Symptoms of aortic stenosis

With aortic stenosis in adults, there is a long latency period during which there is a gradual increase in obstruction and pressure overload of the left ventricular myocardium with complete absence of any symptoms. Cardiac symptoms of acquired aortic stenosis appear usually in the fifth or sixth decade of life and are represented by angina, fainting, shortness of breath and eventually heart failure.

Angina is seen in approximately 2/3 of patients with critical aortic stenosis, about half of which have severe coronary artery obstruction. The clinical symptoms of aortic stenosis in this case are similar to manifestations of angina in IHD. Attacks occur with physical exertion and stop at rest. In the absence of stenosing coronary sclerosis, angina in patients with aortic stenosis occurs with a certain combination of three factors:

• reduction of diastole duration;
• increased heart rate;
• a decrease in the lumen of the coronary vessels.

Occasionally, the cause of angina pectoris may be the calcium embolism of the coronary artery bed.

Syncope states (faints) are the second classic sign of pronounced aortic stenosis. In this case, the syncopal condition implies a transient loss of consciousness caused by inadequate perfusion of the brain with blood enriched with sufficient oxygen. Often, patients with aortic stenosis equivalent to syncopal conditions are dizziness or attacks of unexplained weakness. There are several reasons for the development of syncope (dizziness) in aortic stenosis.

Frequent causes of dizziness and syncope in patients with calcified aortic stenosis:

• Obstruction of the left ventricular outflow tract.
• Violations of rhythm and conductivity.
• Decreased vasomotor tone.
• Carotid sinus hypersensitivity syndrome.
• Hyperactivation of mechanoreceptors of the left ventricle.
• Age-related decrease in the number of pacemaker cells.

Dyspnea with aortic stenosis is represented by two options:

• paroxysmal nocturnal dyspnea due to a decrease in sympathetic and increased parasympathetic tone of the autonomic nervous system (calcification of the conduction system, decrease in the number of pacemaker cells with age);
• attacks of cardiac asthma or alveolar pulmonary edema that occur suddenly, often at night, without other manifestations of chronic heart failure (unspecified neurohumoral mechanisms).

Since cardiac output with severe aortic stenosis persists for many years, symptoms such as fatigue, weakness, peripheral cyanosis, and other clinical manifestations of the "small cardiac output" syndrome tend to remain low until late stages of the disease.

A rare associated symptom of aortic stenosis is gastrointestinal bleeding, both idiopathic and due to angioedema of the intestinal submucosal vessels, described by Neusley in 1958. The most common source of bleeding is the ascending colon. The peculiarity of these bleedings is their disappearance after surgical correction of the blemish.

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

The course of aortic stenosis

Timely timing of the onset of symptoms is the cornerstone of managing patients with aortic stenosis. This is due to two factors. First, the appearance of symptoms dramatically accelerates the progression of the disease, makes the patient worse and significantly reduces the average life expectancy. The rate of progression of aortic stenosis is very variable. The average increase in the transaortic gradient per year is 7 mm Hg. The peak velocity of the transaortal flow is 1 m / s, and the average decrease in the area of the aortic opening ranges from 0.02 to 0.3 cm ² per year. CAS has a much faster rate of progression, in contrast to the "rheumatic" or bicuspid aortic valve. The main predictors of rapid progression; concomitant CHD, AT, hyperlipidemia, and also advanced age and smoking. The study of the natural course of the disease in symptomatic patients made it possible to establish that the prognosis is affected not only by the very fact of the appearance of the symptoms, but also by their combination and the rate of increase in severity, which is accompanied by a sharp increase in the cases of sudden death.

The history of the disease with aortic stenosis

Patient S., 72 years old, complained of cough with discharge of mucous sputum, dyspnea at rest, a feeling of discomfort about the left half of the chest. In the last 2 years, dyspnoea is worried when walking, during the year - discomfort after the sternum with physical exertion, rarely - dizziness. Deterioration of the condition is associated with cooling. When the temperature rose to 37.2 ° C, dyspnea increased, a cough appeared. Outpatient treatment with antibacterial agents without effect. It is directed to hospitalization by the local therapist with the diagnosis: right-sided pneumonia of ischemic heart disease: stenocardia II FC. Hypertensive disease II stage. NK II of Art.

On examination, the condition is severe. Ortopnoe. Acrocyanosis. Pasterness of feet and shins, BHD - 30 per minute. In the lungs to the right of the angle of the scapula, breathing is not audible. The border of the heart is shifted to the left. The heart sounds are muffled, a soft systolic murmur at the top of the heart is heard. The liver is 1.5 cm below the edge of the costal arch,

