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II./4.3.: Aortic regurgitation (AR)
II./4.3.1.: Etiology
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Aortic regurgitation, named also aortic insufficiency, is a disorder of the valve’s closure causing a backflow of blood from the aorta to the left ventricle during diastole. Its development may be due to primary, organic disease of the valvular cusps, or a dilatation or another disorder, such as a dissection in the region of the aortic radix (anulus, sinus Valsalva pouches, ascending aorta). The more frequent organic abnormity of the cusps may be congenital as e.g. in bicuspid aortic valve, or acquired, e.g. senile calcification, rheumatic or myxomatous defect, or destruction of the valve by infective endocarditis.
AR developing in relation to a traumatic injury or systemic diseases (rheumatoid arthritis, syphilis etc.) is much less frequent. In a functional aortic insufficiency e.g. in patients with hypertension, idiopathic aortectasia, or Marfan syndrome, the cusps are usually normal, and the dilation of the radical region, the deformation of its geometry leads secondarily to a regurgitation.
II./4.3.2.: Pathophysiology, symptomatology
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As for the patient’s symptoms and the physical findings, chronic and acute insufficiencies represent separate entities. Chronic aortic regurgitation leads to an increase of the left ventricular end-diastolic and end-systolic volumes, and because of its chronic, gradual development, it can be tolerated well also in the long run due to the compensating mechanisms. The left ventricle that works at an increased volume but with a good pump function is able to maintain the cardiac output with a higher stroke volume, and the patient may be asymptomatic for a longer time.
In the course of time, however, due to the increased preload and afterload, as the contractility of the myocardium decreases and the left ventricle undergoes a progressive dilatation, the symptoms of heart failure will inevitably present themselves. Less frequently angina pectoris or on exceptional occasions syncope may also occur. The clinical picture is much more dramatic and rapid in patients with an acutely developing severe aortic insufficiency (aortic dissection, infective endocarditis). There is no time for developing left ventricular dilatation; the regurgitating blood volume steeply increases the left ventricular end-diastolic pressure, and therefore a severe heart failure, which may even lead to a cardiogenic shock, may develop in a short time. In addition, the classic physical signs of a chronic aortic insufficiency are lacking.
II./4.3.3.: Course
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Although yet few has been elucidated about the factors which determine the progression of chronic AR, but it is well known that the decreasing distensibility of the aorta with the advancing age certainly contributes to an increase of the insufficiency. The systolic function, end-systolic diameter and volume of the left ventricle clearly are determining prognostic factors. In patients with a dilated aortic radix the course depends mainly on the rate of dilation and the underlying disease. As the dilation of the aortic radix’s region develops always in consequence of a structural abnormity of the thoracic aorta’s wall, in such cases the indication of a potential surgical reconstruction depends not only on the extent of the aortic insufficiency, but also on the developed dilation of the ascending aorta.
The systemic blood pressure that strains the ascending aorta increases the tension of the wall proportionally with the radius of the vessel, therefore an elective, preventive surgery may become indicated, such as in patients with Marfan syndrome when the aortic diameter exceeds 45 mm. In case of an acute regurgitation the left ventricle is unable to compensate with a dilation of its chamber, therefore also significant increase of end-diastolic pressure is present what leads to an increase of pulmonary pressure, decrease of perfusion pressure of the subendocardial myocardium, and its consequent ischemia; the prognosis is poor, without a surgical intervention it is very unfavorable.
II./4.3.4.: Diagnostics
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If a significant volume is regurgitated, the patient’s diastolic blood pressure will be low, and signs of widened pulse amplitude are observed such as the Duroziez sign which is a systolo-diastolic murmur over the femoral artery, and the so called Quincke pulse that is capillary pulsation on the finger nails and mucous membranes. The nodding movement of the head (de Musset sign) is also due to the high pulse amplitude. The backflow of blood causes a diastolic regurgitation murmur in the aortic area and elicits the vibration of the anterior cusp of the mitral valve, leading to the appearance of the mesodiastolic so called Austin Flint murmur over the apex. The ECG reveals left ventricular hypertrophy; the prominent Q waves, ST segment depression and T wave inversion in the anterior-lateral thoracic leads are signs of a diastolic strain of the ventricle.
Thoracic X-ray may show left ventricular dilatation, pulmonary venous congestion and pathologic processes of the ascending aorta (aneurysm, calcification). Cardiac catheterization is only performed mostly before surgery, when the equalization of left ventricular end-diastolic and aortic pressures is of diagnostic value. The most important imaging examination of first choice is echocardiography which provides information on both the pathologic mechanism and the degree of severity; however quantification of the insufficiency may pose a challenge, particularly if eccentric jets and left ventricular dysfunction are present.
Differential diagnostics includes, in addition to a few congenital anomalies (coronary arterio-venous fistula, persisting truncus arteriosus etc.) mostly pulmonary regurgitation, persisting ductus arteriosus and ventricular septal defect (VSD) associated with the AR. In this latter the loud pansystolic and early diastolic murmur is caused by the supracristal VSD and the prolapse of the right coronary pouch. Rupture of the sinus Valsalva pouches towards the right ventricular outflow tract or the right atrium is a rare disease which causes an acute chest pain and failure of the right half of the heart, what is uncharacteristic of aortic regurgitation.
II./4.3.5.: Therapy
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For choosing an optimal therapy in patients with aortic insufficiency, similarly to the other diseases of the heart valves, it should be taken into consideration, in addition to the etiology, severity of the lesion and the clinical symptoms, the time aspect of the disease (acute or chronic), the pump function of the heart, the hemodynamic sequels (e.g.: pulmonary hypertension), the expected prognoses in case of a conservative or a surgical therapy, the patient’s underlying disease and accompanying diseases, as well as his/her estimated tolerance for the stress of a surgery. Acute and chronic aortic insufficiencies are to be judged differently also on the base of these aspects. In patients with a significant acute aortic insufficiency and an aortic dissection immediate surgery is indicated. In patients with infective endocarditis and hemodynamic instability a surgery is urgent.
In patients with chronic aortic insufficiency either a medicinal therapy with follow up or surgical solution may be chosen. Medication may include vasodilator agents which, by decreasing the systemic blood pressure, can reduce the extent of regurgitation and slow down the progression of the disease. A surgical solution with implantation of an artificial valve is clearly indicated for patients with a symptomatic significant aortic insufficiency. In some cases plastic surgery of the valves with preservation of the native valves may be feasible. In asymptomatic patients surgery is indicated if their left ventricular function is reduced, there is a significant dilatation (end-systolic diameter 55 mm) or the diameter of the ascending aorta exceeds 55 mm.
In patients with Marfan syndrome or a bicuspid valve a surgical therapy is safer than a conservative one already over 45 mm or 50mm respectively. In addition to the implantation of an artificial valve, reconstruction of the thoracic aorta due to its disease, e.g. aneurysm may also be necessary. Such combined surgeries include, among others, the Bentall procedure, where an artificial valve and an interposed aortic graft are implanted to which the coronaries are reconnected. These extended complex operations are of course much longer and mean a greater burden for patients. Yet no interventional procedure is available for the therapy of patients with aortic insufficiency.
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