الفهرس 
The mitral valveOnly 14 pages are availabe for public view
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Abstract
Acute AR is caused most commonly by infective endocarditis, aortic dissection, or trauma. The characteristic features of acute AR are tachycardia and an increase in LV diastolic pressures. In contrast to the pathophysiological events in chronic AR, in which the left ventricle is able to adapt to the increased hemodynamic load (Alpert JS,2000).
The Echocardiogram reveals a dense diastolic Doppler signal with an end-diastolic velocity approaching zero, and premature closure and delayed opening of the mitral valve LV size and ejection fraction are normal. This contrasts with the findings in chronic AR, in which end-diastolic dimensions and wall motion are increased (Alpert JS,2000). .
While the patient is being prepared for surgery, treatment with an intravenous positive inotropic agent (dopamine or dobutamine) and/or a vasodilator (nitroprusside) is often necessary. The agent and dosage should be selected on the basis of arterial pressure ,Beta-blocking agents and intra-aortic balloon counterpulsation are contraindicated, as either lowering the heart rate or augmenting peripheral resistance during diastole can lead to rapid hemodynamic decompensation (Catherine and Robert ,2007).
Important causes of acute MR are spontaneous rupture of chordae tendineae, infective endocarditis with disruption of valve leaflets or chordal rupture, ischemic dysfunction or rupture of a papillary muscle (Catherine and Robert ,2007). .
Echocardiographic studies demonstrate the etiology of the acute regurgitant lesion: vegetations in patients with infectious endocarditis, ruptured chordae in individuals with mitral valve prolapse, or papillary muscle rupture inacute myocardial infarction (Leonardo and marc ,2007).
IV nitroglycerin is often effective in reducing pulmonary vascular congestion in these patients, particularly if the underlying etiology for MR is ischemic heart disease. Surgical therapy is almost always required in patients with acute severe MR. Intraaortic balloon counterpulsation can be helpful in stabilizing the patient before definitive therapy is instituted The surgical approach and results depend on the underlying pathology. Patients with MR secondary to AMI have a high surgical mortality (Thompson et al,2000).
Although a major risk factor for PVT is inadequate anticoagulation, approximately 40% of patients have adequate prothrombin times at the time of presentation.63 This may be explained by the fact that PVT is a complex process that consists of a significant component of fibrous tissue ingrowth with associated secondary thrombosis. However, the percentage of valves involved with fibrous pannus varies significantly and depending on the study may range from 20% to 80% ( Wellford AL,1994).
A high level of suspicion must be maintained in any patient with a valvular prosthesis who has nonspecific cardiac symptoms and, TTE provides assessment of hemodynamic severity, whereas TEE or fluoroscopy is often used to delineate valve motion and clot burden (Renzulli et al,1993).
The 2006 American College of Cardiology/American Heart Association guideline for valvular disease endorses a class IIA recommendation for emergent surgery of left-sided or fibrinolytic therapy of right-sided PVT that is complicated by either New York Heart Association (NYHA) class III-IV CHF or a large thrombotic burden. Class IIB indications for fibrinolytic therapy include: left-sided PVT with both NYHA class I-II CHF (class III-IV CHF if high surgical risk) and small clot burden; and obstructed left-sided PVT with CHF and large clot burden but high surgical risk. Finally, unfractionated heparin for small
thrombus and class I CHF is also a Class IIb indication (Bonow et al,2006).
Specific management of PVE consists of obtaining blood cultures and initiating empiric antibiotic therapy. Because there is a fairly
well-defined difference between the pathophysiology and type of organisms responsible for early and late PVE, the initial choice of antibiotics will depend on the time of presentation relative to the date of surgical valve replacement; that is, “early” PVE (<60 days) and “late” PVE (>60 days). Staphylococcal, particularly Staphylococcus epidermidis, infections predominate in early PVE, whereas in late PVE there are equal percentages of streptococcal and staphylococcal infections ( Renzulli et al,1993).
In general, the hemodynamic impact of acute tricuspid regurgitation is less significant than that of acute left-sided valvular lesions. However, in the setting of acute massive RV overload, hypotension and shock may ensue. More commonly, persistent, severe, chronic tricuspid regurgitation results in salt and water retention leading to peripheral edema, ascites, and congestive hepatomegaly. Massive RV volume overload secondary to acute tricuspid regurgitation may also lead to a significant reduction in LV ejection fraction due to paradoxic early systolic septal motion that results from ventricular interdependence (Lin SS et al,1994).
The management strategy for acute tricuspid regurgitation should be focused primarily on medical therapy. In general, most patients can be effectively treated with a diuretic alone or in combination with an inotropic agent, such as dobutamine. In rare instances of acute massive tricuspid regurgitation, the patient who is refractory to medical therapy may require immediate surgical intervention. When possible, tricuspid valve repair, often with ring annuloplasty is preferred over valve replacement. However, when valve replacement is required, a bioprosthetic valve is often used ( Stern et al ,1986