Aortic stenosis

From WikiLectures

Template:Infobox - genetic disorder__BEZOBSAHU__ náhled|290px|right|Aortic stenosis – rheumatic heart Stenosis (narrowing) of the aorta occurs in three locations relative to the aortic valve: subvalvular, valvular (most common) and supravalvular . The diffuse narrowing of the ascending aorta is called hypoplasia.

Stenosis is most often congenital, but can also occur due to degenerative changes (often on the congenital bicuspid valve) or after rheumatic endocarditis as part of a combined aorto-mitral defect. Aortic stenosis is a barrier to blood flow from the left ventricle, causing concentric left ventricular hypertrophy, subendocardial fibrosis and subsequent ischemia. The myocardium is more prone to malignant arrhythmias by re-entering the circuit around the ligament. In the late phase of AoS, the left ventricle dilates and systolic dysfunction occurs .

Critical narrowing in the newborn has similar symptoms as a hypoplastic left heart:

At a later age, aortic stenosis may be asymptomatic, the first manifestations of which are syncope or sudden death. Syncope is caused by a critical decrease in minute output during exertion or obstruction of the left ventricular outflow. A dangerous sign of the threat of sudden death is the development of ischemic ECG manifestations. In the natural course, aortic regurgitation occurs over time [1]

Significant stenosis has an aortic orifice area < 1 cm2, mean gradient> 50 mmHg.[2]

The clinical picture[edit | edit source]

  • Curious tip (left ventricular hypertrophy).
  • Tactile vortex over the aortic orifice.
  • Dull I. echo.
  • Early systolic click on the tip and above the aorta (unless the valve is calcified).
  • Ejection systolic murmur over the aorta, crescendo-decrescend, with propagation to the carotid arteries.
  • Heart rate: slow pulse, poor palpation (pulsus parvus et tardus), small systolic-diastolic BP range.

Among the clinical triad includes:

  1. angina pectoris,
  2. exertional dyspnea,
  3. syncope and arrhythmias.

Diagnosis[edit | edit source]

Treatment[edit | edit source]

  • Surgical: aortic valve replacement. After surgery, the systolic and diastolic function of the LV improves. Patients at high surgical risk may undergo valve replacement by TAVR - transcatheter aortic implantation of the aortic valve. In older individuals, bioprostheses are used more. Their lifespan is 10-15 years and the advantage is that the patient does not have to be anticoagulated for a long time. Mechanical prostheses have a longer service life with the disadvantage of long-term anticoagulation. Another possibility, Ross's operation consists in inserting an implanted self-valve into the patient's aortic position, followed by a pulmonary bioprosthesis.
  • Drug treatment: supportive treatment as for heart failure. Studies have not confirmed that statins could inhibit the progression of AoS. Arteriolodilatory drugs - nitrates, iACE could reduce systemic pressure.

Prevention of complications - mainly we prevent complications of endocarditis - proper treatment of respiratory infections is important. A larger one-time load is not recommended for children.

Summary video[edit | edit source]

view|mid|upright=1.6|Video in English, definition, patogenesis, symptoms, complications, treatment.

Auscultation[edit | edit source]

References[edit | edit source]

Related articles[edit | edit source]

External links[edit | edit source]

Sources[edit | edit source]

References[edit | edit source]

  • Incomplete citation of publication. POVÝŠIL, Ctibor. Speciální patologie. I. díl, Patologie oběhového, krevního, mízního a dýchacího ústrojí. Karolinum, 2006. 98 pp. pp. 23. ISBN 80-246-0951-7.
  1. Incomplete citation of publication. ČEŠKA, Richard. Interna. TRITON v Praze, 2015. pp. 116-117. ISBN 9788073878955.
  2. ČEŠKA, Richard, ŠTULC, Tomáš, Vladimír TESAŘ a Milan LUKÁŠ, et al. Interna. 3. vydání. Praha : Stanislav Juhaňák - Triton, 2020. 964 s. ISBN 978-80-7553-780-5.