Rheumocarditis

Rheumocarditis is the most significant symptom of rheumatic fever (RF), determining the severity of the patient's condition and the disease. Carditis usually occurs in isolation or is combined with other main clinical manifestations of RF. Inflammatory and dystrophic changes in the heart with RF can affect all its layers with the development of endocarditis (valvulitis), myocarditis, pericarditis.

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Symptoms of rheumatic carditis

Heart damage in rheumatic carditis	Clinical symptoms
Endocarditis or valvulitis	Apical holosystolic murmur of mitral regurgitation and middiastolic murmur above the apex - mitral valve valvulitis, basal protodiastolic murmur - aortic valve valvulitis In patients with rheumatic heart disease, a change in the character of one of these murmurs or the appearance of a new significant murmur indicates the presence of rheumatic carditis.
Myocarditis	Symptoms of congestive heart failure and/or cardiomegaly, abnormal heart rhythms Myocarditis in the absence of valvulitis is not characteristic of rheumatic fever*
Pericarditis	Pericardial friction rub, muffled heart sounds and cardiomegaly due to pericardial effusion, pain in the cardiac region. In the case of rheumatic pericarditis, the presence of damage to the valve apparatus is a necessary condition Pericarditis is diagnosed with equal frequency both in the first episode and in relapses of rheumatic fever.

* - Although congestive heart failure is almost always directly associated with myocardial involvement in rheumatic fever, deterioration of left ventricular systolic function in rheumatic fever is extremely rare, and its symptoms may be a consequence of severe valvular insufficiency.

In terms of frequency of damage in rheumatic fever, the mitral valve is in the lead, followed in descending order by the aortic, tricuspid and pulmonary valves.

During an objective examination, the pulse character is noticeable. At the earliest stage of the process development, the pulse quickens. Tachycardia does not correspond to the temperature and general condition, does not stop during sleep, and can also persist after the temperature drops and the general condition improves. In rare cases, tachycardia persists for a long time after treatment. Later, the pulse becomes labile. The pulse character can change in response to physical exertion, negative emotions, and then recover for a long time (10-20 minutes).

Bradycardia is also of great clinical significance in rheumatic carditis: along with tachycardia, it is observed much less frequently and indicates the influence of the inflammatory process on the sinus node and a disruption in the conduction of impulses.

Currently, international clinical criteria for rheumatic carditis are identified:

• organic noise(s) not previously heard, or dynamics of previously existing noises;
• enlargement of the heart (cardiomegaly);
• congestive heart failure in young individuals;
• pericardial friction rubs or signs of pericardial effusion.

The most consistent finding in rheumatic carditis is a murmur, which may be difficult to hear in tachycardia and congestive heart failure due to low systolic volume and in pericarditis due to a pericardial friction rub or effusion.

WHO experts consider the following noises to be indicative of the presence of carditis:

• intense systolic murmur;
• mid-diastolic murmur;
• basal protodiastolic murmur,

An intense systolic murmur over the apex is a manifestation of mitral valve valvulitis. A prolonged, blowing, systolic murmur associated with the 1st sound due to the reflection of mitral regurgitation is the leading symptom of rheumatic valvulitis. It occupies most of the systole, is best heard in the region of the apex of the heart and is usually transmitted to the left axillary region. The intensity of the murmur is variable, especially in the early stages of the disease, and does not change significantly with a change in body position and with breathing. This murmur should be distinguished from a midsystolic "click" and / or late systolic murmur in mitral valve prolapse.

Mid-diastolic murmur above the apex (Carey Coombs murmur) is formed as a result of rapid blood flow from the atria to the ventricles during diastole, is heard in the left lateral position with breath holding during exhalation, is transient, often not diagnosed or taken for the 3rd tone. The presence of such murmur makes the diagnosis of mitral valvulitis reliable. This murmur should be distinguished from a low-frequency increasing loud presystolic murmur followed by an increased 1st tone, which indicates formed mitral stenosis, and not current rheumatic carditis.

The basal protodiastolic murmur characteristic of aortic valve valvulitis is a high-pitched, blowing, fading, intermittent murmur.

