Rheumatic carditis

Rheumatic carditis is the most significant sign of rheumatic fever (RL), which determines the severity of the patient's condition and illness. Carditis usually occurs in isolation or is combined with other major clinical manifestations of RL. Inflammatory and dystrophic changes in the heart with RL can affect all its layers with the development of endocarditis (valvulitis), myocarditis, pericarditis.

[1], [2], [3], [4], [5], [6], [7],

Symptoms of rheumatic heart disease

Heart damage in rheumatic carditis	Clinical symptoms
Endocarditis or valvulitis	Apocapic holosystolic murmur of mitral regurgitation and mesodiastolic murmur over the tip - valvulitis of the mitral valve, basal proto-diastolic murmur - valvulitis of the aortic valve In patients with rheumatic heart disease, a change in the nature of one of these noises or the appearance of a new significant noise indicate the presence of rheumatic carditis
Myocarditis	Symptoms of congestive heart failure and / or cardiomegaly, cardiac arrhythmias Myocarditis in the absence of valvulitis is not characteristic of rheumatic fever *
Pericarditis	Noise friction of the pericardium, muted heart sounds and cardiomegaly due to pericardial effusion, pain in the heart. In the case of rheumatic pericarditis, the presence of a valvular lesion is a necessary condition Pericarditis with equal frequency is diagnosed as in the first episode, hack and with relapses of rheumatic fever

* - Although congestive heart failure is almost always directly related to myocardial involvement with RL, worsening of left ventricular systolic function with rheumatic fever is very rare, and its symptoms can be a consequence of severe valve insufficiency.

According to the incidence of rheumatic fever, the mitral valve is the leader, followed by the aortic, tricuspid and pulmonary artery valve.

At objective survey the character of pulse attracts attention. At the earliest stage of the process, the pulse rate increases. Tachycardia does not correspond to temperature and general condition, does not stop during sleep, and can also persist after lowering the temperature and improving the general condition. In rare cases, tachycardia persists for a long time after treatment. Later, the pulse becomes labile. The nature of the pulse can change in response to physical stress, negative emotions, then recover for a long time (10-20 minutes).

Of great clinical importance for rheumatic carditis is also a bradycardia: along with tachycardia is observed much less often, it indicates the effect of the inflammatory process on the sinus node and on the violation, impulses.

Currently, international clinical criteria for rheumatic heart disease are distinguished:

• organic noise (noise), previously unheard, or the dynamics of pre-existing noises;
• augmentation of the heart (cardiomegaly);
• congestive heart failure in young people;
• shui friction of the pericardium or signs of effusion in the pericardial cavity.

The most constant sign of rheumatic heart disease is noise, which can be difficult to hear with tachycardia and congestive heart failure due to low systolic volume and pericarditis due to pericardial friction noise or effusion.

To the noise that indicates the presence of carditis, WHO experts say:

• intensive systolic murmur;
• mesodiastolic murmur;
• basal proto-diastolic murmur,

Intensive systolic murmur over the tip serves as a manifestation of valvulitis of the mitral valve. A prolonged, blowing, systolic noise associated with 1 tone 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 carried to the left axillary region. The intensity of noise is variable, especially in the early stages of the disease, and does not change significantly when the position of the body changes and when breathing. This noise should be distinguished from mesosystolic "click" and / or late systolic noise with mitral valve prolapse.

Mesodiastolic murmur over the tip (Carey Coombs noise) is formed as a result of a rapid discharge of blood from the atria into the ventricles during diastole, is heard in the prone position on the left side, with respiratory retention on expiration, is transient, often not diagnosed or taken for 3 tons. The presence of this noise makes the diagnosis of mitral valvulitis reliable. This noise should be distinguished from a low-frequency rising loud presystolic noise with a subsequent amplified I tone, which indicates a formed mitral stenosis, and not the current rheumatic heart disease.

Basal proto-diastolic noise, typical for valvulitis of the aortic valve, is a high-frequency blowing, damped, unstable noise.

The classification of rheumatic heart disease indicated in the table can be successfully used in patients with primary rheumatic heart disease. Light carditis is diagnosed when there is a noise in the heart without changing its size and function. Medium-sized carditis is determined when cardiac murmur is detected in combination with an increase in heart size, and severe cardiomyopathy in the determination of heart murmurs in combination with cardiomegaly and congestive heart failure and / or pericarditis.

Classification of rheumatic heart disease

Symptom / severity	Organic noise	CardMegaly	Pericarditis	Congestive heart failure
Easy	+	-	-	-
Average	+	+	-	-
Heavy	+	+	+/-	+

Rheumatic carditis of mild degree: the general condition of the patient is insignificant; on examination, tachycardia is detected more than 90 per minute at rest and during sleep, subfebrile or normal body temperature, muffling of sonority, appearance of III and / or IV tones. In the case of a mitral valve, a weakening of the I tone above the tip, a prolonged mean systolic noise, and also a transient mesodiastolic murmur, and in case of aortic valve damage, systolic murmur over the aorta and proto-diastolic murmur.

Rheumedocarditis of moderate severity is characterized by pronounced manifestations in comparison with light carditis in combination with an increase in heart size, confirmed by instrumental diagnostic methods (chest radiography, echocardiography). The general condition of patients is assessed as moderate. There is unmotivated fatigue, a decrease in physical performance, however, signs of congestive heart failure are not determined. The course of rheumatic carditis is characterized by a longer duration, a tendency to exacerbation, heart defects are formed with a greater frequency than with a mild form.

