D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Acute Mitral regurge

--Gravely ill with significant hemodynamic abnormalities that require urgent medical and usually surgical treatment.

Etiology

--Flail leaflet due to myxomatous disease (mitral valve prolapse), infective endocarditis, or trauma.--Chordae tendineae rupture due to trauma, spontaneous rupture, infective endocarditis, or acute rheumatic fever.--Papillary muscle rupture or displacement due to acute myocardial infarction or severe ischemia or trauma

Prosthetic valves

--Tissue valve leaflet rupture due to degeneration, calcification, or endocarditis.--Impaired closure of mechanical valve occluders due to valve thrombosis, infection, or pannus formation.--With older generation mechanical valves, there were instances of strut fracture and disk escape, but these have not been reported with currently implanted valves.--Paravalvular regurgitation due to infection or suture rupture (often related to a calcified or scarred annulus)

PATHOPHYSIOLOGY

--lack of time for the left atrium and left ventricle to adapt increase LA preasure immediately reflected back into the pulmonary circulation, often leading to pulmonary edema--Despite a compensatory increase in heart rate, cardiac output falls, possibly precipitating cardiogenic shock neurohumoral response increase in vascular resistance, which exacerbates the regurgitation

CLINICAL MANIFESTATIONS

--Cardiac emergency with the sudden onset and rapid progression of pulmonary edema, hypotension, and signs and symptoms of cardiogenic shock often not recognized at presentation because the clinical history mimics an acute pulmonary process (such as infection or acute respiratory distress syndrome) consider echocardiography early--May not be so dramatic if acute MR is superimposed upon chronic MR or the patient is younger and physically fit

Physical examination

--Pulmonary edema--Poor tissue perfusion with peripheral vasoconstriction, pallor, and diaphoresis.--The arterial pulse is often rapid and of low amplitude or thready due to the reduction in forward output.--When there is an associated increase in right-sided pressure, the neck veins become distended; they may also become pulsatile with a marked "v" wave if the elevated right ventricular pressure leads to tricuspid regurgitation.--Cardiac impulse is hyperdynamic, normal in location because left ventricular size is normal {unless superimposed upon chronic MR}. --There is often a hyperdynamic precordium with a right ventricular lift due to the acute increase in pressure within this chamber and the development of tricuspid regurgitation.

Cardiac auscultation

--S3 is commonly heard but may be difficult to appreciate if tachycardia is present. --With the development of pulmonary hypertension, P2 is increased in intensity and the murmurs of pulmonary and tricuspid regurgitation may be appreciated--Pressure gradient between the left atrium and ventricle diminishes or disappears by the end of systole {combination of a low systemic blood pressure and elevated left atrial pressure}, the systolic murmur is often soft, low pitched and decrescendo, ending before A2 Approximately 50% of patients with moderate to severe MR have no audible murmur--Best heard along the left sternal border and base of the heart, generally without a thrill, and may radiate to the back. It can be confused with an acute ventricular septal defect

Electrocardiogram

--No electrocardiographic abnormalities specifically associated with acute MR.--Changes that reflect the etiology acute myocardial infarction, left ventricular hypertrophy, or P-mitrale reflecting underlying chronic MR

Chest radiograph

--Normal size cardiac silhouette, with severe left-sided congestive heart failure and pulmonary edema.--An enlarged left ventricle and atrium may be present if chronic MR has been present prior to the acute event.

Echocardiography

--Diagnosis, mechanism, and etiology--Left atrial size may be normal-Left ventricular size is normal-Systolic function is normal or hyperdynamic-The duration of aortic valve opening may be reduced--Findings are related to the etiology of acute MR:*Evidence of a flail mitral leaflet when the etiology is papillary muscle or chordal rupture. {Chordal rupture with rheumatic disease more often affects the anterior leaflet, while chordal rupture with myxomatous disease more often involves the posterior leaflet}.*Vegetations on the leaflets may be seen in patients with endocarditis.--The severity of regurgitation is evaluated with Doppler studies.

--Transthoracic echocardiography can underestimate the severity of MR due to inadequate imaging of the color flow jet TOE

Cardiac catheterization

*2006 ACC/AHA:--Coronary angiography should not be performed before valve surgery in patients who severely hemodynamically unstable.--Coronary angiography was recommended in patients who have or are suspected to have coronary disease (and who may have ischemic MR) and those at risk for coronary disease. At risk was defined as men ≥35 years of age, women ≥35 years of age with coronary risk factors, and postmenopausal women.--The weight of evidence and/or opinion was considered in favor of the usefulness of coronary angiography solely for acute MR in patients undergoing emergency valve surgery*Ventriculography {not recommended} immediate, complete, and usually persistent opacification of the left atrium on the first beat after ventricular injection. Opacification of the pulmonary veins is also frequently seen due to the high atrial pressures during systole

Medical stabilization {till surgery}

--Intravenous nitroprusside can reduce MR, both by reducing systemic vascular resistance and by improving mitral valve competence as the left ventricular size falls increases forward cardiac output and diminishes pulmonary congestion.--Nitroprusside should not be given as monotherapy in patients who are hypotensive at presentation inotropic agent such as dobutamine, intraaortic balloon pump (IABP) is often inserted {can be continued into the early postoperative period until hemodynamics stabilize}

Surgery

--Mortality rates as high as 50%--Chordal rupture:often with mitral valve repair lower operative mortality, improved preservation of left ventricular function, better long-term survival, and risks of a prosthetic valve and anticoagulation are avoided--Endocarditis :*Emergency surgery for acute mitral regurgitation due to endocarditis if refractory heart failure or an intracardiac fistula is present* The 2006 ACC/AHA guidelines recommended that, in the setting of active infection, mitral valve repair should be performed, if possible; mitral valve replacement is associated with a risk of infection of prosthetic materials

-- Ischemic MR:-Percutaneous revascularization may lead to resolution of the MR medical therapy and an IABP may be used during the acute episode with weaning of these modalities as myocardial function improves.-In contrast, surgical intervention is need with papillary muscle rupture- Partial papillary muscle rupture may stabilize the patient and delay surgery for 6-8weeks after myocardial infarction to avoid operating on the necrotic myocardial tissue. Valve repair is preferred, but myocardial necrosis may necessitate valve replacement

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