocardial hypertrophy or without (restrakivny embodiment - HKII).
Chronic carditis characterized by a long asymptomatic, frequent delay in
physical development, recurrent pneumonia, chronic intoxication symptoms,
hepatomegaly, seizures and loss of consciousness, etc. Layering SARS appears
unfolded clinic circulatory failure.
When HKI typical tachypnea, weakened apical impulse, heart hump,
extended mainly to the left border of the heart, systolic murmur of mitral valve
insufficiency, persistent arrhythmias, most deaf tones, enlargement of the liver at a
satisfactory state of health. Heart failure is not a long time, but if is developing
rapidly, from the left ventricle to become total. The ECG high or low voltage teeth
(depending on the degree Cardiosclerosis), various arrhythmias, features moderate
overload atrial and left ventricular hypertrophy. These changes are permanent, it
can be a negative trend even on therapy.
Particularly characteristic for oligosymptomatic HKII. Children behind in
the majority of cases, both in weight and height, draws attention crimson cyanosis,
shortness of breath, lift the apex beat of the heart under normal boundaries.
Auscultated flapping or amplified I tone at the top with a pronounced accent II
tone of the pulmonary artery, less muted tones, noise is absent, but may be
auscultated mezodiastolichesky noise at the apex or in systolic IV, V left intercostal
space. When the breathlessness quickly align signs of right heart failure with
significant enlargement of the liver, the appearance of ascites. The ECG in the
second embodiment, carditis often bradycardia, preferential conduction
disturbances in the form of various closures, features overload both ventricles
(more right) and atria (particularly left), subendocardial hypoxia.
Severitycarditis (Table 1) are heavy - it is a diffuse lesion of the
myocardium, and possibly other membranes of the heart with the rapidly
increasing circulatory failure, often sharp stream. Clear clinical and instrumental
signs of heart disease.
moderately severe - is characterized by moderate clinical and instrumental
signs of heart disease, the frequency of arrhythmias, usually in children of school
age, subacute process may be symptoms of heart failure.
Mild illness no expansion of borders of the heart, heart failure, usually
marked arrhythmias in older children.
Laboratory findings with non-rheumatic carditis little informative and non-
specific: it may be accelerated ESR, leucocytosis with stab shift, the positive C-
reactive protein, high seromucoid indicators, increased 1- and -globulins, IgM in
the first week of the disease, and then IgG (after 3 weeks). But these figures reflect
the current virus infections, and quickly normalized. Designated diagnostic value
has increased activity of the enzymes - aspartic acid and alanine transaminase,
alkaline phosphatase, creatine kinase, lactate dehydrogenase, and especially its
cardiac isoenzymes. But normal numbers of all the indicators do not rule out
cardio. The most reliable confirmation of the diagnosis is 4-hkratnoe increase
neutralizing antibodies in paired sera (range 2-4 weeks) blood of patients with
consequent reduction in titer.
The diagnosis of rheumatic carditis placed on the basis of the above-
described clinical symptoms and laboratory instrumental data.
For the diagnosis algorithm can be recommended carditis Vorontcova IM et
al., in which signs of myocardial lesion quantitatively evaluated by the degree of
importance on a scale and divided into three groups.
Signs of high significance (4 points):
- an increase in the overall size of the heart and its cavities, confirmed by
objective methods of research;
- reduction of myocardial contractility, confirmed by the functional methods
or heart failure;
Signs of secondary importance (2 points)
- the lack of influence of the autonomic nervous system on the heart (rigid
rhythm, absence of respiratory arrhythmia), confirmed intervalografiey. Exception
- the neonatal period;
- detection of cardiac blood antikardialnyh antigen and antibody;
- improving cardiac blood fractions laktatgidrogenazy isozymes, creatine,
etc .;
- a set of ECG signs of hypertrophy of the heart;
- ECG signs of myocardial ischemia.
small signs (1 point):
- pain in the heart;
- weakening sonority I tone;
- tachy or bradycardia;
- gallop;
- apical systolic murmur;
- sinus block;
- disturbance of atrioventricular conduction or intraventricular;
- ectopic rhythm or beats;
- displacement interval ST;
- change of T wave
The diagnosis of myocardial lesion is considered valid if the amount
received 5 points or more (with the mandatory presence of at least one of the
hallmarks of great importance), likely with the total score of 3 (if you have one of
the symptoms of secondary importance).
In formulating diagnosis period indicates the occurrence carditis, etiology,
form (predominant involvement of the conduction system and the myocardium)
during, the severity of the process, step shape and heart failure.
