Combined mitral defect

In ICD-10, in section 108, it is suggested to use the terms "combined" for the lesion of several valves and "combined" for the combination of stenosis and insufficiency of one valve. In Russian clinics, including the Department of Faculty Therapy named after Academician A.I. Nesterov of the Russian State Medical University, the terminology used by Academician A.I. Nesterov and other outstanding Russian clinicians is still used, according to which the combination of two types of defect (stenosis and insufficiency) of one heart valve is designated by the term "combined defect" of the mitral or aortic valve.

In rheumatic etiology of mitral valve disease, as a rule, a combined lesion of the mitral valve with the formation of commissural adhesions and a "fish mouth" deformation is observed. In this case, stenosis or regurgitation may predominate; a situation is also possible when the contribution of stenosis and regurgitation is approximately equal. Treatment should be prescribed taking into account both possible embolic complications and atrial fibrillation, dual to mitral stenosis, as well as chronic left ventricular volume overload, which is characteristic of mitral regurgitation. Simultaneous administration of diuretics and vasodilators can be effective, but not always predictable with respect to hemodynamic effects. Indications for the use of anticoagulants and drugs that control the rhythm in atrial fibrillation are similar to those given above for mitral stenosis and insufficiency. The choice of surgical treatment method depends on the degree of regurgitation and the condition of the valve cusps and the semivalvular apparatus.

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Clinical observation of combined mitral valve disease

Patient T., 44 years old, has been observed at the Department of Faculty Therapy named after Academician A.I. Nesterov since April 2004 for rheumatic heart disease. Currently, the patient complains of irregular heartbeats, palpitations, and shortness of breath during moderate physical exertion.

It is known from the anamnesis that since childhood the patient noted limitations in physical activity due to shortness of breath (in active games he was forced to "stand on the enemies"). He does not remember frequent tonsillitis, pharyngitis, arthralgia/arthritis, or heart pain. After school, he graduated from a construction technical school. He did his military service in the air defense forces as a driver-mechanic. He noticed that forced marches were very difficult in the army. According to the patient, after his military service he suffered from acute tonsillopharyngitis. After the army, he worked as an engineer-technologist in industrial workshops. He did not note limitations in physical activity, since the load was always moderate. At the age of 38, for the first time during a game of football, an attack of severe shortness of breath ("not enough air") with a strong heartbeat occurred, he was forced to interrupt the game. Until that time, such complaints did not arise. Since 2000, due to his professional activities, the intensity of physical activity has increased (he began working as a construction materials supply manager, sometimes he had to unload goods himself). The patient gradually began to notice an increase in shortness of breath under load, weakness, decreased performance, and by 2004 he began to cope with unloading “with difficulty” due to the severity of the described symptoms. However, the patient did not seek medical attention and did not receive any treatment.

On 11/04/2004, while driving out of town (the patient was driving), he suddenly felt weak, the entire right half of his body went numb, and speech reproduction was impaired (he understood speech addressed to him, and his consciousness remained clear). Sensitivity in the extremities was restored within 3 hours, but the patient could not talk. On 12/04/2004, the patient was hospitalized by ambulance to City Clinical Hospital #6 with a diagnosis of "transient ischemic attack in the left carotid basin on 11/04/2004". During examination in the hospital: according to the conclusion of computed tomography of the brain - moderate external hydrocephalus; according to the conclusion of ultrasound diagnostics of the cerebral vessels - initial manifestations of atherosclerosis of the vessels of the main arteries of the head; on ECG - sinus rhythm. Using echocardiography, mitral valve disease (MVD) was detected - stenosis and insufficiency of the left atrioventricular valve. The patient was referred to the Moscow City Rheumatology Center for examination and decision on further treatment tactics. During the examination and checkup, the rheumatologist found that the patient had a narrowing of the mitral orifice to 1 cm ², which corresponded to severe mitral stenosis. A consultation with a cardiac surgeon was recommended, after which the patient was offered surgical correction of the defect. On 16.11.2004, an open mitral commissurotomy was performed under artificial circulation at the Sechenov Research Institute of Thoracic Surgery. The mitral orifice was dilated to 3 cm ². On the second day, the patient began to feel palpitations, and atrial fibrillation was detected using ECG. In the postoperative period, on the 3rd day, the patient developed severe pain in the heart area. To alleviate the condition, the patient took a forced position with a forward bend (possibly due to the development of postoperative adhesive pericarditis). The pain syndrome was relieved with narcotic analgesics. After discharge from the hospital, the patient constantly took acetylsalicylic acid (thrombo ASS) 50 mg / day, digoxin 1/2 tablet 2 times a day 5 days a week. Bicillin prophylaxis was also prescribed: bicillin-5 once every 4 weeks, for life. After the operation, the patient began to feel subjectively worse, there was a "fear of exertion", although, according to the patient, shortness of breath during physical activity became less pronounced. Currently, he constantly takes: digoxin 1/2 tablet per day (2 days a week break); metoprolol (egilok) 100 mg (1/2 tablet 2 times a day daily); acetylsalicylic acid 100 mg/day daily.

