Combined mitral defect

In ICD-10, in the rubric 108, the use of the terms "combined" for the defeat of several clayanones and "combinatorial" is suggested for the combination of stenosis and the inadequacy of a single valve. In Russian clinics, including the department of faculty therapy to them. Acad. A.I. Nesterov RGMU, while applying the terminology used by Acad. A.I. Nesterov and other outstanding domestic clinicians, 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.

With rheumatic etiology of mitral malformation, as a rule, combined mitral valve damage is observed with the formation of commissural adhesions and deformity by the "fish mouth" type. In this case, stenosis or regurgitation may predominate; a situation is also possible where the contribution of stenosis and regurgitation is approximately the same. Treatment should be prescribed taking into account both possible embolic complications and atrial fibrillation, dual to mitral stenosis, hock and chronic left ventricular overload volume, which is characteristic of mitral regurgitation. Simultaneous appointment of diuretics and vasodilators can be effective, but not always predictable for hemodynamic influences. Indications for the use of anticoagulants and drugs that control the rhythm of atrial fibrillation are similar to those given above for mitral stenosis and insufficiency. The choice of the method of surgical treatment depends on the degree of regurgitation and the condition of the valve flaps and half valve.

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

Clinical observation of combined mitral malformation

Patient T., 44, is observed at the Department of Faculty Therapy. Acad. A.I. Nesterova since April 2004 about the rheumatic heart disease. Currently, the patient makes complaints about interruptions in the work of the heart, palpitation, dyspnea with moderate physical exertion.

From the anamnesis it is known that the patient noted from childhood the restriction in physical activity because of dyspnea (in mobile games he was forced to "stand on the winches"), frequent angina, pharyngitis, arthralgia / arthritis, pain in the heart does not remember. After school he graduated from the construction technical school. Military service took place in the air defense troops as a driver-mechanic. I noticed that in the army march-throws were given with great difficulty. According to the patient, after military service he suffered acute tonsillopharyngitis. After the army he worked as an engineer-technologist in industrial shops. There was no restriction in physical activity, since the load was always moderate. At the age of 38, for the first time during the game of football, there was an attack of pronounced dyspnea ("there was not enough air") with a strong palpitation, was forced to interrupt the game. Until this time, there were no such complaints. Since 2000, due to professional activities, the intensity of physical exertion has increased (he began to work as a supply manager for construction materials, sometimes he had to unload the goods on his own). The patient gradually began to notice an increase in dyspnoea with load, weakness, decreased efficiency, and by 2004, with unloading, it was difficult to cope with the severity of the described symptoms. However, the patient did not apply to the doctors, he received no treatment.

