Acquired aortic stenosis
| Classification according to ICD-10 | |
|---|---|
| I35.0 | Aortic stenosis |
| I35.2 | Aortic stenosis with insufficiency |
| ICD-10 online (WHO version 2019) | |
The acquired aortic stenosis , one by inflammation ( endocarditis ), or calcification ( calcification ) caused narrowing of the aortic valve , is now the most common valvular heart disease in humans. The prevalence among those over 75 years of age is more than 3%. The congenital aortic stenosis is described in a separate article, as causes and treatment are very different.
Forms and causes
The most common form of acquired aortic stenosis is primary degenerative, calcified aortic stenosis , which occurs mainly in the elderly. It is caused by progressive sclerosis (commonly known as “calcification”) of the aortic valve, which leads to degeneration and calcification of the valve pouches and gradually to stenosis. The aortic valve sclerosis itself is the result of an inflammatory reaction , the course of which is very similar to that of arteriosclerosis (“hardening of the arteries”). Risk factors of this form are kidney failure and hypercalcaemia, i.e. too high a calcium concentration in the blood. There are also some controversial risk factors such as smoking , high blood pressure and diabetes ( diabetes mellitus ). Genetic factors probably also play a role in the development of aortic valve sclerosis. Certain alleles , such as the B allele of the vitamin D receptor, appear to increase the risk of sclerotherapy.
The second most common cause is misalignment of the aortic valve. Usually the aortic valve consists of three crescent-shaped pockets. In the case of a so-called bicuspid aortic valve , which consists of only 2 crescent-shaped pockets, an incorrect hemodynamic load leads to secondary aortic valve sclerosis with calcification and finally to aortic valve stenosis.
Another cause is acquired aortic valve stenosis as a late sequela of rheumatic fever .
Pathophysiology
The left ventricle ( ventricle , see heart ) pumps blood through the aortic valve into the thoracic artery ( aorta ) with each heartbeat . The opening area of a healthy aortic valve in adults is about 3–4 cm². A narrowing of the aortic valve means that increasingly higher pressure has to be generated in order to convey the same amount of blood. A narrowing to about 25% of the normal opening area results in a significant pressure load on the left ventricle. Severe aortic stenosis, which can be expected to cause symptoms, typically has an opening area of less than 0.75-1 cm². During the valve opening, there is usually a mean pressure difference between the left ventricle and aorta of more than 50 mmHg .
Natural course and symptoms
Since the valve constriction usually only increases slowly or remains unchanged, the heart can adapt to the increased pressure load on the left ventricle by thickening the heart muscle ( hypertrophy ). The valve defect often remains asymptomatic for years and decades .
The occurrence of the typical symptoms, however, is a serious warning:
- Difficulty breathing during exercise or even under resting conditions ( dyspnea ) occurs due to left ventricular hypertrophy , which means that the left heart muscle has grown so much that the pressure in the pulmonary veins increases due to the resulting reduced elasticity of the left ventricle. As a result, the pulmonary circulation is no longer as frequent and what is known as dyspnea occurs.
- A feeling of tightness in the chest ( angina pectoris ), initially mostly during physical exertion, indicates an insufficient supply of the pressure-loaded hypertrophied heart muscle. The mean life expectancy is then about 5 years.
- Sudden loss of consciousness ( syncope ), also occurring mostly during exercise can recognize that the left ventricle can no longer promote through the stenotic aortic valve to the increased demand for blood. The mean survival time is reduced to about 3 years.
- Acute heart failure with pulmonary congestion or even pulmonary edema indicates the beginning of a critical phase with insufficient reserves of the heart muscle. The mean life expectancy is then significantly reduced at around 2 years.
The common occurrence of dyspnea , angina pectoris and syncope is called the triad of symptoms of aortic valve stenosis. If bleeding from the colon as a result of angiodysplasia occurs at the same time , it is called Heyde's syndrome .
The prognosis of an asymptomatic, mostly accidentally discovered aortic valve stenosis cannot be predicted with certainty at first. On average, the valve opening area decreases annually by about 0.12 cm², but more than half of the patients show no or only very little deterioration over the years. The extent of the valve calcifications and, in particular, the course in the first few years can provide clues for a prediction.
Diagnosis
The simplest examination for suspected aortic stenosis is to eavesdrop with a stethoscope ( auscultation ). Typical noise finding of aortic stenosis as in congenital aortic stenosis (in the phonocardiography spindle-shaped) systolic murmur ( systolic ), the above Aortenareal (immediately to the right of the upper sternum third, 2. ICR is lautesten on the right) and in the carotid arteries is propagated. This sound is often described as harsh or hissing. Often a 4th heart sound can be heard. In severe stenoses, the 1st and 2nd heart sounds are almost always very faint or not at all. In the case of moderate to severe stenosis, the palpable findings on the carotid artery (carotid pulse) are usually characteristically changed: With the so-called pulsus parvus et tardus, the pulse wave feels softer due to the changed blood flow. A palpable buzzing on the chest wall to the left of the sternum almost always indicates a severe stenosis.
