Aortic regurgitation

Aortic regurgitation is caused by the unattainability of the aortic valve. Aortic valve insufficiency may be caused dilatation of the aorta root or the valve itself both due to acquired and congenital defects. Aortic regurgitation dominates in pathophysiology volume overload of the left ventricle. The diagnosis of this defect is sometimes complicated many years of asymptomatic period. In addition to clinical examination, it is a basic examination method of echocardiography. Both cardiac surgery and catheterization valve replacement may be used in treatment.

The clinical picture
Aortic regurgitation is long ( to decades ) asymptomatic. It manifests itself fatigue, exertion shortness of breath, loss of performance and less often stenocardiemi. It is characteristic increase in pulse pressure while reducing diastolic pressure while increasing systolic pressure. Patients with aortic regurgitation are poorly tolerated atrial fibrillation and extrasystole due to an increase in postextrasystolic chamber volume. On the contrary, good load tolerance is given to the development of heart failure, when tachycardia shortens the duration of diastole, and thus regurgitation. Patients with acute aortic regurgitation are presented with a picture of pulmonary edema and cardiogenic shock.

Physical findings
We will find out by a consultation blowing diastolic decrescend murmur above the aortic mouth with a maximum in Coat of arms point ( 3.-4. intercostal parasternal ). Alternatively, a diastolic mitral murmur of Austin Flint is heard on the tip, reminiscent of mitral stenosis, which is caused by the premature closure of the anterior tip of the mitral valve by a stream regulating the blood from the aorta. This causes the anterior mitral tip to cause relative stenosis of the mitral mouth. The already mentioned large range of systolic and diastolic blood pressure is typical, which has its correlate in agile Corrigan's pulse on carotid arteries.

Signs of advanced disability are, for example. Quincke's capillary symptom ( pulsates the edge of the lunar ) when the nail is pressed, Musset's symptom ( head shaking with pulsation ) a Müller's symptom ( shaking of the uvula with heart rate ).

Diagnosis:
The basic diagnostic tool for aortic stenosis is transthoracic and esophageal echocardiography. It is no exception that aortic regurgitation is also an accidental finding in asymptomatic patients in the case of this examination.

X-ray of the chest usually reveals an increase in the heart shadow, dilation in the area of the ascendant aorta, or signs of congestion in small circulation. ECG is also non-specific, mostly signs of hypertrophy and left ventricular load, or the slope of the heart axis to the left are found. Examination by magnetic resonance imaging or computed tomography is used primarily to assess the dilatation of the aorta or a more detailed representation of other structures. Cardiac catheterization serves to rule out ischemic heart disease.

They are a sovereign diagnostic method transthoracic ( TTE ) and esophageal ( TAE ) echocardiography. The test is largely able to reveal the etiology of aortic regurgitation ( e.g. bicuspid valve ). The dimensions and functions of the heart sections ( the haemodynamic impact of the defect ), as well as the morphology of the valve and by Doppler the display can not only be detected, but also quantify various parameters of regurgitation, such as regurgitation fraction and volume. Oesophageal echocardiography also offers the possibility of a detailed 3D display of the valve.

Examination of natriuretic peptides is also appropriate in selected patients.

Therapy
Patients with haemodynamically insignificant and asymptomatic aortic regurgitation usually do not require specific therapy. However, this is necessary in the case of arterial hypertension. In hypertensive patients and incipient dilatation of the left ventricle, we try to medically reduce distolic hypertension by administration ACE inhibitors, which also positively affect remodeling, further calcium channel blockers and in symptomatic patients i diuretics. Beta-blockers should be used with caution due to possible bradycardia, which is poorly tolerated by patients.

Therapeutic methods of significant aortic regurgitation are cardiac surgery aortic valve replacement or aortic valve and root replacement (Bental's operations) in bulb dilation and ascendant aorta. It is also possible to perform valve rescue operations in indicated cases, eg for aortic dilatation in normal aortic valve tip morphology. An operational solution is indicated in symptomatic patients with significant aortic regurgitation, u asymptomatic patients with systolic dysfunction or significant dilation of the left ventricle, possibly also in the significant dilation of the ascendant aorta. Moderate aortic regurgitation can be resolved in some patients by surgery while exercising on another valve, aorta or aorticoronary bypass. An increasingly developing technique that is used primarily in at-risk patients is a catheter replacement of the aortic valve (TAVI, resp. TAVR ).

The prognosis of asymptomatic aortic regurgitation without systolic left ventricular dysfunction is good. In symptomatic patients with the development of heart failure or significant dilatation of the left ventricle, the prognosis is worse, without surgery the mortality is about 20% per year. It is therefore essential correct timing of the intervention solution, ideally before the symptoms develop and significant systolic dysfunction, when the prognosis of patients is best.

Ethiopogenesis
The causes of the development of aortic regurgitation can be divided into two main categories - dilatation of the aortic root and involvement of the valve itself. For aortic dilation ( not only its root ) may be the result of genetic syndromes, especially Marfanova and Ehlers-Danlos syndrome. There is also an increased incidence in ankylosing spondyloarthritis. Another important cause of aortic root dilation is hypertension with consequences in the form of increased stiffness of the aortic wall, loss of elasticity and atherosclerotic impairment. Aortic regurgitation also often occurs on the basis of infectious endocarditis, bicuspid valves, within post-revumatic involvement, myxomatous involvement, calcification ( degenerative ) valve disease, chest trauma or aortic dissection. Other less common causes are aortic valve involvement in systemic inflammatory diseases ( SLE ), infiltrative and spawning diseases or aortitis. It also occurs often together with aortic stenosis.

Aortic regurgitation dominates in pathophysiology volume overload of the left ventricle, which is chronically progressing in most cases. Thus, the left ventricle dilates over time and the image of eccentric hypertrophy develops. In the initial phases, sometimes several years, dilatation may not be accompanied by a reduction in the systolic function of the left ventricle or a significant increase in the filling pressures of the chamber, and thus diastolic dysfunction. This defect therefore remains very long asymptomatic, which complicates not only diagnosis but also treatment, because it remains only relatively limited time period for effective intervention even before the irreversible impairment of the systolic function of the chamber. Dilatation of the left ventricle leading to increased myocardial consumption, its systolic ( and later diastolic ) dysfunction together with reduced diastolic blood pressure eventually lead to hypoxic myocardial involvement and left heart failure. This can be further complicated by secondary mitral regurgitation, which, together with the reduced flexibility of the chambers due to progressive dilatation, leads to increased pressures in the left atrium.

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