Aortenklappeninsuffizienz

The aortic valve (AI) is the inability of the aortic valve closing, which leads to a return flow of blood from the aorta into the left ventricle during diastole. The causes include degeneration of the heart valves and dilatation of the aortic root (with or without bicuspid valve), rheumatic fever, endocarditis, myxomatous degeneration, dissection of the aortic root and connective tissue disorders (eg. As Marfan syndrome) or rheumatic diseases. Symptoms include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, palpitations and chest pain. Signs are a high pulse amplitude and an early diastolic murmur. The diagnosis is made because of the physical examination and echocardiography. The treatment is surgical aortic valve replacement or by Aortenklappenrekonstruktion. The effectiveness of percutaneous valve replacement is evaluated.

The aortic valve (AI) is the inability of the aortic valve closing, which leads to a return flow of blood from the aorta into the left ventricle during diastole. The causes include degeneration of the heart valves and dilatation of the aortic root (with or without bicuspid valve), rheumatic fever, endocarditis, myxomatous degeneration, dissection of the aortic root and connective tissue disorders (eg. As Marfan syndrome) or rheumatic diseases. Symptoms include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, palpitations and chest pain. Signs are a high pulse amplitude and an early diastolic murmur. The diagnosis is made because of the physical examination and echocardiography. The treatment is surgical aortic valve replacement or by Aortenklappenrekonstruktion. The effectiveness of percutaneous valve replacement is evaluated.

