STS E Book - The Mitral Valve Flashcards

1
Q

What are the trigones of the mitral valve

A

The two fibrous components whose limits define the fibrous portion of the mitral annulus

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2
Q

The right fibrous trigone of the mitral valve is part of the central fibrous body of the heart, in continuity with what structures (3)?

A

The aortic valve, the tricuspid valve, and membranous septum

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3
Q

What are the important markers of the mitral valve used for annuloplasty ring sizing? Why?

A

Intertrigonal distance, because the fibrous annulus remains unchanged across the spectrum of mitral disease

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4
Q

What are the papillary muscles that support the mitral valve? What is their blood supply?

A

Anterolateral - LAD and Cx
Posteromedial - PDA

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5
Q

What is the usual etiology of mitral stenosis?

A

Rheumatic fever in childhood or adulthood - definitive history can be obtained in about 50-60%.

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6
Q

Does rheumatic fever affect women or men more?

A

Women by a 2:1 to 3:1 ratio, usually acquired before 20, becomes evident 1-3 decades later

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7
Q

What is the underlying bacteria that causes rheumatic fever and thus rheumatic mitral stenosis?

A

Group A beta-hemolytic strep -> mimicry b/w strep antigens and heart tissue proteins -> antigen cross-reactivity + high inflam cytokine + low IL-4 -> auto-immune pancarditis -> valve leaflet (MV most common), endocardium, and myocardium damage -> commissural fusion, chordial fusion and shortening, leaflet fibrosis, calcifications

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8
Q

What are the physiologic adaptations of mitral stenosis?

A

Ventricular filling restriction -> LA pressure inc -> TV gradient increase during diastole -> … -> chronic and progressive stenosis -> inc PVR and pulm HTN

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9
Q

What are the valve area and transvalvular gradient consistent with mitral stenosis?
Diastolic pressure half time?

A

MVA < 1.5 cm^2 (MVA < 1 is very severe)
TVG >10 mm Hg

Other dx criteria: diastolic half-time >150 ms

Will cause elevated PASP >30

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10
Q

How is mitral transvalvular gradient dynamic as it relates to heart rate?

A

With increased HR -> dec duration of LV filling during diastole -> inc mean TVG and LA pressure.
This can create situations where the TVG is only significant (and thus symptomatic) during exercise.

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11
Q

Why is maintenance of sinus rhythm important for mitral stenosis patients?

A

Atrial contraction augments flow through the stenotic valve, thereby helping to sustain adequate forward cardiac output

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12
Q

Why does maintaining sinus rhythm become difficult for MS patients?

A

High LA pressure -> LA hypertrophy and dilation -> disorganized atrial muscle fibers -> abnormal conduction velocities -> nonhomogenous refractory periods -> inc automaticity or re-entry -> AF -> atrial thrombus and dec hemodynamic stability.

Eventually PASP >30.
MS = MVA < 1.5 or DP1/2t > 150 ms.

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13
Q

Describe the pathophysiology of pHTN in MS.

A

Passive transmission of high LA pressure (w/ severe enlargement of LA) -> PV HTN, pulm arteriole constriction -> pulm vasc obliterative changes -> PA systolic P >60 -> inc impedance to RV emptying -> RHF and TR.

Elevated PASP >30 is a hemodynamic consequence of severe MS.

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14
Q

How is frailty caused by MS?

A

“Cardiac cachexia” can be caused by the low CO, CHF, and lethargy associated w/ MS

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15
Q

Describe the TTE findings of rheumatic mitral stenosis

A

Reduced diastolic excursion of the leaflets, thickening or calcification of the valvular and subvalvular apparatus; M-mode can show thickening, reduced motion, parallel movement of the anterior and posterior leaflets during distole

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16
Q

How might a cardiac cath help with mitral stenosis workup?

A

LHC for coronary anatomy for older pts that have CAD risk; RHC for CI and pHTN.

17
Q

What are the three general pathoanatomic types of MR based on leaflet motion (Carpentier)?

A

I: normal leaflet
II: prolapse or excess motion
III: restricted motion
- a: diastole
- b: systole

18
Q

Most common cause of primary MR?

A

myxomatous degeneration - thickened and opaque and the degenerative process may extend down the chordae and out onto the annulus. Histologically, elastic fiber and collagen fragmentation and disorganization are present, and acid mucopolysaccharide material accumulates in the leaflets

PICTURE: Gross view of the surgical specimen from an insufficient mitral valve represented by the anterior leaflet. A - The atrial aspect; B - The ventricular aspect. Note the diffuse thickening of the redundant leaflet with focal bulging towards the atrial aspect (asterisks) flagged as areas of valvar prolapse by the imaging exams. The chordae tendineae are also thickened. One of them shows a rounded tail end, which is characteristic of a secondary lesion due to its rupture (arrows); C and D - Photomicrography of the valve leaflet. In C, a central area of dense fibrous tissue (F) is shown, surrounded by a thick layer of loose connective tissue with myxomatous appearance (M). Hematoxylin-eosin stain, objective magnification 10X. In D, the valve section stained with Movat pentachrome is shown, revealing pale blue areas corresponding to myxomatous stroma. Black areas correspond to elastic fibers, focally disrupted (black arrowhead). Objective magnification 2.5X.

