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Valvular Heart Disease: Difference between revisions
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# An asymptomatic adolescent with chronic severe AR* with onset of ST depression or T-wave inversion over the left precordium on ECG at rest may be considered for aortic valve repair or replacement. (Level of Evidence: C) | # An asymptomatic adolescent with chronic severe AR* with onset of ST depression or T-wave inversion over the left precordium on ECG at rest may be considered for aortic valve repair or replacement. (Level of Evidence: C) | ||
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== Mitral Stenosis == | |||
=== Etiology and pathology === | |||
The leading cause of mitral stenosis is rheumatic fever, causing postrheumatic deformities. Other rare aetiologies of left atrial outflow obstruction include congenital and degenerative mitral valve stenosis, severe mitral annular and/or leaflet calcification carcinoid disease, neoplasm, left atrial thrombus, infective endocarditis with large vegetations, certain inherited metabolic disorders such as Fabry’s disease, mucopolysaccharidosis, Whipple’s disease, gout, rheumatic arthritis, lupus erythematosus, methysergide therapy, and cases related to previous implanted prosthesis or commisurotomy. | |||
Rheumatic valvular disease causes diffuse thickening of the valve leaflets by fibrous, or fibrocalcific distortion, with fusion of one or more commisures valve commisures, and fusion and shortening of the subvalvular apparatus. This combined with increasingly rigid cusps results in narrowing of the valve. chordae tendineae, with or without annular or papillary muscle deformities. | |||
The area of the normal mitral valve orifice is 4-6 cm2. In patients with mitral stenosis, when the valve area approaches 2 cm2 or less, an early, mid and late diastolic transvalvular gradient is present between the left atrium and ventricle. With progressive mitral stenosis, transvalvular pressure gradient increases. Mitral transvalvular flow depends on cardiac output and heart rate. Shortening of diastolic phase in increased heart rate causes symptoms by reducing forward cardiac output. Mitral stenosis develops gradually, and may be asymptomatic for years. | |||
=== Clinical presentation === | |||
Patients with mitral stenosis may be asymptomatic for years. Mean age of presentation of symptoms is fifty to sixty years old. The presenting symptom in patients with mild mitral stenosis is typically dyspnea precipitated by stress or atrial fibrillation. Progression of disease with increasing left atrial and pulmonary venous pressures will cause progressive symptoms of dyspnea. | |||
== Mitral regurgitation == | |||
Mitral valve regurgitation results from inadequate mitral leaflet coaptation during systole. This allows the systolic regurgitation of blood from the high-pressure LV to the normally low-pressure LA. The regurgitating volume depends on both the size of the regurgitant orifice and the pressure gradient between the left ventricle and the left atrium. In primary mitral regurgitation, inadequate mitral leaflet coaptation results from an abnormality in any of the functional components of the mitral apparatus. Secondary or functional mitral regurgitation results from left ventricle disease and remodeling. | |||
During systole, combined papillary muscle contraction and contraction of the dynamic annulus promote leaflet coaptation. Calcification of the annulus may hinder the sphincter-like contraction of the annulus allowing regurgitation. Secondary mitral regurgitation may be due to annulus dilation, caused by ischemic or dilated cardiomyopathy. The regurgitant volume causes left ventricular enlargement and contractile dysfunction. Left ventricle dilation may enlarge the mitral annulus and the regurgitant orifice, increasing the mitral regurgitation. Positive inotropes, diuretics and vasodilators reduce the size of the left ventricle and the regurgitant orifice, and decreases the the regurgitant flow. | |||
=== Etiology === | |||
Three different types of primary mitral regurgitation can be defined; leaflet retraction from fibrosis and calcification, annular dilatation and chordal abnormalities (including rupture, elongation, or shortening). Functional mitral regurgitation results from LV dysfunction with or without annular dilation. Mitral regurgitation was classified by Carpentier into three types based on leaflet and chordal motion: normal leaflet motion (type I), leaflet prolapse or excessive motion (type II), and restricted leaflet motion (type III). <cite>FannIngelsMiller</cite> | |||
