Aortic regurgitation

from Wikipedia, the free encyclopedia
Classification according to ICD-10
I35.1 Aortic regurgitation
ICD-10 online (WHO version 2019)

In medicine, aortic valve insufficiency or aortic insufficiency for short is the inadequate closure of the aortic valve of the heart with the resulting diastolic return of blood from the aorta into the left ventricle.

Mild forms of aortic regurgitation can often be seen on an ultrasound scan of the heart. Moderate and severe forms have become rarer in recent years, as rheumatic fever, the most common cause of this second most common valve disease, is recognized earlier and treated with antibiotics .

causes

Inflammatory processes are the most common cause of aortic regurgitation. Bacterial inflammation ( endocarditis ) can affect the aortic valve and cause insufficiency by destroying its structure. Rheumatic valve defects arise as a late consequence of an infection. In the event of an infection, the body forms antibodies against the bacteria (usually streptococci ); these antibodies can then attack the tissue of the heart valves and cause shrinkage or accelerated wear and tear. These valve defects have become rare in Central Europe, as the bacterial infections are usually treated early enough with antibiotics . Other autoimmune diseases can lead to aortic valve insufficiency in a similar way. Aortic valve insufficiency can also result from overstretching the valve elements (valve pockets ); this mostly affects people over the age of 60.

Congenital aortic valve insufficiency is rare. Congenital valve defects, such as the bicuspid or unicuspid anchoring (double-sided or single-sided) of the aortic valve can lead to relevant insufficiency as early as the 2nd or 3rd decade due to accelerated wear and tear. This is particularly true of the aortic valves, which in infancy or early childhood are caused by congenital aortic valve stenosis with balloon valvuloplasty (the "bursting" of the narrowed aortic valves with the help of a balloon catheter) or a commissurotomy (the surgeon cuts or splits the fused heart valves with the finger or the surgeon) an instrument).

Another important mechanism that leads to aortic valve insufficiency is the expansion of the aorta ( aortic aneurysm ), especially the ascending aorta (ascending aorta). The flap is then pulled apart, so to speak, and the flap pockets lose the necessary contact. Common causes for this are atherosclerosis or connective tissue diseases (e.g. Marfan syndrome or Ehlers-Danlos syndrome ). Recently, inflammation of the aorta in the context of autoimmune diseases has also been observed increasingly. A special form is mesaortitis luetica (syn. Mesaortitis luica, mesaortitis syphilitica) in syphilis . Even with the aortic dissection is a distortion and leakage of the valve can occur.

Pathophysiology

Depending on the extent of chronic aortic valve insufficiency and the level of voiding resistance in the aorta, the return flow volume can be up to 2/3 of the ejection volume (normal stroke volume 40–70 ml) of the left ventricle, sometimes also referred to as diastolic aortic tap syndrome. This leads to a characteristically high amplitude of blood pressure . This pendulum blood increases the diastolic filling of the left ventricle, especially when the heart rate is too low, and leads to volume loading of this heart section with the consequence of eccentric hypertrophy . The ratio of wall thickness to volume initially remains within the norm. Increased extensibility enables the left ventricle to absorb larger volumes without increasing the end-diastolic pressure. After a course that often lasts for decades, the overstrain leads to muscular dysfunction of the heart muscle, gradually leading to severe left heart failure . - Instead of the return flow volume one also speaks of the blood return flow, the pendulum volume, the return flow (return flow, reflux) or the regurgitation.

In the case of acute aortic regurgitation (e.g. after aortic valve rupture, valve perforation or sudden inability to close the aortic dissection), there is an immediate increase in end-diastolic pressure in the left ventricle (possibly up to 60 mm Hg!). This leads to pulmonary congestion, pulmonary edema and a reduction in cardiac output . Due to the high pressure increase, the mitral valve closes prematurely - a characteristic sign of severe AI. In contrast to chronic AI, the blood pressure amplitude can remain the same, especially when the patient is tachycardiac .

Symptoms and Examination Findings

Lighter forms are not noticed by the person concerned. In more pronounced forms, shortness of breath is the decisive symptom. Other possible symptoms or findings are:

  • large blood pressure amplitudes with low diastolic blood pressure e.g. B. 150/60 mm Hg
  • weakened 2nd heart sound in severe insufficiency
  • Heart murmurs :
  1. Early diastolic, "pouring" decrescendo noise directly after the 2nd heart sound with punctum maximum above the Erb point
  2. Austin-Flint sound , rumbling mid-diastolic to presystolic sound with punctum maximum above the apex of the heart
  • Pulse: pulsus celer et Altus (et frequens) ( water hammer pulse ) with extra beats , Homo pulsans , pulssynchronem nod ( Musset-mark ), clearly visible Karotidenpulsation (Corrigan-mark), visible Kapillarpuls (Quincke's characters or Quinckescher Kapillarpuls)
  • mostly noticeably pale complexion
  • strong left widening of the heart during percussion ("shoe shape")
  • ECG changes with signs of left heart strain ( Sokolow-Lyon index )
  • X-ray image : enlargement of the left ventricle as a so-called "shoe shape", rounded apex of the heart
  • Fever in endocarditis

