mitral regurgitation mitral regurgitation mitral regurgitation (mr), also known as mitral insufficiency or mitral incompetence, is a form of valvular heart disease in which the mitral valve is insufficient and does not close properly when the heart pumps out blood. it is the abnormal leaking of blood backwards – regurgitation from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts. mitral regurgitation is the most common form of valvular heart disease. mitral regurgitationother namesmitral incompetence, mitral insufficiencymitral regurgitation (schematic drawing)during systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left atrium.1 mitral valve2 left ventricle3 left atrium4 aortaspecialtycardiologysymptomsheart murmur, shortness of breath during exercise or laying down, fatigue, palpitations, swollen feet or anklescomplicationsin severe cases: congestive heart failure, arrhythmias (atrial fibrillation), pulmonary hypertensiontypesacute mitral regurgitation, chronic compensated mitral regurgitation, chronic decompensated mitral regurgitationcausesmitral valve prolapse, ageing, rheumatic fever, mitral annular calcification, infective endocarditis, hypertrophic cardiomyopathytreatmentmedication, mitral valve repair, mitral valve replacement, mitraclip definition mitral regurgitation, also known as mitral insufficiency or mitral incompetence, is the backward flow of blood from the left ventricle, through the mitral valve, and into the left atrium, when the left ventricle contracts, resulting in a systolic murmur radiating to the left armpit. signs and symptoms phonocardiograms from normal and abnormal heart sounds mitral regurgitation may be present for many years before any symptoms appear. the symptoms associated with mr are dependent on which phase of the disease process the individual is in. individuals with acute mr are typically severely symptomatic and will have the signs and symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea). in acute cases, a murmur and tachycardia may be the only distinctive signs. individuals with chronic compensated mr may be asymptomatic for long periods of time, with a normal exercise tolerance and no evidence of heart failure. over time, however, there may be decompensation and patients can develop volume overload (congestive heart failure). symptoms of entry into a decompensated phase may include fatigue, shortness of breath particularly on exertion, and leg swelling. also, there may be development of an irregular heart rhythm known as atrial fibrillation. findings on clinical examination depend on the severity and duration of mr. the mitral component of the first heart sound is usually soft and with a laterally displaced apex beat, often with heave. the first heart sound is followed by a high-pitched holosystolic murmur at the apex, radiating to the back or clavicular area. its duration is, as the name suggests, the whole of systole. the loudness of the murmur does not correlate well with the severity of regurgitation. it may be followed by a loud, palpable p2, heard best when lying on the left side. a third heart sound is commonly heard. patients with mitral valve prolapse may have a holosystolic murmur or often a mid-to-late systolic click and a late systolic murmur. cases with a late systolic regurgitant murmur may still be associated with significant hemodynamic consequences. mitral regurgitation as a result of papillary muscle damage or rupture may be a complication of a heart attack and lead to cardiogenic shock. cause illustration comparing mitral valve regurgitation to mitral valve stenosis the mitral valve apparatus comprises two valve leaflets, the mitral annulus, which forms a ring around the valve leaflets, and the papillary muscles, which tether the valve leaflets to the left ventricle and prevent them from prolapsing into the left atrium. the chordae tendineae is also present and connects the valve leaflets to the papillary muscles. dysfunction of any of these portions of the mitral valve apparatus can cause regurgitation. the most common cause of mr in developed countries is mitral valve prolapse. it is the most common cause of primary mitral regurgitation in the united states, causing about 50% of cases. myxomatous degeneration of the mitral valve is more common in women as well as with advancing age, which causes a stretching of the leaflets of the valve and the chordae tendineae. such elongation prevents the valve leaflets from fully coming together when the valve closes, causing the valve leaflets to prolapse into the left atrium, thereby causing mr. ischemic heart disease causes mr by the combination of ischemic dysfunction of the papillary muscles, and the dilatation of the left ventricle. this can lead to the subsequent displacement of the papillary muscles and the dilatation of the mitral valve annulus. rheumatic fever (rf), marfan's syndrome and the ehlers–danlos syndromes are other typical causes. mitral valve stenosis (mvs) can sometimes be a cause of mitral regurgitation (mr) in the sense that a stenotic valve (calcified and with restricted range of movement) allows backflow (regurgitation) if it is too stiff and misshapen to close completely. most mvs is caused by rf, so one can say that mvs is sometimes the proximal cause of mi/mr (that is, stenotic mi/mr) and that rf is often the distal cause of mvs, mi/mr, or both. mr and mitral valve prolapse are also common in ehlers–danlos syndromes. secondary mitral regurgitation is due to the dilatation of the left ventricle that causes stretching of the mitral valve annulus and displacement of the papillary muscles. this dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy including aortic insufficiency, nonischemic dilated cardiomyopathy, and noncompaction cardiomyopathy. because the papillary muscles, chordae, and valve leaflets are usually normal in such conditions, it is also