In the clinical analysis of the blood: hemoglobin - 149 g / l, red blood cells - 4,2х10 ⁹ / l, leukocytes - 10,0х10 ⁹ / l, polymorphonuclear - 5%, segment- nuclear - 49%, eosinophils - 4%, basophils - 2% lymphocytes - 36%, macrophages - 4%, ESR - 17 mm / h. In the biochemical analysis of blood: total protein - 68 g / l, glucose - 4.4 mmol / l, urea - 7.8 mmol / l, creatinine - 76 μmol / l, total cholesterol - 4.6 mmol / l, triglycerides - 1.3 mmol / l, HDL cholesterol 0.98 mmol / L, LDL cholesterol 3.22 mmol / l, VLDLP cholesterol 0.26 mmol / L, lipoprotein-a (LPa) 25 mg / dL, atherogenicity index - 3,7, total bilirubin 15,8 mkmol / l, ACT - 38 U / l, ALT - 32 U / l, calcium - 1,65 mmol / l, alkaline phosphatase - 235 U / l, creatine phosphokinase (CK) - 130 ME / l, LDH - 140 IU / l, vitamin D - 58 nmol / l; parathyroid hormone - 81 pg / ml.

ECG: sinus rhythm, heart rate - 90 per minute. Left ventricular hypertrophy.

2Dehogh: the aorta is compacted, not expanded. Calcinates in the base of the valves of the fibrous ring of the aortic valve. The valves are compacted, mobile, the commissure is not welded. Stenosis of the aortic valve (systolic opening of the valves is 8 mm, transaortal pressure gradient is 70.1 mm Hg, maximum speed is 4.19 m / s). The mitral valve is not changed. The finite-diastolic size (CDR) is 50 mm, the finite-systolic size (CSF) is 38 mm, the end-diastolic volume (BDW) is 155 ml, the finite-systolic volume (CSR) is 55 ml. Signs of pulmonary hypertension, the thickness of the back wall of the left ventricle is 12 mm, the interventricular septum is 14 mm. The ratio of the rate of early diastolic filling (peak E, m / s) to the rate of late diastolic filling of the left ventricle (peak A, m / s) (E / A) - 0.73, FV - 54%. AS - 23%. A zone of hypo- and akinesia is not revealed.

Started treatment with diuretics, beta-blockers in small doses, ACE inhibitors, nitrates. The second day of hospitalization was followed by the death of the patient.

Clinical diagnosis: calcified aortic stenosis of severe degree, ischemic heart disease, atherosclerotic cardiosclerosis NK II B, III FC.

At autopsy: the lungs are swollen, with a brownish hue, in the right pleural cavity 1000 ml of serous fluid, in the pericardial cavity - 100 ml. The blood supply to the heart is uniform. The venous arteries are stenosed with fibrous and calcified plaques by 20-30%. The valves of the mitral valve are not changed. The perimeter of the mitral orifice is 8 cm. The valves of the aortic valve are calcified, deformed, and lack mobility.

The aortic opening is slit-shaped. Valves of the right heart without apparent pathology. In the left ventricle, the myocardium with interlayers of fibrous tissue. Pronounced left ventricular myocardial hypertrophy (heart mass - 600 g, the thickness of the wall of the left ventricle - 2.2 cm).

Subsequently, a microscopic study of the sections of the valves of the aortic valve of patients with CAS was performed.

Pathological and anatomical diagnosis: calcified aortic valvular stenosis of severe degree, eccentric hypertrophy of left ventricle myocardium, venous plethora of internal organs, fine-focal diffuse cardiosclerosis.

The death of the patient ensued from heart failure as a complication of calcified aortic malformation.

In this clinical example, the cause for treatment was signs of progressive heart failure. Given the hemodynamic significant stenosis, the risk of sudden death in this patient was very high. Attention is drawn to the absence of significant stenosis of the coronary arteries during pathomorphological examination, therefore, the clinical symptoms of the disease (discomfort in the heart, dyspnea, dizziness) were most likely caused by CAS, rather than by IHD. In favor of this assumption, there is no evidence of myocardial infarction and / or acute cerebrovascular accident (DCM), dyslipidemia, diabetes mellitus, and other IHD risk factors.

It was noted that the parameters of systemic calcium metabolism are involved in increasing the values of gatrathyroid hormone, alkaline phosphatase, decreasing total calcium at normal vitamin D concentrations, which was associated with the expansion of the heart cavities and the presence of eccentric left ventricular myocardial hypertrophy, confirmed by autopsy. In histomorphological studies of valves of the aortic valve, lymphohistiocyte infiltration, neoangiogenesis, lobrocyte aggregates and calcification foci were detected. The described picture is evidence in favor of the regenerative and not degenerative character of calcification of the aortic valve in CAS patients and requires further study.

Given the difficulties experienced by practicing physicians, and the specifics of the revision of ICD-10, below we give examples of the formulation of the clinical diagnosis of various variants of CAS:

• I 35.0 - Calcified aortic (valve) stenosis of mild (moderate, severe) degree, asymptomatic (decompensated) form. NC II A, III FC (HYNA),
• I 06.2 - Rheumatic heart disease: a combined aortic disorder with a predominance of aortic valve stenosis (or failure). NK I, II FC (NYHA).
• Q 23.1 - Congenital bicuspid aortic valve with stenosis (and / or insufficiency), stenosis of mild (moderate, severe) degree, asymptomatic (decompensated) form. NC II A, III FC (NYHA).