Symptoms of aortic stenosis

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

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

• reduction in the duration of diastole;
• increase in heart rate;
• narrowing of the lumen of the coronary vessels.

Rarely, calcium embolism of the coronary artery bed can cause angina.

Syncopal states (fainting) are the second classic sign of severe aortic stenosis. Syncopal state is understood as a transient loss of consciousness caused by inadequate perfusion of the brain with blood enriched with sufficient oxygen. Often, in patients with aortic stenosis, the equivalent of syncopal states is dizziness or attacks of unexplained weakness. There are several reasons for the development of fainting states (dizziness) in aortic stenosis.

Common causes of dizziness and syncope in patients with calcific aortic stenosis:

• Left ventricular outflow tract obstruction.
• Rhythm and conduction disturbances.
• Decreased vasomotor tone.
• Carotid sinus hypersensitivity syndrome.
• Hyperactivation of left ventricular mechanoreceptors.
• Age-related decline in pacemaker cells.

Shortness of breath in aortic stenosis is presented in two variants:

• paroxysmal nocturnal dyspnea due to a decrease in sympathetic and an increase in parasympathetic tone of the autonomic nervous system (calcification of the conduction system, a 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 in severe aortic stenosis remains at a sufficient level for many years, symptoms such as fatigue, weakness, peripheral cyanosis and other clinical manifestations of the "low cardiac output" syndrome usually remain poorly expressed until the late stages of the disease.

A rare associated symptom of aortic stenosis is gastrointestinal bleeding, both idiopathic and due to angiodysplasia of the vessels of the intestinal submucosa, described by Neusle in 1958. The most common source of bleeding is the ascending colon. A feature of these bleedings is their disappearance after surgical correction of the defect.

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

Course of aortic stenosis

Timely identification of the onset of symptoms is the cornerstone of the management of patients with aortic stenosis. This is due to two factors. Firstly, the onset of symptoms dramatically accelerates the progression of the defect, aggravates the condition of patients and significantly reduces the average life expectancy. The rate of progression of aortic stenosis is highly variable. The average increase in the transaortic gradient per year is 7 mm Hg, the peak velocity of transaortic flow is 1 m/s, and the average decrease in the area of the aortic orifice varies from 0.02 to 0.3 cm ² per year. CAS has a significantly faster rate of progression, in contrast to the "rheumatic" or bicuspid aortic valve. The main predictors of rapid progression are concomitant coronary heart disease, AT, hyperlipidemia, as well as old age and smoking. A study of the natural course of the disease in symptomatic patients has established that the prognosis is influenced not only by the very fact of the appearance of symptoms, but also by their combination and the rate of increase in severity, which is accompanied by a sharp increase in cases of sudden death.

Medical history of aortic stenosis

Patient S., 72 years old, was admitted with complaints of cough with mucous sputum, shortness of breath at rest, and discomfort in the left half of the chest. In the last 2 years, she has been bothered by shortness of breath when walking, during the year - discomfort behind the sternum during physical exertion, and rarely - dizziness. She associates the deterioration of her condition with cooling. When the temperature rose to 37.2 °C, shortness of breath increased and a cough appeared. Outpatient treatment with antibacterial agents was ineffective. She was referred to hospital by a local therapist with the diagnosis: right-sided pneumonia, coronary heart disease: angina pectoris II FC. Hypertension stage II. NC II st.

On examination, the condition is severe. Orthopnea. Acrocyanosis. Swelling of the feet and shins, respiratory rate - 30 per minute. Breathing is not heard in the lungs to the right of the angle of the scapula. The borders of the heart are shifted to the left. Heart sounds are muffled, a soft systolic murmur is heard at the apex of the heart. The liver is 1.5 cm below the edge of the costal arch,

In the clinical blood test: hemoglobin - 149 g/l, erythrocytes - 4.2x10 ⁹ /l, leukocytes - 10.0x10 ⁹ /l, polymorphonuclear - 5%, segmented - 49%, eosinophils - 4%, basophils - 2%, lymphocytes - 36%, macrophages - 4%, ESR - 17 mm/h. In the biochemical blood test: 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, VLDL cholesterol - 0.26 mmol / l, lipoprotein-a (LPa) - 25 mg / dl, atherogenic index - 3.7, total bilirubin 15.8 μmol / l, AST - 38 U / l, ALT - 32 U / l, calcium - 1.65 mmol / l, alkaline phosphatase - 235 U / l, creatine phosphokinase (CPK) - 130 IU/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.