Treatment- a comprehensive, phased. In the acute phase and during
exacerbation requires bed rest, the duration of which an average of 2-4 weeks and
is determined by positive dynamics influenced by therapy. A diet enriched with
vitamins and potassium salts. In severe cases, - oxygen therapy. In the initial phase,
the bacterial etiology carditis recommended antibiotics penicillin for 10-14 days.
In chronic course bitsillin prescribed for 2-3 months. and more. When viral carditis
recommended assignment antiviral drugs: interferon, deoxyribonuclease and
ribonuclease 0.05% solution of 2-3 drops every 2 hours a nose for 3 days, or by
inhalation, intron A. Within 1-2 months . held anti-inflammatory therapy: Aspirin
0.2 g per year of life per day or Voltaren,
The criterion for efficacy and dose reduction or discontinuation of therapy is
the positive dynamics of clinical, instrumental and laboratory parameters.
Mixed views on the use of steroids in the treatment of non-rheumatic
carditis. Some pediatricians (DP Murray et al., 1995) strongly opposed the
appointment, especially in the first 10 days of illness. However, other authors have
recommended their appointment if severe, especially in young children.
Glucocorticosteroid drugs are prescribed on the basis of 1-1,5mg / kg per
day, with a gradual decrease in achieving positive clinical dynamics. hormone
therapy can be from several weeks to several months. They are prescribed in
diffuse during circulatory insufficiency, chronic process, with a primary lesion
conducting system; as well as in allergic genesis of carditis. Assign also
desensitizing drugs: promethazine, diphenhydramine, suprastin, fenkarol, peritol in
age dosages. If signs of hypercoagulability recommended that heparin at a dose of
10-150 IU / kg per day and drugs reducing platelet adhesion and aggregation -
Curantylum at a dose of 3-5 mg / kg per day orally or intravenously xantinol
nicotinate.
In the complex treatment of patients carditis include potassium preparations
Riboxinum, ATP, vitamin B, E, A, sedatives.
When the process of synchronization to the above formulations was added
aminohinolinovogo derivatives of (delagil, Plaquenil of 5-10mg / kg per day),
inhibitors of kinin system (anginin, Protektin 0.25 g 3-4 times a day within a
month), as well as drugs anabolic action (nerabol, retabolil). When heart failure
appointed glycosides, diuretics, but it must be remembered that in patients with
carditis phenomenon glycoside intoxication, ectopic arrhythmias, conduction
abnormalities occur soon. Therefore, you should be careful when assigning these
funds.
When arrhythmic embodiment carditis in acute rhythm can be normalized
under the effect of anti-inflammatory, desensitizing agents, potassium preparations.
While maintaining arrhythmia stihaniya process acuity prescribed antiarrhythmic
agents, the choice of which depends on the type of arrhythmia.
The convalescence period of patients gradually expanded mode under the
control of functional tests, periodically uses anabolic agents (potassium orotate,
Riboxinum, nerabol, retabolil et al.), Run courses hyposensitizing therapy, physical
therapy.
After discharge from the hospital, where patients with non-rheumatic carditis
is the average for 1-1.5 months, the child's best finish the cure in the local
cardiorheumatological sanatorium, where under the control of functional tests
expanding patient treatment, although on physical exercise in the study group as
the children are exempt at least 1 year (even in mild carditis), but not necessarily
assigned LFK, on the testimony of drug therapy (diuretics, glycosides, drugs
aminohinolinovogo series, etc.). After sanatorium child is under medical
supervision of a cardiologist for 3-5 years. Children with acute carditis without
circulatory failure, are observed with quarterly mandatory testing (ECG, PCG,
blood and urine tests, X-ray and ultrasound study is not more than 1 time per year),
conducted sanitation foci of infection.
Children with subacute, chronic course of carditis, and circulatory
insufficiency are inspected and surveyed on a monthly basis. Continues on the
testimony of medical therapy for all children who have suffered cardio 2-4 times a
year are assigned courses kardiotroficheskoy therapy. Children with acute and
subacute carditis, preventive vaccination is contraindicated for 3-5 years. Chronic
carditis is an absolute contraindication for vaccination. If after 3 years of clinical
supervision for a child who suffered cardio, his condition is satisfactory, no
abnormal ECG changes, it can be removed from the register. If there are subjective
symptoms, ECG changes (violations of myocardial polarization, rhythm, or
conductivity), the medical check-up continued up to 5 years.
Question of bitsillinoprofilaktiki controversial. V.A.Nasonova (1980)
recommended a year-round bitsillinoprofilaktiku (bicillin 5 bitsillin-1) in 1-3 years,
depending on the severity of carditis, presence of foci of chronic infections (solved
individually) N.A.Belokon (1987) does not It recommends the introduction of
bitsillina.