Left atrial myxoma can cause a diastolic murmur and a tumour plop may resemble the OS and can mimic MS. Hypertrophic cardiomyopathy can cause a diastolic rumble due to early diastolic flow into a hypertrophied stiff left ventricle. A mid-diastolic rumble, the Austin Flint murmur, can be heard in aortic regurgitation when an eccentric jet of AR hits the anterior leaflet of the mitral valve causing it to reverberate generating an apical rumble.
There is also some suggestion that this murmur may not be due to reverberation of the anterior leaflet and may actually be due to an AR jet preventing the mitral valve from opening fully [5]. Amyl nitrate inhalation has been used in the past to differentiate between the two. A diastolic murmur mimicking MS can also be heard in cor triatriatum sinister, a rare congenital abnormality where the LA is divided into two chambers usually by a thick fibromuscular septum, but in this case S1 will not be loud and there will be no OS [7].
The mitral valve apparatus consists of mitral annulus, valve leaflets, chordae tendineae and papillary muscles. Abnormalities of one or a combination of these structures can cause MR. MR is commonly caused by mitral valve prolapse, ischaemic heart disease, cardiomyopathy, infective endocarditis, rheumatic heart disease and annular calcification. As mentioned before, the examinational findings of mitral regurgitation will depend upon the severity and aetiology as well as the chronicity of the development of MR.
A significant MR will cause a sharp carotid upstroke, and a downward and outwardly displaced brisk hyperdynamic apical impulse. Expansion of the large left atrium during systole may cause a late systolic thrust in the parasternal region and this may mimic right ventricular enlargement. If MR is caused by defective leaflets, the S1 is usually soft. The S2 can be widely split because of earlier A2 due to shortened LV ejection as well as reduced resistance to LV ejection.
The P2 is louder if there is significant pulmonary hypertension. The increase in diastolic flow across the mitral orifice during the rapid filling phase may produce S3. Single or multiple non-ejection systolic clicks can be heard if the cause of MR is mitral valve prolapse described in detail later in the mitral valve prolapse [MVP] section.
The systolic murmur is the most important auscultatory finding. In severe MR, the systolic murmur starts immediately after a soft S1 and may continue beyond A2 as the pressure difference between LV and LA persists even after aortic valve closure. The holosystolic murmur of MR is blowing, high-pitched and best audible at the apex with radiation to the left axillary and infrascapular area. The murmur can radiate anteriorly towards the left parasternal area in case of mitral valve prolapse with involvement of the posterior leaflet.
There is weak correlation between the intensity of the murmur and the severity of MR. In patients with severe MR due to LV dilatation, acute myocardial infarction, paraprosthetic valvular regurgitation and in patients with severe emphysema, obesity and chest deformity, the systolic murmur may be very faint or even not audible [3].
Murmurs of shorter duration usually correspond to mild MR. The late systolic murmur of papillary muscle dysfunction may become holosystolic during acute ischaemia and may disappear when ischaemia is relieved.
A low-pitched diastolic murmur may be heard at the apex following S3 in severe MR because of increased flow across the mitral inflow in the absence of any mitral stenosis. An acute MR will produce only a short early systolic murmur, making the diagnosis clinically challenging.
This happens because a large v wave is generated in a non-compliant left atrium and LA and LV pressure essentially equalise in systole removing any reverse gradient across the mitral valve after the early part of systole. A left-sided S4 is usually heard. An abrupt rise in LA pressure leads to pulmonary oedema and increased pulmonary vascular resistance and even right heart failure.
Pulmonary hypertension can cause a loud P2, and rarely a large v wave in the pulmonary artery pressure pulse in acute severe MR can prematurely close the pulmonary valve leading to paradoxical splitting of the S2. The intensity of the aortic stenosis murmur increases after a premature beat or in the beat after a long cycle length in AF. This helps in differentiating AS from MR, particularly in older patients where the AS murmur may be prominent in the apex Gallavardin effect.
The systolic murmur of AS increases in the beat following a premature beat because of the combined effect of increased LV filling and post extra-systolic potentiation of ventricular contraction.
The intensity of the MR murmur does not change after a premature beat, can decrease papillary muscle dysfunction or become shorter after a premature beat MVP. The holosystolic murmur of a VSD may resemble MR but the former is usually loudest at the left sternal border and can be accompanied by parasternal thrill.
The murmur of TR may appear in the differential diagnosis but is usually best heard at the left sternal border. Its intensity increases during inspiration and it is associated with prominent v wave and y descent in the jugular venous pulse. Dynamic auscultation helps to differentiate MR from other systolic murmurs. The holosystolic murmur of MR does not vary much with respiration.
Sudden standing diminishes the murmur and squatting increases the murmur. The late systolic murmur of MVP behaves in another way, decreasing after squatting and increasing with standing mechanism and haemodynamics explained in the MVP section. The holosystolic murmur of MR is reduced during the strain phase of the Valsalva manoeuvre. The holosystolic murmur of MR will increase with hand grip compared to the murmur of AS and hypertrophic cardiomyopathy, both of which will reduce with hand grip.