The classification of rheumatic carditis indicated in the table can be successfully used in patients with primary rheumatic carditis. Mild carditis is diagnosed when murmurs appear in the heart without changes in its size and function. Moderate carditis is determined when murmurs in the heart are detected in combination with an increase in the size of the heart, and severe carditis is determined when murmurs in the heart are detected in combination with cardiomegaly and congestive heart failure and/or pericarditis.

Classification of rheumatic carditis

Symptom/Severity	Organic noise	Cardiomyomagaly	Pericarditis	Congestive heart failure
Easy	+	-	-	-
Average	+	+	-	-
Heavy	+	+	+/-	+

Mild rheumatic carditis: the general condition of the patient suffers slightly, examination reveals tachycardia over 90 per minute at rest and during sleep, subfebrile or normal body temperature, muffled sonority of tones, appearance of III and/or IV tones. In case of mitral valve damage - weakening of the first tone above the apex, prolonged medium-intensity systolic murmur, transient mesodiastolic murmur is also possible, and in case of aortic valve damage - systolic murmur above the aorta and protodiastolic murmur.

Moderate rheumatic carditis is characterized by pronounced manifestations in comparison with mild carditis in combination with an increase in the size of the heart, confirmed by instrumental diagnostic methods (chest X-ray, echocardiography). The general condition of patients is assessed as moderate. There is unmotivated fatigue, decreased physical performance, but no signs of congestive heart failure are determined. The course of rheumatic carditis is characterized by a longer duration, a tendency to exacerbations, heart defects are formed with a higher frequency than in the mild form.

In severe rheumatic carditis, in addition to organic noise and cardiomegaly, congestive heart failure of varying degrees develops. In this case, fibrinous or exudative pericarditis may occur. The general condition is assessed as severe or extremely severe. In diffuse rheumatic carditis or pancarditis, a fatal outcome may occur. In most cases, severe rheumatic carditis takes a protracted course, ending in the formation of valvular heart disease. However, complete recovery is possible even with severe rheumatic carditis. The specified classification of rheumatic carditis can be successfully used in patients with primary rheumatic carditis.

Recurrent rheumatic carditis against the background of formed valvular heart disease is much more difficult to diagnose. In this case, evidence of a recent streptococcal infection and knowledge of the state of the cardiovascular system in the period preceding the relapse, which is ensured by dispensary observation of the patient, are of decisive importance. The appearance of a new noise or a change in the intensity of a previously existing noise (noises), an increase in the size of the heart compared to the initial size, the appearance or increase in signs of congestive heart failure, the development of pericarditis in the presence of criteria for rheumatic fever and changes in laboratory parameters make it possible to diagnose recurrent rheumatic carditis and determine its severity.

Rheumatic heart disease develops as a result of rheumatic carditis. In the first 3 years from the onset of the disease, the frequency of heart defects is maximum. The most common are stenosis of the left atrioventricular orifice, mitral regurgitation, aortic valve insufficiency and aortic stenosis, as well as combined and combined heart defects.

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Diagnosis of rheumatic carditis

Rheumatic carditis, especially if it turns out to be the leading or only manifestation of suspected rheumatic fever, must be differentiated from the following diseases:

• infective endocarditis;
• non-rheumatic myocarditis;
• neurocirculatory asthenia;
• idiopathic mitral valve prolapse;
• cardiomyopathy;
• cardiac myxoma;
• primary antiphospholipid syndrome;
• nonspecific aortoarteritis.

A good instrumental method for diagnosing rheumatic carditis is two-dimensional echocardiography using Doppler technology, since in 20% of patients, echocardiography can reveal changes in the valves that are not accompanied by a heart murmur. Echocardiography provides information on the size of the atria and ventricles, the thickness of the valves, the presence of valve prolapse, limited mobility of the valves and ventricular dysfunction, and the presence of effusion in the pericardial cavity.

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Endomyocardial biopsy

Endomyocardial biopsy does not provide additional diagnostic information in patients with clinical features of carditis in the first episode of rheumatic fever. It should be noted that the occurrence of unexplained congestive heart failure in patients with an established diagnosis of RHD, who have only minor manifestations of RL and an elevated ASL-O titer, indicates a high probability of ongoing rheumatic carditis, and myocardial biopsy, as an invasive test, is not necessary for diagnosis and can be used only for scientific purposes.

