Mitral regurgitation

Mitral regurgitation . Mitral regurgitation decreases resistance to ventricular emptying. The volume of blood regurgitated at the beginning of the ejection reduces the tension of the ventricle, so the atrium acts as a decompression chamber for the ventricle.


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  • 1 Etiology
  • 2 Pathophysiology
  • 3 Clinical picture
  • 4 Physical examination
    • 1 Radiology
    • 2 Electrocardiogram
    • 3 Echocardiogram
    • 4 Catheterization
  • 5 Sources


Mitral regurgitation is rheumatic in half of the cases. The anatomical alterations that determine valve incompetence are stiffness and retraction of the leaflets and shortening and fusion of the tendon cords. Unlike pure mitral stenosis , rheumatic mitral regurgitation is more common in males. In ischemic heart disease, mitral regurgitation may occur due to rupture or dysfunction of a papillary muscle and / or dilation of the ventricle, with or without aneurysm . Dilatation of the left ventricle of any etiology, but particularly in cardiomyopathyDilated, it causes mitral regurgitation due to widening of the ring and outward movement of the papillary muscles. Calcification of the mitral annulus, more common in the elderly, may also determine valve incompetence. In bacterial endocarditis , mitral regurgitation, which is established acutely, is due to involvement of the leaflets themselves (which can be perforated) or of the tendon cords. It can also occur as a result of inadequate commissurotomy or due to dehiscence of a mitral prosthesis. Another important cause of mitral regurgitation is mitral prolapse syndrome., whose anatomical substrate the myxomatous degeneration of the mitral valve determines an abnormal elongation of the tendon cords and an increase in size of the posterior leaf that, in systole, partially projects into the interior of the atrium. Less frequent causes of mitral regurgitation are hypertrophic cardiomyopathy , rheumatoid arthritis , ankylopoietic spondyloarthritis, and certain congenital abnormalities (endocardial cushion defect, “parachute” mitral valve, endocardial fibroelastosis, and transposition of the great vessels).


Cardiac output is usually maintained, even in severe mitral regurgitation, as contractile activity is used to produce more complete ventricular emptying. When ventricular function deteriorates, the volume of the ventricle increases and, in advanced stages, cardiac output decreases. The atrial pressure curve usually shows a high v wave that translates the increase in filling, and a decrease and marked, due to the speed of emptying. For a given regurgitation volume, the elevation of the mean atrial pressure, and therefore of the pulmonary pressures, depends primarily on the compliance of the atrium (i.e. the passive pressure-volume ratio). When atrial compliance is normal or reduced, the atrium is poorly enlarged and its pressure is high, particularly the v wave. An example of this is provided by acute mitral regurgitation due to rupture of the posterior pillar in a heart attack or bacterial endocarditis; the sudden elevation of the pressure can determine the appearance of an acute edema of the lung and, sometimes, right failure, maintaining the patient a sinus rhythm. The opposite situation corresponds to patients with chronic mitral regurgitation, a giant left atrium, and normal or only slightly elevated pressures in the pulmonary tree. Therefore, signs of pulmonary congestion are few or absent; on the other hand, cardiac output is usually low, so that fatigue and muscle weakness predominate. All of these patients are in atrial fibrillation. The largest group of patients, however, it presents a moderate elevation of atrial compliance and its situation is intermediate between the aforementioned extremes; consequently, they present a variable degree of atrial dilation, together with a more or less significant increase in mean atrial pressure. In severe mitral regurgitation, the end-diastolic pressure of the left ventricle increases, although the elevation also depends on the compliance of the ventricle wall. As in the atrium, chronic volume overload seems to modify the ventricular diastolic pressure-volume ratio in the sense of increasing compliance. The end-diastolic pressure of the left ventricle increases, although the elevation also depends on the compliance of the ventricle wall. As in the atrium, chronic volume overload seems to modify the ventricular diastolic pressure-volume ratio in the sense of increasing compliance. The end-diastolic pressure of the left ventricle increases, although the elevation also depends on the compliance of the ventricle wall. As in the atrium, chronic volume overload seems to modify the ventricular diastolic pressure-volume ratio in the sense of increasing compliance.