Diagnosis

Severity classification

Severity I ° II ° III ° IV °
Blood pressure amplitude <60 mmHg increased, on average 75 mmHg mean 110 mmHg, in diastole <60 mmHg like III
EKG Link type Left ventricular hypertrophy, possible damage Left ventricular hypertrophy and injury like III, possibly atrial fibrillation
Chest x-ray Normal heart shape, slight aortic elongation, increased pulsations Left ventricle enlarged Aortic heart configuration, posterior space narrowed Large LV, pulmonary congestion with beginning stress on the right heart
Echocardiography no changes to the left ventricle Left ventricle slightly dilated, normal wall thickness LV dilated, increased contraction amplitude, normal wall thickness, increased muscle mass Very large LV, septum thickness> 0.7 cm, in acute AI premature mitral valve closure, normal wall thickness, very large muscle mass
Color Doppler Small insufficiency jet to the middle of the left ventricle Moderate jet of insufficiency up to the middle of the left ventricle 50–75% return blood flow to the apex of the heart 75% blood return to the apex of the heart
Cardiac catheter Backflow of blood up to the middle of the LV visible Immediately filled after the administration of contrast medium in the aorta LV, but the contrast density is lower than in the aorta Filling of the entire LV with contrast density like aorta Contrast density in the LV higher than in the aorta, e.g. T. Mitral regurgitation

therapy

Therapy is not required if the reflux is low. There is no evidence of effectiveness for drug therapy with afterload -lowering drugs ( calcium antagonists , nitro preparations , ACE inhibitors, etc.) unless arterial hypertension is also present. Surgical treatment with an artificial heart valve should be considered if symptoms (e.g. shortness of breath) or signs of overloading of the left heart ( ejection fraction less than 50%, end-systolic diameter of the left ventricle greater than 50 mm). Acute aortic valve insufficiency usually requires immediate surgery.

The long-term effective therapy options normalize the function of the valve. Traditionally, the standard treatment is to replace the aortic valve ; A mechanical heart valve is recommended for younger people and a biological prosthesis for older people (> 60 to 65 years). The bioprostheses are made of biological material, either a porcine aortic valve or a stitched flap of other material such as tissue of an animal pericardium (pericardium). In the last few decades, reconstructive procedures have been developed for many causes of aortic regurgitation. Aortic valve reconstruction is particularly promising in the presence of an aortic aneurysm, bicuspid aortic valve or overstretching of a valve pocket and leads to good long-term results. In contrast, the implantation of a valve prepared by tissue engineering is still experimental. The same applies to the use of catheter valves.

See also

literature

  • Hans Joachim Schäfers: Clinical basics of cardiac and thoracic surgery . ABW Wissenschaftsverlagsgesellschaft; 4th update u. additional edition (October 1, 2011)
  • Hans Joachim Schäfers. Current treatment of aortic regurgitation . UNI-MED; Edition: 1st edition (August 26, 2013)
  • Guidelines on the management of valvular heart disease. In: European Heart Journal . The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology, 2007, accessed March 26, 2009 ( PMID 17259184 ).
  • S2k guideline for aortic valve insufficiency of the German Society for Pediatric Cardiology (DGPK). In: AWMF online (as of 2013)
  • Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York et al. 1999, ISBN 3-540-65024-5 , pp. 260-268.
  • Klaus Holldack, Klaus Gahl: Auscultation and percussion. Inspection and palpation. Thieme, Stuttgart 1955; 10th, revised edition ibid 1986, ISBN 3-13-352410-0 , pp. 163-167, 171 f., 178 f. and 196 f.

Web links

Individual evidence

  1. ↑ balloon expansion
  2. ↑ FA Flachskampf, W. Fehske, H. Reichenspurner, K. Rybak, WG Daniel: Commentary on the European guideline "valvular heart disease" . In: German Society for Cardiology (Hrsg.): The cardiologist . tape 3 , no. 2 . Heidelberg February 17, 2009, p. 101-107 ( dgk.org [PDF; accessed March 26, 2009]). doi: 10.1007 / s12181-008-0133-6 ISSN 1864-9718  
  3. ↑ Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York et al. 1999, ISBN 3-540-65024-5 , pp. 260-268 ( aortic insufficiency ); here: pp. 264–266.
  4. ↑ Hans Joachim Schäfers: Current treatment of aortic regurgitation. In: UNI-MED. August 26, 2013.
  5. ^ Tissue engineering: (Tissue Engineering) of heart valves. In: Deutsches Ärzteblatt. February 25, 2000, accessed October 11, 2014 .