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

Recurrent rheumatic carditis on the background of the formed valvular heart disease is much more difficult to diagnose. In this case, the evidence of a recently transferred streptococcal infection and the knowledge of the data on the state of the cardiovascular system in the period preceding the relapse are crucial, which is ensured by dispensary observation of the patient. The appearance of a new noise or a change in the intensity of the noise (noise) that occurred before, an increase in 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 is formed as the outcome of rheumatic heart disease. In the first 3 years from the onset of the disease, the incidence of heart disease is maximal. The most common stenosis is the left atrioventricular orifice, mitral regurgitation, aortic valve insufficiency, and aortic stenosis, as well as combined and combined heart defects.

[8], [9], [10],

Diagnosis of rheumatic heart disease

Rheumatic heart disease, especially if it proves to be the leading or only manifestation of the alleged rheumatic fever, must be differentiated with the following diseases:

• infective endocarditis;
• non-rheumatic myocarditis;
• neurocirculatory asthenia;
• idiopathic prolapse of the mitral valve;
• cardiomyopathy;
• myxoma heart;
• primary antiphospholipid syndrome;
• nonspecific aortoarteriitis.

A two-dimensional echocardiography using Doppler technique serves as a good instrumental method for diagnosing rheumatic carditis, as in 20% of patients with echocardiography it is possible to detect valve changes that are not accompanied by noise in the heart. Echocardiography provides information on the dimensions of the atria and ventricles, the thickness of the valves, the presence of prolapse of the valves, the limitation of the mobility of the valves and ventricular dysfunction, and the presence of effusion in the pericardial cavity.

[11], [12], [13], [14], [15]

Endomyovascular biopsy

Endomiocardial biopsy does not provide additional diagnostic information in patients with clinical signs of carditis in the first episode of rheumatic fever. It should be noted that the occurrence of unexplained congestive heart failure in patients with established RBS diagnosis, which have only small manifestations of RL and elevated titre ACL-O, indicates a high probability of current rheumatic heart disease, and myocardial biopsy as an invasive test is not necessary for setting diagnosis and can be used only for scientific purposes.

Morphological criteria for rheumatic heart disease include:

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

Ashot-Talalay's granulomas are markers of the rheumatic process and are usually localized in the myocardium, endocardium and perivascular in the connective tissue of the heart, and they are not found in other organs and tissues. "Active" is considered granulomas with exudative inflammatory reaction, alternative changes in collagen fibers and degenerative changes in the myocardium. In the absence of signs of fibrinoid necrosis against the background of pronounced peri-vascular sclerosis, granulomas are considered as "old", "inactive". The latter can persist for many years and represent residual phenomena of previous activity without connection with continuing activity and further prognosis.

[16], [17], [18], [19]

Treatment of rheumatic heart disease

The regime of physical activity of a patient with rheumatic fever is determined by the presence of rheumatic heart disease and by the degree of its severity. When rheumatic carditis mild, bed rest is recommended for a period of at least 4 weeks. In the case of persisting or increasing symptoms of rheumatic carditis, bed rest is prescribed at least up to 6 weeks. In the future, the regime expands; in general, the load limitation is recommended for at least 12 weeks. In rheumatic heart disease, a strict bed rest is prescribed for the first 2 weeks - for the period of cardiomegaly; then - bed for 4 weeks and then - ward and outpatient for 6-8 weeks, until the disappearance of signs of rheumatic heart disease. In severe rheumatic heart disease, strict bed rest is prescribed for the period until the disappearance of symptoms of heart failure and cardiomegaly - 2-3 weeks, bedtime - 4-6 weeks, ward (home) - for 4-6 weeks and ambulatory - for 8-10 months. At the end of the rheumatic attack, the physical activity regimen is recommended taking into account the effects of rheumatic heart disease. The diet of a rheumatic fever patient does not present any peculiarities. In severe rheumatic heart disease, you must limit the intake of table salt. The restriction in the use of salt is also shown in the treatment of glucocorticoids - in connection with their ability to increase sodium reabsorption. At the same time, the use of foods high in potassium (potatoes, tomatoes, melons, apricots, dried apricots) should be envisaged.

Symptomatic treatment of rheumatic heart disease is performed by NSAIDs and glucocorticoids.

With mild rheumatic cardiovascular and extracardiac manifestations of rheumatic fever, acetylsalicylic acid is 3-4 g / day, and when it is intolerant - diclofenac (voltaren, orthophene) at a dose of 100 mg / day. In severe and persistent, unresponsive mediocris, moderate rheumatic heart disease, whose markers are cardiomegaly, congestive heart failure, the appearance of intracardiac blockades, as well as rhythm disturbances of high grades, it is recommended to prescribe prednisolone at an average daily dose of 1.0-1.5 mg / kg in for 2 weeks. Subsequently, gradually reduce the dose and prescribe NSAIDs, which the patient should take within 4 weeks after the abolition of prednisolone, which can improve the immediate prognosis of the disease. Some researchers suggest that in severe rheumatic heart disease, pulse therapy with methylprednisolone (methylpred).

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

Treatment of relapses in rheumatic heart disease does not differ from the treatment of the first attack, but in the presence of symptoms of cardiac decompensation, especially in patients with previously formed heart defects, ACE inhibitors, diuretics and, according to indications, cardiac glycosides are included in the plan.

Prognosis for rheumatic heart disease

The defeat of the valvular apparatus is due to the development of heart disease in 20-25% of patients who underwent primary rheumatic carditis. Repeated attacks of rheumatic fever can occur secretly, increasing the incidence of heart disease to 60-70%. In addition, even hemodynamically insignificant damage to the valves increases the risk of infective endocarditis.