The morphological criteria for rheumatic carditis are:

• subendocardial or myocardial granulomas of Aschoff-Talalaev;
• warty endocarditis of the valves;
• auriculitis of the posterior wall of the left atrium;
• lymphohistiocytic infiltration.

Aschoff-Talalaev granulomas are markers of the rheumatic process and are usually localized in the myocardium, endocardium and perivascularly in the connective tissue of the heart, while they are not found in other organs and tissues. Granulomas with an exudative inflammatory reaction, alternative changes in collagen fibers and degenerative changes in the myocardium are considered "active". In the absence of signs of fibrinoid necrosis against the background of pronounced perivascular sclerosis, granulomas are considered "old", "inactive". The latter can persist for many years and represent residual phenomena of previous activity without connection with ongoing activity and further prognosis.

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Treatment of rheumatic carditis

The physical activity regimen for patients with rheumatic fever is determined by the presence of rheumatic carditis and its severity. In case of mild rheumatic carditis, bed rest is recommended for at least 4 weeks. If rheumatic carditis symptoms persist or worsen, bed rest is prescribed for at least 6 weeks. The regimen is then expanded; in general, limiting exercise is recommended for at least 12 weeks. In case of moderate rheumatic carditis, strict bed rest is prescribed for the first 2 weeks - for the period of cardiomegaly; then - bed rest for 4 weeks and subsequently - ward and outpatient for 6-8 weeks, until the signs of rheumatic carditis disappear. In severe rheumatic carditis, strict bed rest is prescribed until the symptoms of heart failure and cardiomegaly disappear - 2-3 weeks, bed rest - for 4-6 weeks, ward (home) - for 4-6 weeks and outpatient - for 8-10 months. After the end of a rheumatic attack, a physical activity regimen is recommended taking into account the consequences of rheumatic carditis. The diet of a patient with rheumatic fever does not present any special features. In severe rheumatic carditis, it is necessary to limit the consumption of table salt. Limiting salt intake is also indicated during treatment with glucocorticoids - due to their ability to increase sodium reabsorption. At the same time, it is necessary to provide for the use of foods with a high potassium content (potatoes, tomatoes, melons, dried apricots, dried apricots).

Symptomatic treatment of rheumatic carditis is carried out with NSAIDs and glucocorticoids.

In mild rheumatic carditis and extracardiac manifestations of rheumatic fever, acetylsalicylic acid 3-4 g/day is effective, and in case of its intolerance - diclofenac (voltaren, orthofen) at a dose of 100 mg/day. In severe and persistent, refractory to treatment, moderate rheumatic carditis, the markers of which are cardiomegaly, congestive heart failure, the appearance of intracardiac blocks, as well as high-grade rhythm disturbances, it is recommended to prescribe prednisolone in an average daily dose of 1.0-1.5 mg/kg for 2 weeks. Subsequently, the dose is gradually reduced and NSAIDs are prescribed, which the patient must take for 4 weeks after the withdrawal of prednisolone, which can improve the immediate prognosis of the disease. Some researchers suggest pulse therapy with methylprednisolone (methylpred) in severe rheumatic carditis.

In cases where heart failure in rheumatic carditis occurs as a result of severe valvulitis and the resulting disturbances in intracardiac hemodynamics, WHO experts recommend considering the issue of heart surgery (valvuloplasty) and even valve replacement.

Treatment of relapses in rheumatic carditis is no different from treatment of the first attack, however, in the presence of symptoms of decompensation of cardiac activity, especially in patients with previously formed heart defects, the plan includes ACE inhibitors, diuretics and, if indicated, cardiac glycosides.

Prognosis for rheumatic carditis

Damage to the valve apparatus occurs as a result of the development of heart defects in 20-25% of patients who have had primary rheumatic carditis. Repeated attacks of rheumatic fever can proceed latently, increasing the frequency of heart defects to 60-70%. In addition, even hemodynamically insignificant damage to the valves increases the risk of infective endocarditis.