Mitral regurgitation

Pratap Sagar Tiwari, MD

Pic source: www.brown.edu

Overview• Mitral regurgitation (MR) is defined as an

abnormal reversal of blood flow from the leftventricle (LV) to the left atrium (LA).

• It is caused by disruption in any part of the mitralvalve (MV) apparatus.

• Mitral regurgitation can be divided into 3 stages:

1. acute

2. chronic compensated

3. chronic decompensated

Pic source: www.abbottvascular.com

Anatomy: Mitral valve

The mitral apparatus is composed of

1. the left atrial wall

2. the annulus

3. the leaflets

4. the chordae tendineae

5. the papillary muscles

6. the left ventricular wall

• The mitral valve connects the left atrium (LA) and the left ventricle (LV).

• The mitral valve opens during diastole to allow the blood flow from the LA to the LV.

• During ventricular systole, the mitral valve closes and prevents backflow to the LA.

Pic source: www.heart-valve-surgery.com

Anatomy: MV Annulus

1. Figure2: http://emedicine.medscape.com

• The mitral annulus is a fibrous ring thatconnects with the leaflets.

• The annulus functions as a sphincter thatcontracts and reduces the surface area ofthe valve during systole to ensurecomplete closure of the leaflets.

• Annulus contraction during systolepromotes valve competence

• Thus, annular dilatation of the mitral valvecauses poor leaflet apposition, whichresults in mitral regurgitation.

• Annulus may dilate in ischemic or dilatedcardiomyopathy.

Anatomy: Mitral valve leaflets

1. Picture source: http://emedicine.medscape.com2. Harken DE, Ellis LB, Dexter L, Farrand RE, Dickson JF. The responsibility of the physician in the selection of patients with mitral stenosis for surgical treatment.Circulation. Mar 1952;5(3):349-62.

Harken et al have described the mitral valve as acontinuous veil inserted around thecircumference of the mitral orifice.[2]The free edges of the leaflets have severalindentations.Two of these indentations, the anterolateral andposteromedial commissures, divide the leafletsinto anterior and posterior .These commissures can be accurately identifiedby the insertions of the commissural chordaetendineae into the leaflets.• Inflammatory, degenerative, or infectious diseases

can result in perforation or poor coaptation ofleaflets

1

Anatomy: Chordae tendineae

1. Pic source: http://emedicine.medscape.com

• These are small fibrous strings thatoriginate either from the apicalportion of the papillary muscles ordirectly from the ventricular wall andinsert into the valve leaflets or themuscle.

• Chordal rupture or foreshorteningprevents leaflet coaptation

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Anatomy: Papillary muscles and left ventricular wall

1. http://emedicine.medscape.com2. Harken DE, Ellis LB, Dexter L, Farrand RE, Dickson JF. The responsibility of the physician in the selection of patients with mitral stenosis for surgical treatment.Circulation. Mar 1952;5(3):349-62.

• These 2 structures represent the muscularcomponents of the mitral apparatus.

• PM normally arise from apex and mid thirdof the LV wall.

• The anterolateral PM is normally larger thanthe posteromedial PM & is supplied by LADartery or LCX artery.

• The posteromedial PM is supplied by theRCA.

• Rupture of a PM, usually the complication ofAMI, will result in acute MR.

• Infarction or LV wall motion abnormalitiesmay lead to valve incompetence.

• Infarction of PM itself more likely to causeacute MR.

1

Anatomy: Mitral valve

1. Figure2: http://emedicine.medscape.com2. Perloff JK, Roberts WC. The mitral apparatus. Functional anatomy of mitral regurgitation. Circulation. Aug 1972;46(2):227-39.

Left atrial wall• The left atrial myocardium

extends over the proximal portionof the posterior leaflet.

• Thus, left atrial enlargement canresult in MR by affecting theposterior leaflet. The anteriorleaflet is not affected, because ofits attachment to the root of theaorta.2

Mitral regurgitation: etiologyAcute Chronic Primary MR

Endocarditis Papillary muscle rupture (post-MI) Trauma Chordal rupture/leaflet flail (MVP, IE)

Myxomatous (MVP) Rheumatic fever Endocarditis (healed)Mitral annular calcification Congenital (cleft, AV canal) \HOCM with SAM Radiation

Chronic secondary MR

Ischemic (LV remodeling) Dilated cardiomyopathy

The abnormal and dilated left ventricle causes papillary muscle displacement, which in turn results in leaflet tethering with associated annular dilation that

prevents coaptation.

Laplace Law

• The hemodynamic changes inacute MR are more severethan those in chronic MR duein part to the lack of time forthe left atrium and leftventricle to adapt to the MR.

• This is in contrast to chronicMR where these adaptationshave time to develop andtypically preservehemodynamic stability.

