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Valvular Heart Diseases

MITRAL STENOSIS
ETIOLOGY AND PATHOLOGY Two-thirds are female. generally rheumatic in origin; very rarely, MS is congenital. 40% rheumatic heart disease MS . In rheumatic stenosis the valve leaflets are diffusely thickened by fibrous tissue and/or calcific deposits. the valvular cusps become rigid, (fish-mouth) valve. Calcification of the stenotic mitral valve . Thrombus formation and arterial embolization may arise from the calcific valve itself, but more frequently arise from the dilated left atrium (LA) in patients with atrial fibrillation (AF)

PATHOPHYSIOLOGY
normal adults the mitral valve orifice is 4 to 6 cm2.
In the presence of significant obstruction, less than 2 cm2, blood can flow from the LA to the left ventricle (LV) only if propelled by an abnormally elevated left atrioventricular pressure gradient When the mitral valve opening is reduced to 1 cm2, often referred to as critical MS, a LA pressure of approximately 25 mmHg is required to maintain a normal cardiac output (CO). The elevated pulmonary venous and pulmonary arterial (PA) wedge pressures reduce pulmonary compliance, contributing to exertional dyspnea. dyspnea are usually precipitated by clinical events that increase the rate of blood flow across the mitral orifice, tachycardia including that resulting from atrial fibrillation augments the transvalvular gradient and elevates further the LA pressure. tricuspid stenosis.

Cardiac Output moderately severe MS (mitral valve orifice 1.2 cm2 to 1.7 cm2), the CO is normal or almost so at rest but rises subnormally during exertion. critical MS --- pulmonary vascular resistance

Pulmonary Hypertension The clinical and hemodynamic features of MS


importantly -- level of the PAP. Pulmonary hypertension results from : (1) passive backward transmission of the elevated LA pressure; (2) pulmonary arteriolar constriction -- triggered by LA and pulmonary venous hypertension (reactive pulmonary hypertension) (3) interstitial edema in the walls of the small pulmonary vessels (4) organic obliterative changes in the pulmonary vascular bed. Severe pulmonary hypertension --- tricuspid regurgitation (TR) & pulmonary incompetence ----- right-sided heart failure.

SYMPTOMS
valvular obstruction is mild, --- physical signs of MS may be present without symptoms. dyspnea and cough, fever, severe anemia, paroxysmal atrial fibrillation and other tachycardias, sexual intercourse, pregnancy, and thyrotoxicosis.

dyspnea, -- orthopnea and paroxysmal nocturnal dyspnea.


Pulmonary edema, atrial arrhythmias

Hemoptysis
results from rupture of pulmonary-bronchial venous connections secondary to pulmonary venous hypertension. elevated pulmonary vascular resistances----- never fatal. Recurrent pulmonary emboli , sometimes with infarction, --- important cause of morbidity and mortality Pulmonary infections, i.e., bronchitis, bronchopneumonia, and lobar pneumonia, commonly complicate untreated MS. Infective endocarditis

Pulmonary Changes
pulmonary vascular bed : fibrous thickening of the walls of the alveoli and pulmonary capillaries occurs commonly in MS. vital capacity, total lung capacity, maximal breathing capacity, and oxygen uptake per unit of ventilation are reduced pulmonary capillary pressure rises during exercise. airway resistance is abnormally increased the diffusing capacity may be reduced. transudation of fluid from the pulmonary capillaries into the interstitial and alveolar spaces. the increased capacity of the pulmonary lymphatic system to drain excess fluid ------- retards the development of alveolar edema.

Thrombi and Emboli Thrombi may form in the left atria, particularly in the enlarged atrial appendages of patients with MS. Embolization occurs much more frequently in patients with AF, in older patients, and in those with a reduced cardiac output (CO). systemic embolization may be the presenting complaint in otherwise asymptomatic patients with mild MS. thrombus may suddenly obstruct the stenotic mitral orifice and cause syncope, angina, and changing auscultatory signs with alterations in position.

PHYSICAL FINDINGS Inspection and Palpation blue facies the jugular venous pulse reveals prominent a waves due to vigorous right atrial systole.

Auscultation The first heart sound (S1) generally snapping, and slightly delayed. The pulmonary component of the second heart sound (P2) is often accentuated, the second heart sound (S2) are closely split or fixed. A pulmonary systolic ejection click may be heard in patients with severe pulmonary hypertension. Opening snap (OS) -- audible in expiration low-pitched, rumbling, diastolic murmur

Associated Lesions
pansystolic this murmur is accentuated by inspiration and diminishes during forced expiration (Carvallos sign) pansystolic murmur of MR. When the CO is markedly reduced in MS, the typical auscultatory findings, including the diastolic rumbling murmur, may not be detectable (silent MS), but they may reappear as compensation The Graham Steell murmur of pulmonary regurgitation (PR), a high-pitched, diastolic, decrescendo blowing murmur along the left sternal border, results from dilatation of the pulmonary valve ring and occurs in patients with mitral valve disease and severe pulmonary hypertension.