=== Chronic mitral valve regurgitation === | |||
Degenerative mitral valve disease is the most common cause of mitral regurgitation in Europe. | |||
Myxomatous mitral valve degeneration is also known as floppy mitral valve or mitral valve prolapse. Prolapse is defined as excursion of one or both leaflets above the plane of the annulus during systole. <cite>Gilbert</cite> Prolapse of the middle portion of the posterior leaflet is the most common finding in degenerative MR. <cite>Carpentier</cite>. | |||
Mitral regurgitation in Barlow syndrome or parachute mitral valve is due to annular dilatation and extensive hooding of leaflets with large amounts of excessive leaflet tissue. In mitral regurgitation, the mass-to-volume ratio of the enlarged, thin walled left ventricle is less than 1 <cite>FeiringRumberger</cite>. | |||
=== Clinical Presentation === | |||
Patients with mild to moderate compensated chronic mitral regurgitation may remain asymptomatic for many years. The adapted left ventricle maintains normal forward cardiac output. The left ventricle ejection fraction in chronic mitral regurgitation may be greater than normal due to the compensatory cardiac adaptations. Progression of severity depends on etiology of regurgitation; in patients with connective tissue disease regurgitation tends to progress more rapidly than patients with mitral valve prolapse or rheumatic mitral regurgitation. Progression in acute rheumatic fever is often rapid. Acute progression may by caused by endocarditis or chordae rupture. | |||
Gradual progression and eventually decompensation results in decreased cardiac output with physical activity and pulmonary congestion. Patients present with weakness, fatigue, palpitations, dyspnea on exertion. Hepatomegaly, peripheral edema and ascites due to right sided heart failure can be associated with rapid clinical deterioration. | |||
Acute mitral regurgitation is associated with sudden pulmonary congestion and edema. | |||
On physical examination the apical impulse is displaced laterally, indicating left ventricular enlargement. S1 is normal or diminished. S2 may be single, closely split, normally split, or even widely split as a consequence of the reduced resistance to LV ejection. A widely split S2 is often audible, due to shortening of LV systole and early closure of the aortic valve. The P2 component of the second heart sound may be increased if pulmonary hypertension has developed. The apical systolic murmur is typically holosystolic and radiates to the axilla, depending on the direction of the regurgitant jet. It can be blowing, moderately harsh, or even soft. An S3 gallop often is present, reflecting the transmitral diastolic flow during the rapid filling phase. | |||
Early in the disease process of patients with Barlow syndrome, a characteristic midsystolic click can be appreciated, followed by a late systolic murmur; with disease progression the murmur becomes holosystolic, and the midsystolic click may become inaudible. <cite>FannIngelsMiller</cite> | |||
=== Acute mitral regurgitation === | |||
Immediate intervention is often necessary in acute mitral regurgitation. Etiology can be organic or functional. Organic causes includes rupture of a major chorda tendinea (in myxomatous mitral valve disease) or papillary muscle (due to myocardial infarction), leaflet perforation (of endocarditic origin), and dysfunction of a prosthetic valve due to endocarditis or paravalvular regurgitation. Regurgitation of functional etiology results from left ventricular abnormalities such as dyskinetic wall due to ischemia or dilated ventricle due to cardiomyopathy. | |||
Acute mitral regurgitation is associated with dyspnea and orthopnea, caused by sudden pulmonary congestion and edema. Acute papillary muscle rupture may mimic the presentation of a patient with a postinfarction ventricular septal defect.(Harrison et al. 697-701) | |||
On physical examination no signs of cardiac compensatory mechanisms are present. The increase in left atrial pressure diminishes the pressure gradient between the left ventricle and left atrium by midsystole. The murmur of mitral regurgitation is shortened and of decreased intensity, it may be soft, short of even inaudible. an S3 gallop usually is present. The volume overload is increasing the severity of MR over time leads to a greater percentage of the LV stroke volume being ejected in a retrograde fashion. | |||