As stated by Laplace law: LV wall stress isdirectly proportional to the cavitypressure and inversely proportional towall thickness. Due to the addedregurgitant vol there is ↑ in LV volumethat leads to an ↑ in LV cavity pressureand it causes an ↑in wall stress.If a hypertrophic response occurs, ↑↑

thickness can return wall stress to N.

Chronic MR: Pathophysiology

Vol load imposed on LA & LV (usually it gradually ↑ over time)

Large total SV (supra normal EF) and normal forward SV

MR begets MR (viscious cycle in which further LV/annular dilatation ↑ MR

↑ Preload, LV hypertrophy, & reduced or normal afterload (low resistance LA provides unloading of LV)

↑ LVEDP &↑ LAP

Compensatory dilatation of LA & LV to accommodate vol load at lower pressure; this helps relieve pul congestion

LV hypertrophy (eccentric) stimulated by LV dilatation (↑ wall stress- Laplace Law)

Chronic MR: Pathophysiology..continue

Reduced forward SV/CO

MR begets MR (viscious cycle in which further LV/annular dilatation ↑ MR

Pul congestion & pHTN

Contractile

dysfunction↓ EF, ↑ end-systolic volume ↑ LVEDP/ vol, ↑ LAP

Basic mechanisms of acute native valve acute MR

1. Flail leaflet due to myxomatous disease(MVP), IE, or trauma.

2. Chordae tendineae rupture due to trauma,IE, or acute rheumatic fever.

3. Papillary muscle rupture or displacementdue to AMI or severe ischemia or trauma.

Pathophysiology: AMR

• Flail leaflet• Chordae tendineae rupture• Papillary muscle rupture

MRAbnormal reversal of

blood flow from :LV LA.

Sudden large Vol load imposed on LA & LV of normal size &

compliance

↑ LA volume /LAP

Pulmonary congestion

↓ Forward SV

Neurohumoral Response :↑Vascular resistance

↓ CO

Compensatory ↑ HR

Shock

Neurohumoral Responses

Activation of RAAS

Low output state

Contribute to maintenance of perfusion of vital organs :1. Maintenance of systemic pressure by

vasoconstriction, resulting in redistribution of bloodflow to vital organs

2. Restoration of CO by ↑ myocardial contractility andHR and by expansion of the ECF volume

• Catecholamine-stimulated contractility and ↑ HR.• Volume expansion ↑ venous return ↑ EDV ↑SV(via FSM)

Activation of SNS

Neurohumoral Maladaptive Responses

Activation of RAAS

Low output state

• Catecholamine-stimulated contractility and ↑ HR.• Volume expansion ↑ venous return ↑ EDV ↑SV(via FSM)

Activation of SNS

Maladaptive responses as below

• The ↑ in diastolic pressures transmitted to the atria and to the pulmonary circulations↑ in capillary pressures pulmonary congestion & peripheral edema

• The ↑ in LV afterload induced by the ↑ in PVR can both directly depress cardiac fn and enhance the rate of deterioration of myocardial function .

• Catecholamine-stimulated contractility & ↑HR worsen coronary ischemia (also ↑HR ↓EDFilling ↓EDV ↓ SV/CO

• Catecholamines and ATII promote the loss of myocytes by apoptosis, and hypertrophy

Eccentric vs concentric hypertrophy

EH :where the walls andchamber of a hollow organundergo growth in which theoverall size and volume areenlarged.It is applied especially to theLV.Sarcomeres are added inseries, as for example in DCM(in contrast to HOCM, a type ofCH, where sarcomeres areadded in parallel).

Pic source: www.revespcardiol.org

Functional mitral regurgitation

In patients with functional or secondary mitral regurgitation (MR), thepapillary muscles, chordae, and valve leaflets are normal.• There are two major causes of this problem:1. ischemia2. any cause of dilated left ventricle.

In these settings, MR may result from one or both of the following [1]:• Annular enlargement secondary to left ventricular dilatation• Papillary muscle displacement due to left ventricular remodeling,

which results in tethering and excess tenting of the leaflet .21. Trichon BH, O'Connor CM. Secondary mitral and tricuspid regurgitation accompanying left ventricular systolic dysfunction: is it

important, and how is it treated? Am Heart J 2002; 144:373.2. Yiu SF, Enriquez-Sarano M, Tribouilloy C, et al. Determinants of the degree of functional mitral regurgitation in patients with systolic

left ventricular dysfunction: A quantitative clinical study. Circulation 2000; 102:1400.

PREVALENCE of FMR

• Some degree of functional MR is almost always present inpatients with severe dilated cardiomyopathy, regardless ofetiology [1,2,3].