LABORATORY EXAMINATION EKG In MS and sinus rhythm, the P wave usually suggests LA enlargement , tall and peaked in lead II and upright in lead V1 RA enlargement The QRS complex is usually normal. right axis deviation and RV hypertrophy

Echocardiogram the most sensitive and specific noninvasive method for diagnosing MS.
Transthoracic two dimensional color flow Doppler echocardiographic imaging and Doppler ultrasound provide, including an estimate of the transvalvular gradient and of mitral orifice size, the presence and severity of accompanying MR, , echocardiography provides an assessment of the size of the cardiac chambers, an estimation of the LV function, an estimation of the PAP, and an indication of the presence and severity of associated valvular lesions. Transesophageal echocardiography provides superior images and should be employed when transthoracic imaging is inadequate for guiding therapy.

Roentgenogram
The earliest changes are straightening of the left border of the cardiac silhouette, Prominence of the main pulmonary arteries, Dilatation of the upper lobe pulmonary veins, Backward displacement of the esophagus by an enlarged LA. In severe MS, however, all chambers and vessels upstream to the narrowed valve are prominent. Kerley B lines are fine, dense, opaque, horizontal lines that are most prominent in the lower and midlung fields and that result from distention of interlobular septa and lymphatics with edema when the resting mean LA pressure exceeds approximately 20 mmHg.

DIFFERENTIAL DIAGNOSIS
Atrial septal defect may be mistaken for MS; in both conditions there is often clinical, EKG, and roentgenographic evidence of RV enlargement and accentuation of the pulmonary vascularity. The widely split S2 of atrial septal defect may be confused with the mitral OS, and the diastolic flow murmur across the tricuspid valve may be mistaken for the mitral diastolic murmur. However, the absence of LA enlargement and of Kerley B lines and the demonstration of fixed splitting of S2 all favor atrial septal defect over MS. Left atrial myxoma may obstruct LA emptying, causing dyspnea, a diastolic murmur, and hemodynamic changes resembling those of MS. However, patients with an LA myxoma often have features suggestive of a systemic disease, such as weight loss, fever, anemia, systemic emboli, and elevated serum IgG concentrations. The auscultatory findings may change markedly with body position. The diagnosis can be established by the demonstration of a characteristic echo-producing mass in the LA with two-dimensional echocardiography.

TABLE : Summary of Useful Medical Treatments in Valvular Heart Disease


Source: NA Boon, P Bloomfield: The medical management of valvular heart disease. Heart 87:395, 2002, with permission

Lesion
Mitral stenosis

Symptom Control

Secondary Prevention and Natural History Penicillin prophylaxis against recurrent episodes of rheumatic fever; Anticoagulants to prevent systemic thromboembolism.

Diuretics for heart failure; Digoxin, Beta blockers, calcium antagonists control atrial fibrillation

Mitral regurgitation

Diuretics and vasodilators (usually ACE inhibitors) for heart failure Diuretics for heart failure; nitrates and blockers for angina Diuretics and vasodilators (usually ACE inhibitors) for heart failure

No proven treatment

Aortic stenosis

No proven treatment but lipid lowering therapy may slow progression of calcific aortic stenosis Vasodilators (nifedipine or ACE inhibitors) to protect the left ventricular myocardium and delay the need for surgery

Aortic regurgitation

Penicillin prophylaxis of -hemolytic streptococcal infections prevent rheumatic fever and prophylaxis for infective endocarditis restriction of sodium intake and maintenance doses of oral diuretics. Digitalis glycosides usually do not benefit patients with MS and sinus rhythm but are helpful in slowing the ventricular rate of patients with AF. Beta blockers or nondihydropyridine calcium antagonists (e.g., verapamil or diltiazem) are useful in this regard. Warfarin to an INR of 2-3:1 should be administered for at least 1 year to patients with MS who have suffered systemic and/or pulmonary embolization and permanently to those with AF. If AF is of relatively recent origin in a patient whose MS is not severe enough to warrant balloon mitral valvotomy or surgical valvotomy, reversion to sinus rhythm pharmacologically or by means of electrical countershock is indicated. Usually this reversion should be undertaken after the patient has had 3 weeks of anticoagulant treatment.

Mitral Valvotomy
effective if orifice is less than approximately 1.0 cm2/m2 body surface area, or 1.7 cm2 in normal-sized adults.
two techniques: percutaneous balloon mitral valvotomy and surgical valvotomy. balloon mitral valvotomy , a catheter is directed into the LA after transseptal puncture and a single or double balloon (Inoue balloon) is directed across the valve and inflated in the valvular orifice. Ideal patients have relatively mobile, thin leaflets with no or little calcium, without extensive subvalvular thickening and with no or mild MR. surgical valvotomy,. In patients in whom percutaneous valvotomy is not possible, unsuccessful, or in those with restenosis,

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