If there is a suspicious noise finding, an ultrasound examination of the heart ( echocardiography ) is carried out, with the help of which the aortic valve can usually be reliably assessed. If the sound conditions are sufficiently good, the aortic stenosis can already be reliably quantified by calculating the pressure gradients and the valve opening area (KÖF) using the Doppler technique.
A cardiac catheter examination including coronary angiography is almost always carried out for patients in need of surgery in order to rule out accompanying coronary artery disease before the heart operation , which would otherwise require a simultaneous bypass operation. If the echocardiography results are unclear, the exact extent of the aortic stenosis can also be determined during the cardiac catheter examination.
Complications
In the event of misdiagnosis, too late a diagnosis, a very acute occurrence of a previously asymptomatic aortic valve stenosis or inadequately rapid action, small blood clots can develop due to the turbulent flows in the calcified aortic valve, which, for example , can clog the fine capillaries of the brain and lead to a stroke. Cardiac arrhythmias can also occur, accompanied by sudden cardiac death.
therapy
Asymptomatic aortic valve stenosis does not usually require any special treatment, but should be checked regularly by the cardiologist. If, based on the observation of the progress, it is suspected that severe aortic stenosis will soon become symptomatic, surgery can be advised at this point in time.
surgery
Symptomatic acquired aortic valve stenosis usually requires surgical treatment. The diseased valve is removed and replaced with a biological or artificial valve prosthesis . This operation is also carried out on very old people (up to the age of 90), because the prognosis can be improved for them too . In the 1990s, great hopes had been placed in the technically feasible balloon dilatation of the aortic valve via a cardiac catheter , which could save the patient the costly heart operation. Today, however, this method is limited to patients with a very high surgical risk, since after successful dilation a narrowing usually occurs again very quickly, and is increasingly being displaced by procedures of minimally invasive valve replacement.
In recent years it has also become possible to implant a replacement valve ( transfemoral aortic valve replacement, transcatheter aortic valve implantation (TAVI) or transcatheter aortic valve implantation) into a narrowed aortic valve using an interventional catheter procedure (via access via the inguinal vessels or via a small thoracic incision ). transapical valve replacement). The implantable valve is pressed into the calcified valve by means of a balloon (balloon-dilated valve) or it unfolds itself (self-expanding valve). This procedure is currently only used in patients for whom open aortic valve surgery appears to be too risky. In a study with selected, particularly severely ill (and thus conventionally inoperable) patients, the one-year mortality rate was reduced from 50.7% (without surgery) to 30.7% (catheter procedure).
Medication
There is no reliable indication for drug treatment. Patients with heart failure for whom surgery is not an option are usually given diuretics and, if indicated, digitalis glycosides . The use of diuretics must be carried out very carefully, since in aortic stenosis the cardiac output is maintained via the increased intravascular volume (preload). The use of circulatory drugs takes place very carefully in extremely low initial doses. ACE inhibitors are contraindicated in aortic stenosis, as are calcium antagonists and nitrates. The reason for this is a reduced perfusion of the coronary arteries due to the lowering of the afterload in the circulation with a simultaneous increased preload and thus increased wall tension. In the case of atrial fibrillation , anticoagulation is carried out to prevent embolism. The attempt to stop the progressive narrowing of calcified aortic stenoses by statins cannot yet be conclusively assessed due to contradicting study results.
General measures
Asymptomatic patients with a mild aortic stenosis can exercise normally; if the stenosis is moderate, competitive sports should be avoided. In the case of severe stenosis, high and sudden physical exertion is not recommended, but endurance sports may be permitted if the stress ECG results are normal .
Web links
Literature and Sources
- H. Renz-Polster among others: Basic textbook internal medicine. 4th edition. Urban & Fischer-Verlag, Munich 2008, ISBN 978-3-437-41053-6 .
- Thomas Christen among others: The aortic valve stenosis in adults. In: Switzerland Med Forum. 6, 2006, pp. 626-632. Part 1 (PDF; 470 kB) and Part 2 (PDF; 204 kB)
- Wolfgang Scheider: Aortic valve stenosis. In: Medical Practice. 2007.
Individual evidence
- ^ Klaus Holldack, Klaus Gahl: Auscultation and percussion. Inspection and palpation. 1986, p. 196 f.
- ↑ Aortic stenosis: valve replacement via catheter lowers mortality rate. ( Memento of the original from September 26, 2010 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. In: Deutsches Ärzteblatt. September 23, 2010.
- ^ A b W. G. Daniel et al.: Valve vitia in adulthood. In: Clinical Research in Cardiology . 95, 2006, pp. 620-641. PMID 17058154 .
- ↑ L. Thiago, S. Tsuji et al: Statins for aortic valve stenosis. Cochrane Library, September 5, 2015.