2D echocardiography: the aorta is compacted, not dilated. Calcifications at the base of the cusps of the fibrous ring of the aortic valve. The cusps are compacted, mobile, the commissures are not fused. Aortic valve stenosis (systolic opening of the cusps is 8 mm, transaortic pressure gradient is 70.1 mm Hg, maximum velocity is 4.19 m/s). The mitral valve is unchanged. End-diastolic dimension (EDD) is 50 mm, end-systolic dimension (ESD) is 38 mm, end-diastolic volume (EDV) is 155 ml, end-systolic volume (ESV) is 55 ml. Signs of pulmonary hypertension, thickness of the posterior wall of the left ventricle is 12 mm, interventricular septum is 14 mm. The ratio of the early diastolic filling velocity (peak E, m/s) to the late diastolic filling velocity of the left ventricle (peak A, m/s) (E/A) is 0.73, EF is 54%. AS is 23%. No hypo- or akinesia zones were detected.

Treatment with diuretics, beta-blockers in small doses, ACE inhibitors, and nitrates was started. The patient died on the second day of hospitalization.

Clinical diagnosis: severe calcified aortic stenosis, coronary artery disease, atherosclerotic cardiosclerosis NC II B, III FC.

At autopsy: the lungs are edematous, with a brownish tint, in the right pleural cavity there is 1000 ml of serous fluid, in the pericardial cavity - 100 ml. The blood supply to the heart is uniform. The coronary arteries are stenotic with fibrous and calcified plaques by 20-30%. The mitral valve cusps are unchanged. The perimeter of the mitral orifice is 8 cm. The aortic valve cusps are calcified, deformed, and immobile.

The aortic orifice is slit-like. The valves of the right heart are without visible pathology. The left ventricle contains myocardium with layers of fibrous tissue. Pronounced hypertrophy of the left ventricle myocardium (heart weight is 600 g, left ventricular wall thickness is 2.2 cm).

Subsequently, a microscopic study of sections of the aortic valve cusps of patients with CAS was carried out.

Pathological diagnosis: severe calcified aortic valve stenosis, eccentric hypertrophy of the left ventricular myocardium, venous congestion of internal organs, small focal diffuse cardiosclerosis.

The patient died from heart failure as a complication of calcified aortic valve disease.

In this clinical example, the reason for seeking medical help was signs of progressive heart failure. Given the hemodynamically significant stenosis, the risk of sudden death in this patient was very high. It is noteworthy that the pathomorphological examination showed no significant stenosis of the coronary arteries, therefore, the clinical symptoms of the disease (discomfort in the heart, shortness of breath, dizziness) were most likely due to CAS, not ischemic heart disease. This assumption is supported by the absence of previous myocardial infarctions and/or acute cerebrovascular accidents (ACVA), dyslipidemia, diabetes mellitus, and other risk factors for ischemic heart disease.

The involvement of systemic calcium metabolism parameters was noted, consisting in an increase in the values of g-thyroid hormone, alkaline phosphatase, a decrease in total calcium with a normal concentration of vitamin D, which was associated with the expansion of the heart cavities and the presence of eccentric hypertrophy of the left ventricle myocardium, confirmed at autopsy. Histomorphological studies of the aortic valve cusps revealed lymphohistiocytic infiltration, neoangiogenesis, accumulations of labrocytes and foci of calcification. The described picture testifies in favor of the regenerative, rather than degenerative nature of aortic valve calcification in patients with CAS and requires further study.

Taking into account the difficulties encountered by practicing physicians and the peculiarities of the revision of ICD-10, below we provide examples of the formulation of clinical diagnosis of various variants of CAS:

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