1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Acute Mitral regurge

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

3. 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

4. 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)

5. 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

6. 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

7. 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.

8. 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

9. 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

10. 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.

11. 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.

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

16. 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

17. 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}

18. 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

19. -- 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

20. Thank you