(See also Overview of the heart valve diseases.) The aortic valve insufficiency (AI) is the final failure of the aortic valve, leading to a return flow of blood from the aorta into the left ventricle during diastole. The causes include degeneration of the heart valves and dilatation of the aortic root (with or without bicuspid valve), rheumatic fever, endocarditis, myxomatous degeneration, dissection of the aortic root and connective tissue disorders (eg. As Marfan syndrome) or rheumatic diseases. Symptoms include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, palpitations and chest pain. Signs are a high pulse amplitude and an early diastolic murmur. The diagnosis is made because of the physical examination and echocardiography. The treatment is surgical aortic valve replacement or by Aortenklappenrekonstruktion. The effectiveness of percutaneous valve replacement is evaluated. Etiology The AI ??can be acute (very rare) or chronic. The primary cause of acute AortenregurgitationI are infectious endocarditis dissection of the ascending aorta, the primary causes of chronic aortic insufficiency in adults are degeneration of the aortic valve and root (with or without bicuspid valve) Rheumatic fever Infectious endocarditis myxomatous degeneration injuries Thoracic aortic aneurysm in children is the ventricular septal defect with prolapse the aortic valve is the most common cause of chronic aortic regurgitation. Rarely is the aortic regurgitation by a seronegative spondyloarthropathy (ankylosing spondylitis, reactive arthritis, Psoriasarthritis), rheumatoid arthritis, systemic lupus erythematosus, a Arthriitis associated with ulcerative colitis, a syphilitic (syphilitic) aortitis, an osteogenesis imperfecta, supravalvular aortic stenosis, or discrete membranous subaortic stenosis, a Takayasu’s arteritis, a rupture of the sinus of Valsalva, an acromegaly or a giant cell (temporal) -Arteriitis caused. An AI due to myxomatous degeneration can develop in patients with Marfan syndrome or Ehlers-Danlos syndrome. Pathophysiology of aortic regurgitation occurs a volume overload of the left ventricle (LV), since the LV takes up the regurgitated during diastole blood from the aorta in addition to the blood from the left atrium. In acute AR, the LV does not have time to expand and accommodate the increased volume, which then causes a rapid increase in left ventricular pressure and subsequent pulmonary edema and reduced cardiac output. In chronic AR, LV hypertrophy and dilation can be done gradually, so that the normal left ventricular pressure and cardiac output can be maintained. Finally, a decompensation and developed causing arrhythmias, impaired ventricular function and heart failure. Aortenklappeninsuffizienz var model = {thumbnailUrl: ‘/-/media/manual/professional/images/aortic_regurgitation_high_blausen_de.jpg?la=de&thn=0&mw=350’ imageUrl: /-/media/manual/professional/images/aortic_regurgitation_high_blausen_de.jpg ‘? lang = en & thn = 0 ‘, title:’ aortic ‘description:’ ‘credits”, hideCredits: false, hideTitle: false, hideFigure: false, hideDescription: true}; var panel = $ (MManual.utils.getCurrentScript ()) Closest ( ‘image-element-panel.’). ko.applyBindings (model, panel.get (0)); Symptoms and signs Acute aortic regurgitation caused symptoms of heart failure (dyspnea, fatigue, weakness, edema) and cardiogenic shock (low blood pressure with the resulting multi-system organ damage). The chronic aortic regurgitation is typically asymptomatic for years; an increasing exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea and palpitations develop insidiously. Symptoms of heart failure correlate poorly with objective measurements of left ventricular function. A chest pain (angina) affects only 5% of patients who do not have co-existing coronary artery disease (CAD); if it occurs, especially at night. Patients may present with endocarditis (eg., Fever, anemia, weight loss, embolic phenomena), because the altered aortic valve predisposed to bacterial colonization. The findings vary with the severity and acuity. The findings in aortic regurgitation reflect heart failure and cardiogenic shock and usually include tachycardia, cool extremities, Lungenknistern and low blood pressure. The first heart sound (S1) is usually missing (because the diastolic pressure in the aorta and LV offset) and a third heart sound (S3) often occurs. An AI sound may be missing, even if the AI ??is hard, but an Austin Flint murmur occurs frequently. If the chronic disease progresses, increased systolic blood pressure, while diastolic blood pressure drops, resulting in a high pressure amplitude. Over time, the LV chest wall impact can be stronger and higher in amplitude and down and are moved laterally; with a lowering of the systolic entire left Sternumseite this leads to a rocking movement of the left chest. A systolic apical buzz or a thrill through the carotid arteries can be palpated in the later stages of AI; it is caused by the high ejection stroke volume and the low diastolic aortic pressure. The auscultatory findings are a normal S1 and a non-split, louder, sharp 2. heart sound (S2), which is caused by the increased elastic Aortenrückstoß. The murmur of AI is often inconspicuous. The noise is blowing, high frequency, diastolic, and has a decrescendo character, it starts soon after the aortic component of S2 (A2) and it is the loudest in the 3rd or 4th ICR. The sound is best heard with the diaphragm of the stethoscope when the patient while leaning forward and holding its breath at end expiration. The noise increases in volume during maneuvers that increase the afterload (z. B. squat position, isometric handgrip). If the AI ??is leichtgradig, the noise may occur even in early diastole. If the diastolic LV pressure is very high, the sound is short because of the aortic and LV pressure sooner converge in diastole. Sound of a normal S1 followed by a sharp or beating S2 and a blowing, high-frequency, diastolic decrescendo noise. var player panel = $ (MManual.utils.getCurrentScript ()) Closest ( ‘player..’); ko.applyBindings ({MediaUrl ‘/-/media/manual/professional/sounds/aortic_regurgitation_de.mp3?la=de&thn=0&mw=350’, Mime Type: ‘audio / wav’}, playerPanel.get (0)); Aortic valve insufficiency recording provided by Jules Constant, M.D. Other pathological noises are a Vorwärtsaustreibungs – and reverse flow noise ( “to-and-fro”), a Austreibungsklick soon after S1 and a Aortenaustreibungsgeräusch. A diastolic noise that is heard near the axilla or in the middle left side of the thorax (Cole-Cecil-noise) caused by the fusion of the Aortengeräusches with S3, which is the consequence of simultaneous filling of LV from the left atrium and the AI , A medium to late diastolic rumble, which is heard at the apex (Austin Flint murmur), can be caused by the rapid current insufficiency in the LV, and causes a vibration of the mitral valve during the maximum atrial flow; This noise mimics the diastolic murmur of mitral stenosis. S1 is quiet; S2 is overlaid by a slight insufficiency sound and a loud, low frequency late diastolic noise. The diastolic murmur mimics a mitral after and the vibration of the mitral valve or a low concentration by rapid failure current is attributed. var player panel = $ (MManual.utils.getCurrentScript ()) Closest ( ‘player..’); ko.applyBindings ({MediaUrl ‘/-/media/manual/professional/sounds/austin_flint_murmur_de.mp3?la=de&thn=0&mw=350’, Mime Type: ‘audio / wav’}, playerPanel.get (0)); Austin Flint murmur recording provided by Jules Constant, M.D. Other characters are not common; the sensitivity and specificity are low or unknown. Visible signs are a head swings (Musset’s sign), a pulsation of Fingernägelkapillaren (angioneurotic character best seen in exercising a slight pressure) or the uvula (Mueller characters). Tactile signs are a high pulse amplitude with a rapid rise and fall (slap, water hammer – or coincident pulse) and a pulsation of the carotid arteries (Corrigan mark), retinal arteries (Becker-characters), the liver (Rosenbach-mark) or the spleen ( Gerhard characters). The blood pressure findings can have a popliteal systolic pressure difference of ? 