called functional mitral regurgitation. acute mr is most often caused by endocarditis, mainly s. aureus. rupture or dysfunction of the papillary muscle are also common causes in acute cases, dysfunction, which can include mitral valve prolapse. pathophysiology the pathophysiology of mr can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase. mild mitral regurgitation. the colored cloud symbolizes the return blood flow. 1. left ventricle, 2. left atrium acute phase acute mr (as may occur due to the sudden rupture of the chordae tendinae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. the left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume) but also the blood that regurgitates into the left atrium (the regurgitant volume). the combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle. in the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction); this happens because of more complete emptying of the heart. however, as it progresses the lv volume increases and the contractile function deteriorates, thus leading to dysfunctional lv and a decrease in ejection fraction. the increase in stroke volume is explained by the frank–starling mechanism, in which increased ventricular pre-load stretches the myocardium such that contractions are more forceful. the regurgitant volume causes a volume overload and a pressure overload of the left atrium and the left ventricle. the increased pressures in the left side of the heart may inhibit drainage of blood from the lungs via the pulmonary veins and lead to pulmonary congestion. compensated if the mr develops slowly over months to years or if the acute phase cannot be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. in this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. the eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward stroke volume (forward cardiac output) approaches the normal levels. in the left atrium, the volume overload causes enlargement of the left atrium, allowing the filling pressure in the left atrium to decrease. this improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease. these changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease. individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances. decompensated an individual may be in the compensated phase of mr for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mr. it is currently unclear what causes an individual to enter the decompensated phase of this disease. however, the decompensated phase is characterized by calcium overload within the cardiac myocytes. in this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. the decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. the increased end-systolic volume translates to increased filling pressures of the left ventricle and increased pulmonary venous congestion. the individual may again have symptoms of congestive heart failure. the left ventricle begins to dilate during this phase. this causes a dilatation of the mitral valve annulus, which may worsen the degree of mr. the dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well. while the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase, it may still be in the normal range (i.e.: > 50 percent), and may not decrease until late in the disease course. a decreased ejection fraction in an individual with mr and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase. diagnosis there are many diagnostic tests that have abnormal results in the presence of mr. these tests suggest the diagnosis of mr and may indicate to the physician that further testing is warranted. for instance, the electrocardiogram (ecg) in long-standing mr may show evidence of left atrial enlargement and left ventricular dilatation. atrial fibrillation may also be noted on the ecg in individuals with chronic mitral regurgitation. the ecg may not show any of these findings in the setting of acute mr. comparison of acute and chronic phases of mr acute chronic electrocardiogram normal p mitrale, atrial fibrillation, left ventricular hypertrophy heart size normal cardiomegaly, left atrial enlargement systolic murmur heard at the base, radiates to the neck, spine, or top of head heard at the apex, radiates to the axilla apical thrill may be absent present jugular venous distension present absent the quantification of mr usually employs imaging studies such as echocardiography or magnetic resonance angiography of the heart. chest x-ray the chest x-ray in individuals with chronic mr is characterized by enlargement of the left atrium and the left ventricle, and then maybe calcification of the mitral valve. echocardiogram transesophageal echocardiogram of mitral valve prolapse severe mr legend 1 left atrium (la) – 2 mr jet, lv left ventricle – rv right ventricle – ra right atrium animation of a mitral valve regurgitation in a dog, left apical view an echocardiogram is commonly used to confirm the diagnosis of mr. color doppler flow on the transthoracic echocardiogram (tte) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole. also, it may detect a dilated left atrium and ventricle and decreased left ventricular function. a transesophageal echocardiogram can give clearer images if needed as the back of the heart can also be viewed. electrocardiography p mitrale is a broad, bifid notched p wave in several or many leads with a prominent late negative component to the p wave in lead v1, and may be seen in mr, but also in mitral stenosis, and, potentially, any cause of overload of the left atrium. quantification of mitral regurgitation the degree of severity of mr can be quantified by the regurgitant fraction, which is the percentage of the left ventricular stroke volume that regurgitates into the left atrium. regurgitant fraction = v m i t r a l − v a o r t i c v m i t r a l × 100 % -v_\times 100\%} where vmitral and vaortic are, respectively, the volumes of blood