11.04.2004 During a trip outside the city (the patient was behind the wheel of the car) suddenly appeared weakness, the entire right half of the body was numb, the reproduction of speech was disrupted (the spoken speech was understood, the consciousness remained clear). Sensitivity in the limbs recovered within 3 hours, but the patient could not talk. On 12.04.2004 the patient was hospitalized in the Emergency Hospital No. 6 with the diagnosis "transient ischemic attack from 11.04.2004 in the left carotid basin". In a hospital at inspection: on the conclusion of a computer tomography of a brain - the moderate external hydrocephalus; on the conclusion of ultrasound diagnosis of cerebral vessels - the initial manifestations of arteriosclerosis of the vessels of the main arteries of the head; on the ECG - rhythm sinus; with the help of echocardiography, a mitral cardiac defect (MPS) was detected-stenosis and left atrioventricular valve insufficiency. The patient was referred to the Moscow City Rheumatology Center for examination and resolution of the issue of further tactics of reference. During the examination and examination, the rheumatologist detected a narrowing of the mitral orifice up to 1 cm ², which corresponded to severe mitral stenosis. A consultation of a cardiac surgeon was recommended, after which the patient was offered a surgical correction of the defect. 16.11.2004 in the Research Institute of Breast Surgery. Sechenov performed an open mitral commissurotomy in conditions of artificial circulation. The mitral orifice is widened to 3 cm ². On the second day the patient had a feeling of palpitations, with the help of an electrocardiogram found atrial fibrillation. In the postoperative period on the 3rd day, the patient developed severe pains in the heart area, to ease the condition, the patient took a forced position with a forward slope (possibly due to the development of postoperative adhesive pericarditis). The pain syndrome was stopped by narcotic analgesics. After discharge from the hospital, the patient constantly took acetylsalicylic acid (thrombotic ACC) at 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, "fear of exercise" appeared, although, according to the patient, shortness of breath during physical activity became less pronounced. Now constantly accepts: digoxin on 1/2 tablets in day (2 days in a week a break); metoprolol (egilok) for 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. Skin covers pale, visible mucous membranes of normal color. The skin turgor is preserved. Peripheral edema is absent. Body temperature 36.6 C. Lymph nodes are not enlarged. In the lungs, vesicular breathing is carried out in all departments. The wheezing is not heard, the percussion is clear, the pulmonary sound. Respiration rate 16 per minute. The apical impulse is determined by the anterior axillary line, spilled. Heart push, not determined. The left border of the relative dullness of the heart 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 III rib. The diameter of the relative stupidity of the heart is 21 cm, the absolute one is 10 cm, the width of the vascular bundle is 7.5 cm. The heart sounds are muffled, the rhythm is incorrect, the tone above the tip is strengthened, the accent is II tone above the pulmonary artery. A systolic murmur is heard that occupies the entire systole with a maximum over the tip, gradation III with the aorta, pulmonary artery and the entire left margin of the sternum. Heart rate - 104 per minute. Deficiency of pulse - 12. AD - 122/80 mm. Hg. The abdomen is soft, painless. The right border of the liver at the edge of the costal arch, the left one 1/3 of the distance from the xiphoid process to the navel. The margin of the liver is soft, rounded, Symptom pokolachivayaya negative on both sides. Physiological administration is normal.

To assess the severity of the defect, its compensation, assessment of the dynamics of the state, the following examinations were carried out.

ECG - atrial fibrillation. Heart rate - 102-111 per minute. Incomplete blockade of the right leg of the bundle.

Radiography of chest organs; the pulmonary fields are transparent, signs of moderate stagnation in the ICC, the roots are not expanded. The shadow of the heart is widened to the left, the arcs are smoothed with the tendency of bulging II, III arcs.

Phonocardiogram: amplitude I of tone unstable at the top, II tone 2L> II tone 2R. Systolic murmur of medium amplitude, for the whole systole. On the left side, the amplitude of I tone is unstable, systolic murmur for the entire systole of medium amplitude, diastolic noise.

EchoCG from 13.02.2006 and later on in dynamics from 11.01.2007, the marginal thickening and monophasic movement of the mitral valve flaps was found, the diameter of the opening was 3 cm. The left atrium enlargement was up to 5 cm with practically normal left ventricular parameters, as well as an increase in the right heart. Systolic pressure in the pulmonary artery 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 rheology of blood. The study of hemostasis did not reveal any significant deviations from normal values. When studying the indices of blood rheology, an increase in the level of hematocrit, viscosity of blood and plasma, which serve as indirect markers of endothelial dysfunction, was determined. Indices of blood structuring and erythrocyte elasticity, reflecting tissue hypoxia, also appeared to be elevated.

On the basis of patient complaints, anamnesis, data of fiscal examination, laboratory and instrumental studies, a diagnosis is made.

Clinical diagnosis: rheumatic heart disease. Combined mitral defect with predominance of stenosis. Mitral stenosis of mild degree. Mitral regurgitation of mild degree. Atrial fibrillation, permanent form, tachysystole, pulmonary hypertension I degree, II FK (according to WHO). ND I degree, II FC.

Analyzing the patient's medical history, anamnestic data, in particular the limitation of exercise tolerance from school age due to dyspnea, we can assume the formation of mitral heart disease since childhood. However, due to the long asymptomatic course of the defect, the patient did not apply for help to the specialist doctors. The clinical manifestation of MPS in this patient was characterized by a sharp appearance of symptoms of cerebral ischemia with right-sided hemiparesis and aphasia. Presumed reasons for transient ischemic attack could be both asymptomatic, short-term paroxysm of atrial fibrillation, and coagulopathy (increased viscosity of blood and plasma, increase in hematocrit).

[8], [9], [10], [11]