On examination: the patient's condition is satisfactory. Height 145 cm, weight 88 kg. The skin is pale, visible mucous membranes are of normal color. Skin turgor is preserved. There is no peripheral edema. Body temperature is 36.6 C. The lymph nodes are not enlarged. In the lungs, vesicular breathing is conducted to all sections. Wheezing is not heard, percussion reveals a clear pulmonary sound. Respiratory rate is 16 per minute. The apical impulse is determined by the anterior axillary line, diffuse. Cardiac impulse is not determined. The left border of relative cardiac dullness is determined by the anterior axillary line, the right one protrudes 1 cm from the right edge of the sternum, the upper one - along the upper edge of the 3rd rib. The diameter of the relative cardiac dullness is 21 cm, absolute - 10 cm, the width of the vascular bundle is 7.5 cm. Heart sounds are muffled, the rhythm is irregular, the 1st sound above the apex is strengthened, the accent of the 2nd sound above the pulmonary artery. A systolic murmur is heard, occupying the entire systole with a maximum above the apex, gradation III with conduction to the aorta, pulmonary artery and along the entire left edge of the sternum. Heart rate is 104 per minute. Pulse deficit is 12. Blood pressure is 122/80 mm Hg. The abdomen is soft, painless. The right border of the liver is at the edge of the costal arch, the left is at 1/3 of the distance from the xiphoid process to the umbilicus. The edge of the liver is soft, rounded, the percussion symptom is negative on both sides. Physiological functions are normal.

To assess the severity of the defect, its compensation, and to evaluate the dynamics of the condition, the following examinations were carried out.

ECG - atrial fibrillation. Heart rate - 102-111 per minute. Incomplete right bundle branch block.

Chest X-ray: lung fields are transparent, signs of moderate congestion in the pulmonary artery, roots are not dilated. The heart shadow is dilated to the left, the arches are smoothed with a tendency for the II and III arches to bulge.

Phonocardiogram: the amplitude of the first tone is inconstant at the apex, the second tone 2L > the second tone 2R. Systolic murmur of medium amplitude, throughout the systole. On the left side, the amplitude of the first tone is inconstant, systolic murmur of medium amplitude throughout the systole, diastolic murmur.

EchoCG from 13.02.2006 and further in dynamics from 11.01.2007 revealed marginal thickening and monophasic movement of the mitral valve leaflets, the diameter of the opening is 3 cm. Enlargement of the left atrium to 5 cm with practically normal indicators of the left ventricle, as well as an increase in the right chambers of the heart. Systolic pressure in the pulmonary artery is 36 mm Hg,

To determine the risk of thrombotic complications, the contribution of endothelial dysfunction to the progression of pulmonary hypertension, and, accordingly, CHF, hemostasis and blood rheology were studied. The hemostasis study did not reveal any significant deviations from normal values. When studying blood rheology indices, an increase in the hematocrit level, blood and plasma viscosity, which serve as indirect markers of endothelial dysfunction, was determined. Blood structuring indices and erythrocyte elasticity, reflecting tissue hypoxia, were also elevated.

Based on the patient's complaints, medical history, fiscal examination data, laboratory and instrumental studies, a diagnosis was made.

Clinical diagnosis: rheumatic heart disease. Combined mitral valve defect with predominant stenosis. Mild mitral stenosis. Mild mitral regurgitation. Atrial fibrillation, permanent form, tachysystole, pulmonary hypertension grade I, FC II (according to WHO). pulmonary hypertension grade I, FC II.

Analyzing the patient's medical history, anamnestic data, in particular, limited tolerance to physical activity since school age due to dyspnea, it is possible to assume the development of mitral valve disease since childhood. However, due to the long asymptomatic course of the defect, the patient did not seek help from medical specialists. The clinical manifestation of MPS in this patient was characterized by the acute onset of symptoms of cerebral ischemia with right-sided hemiparesis and aphasia. The presumed causes of transient ischemic attack could be both asymptomatic, short-term paroxysm of atrial fibrillation and coagulopathy (increased blood and plasma viscosity, increased hematocrit).

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