19
Q

Affecting 2-3% of the population, MR can be congenital/heritable or acquired. What is the congenital/heritable type?

A

Barlow valve in younger pts (A). Tend to have more myxomatous changes - thick, opaque.

20
Q

Affecting 2-3% of the population, MR can be congenital/heritable or acquired. What is the acquired type?

A

fibroelastic deficiency in older pts

21
Q

A minority of pts w/ MVP progress to sx mitral insufficiency (5-10%). What are the general etiologies of the mitral insufficiency in these pts?

A

chordal rupture and/or annular dilation

22
Q

What is the most common chordal rupture for the mitral valve?

A

P2.

23
Q

What is the difference in hemodynamic pathophysiology b/w acute MR and chronic MR?

A

Acute: LA is not as compliant -> high LA pressure -> rapid pulm edema and sx.
Chronic: compensatory changes inc LA and pulm bed venous compliance -> sx may not occur for years.

24
Q

How does MR affect preload and afterload?

A

preload is increased because of the backwards volume, and afterload is decreased d/t a parallel outflow track across the MV -> inc LV EF, inc LV EDV

25
Q

What EF in the presence of severe MR would indicate an advanced degree of myocardial dysfunction?

A

<55%

26
Q

Does atrial fibrillation occur more often in MR or MS?

A

MS

27
Q

What is the prognosis of those with rheumatic anterior leaflet MR as opposed to those with posterior?

A

Anterior rheumatic MR tends to improve with medical mgmt.

28
Q

How did Replogle subclassify ischemic mitral regurgitation?

A

1) sudden onset insufficiency d/t acute MI and papillary muscle rupture w/ or w/o LV wall dysfx
2) MR assd w/ CAD w/ normal leaflets
3) MR caused by end-stage ischemic dilated CM

29
Q

Boltwood found that in patients with nonischemic cardiomyopathy and mean EF of 25%, what echo measurement was the chief determinant mitral insufficiency?

A

Annular size, especially in the septal-lateral dimension correlates with the degree of LV systolic dysfunction in those with dilated cardiomyopathy

30
Q

What represents the sum effect of annular and subvalvular geometric deformations on leaflet coaption and is consistently identified in FMR and iMR as the main predictor of MR severity?

A

Leaflet tenting

31
Q

What is the trend seen in the difference in MR caused by anterior vs inferior MI?

A

Anterior MI:
More significant LV dysfunction and dilation - more like idiopathic dilated cardiomyopathy with leaflets widely tethered toward the ventricle with greater LV and mitral dilation.
Infarction of the anterior wall and the anterior papillary muscle does not result in MR until advanced LV dilatation and systolic dysfunction develop.

Inferior MI:
More localized tethering, more substantial perturbation of the mitral valve apparatus.
Systolic dysfunction of the posterior/inferior LV wall inclusive of the posterior papillary muscle with subsequent leaflet tethering appears to be the prerequisite lesion for the evolution of experimental IMR.

32
Q

In a recent report from the Cardiothoracic Surgical Trials Network of 301 patients with moderate IMR randomized to coronary artery bypass grafting alone or combined coronary artery bypass grafting with valve repair, the rate of death was 7.3% and 6.7% at 1 year, respectively.
What were some of the other outcomes?
What are the likely determinants of outcomes?

A

The combined group had longer bypass time, longer hospital stays, and more neurologic events.
In terms of the best type of valve surgery for patients with IMR, it is likely that the patient clinical condition and LV functional status are more powerful determinants of outcome, as opposed to whether a patient undergoes repair or replacement.

33
Q

The Cardiothoracic Surgical Trials Network multi-institutional randomized trial of 251 patients with severe IMR comparing complete rigid or semi-rigid ring annuloplasty with mitral valve replacement demonstrated what?

A

no difference in LV reverse remodeling or survival at 12 months

34
Q

Pt has severe symptomatic MS with AF and LA thrombus. What do you do?

A

Surgery.
PMBC is normally first line, but not in pts with LA thrombus and moderate to severe thrombus.

35
Q

Pt has severe symptomatic MS with moderate MR, and AF. What do you do?

A

Surgery.
PMBC is normally first line, but not in pts with LA thrombus and moderate to severe regurgitation.

36
Q

In the context of rheumatic mitral stenosis, the morphologic favorability of a stenotic valve for PMBC can be assessed using what?

A

the Wilkins Score

37
Q

What is the Wilkins Score (context of MS)?

A

Score to predict PMBC success when evaluating favorable valve anatomy. Consists of degree of leaflet mobility, valve thickness, subvalvular thickening, and valvular calcification are evaluated by echocardiography and each scored from 0 to 4.
Using this system, a total score of 8 or less is predictive of successful PMBC, with 72% sensitivity and 73% specificity.