60 mmHg between the popliteal artery and the brachial artery (Hill’s sign) show and a drop in diastolic blood pressure of> 15 mmHg at lifting the arm (Mayne characters). Auscultatory signs are a sharp tone, via the femoral artery (Pistolenschusston or grape character) is heard, and a systolic and a diastolic propagation distal propagation proximal arterial compression in the femoral artery (Duroziez characters). Diagnosis Echocardiography diagnosis of aortic regurgitation is suspected aufgund the medical history and the findings on physical examination and confirmed by echocardiography. The Doppler echocardiography is the investigation of choice to detect the strength of the regurgitant blood flow and quantify and determine the general severity of AI. The two-dimensional echocardiography can quantify the size of the aortic root and the anatomy and LV function. A severe aortic regurgitation is believed due to the following: color Doppler beam width> 65% of the diameter of the LV outflow tract vena contracta> 6 mm (the narrowest diameter of the liquid flow, if an abnormal flap opening) Holodiastolische flow reversal in the abdominal aorta regurgitant> 60 ml / heartbeat Regurgitationsfraktion> 50% In the event of a serious AI (and therefore the need for a surgical procedure) indicated by each of the following findings decompensation of the left ventricle: end-systolic LV volume> 60 ml / m2 end-systolic LV diameter> 50 mm LV -Ejektionsfraktion (LVEF) <50% echocardiography can also determine the severity of pulmonary arterial hypertension secondary to LV failure, and pericardial vegetations seen (eg. B . In aortic dissection) and provides information on the prognosis. Isthmus stenosis is connected to the bicuspid valve, and is determined by the placement of the ultrasonic transducer to the choke groove. A transesophageal echocardiography provides additional information for differentiation of aortic dilatation and valve anatomy, which is particularly useful when surgery is contemplated. If the aorta is enlarged, CT or MRI are recommended to evaluate the entire thoracic aorta. An MRI can also help to assess LV function and the degree of AI if the quality of the echocardiographic images is less than optimal. Scintigraphy can be used for the determination of left ventricular Ejectionsfraktions when the echocardiographic results are borderline or changed when the echocardiography is technically difficult. An EKG and a chest X-ray absorption should be performed. The ECG can show Repolarisationsveränderungen with or without QRS criteria of LV hypertrophy, a magnification of the left atrium and inversions of the T-wave with ST depression in the precordial leads. The chest x-ray recording can cardiomegaly and a prominent aortic root in patients with chronic progressive show AI. If the AI ??is hard signs of pulmonary edema or heart failure may be present. A stress test may be helpful to determine the functional capacity and symptoms in patients with documented AI and unclear symptoms. Coronary angiography should be performed prior to surgery even if no angina is present, since 20% of patients with severe AI have a significant CAD, which may require concomitant coronary artery bypass surgery. First-degree relatives of patients with a bicuspid valve echocardiography should undergo because 20-30% are similarly affected. Prognosis With treatment is the 10-year survival rate for patients with mild to moderate aortic regurgitation 80 to 95%. With a valve replacement at the appropriate time (i. E. H before failure and using the accepted Kriterein for engaging) the long-term prognosis for patients is good with moderate or severe AI. The prognosis of patients with severe heart failure and AI is considerably worse. Treating aortic valve replacement or reconstruction Sometimes vasodilators, diuretics and nitrates If the dilatation of the aortic root is part of the mechanism of aortic regurgitation, angiotensin antagonists may slow the progression, for which reason they constitute the preferred substance for treatment of patients with concomitant hypertension. The Intenvetion done either by surgically aortic valve replacement, or (rarely) valve repair. Percutaneous options are developed. A bioprosthetic aortic valve required except in the period immediately after surgery no anticoagulation, but a mechanical valve makes lifelong anticoagulation with warfarin necessary. Newer novel oral anticoagulants (NOAC) are ineffective and should not be used. Patients who are not candidates for surgery, benefit from treatment of HI. The insertion of an intra-aortic balloon pump is contraindicated because the diastolic balloon inflation worsens the AI. Beta blockers should be used with caution because they block the compensatory tachycardia and AI worse by extending the diastole. Patients with severe AR who do not meet the criteria for intervention, should every 6 to 12 months re-evaluated by physical examination and echocardiography. Antibiotic prophylaxis against endocarditis is no longer recommended for aortic regurgitation, except in patients in which a heart valve replacement was performed (see Table: Recommended endocarditis during dental procedures or surgery of the airways *). Criteria for the Intervention Intervention is displayed when AR is severe and causes symptoms AI is hard, causing LV dysfunction (EF <50%, left ventricular end-systolic diameter> 50 mm or left ventricular end-diastolic diameter> 65-75 mm) caused. Sometimes an intervention is made before aortic regurgitation is severe when the dilation of the aorta is ascending> 55 mm (> 50 mm in patients with Marfan syndrome and perhaps a bikuspidaler aortic valve). If heart surgery is performed because of other indications, simultaneous Aortenklappenintervention is indicated if the AI ??is moderate or severe. Summary The main causes of acute AI are ascending infective endocarditis and aortic dissection. Chronic AI is used in adults usually caused by degeneration of the aortic valve or -wurzel. The acute AI causes symptoms of heart failure and cardiogenic shock, but symptoms of AI may be missing. Chronic AI is typically asymptomatic for years; followed by an increasing exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Typical heart sounds are a normal S1 followed by a sharp S2 and a blowing shrill diastolic murmur with decrescendo character. Acute AI requires immediate valve replacement or reconstruction. In chronic AI are aortic valve replacement or reconstruction required if symptoms develop or become an LV dysfunction. In patients who meet these criteria but are not eligible for surgery, treatment of HI can be helpful.

Health Life Media Team

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