In patients with mixed rheumatic mitral valve disease, careful auscultation may help to find the predominant lesion. MVP, or degenerative mitral valve disease as it is sometimes called in a broader sense, is defined by a spectrum of mitral valve lesions involving one or more components of the mitral valve apparatus.
It can vary from simple chordal rupture with prolapse of an isolated segment of the posterior leaflet P2 in an otherwise normal valve to multi-segment prolapse affecting one or both leaflets in a valve with significantly excess tissue and a larger annulus [2].
As expected, on auscultation MVP produces some characteristic but at the same time varied features. The characteristic auscultatory feature of MVP is a mid-systolic click, a high-pitched sound.
It results from sudden tensing of the mitral valve apparatus as the leaflets prolapse into the left atrium in systole.
Multiple clicks can be heard as different parts of the mitral leaflets prolapse at different times of systole. The significantly increased opening pressure causes an opening snap to occur when the mitral valve leaflets suddenly tense and dome into the left ventricle. This high frequency sound is best heard at the apex. Echocardiography is the primary means to both diagnose and evaluate the severity of mitral stenosis. The mitral leaflet tips become calcified and thickened.
The two most important measurements made on echocardiography include the pressure gradient between the left ventricle and left atrium and the mitral valve area.
Because transmitral velocities can be determined, the transmitral pressure gradient can be calculated using the modified Bernoulli equation, as described above. The mitral valve area can be found using the continuity equation, and the pulmonary artery pressure can be calculated to assess the severity of pulmonary hypertension.
Cardiac catheterization can also measure the mitral valve area using the Gorlin equation:. Mitral valvular flow is proportional to cardiac output. This equation assumes that no mitral regurgitation is present and the mitral valve area remains constant. With this equation, it is clear that if the mitral valve area remains constant and the cardiac output increases, the mitral valve gradient will increase exponentially — as previously described using the modified Bernoulli equation.
Mitral stenosis is categorized as mild, moderate or severe. The parameters associated with the severity are summarized below. The ECG in mitral stenosis is often normal early in disease. The most common finding is left atrial enlargement P mitrale , but this finding disappears if the patient enters atrial fibrillation.
Right heart strain may produce findings of right axis deviation and right ventricular hypertrophy on ECG. In pure mitral stenosis, left ventricular hypertrophy would be absent. The chest radiograph will again show left atrial enlargement. Both ECG and chest radiograph, however, are non-specific for mitral stenosis. The treatment of mitral stenosis relies on the prevention or early recognition of rheumatic heart disease.
Prophylactic penicillin treatment for patients known to have rheumatic heart disease successfully reduces exacerbations and will limit the damage done to the mitral valve. Anticoagulation is of great importance to prevent the formation of a left atrial thrombus and embolic events.
Even in the absence of atrial fibrillation, patients with certain risk factors including hypertension or hypercoagulable states should be anticoagulated.
Antibiotic prophylaxis before dental procedures and certain surgeries is no longer recommended to prevent bacterial endocarditis unless a prosthetic valve is present. Preload reduction with diuretics and salt restriction can relieve symptoms if mitral stenosis if pulmonary hypertension is present. Many patients experience symptoms only when the heart rate is elevated, as tachycardia decreases diastolic filling time significantly.
Therefore, the use of beta blockers can be beneficial, at times, especially in patients with predominantly exertional symptoms. In this procedure, a catheter is inserted through the femoral vein into the right heart, then across the interatrial septum into the left atrium, and finally down across the stenotic mitral valve.
A balloon is then inflated, fracturing the calcium deposits and relieving the stenosis. Unlike valvuloplasty in the setting of aortic stenosis , PBMV is highly successful with a low rate of restenosis.
Complications include residual mitral regurgitation, a persistent atrial septal defect and, rarely, calcium embolization. PBMV is indicated for patients who are symptomatic with moderate to severe mitral stenosis in the absence of a pre-existing LA thrombus and mitral regurgitation. PBMV is also indicated for patients who are asymptomatic with severe mitral stenosis and a Wilkins Abascal echocardiographic score of 8 or less. Surgical approaches to manage mitral stenosis include closed commissurotomy, open commissurotomy and mitral valve replacement.
This similar to PBMV in that the mitral valve is not directly visualized, and a balloon is used to dilate the stenotic mitral valve. As a thank-you for using our site, here's a discounted rate for renewal or upgrade.
Not now - I'd like more time to decide. Renew my subscription. Washington Manual of Medical Therapeutics. Tags Type your tag names separated by a space and hit enter. Mitral stenosis MS is characterized by incomplete opening of the mitral valve during diastole, which limits antegrade flow and yields a sustained diastolic pressure gradient between the left atrium LA and the left ventricle LV.
Citation Bhat, Pavat, et al. Washington Manual , www. Mitral Stenosis. Wolters Kluwer Health; Accessed November 14, In Bhat, P.
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