Aortic insufficiency. Aortic regurgitation (IA), also known as aortic regurgitation, may be due to abnormalities both in the valve itself and in the proximal portion of the aorta.
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- 1 Etiology
- 2 Pathophysiology
- 3 Clinical picture
- 4 Physical examination
- 1 Radiology
- 2 Electrocardiogram
- 3 Echocardiogram
- 4 Catheterization
- 5 Treatment
- 6 Sources
Pure aortic regurgitation is more common in males; in women it is usually associated with mitral valve disease. The most common cause of pure or associated aortic regurgitation is rheumatic valve disease, which can lead to thickening, deformation, and shortening of the sigmoids, causing them to not coappt properly.
Other causes of aortic regurgitation due to a primary valve condition are bacterial endocarditis and traumatic valve rupture that are examples of acute insufficiency and certain congenital anomalies, such as the bicuspid valve, the fenestrated valve, the prolapse of a sigmoid, associated in occasions to a ventricular septal defect, and membranous subaortic stenosis, often accompanied by a thickening of the sigmoids that become incompetent.
In any case of primary sigmoid involvement, secondary valve ring dilation may increase the degree of regurgitation.
Occasionally, both acute and chronic aortic regurgitation depends primarily on dilation of the aortic root , which will eventually determine a widening of the valve annulus and sigmoid separation. This group includes idiopathic dilation of the aorta, median cystic necrosis (associated or not with a florid Marfan syndrome ), dissecting aneurysm (due to retrograde dissection), severe arterial hypertension , syphilis (which can also affect coronary ostia) and certain diseases of autoimmune origin, such as ankylopoietic spondyloarthritis , rheumatoid arthritis and arteritis ofgiant cells .
Regurgitation of blood from the aorta to the left ventricle represents a volume overload for this cavity, which in the following systole must eject more blood. Dilatation of the ventricle allows its expulsion volume to be increased without increasing the shortening of each contractile unit. Therefore, severe aortic regurgitation can occur with a normal heartbeat volume and ejection fraction, and with increased end-diastolic pressure and volume.
When ventricular function deteriorates, increased end-diastolic volume does not increase expulsion volume , and the ejection fraction is reduced. Cardiac output can be maintained at rest, even in advanced stages of the disease.
The pressure gradient between the aorta and the left ventricle, which, due to valve incompetence, is responsible for regurgitation, progressively decreases throughout diastole. This phenomenon explains the character of the murmur, which is decrescendo. At the end of diastole, the left aortic and left ventricular pressure may coincide, particularly when the heart rate is slow. The elevation of ventricular filling pressure explains the symptoms of pulmonary congestion. When the end-diastolic pressure of the left ventricle is very high, it can exceed the atrial pressure in the mesodiastole; the existence of an inverted transmitral gradient can determine the early closure of this valve or a diastolic mitral regurgitation. This usually occurs in severe acute aortic regurgitation.
The myocardial ischemia that these patients can develop is due, on the one hand, to the increase in myocardial oxygen demands derived from the increased tension on the wall and, on the other hand, to the decrease in perfusion pressure as a consequence of the reduction in diastolic pressure gradient between the aorta and the left ventricle .
Chronic aortic regurgitation is usually asymptomatic for many years. When its origin is rheumatic, the free interval between the outbreak of rheumatic fever and the development of significant regurgitation is about 10 years, and another 10 may elapse before symptoms appear. The first clinical manifestation is the palpitations, which do not necessarily translate into the existence of an arrhythmia, but are due to the patient becoming aware of the vigorous heartbeat resulting from the greater volume of blood ejected from the ventricle. This sensation is more noticeable in decubitus and is particularly bothersome during exercise or emotions.
Symptoms derived from left ventricular failure, exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea then appear. Acute lung edema, which can be the cause of death in these patients, is usually the initial symptom in acute aortic regurgitation. Chest pain is less common (about 20% of cases) than symptoms of pulmonary congestion and can appear both at rest and during exertion; it is usually prolonged and the response to nitroglycerin is poor. When claudication of the right ventricle occurs, the typical symptoms of low cardiac output appear (fatigability, asthenia, etc.).
Often the Anamnesis helps determine the cause of aortic regurgitation. Thus, there is usually a remote history of rheumatic fever when this is its origin, while detection of a murmur from childhood suggests a congenital valve malformation, and a recent history of fever supports infectious endocarditis. In the case of rheumatoid arthritis or ankylopoietic spondyloarthritis , clinical data generally allow the diagnosis of the fundamental disease. When the cause is not evident, the patient should be questioned about her medical history or possible chest trauma. In Marfan syndrome there is usually a family history.
In severe aortic regurgitation, inspection can reveal rocking of the chest and even the head (Musset’s sign), synchronous with the heartbeat. Sudden distension and collapse of the arteries more accessible to inspection (Corrigan’s pulse) may also be visible.