Clinical picture

The pathophysiological considerations presented explain that the natural history of mitral regurgitation is not uniform. Symptoms that depend on pulmonary congestion (dyspnea) are progressive and less episodic than in the case of mitral stenosis . Thus, hemoptysis and acute lung edema are rare, except in acute mitral regurgitation. In the less frequent cases in which the reduction in cardiac output predominates, the characteristic clinical manifestations are fatigue and muscle weakness, which also appear when right failure occurs as a consequence of pulmonary hypertension. In pure mitral regurgitation, systemic embolism is rare.

Physical exploration

Jugular venous pulse is normal, in the absence of congestive heart failure. The carotid pulse usually shows a rapid rise. The tip beat is usually broad, corresponding to a volume overload, and is displaced out and down. In the lower left parasternal area, the left atrium can be palpated when, at the end of systole, it reaches its maximum distension. When there is pulmonary hypertension, the pulmonary closure and the hypertrophic right ventricular beat are palpable. Auscultation reveals a first noise of decreased intensity, which is practically included in a generally long systolic murmur (holosystolic), of high frequency, in a jet of steam, irradiated to the armpit and that is better detected with the membrane of the stethoscope . The second noise usually has a physiological split, although in severe mitral regurgitation, early aortic closure can determine a wide split (both on inspiration and expiration). When pulmonary hypertension is present, the pulmonary component of the second noise is reinforced and an ejection click may appear. The presence of a mitral opening snap indicates the existence of an associated stenosis. In severe mitral regurgitation, rapid ventricular filling produces a third noise, which may be followed by a hyperaflow mesodiastolic murmur (not indicative of associated stenosis). The existence of a first intense noise, as well as the absence of a third noise, exclude severe mitral regurgitation. The main characteristic of this is the long systolic murmur, of intensity III / VI or greater, frequently accompanied by thrill. The most common irradiation of the frequently accompanied by frémito. The most common irradiation of the frequently accompanied by frémito. The most common irradiation of thesystolic murmur of mitral regurgitation is towards the armpit, although in certain patients (with ruptured tendons or with a preferential involvement of the posterior leaflet) it can be transmitted to the base and be confused with a murmur of aortic stenosis . In acute mitral regurgitation, the murmur may decrease and be accompanied by a fourth noise.


The characteristic radiological signs are dilation of the left atrium and ventricle and, where appropriate, the appearance of images of pulmonary congestion. In pure mitral regurgitation, valve calcifications are not usually observed, contrary to what happens in the case of stenosis. Although both forms of valve disease can determine significant dilatation of the left atrium, this is usually more pronounced in chronic severe mitral regurgitation. Fluoroscopic examination with the image amplifier allows observing the systolic expansion of the atrium.


As the patient maintains sinus rhythm, atrial dilation results, as in the case of stenosis, by the widening of the P wave and its bimodal appearance. Left ventricular growth is manifested by the presence of deep Q waves and high R waves with positive T (diastolic overload pattern); these signs become less evident when there is right ventricular growth due to pulmonary hypertension.


The echocardiogram shows indirect images of mitral regurgitation, which are expressed by atrial dilation accompanied by signs of volume overload of the left ventricle (dilation of the cavity with increased systolic excursion of the septum and the posterior wall). In the rupture of the tendon cords, an erratic movement of the mitral valve is observed in diastole and the existence of multiple echoes in systole. In infective endocarditis the presence of warts can be detected; if these are not visible on the transthoracic echocardiogram, a transesophageal ultrasound should be performed , which is more sensitive.

The diagnosis of mitral regurgitation by Doppler is based on the detection of turbulent flow in the left atrium during systole. Regurgitation severity is established by the distance traveled by the turbulent jet within the atrium and the size of the atrium. With Doppler it can be seen that the turbulence of the regurgitant jet causes a color mosaic that is also correlated with the severity of the regurgitation. An eccentric regurgitation jet, which reaches the pulmonary veins, is usually indicative of severe mitral regurgitation.


The height of the v waves in the left atrium is increased, as is the mean atrial pressure and the end-diastolic pressure of the left ventricle. The measure of compliance of the atrium and ventricle is indicated, for a given volume of regurgitation, the elevation of these pressures. Angiography allows quantification of mitral regurgitation. Indeed, the injection of contrast into the left ventricle allows the atrium to be seen, to a greater or lesser extent, depending on the degree of valve incompetence. Prior to valve replacement, cardiac catheterization should be performed to confirm the severity of regurgitation, assess the status of ventricular function, and rule out associated valve injury or ischemic heart disease.


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