Frequently, palpation of the pulse reveals a double beat (pulse bisferiens) and the distal pressure of the nails allows us to appreciate the capillary pulse (Quincke’s sign, characterized by the alternation of paleness and flushing with each beat). Differential pressure is wide, with high maximum figures and persistence of Korotkov noises up to 0 mm Hg; in reality, the values of the diastolic pressure correspond to the moment in which these noises are damped.
The magnitude of the pulse pressure is not always a good index of the severity of the regurgitation, since vasoconstriction secondary to heart failure can raise diastolic pressure; Furthermore, the end-diastolic pressure of the left ventricle is increased and the peripheral diastolic pressure cannot be lower than it. Jugular venous pulse is normal unless there is congestive heart failure.
When aortic regurgitation is moderate or severe, there is left ventricular dilation, except in the acute forms. The root of the aorta appears dilated and on fluoroscopic examination shows a broad pulsatility opposite to that of the ventricle. Aortic elongation is more pronounced when this is the cause of valve incompetence. If there is left ventricular failure, the lung fields will show the characteristic images.
The rhythm is almost always sinus, except when associated with mitral valve disease. Although the ECG is normal in mild aortic regurgitation, signs of left ventricular growth of the type of diastolic overload (deep q, high R, and pointed T) are observed in the remaining cases. In the more advanced stages, ST segment depression usually occurs. The electrical axis deviates to the left and there may be an extension of the PR interval.
The echocardiographic signs of aortic regurgitation are indirect. The most characteristic image is the appearance of a diastolic (flutter) vibration in the anterior mitral leaflet, produced by the collision of the regurgitated blood stream with said structure. It is a practically constant and independent sign of the importance of regurgitation. In acute aortic regurgitation, the echocardiogram also shows the early closure of the mitral valve, secondary to the elevation of ventricular filling pressure.
The increase in the dimensions of the ventricular cavity is due to volume overload and does not indicate ventricular failure if the dynamics of the walls is preserved. In case of endocarditis, the echocardiogram allows us to appreciate the existence of warts and associated lesions. Doppler examination is the most sensitive diagnostic method of aortic regurgitation, since it allows detecting minor degrees of regurgitation, sometimes inaudible. As in the case of mitral regurgitation , the quantification of valve incompetence is based on the path of the regurgitation jet and the size of the left ventricle.
Angiography allows us to appreciate the status of the ascending aorta and determine the importance of regurgitation, which is particularly important when ventricular function deteriorates and peripheral signs of aortic regurgitation disappear or become less evident. Coronary angiography should always be performed in patients with angina pectoris. In acute aortic regurgitation, catheterization will rule out a dissection or, in the case of endocarditis, the rupture of a Valsalva sinus aneurysm in the heart chambers.
Medical treatment of chronic aortic regurgitation is limited to the use of ACE inhibitors, digitalis, and diuretics, along with reduced sodium intake when the patient develops heart failure. The administration of arterial vasodilators is useful since, by decreasing vascular resistance (afterload), it reduces the degree of regurgitation of blood to the left ventricle during diastole.
Although the response to nitroglycerin is poor, its administration is indicated in the patient with angina pectoris. Diastolic hypertension should be treated as it can increase the regurgitant volume. However, drugs that depress ventricular function, such as beta-adrenergic blockers, are contraindicated.
Discovery of an untreated lus requires administration of penicillin. The prevention of endocarditis with antibiotics should not be forgotten. Arrhythmias should always be treated, as their tolerance is poor. In asymptomatic patients with severe aortic regurgitation and normal ventricular function who follow medical treatment, ventricular function should be evaluated every 6 months and surgery should be indicated if it deteriorates.
Definitive regurgitation correction requires implantation of a valve prosthesis. Given the surgical risks, this treatment should be offered to patients whose aortic insufficiency determines a limitation of at least their usual physical activity. Long-term mortality depends on the state of ventricular function at the time of the intervention; thus, when the ventricle is very dilated, the annual mortality is 5%. In acute aortic regurgitation, urgent surgical treatment is imperative.
In these circumstances, the patient may temporarily benefit from an intravenous vasodilator treatment (nitroprusside), which must always be administered under hemodynamic monitoring. In a dissecting aneurysm , its repair and suspension of the valve floor are often not sufficient to control regurgitation, therefore the implantation of an aortic prosthesis should be associated with treatment.
The advisability of indicating surgery in the case of severe aortic insufficiency in asymptomatic or oligosymptomatic patients is debatable. In general, it is considered that the intervention will be beneficial when the ejection fraction is decreased (less than 50%), the LV end-diastolic volume increased (more than 55 mL / m2) and the shortening fraction (determined by echocardiogram). reduced (less than 30%).