• A review of 50 patients with DCM(36 idiopathic, 14ischemic) referred for heart transplantation found that allpatients had at least moderate MR by Doppler echo [2].

• Functional MR is also a common problem in patients withESRD on maintenance HD. In this setting, volume expansionrather than intrinsic cardiac disease is primarily responsiblefor the cardiac enlargement.

1. Trichon BH, O'Connor CM. Secondary mitral and tricuspid regurgitation accompanying left ventricular systolic dysfunction:is it important, and how is it treated? Am Heart J 2002; 144:373.

2. Strauss RH, Stevenson LW, Dadourian BA, Child JS. Predictability of mitral regurgitation detected by Dopplerechocardiography in patients referred for cardiac transplantation. Am J Cardiol 1987; 59:892.

3. Koelling TM, Aaronson KD, Cody RJ, et al. Prognostic significance of mitral regurgitation and tricuspid regurgitation inpatients with left ventricular systolic dysfunction. Am Heart J 2002; 144:524.

Ischemic mitral regurgitation

• Ischemic MR is a complication of coronary heartdisease.

• It primarily occurs in patients with a priormyocardial infarction (MI).

• MR may also occur with acute ischemia, a settingin which the MR typically resolves after theischemia resolves.

• Following an MI, the MR is usually due toinfarction with permanent damage to thepapillary muscle or adjacent myocardium.

IMR:classified by the mechanism of the valve dysfunction

1. IMR secondary to papillary muscle rupture is a life-threatening complication of acute MI that accountsfor 5 % of deaths in these patients . This complicationusually occurs 2-7days after the infarct.

2. The papillary muscle may be infarcted with acute MI,but not ruptured.

3. The vast majority of patients have "functional"ischemic MR. In these individuals, the papillarymuscles, chordae, and valve leaflets are normal .However, the leaflets do not coapt and restrictedleaflet motion is frequently noted on echo.

IMR: papillary muscle dysfunction

• The term "papillary muscle dysfunction" has been usedin the literature to describe patients with functionalischemic MR, but this is a misnomer since papillarymuscle dysfunction does not explain the mechanism ofthis disorder [1,2,3].

• The mechanism for MR in this setting is betterdescribed as "papillary muscle displacement" due todysfunction of underlying left ventricular wall andassociated alteration of ventricular geometry.

1. Levine RA, Schwammenthal E. Ischemic mitral regurgitation on the threshold of a solution: from paradoxes to unifying concepts.Circulation 2005; 112:745.

2. Kaul S, Spotnitz WD, Glasheen WP, Touchstone DA. Mechanism of ischemic mitral regurgitation. An experimental evaluation.Circulation 1991; 84:2167.

3. Uemura T, Otsuji Y, Nakashiki K, et al. Papillary muscle dysfunction attenuates ischemic mitral regurgitation in patients with localizedbasal inferior left ventricular remodeling: insights from tissue Doppler strain imaging. J Am Coll Cardiol 2005; 46:113.

Auscultation

• S1 is generally absent, soft, or buried in the holosystolicmurmur of chronic MR.

• In patients with severe MR, the AV may close prematurely,resulting in wide but physiologic splitting of S2.

• A low-pitched S3 occurring 0.12–0.17 s after the AV closuresound, i.e., at the completion of the rapid-filling phase ofthe LV, : DUE TO sudden tensing of the papillary muscles,chordae tendineae, and valve leaflets. It may be followedby a short, rumbling, mid-diastolic murmur, even in theabsence of structural MS.

• S4 is often audible in ps with acute severe MR who are insinus rhythm.

Auscultation

• Chronic severe MR: A systolic murmur of atleast grade III/VI intensity and is usuallyholosystolic.

• The systolic murmur of chronic MR is usuallymost prominent at the apex and radiates tothe axilla.

• Acute severe MR: is decrescendo and ceasesin mid- to late systole .

Auscultation

• Ruptured chordae tendineae or primary involvement of theposterior mitral leaflet with prolapse or flail : regurgitantjet is eccentric, directed anteriorly, and strikes the LA wallthe systolic murmur is transmitted to the base of theheart (therefore, may be confused with the murmur of AS).

• ruptured chordae tendineae, the systolic murmur mayhave a cooing or "sea gull" quality.

• A flail leaflet: murmur with a musical quality.• The systolic murmur of chronic MR not due to MVP is

intensified by isometric exercise (handgrip:↑LVV) but isreduced during the strain phase of the Valsalva maneuverbecause of the associated decrease in LV preload.

Mitral valve prolapse

• The most important finding is the mid- or late (nonejection) systolic click,which occurs 0.14 s or more after S1 and is thought to be generated by thesudden tensing of slack, elongated chordae tendineae or by the prolapsingmitral leaflet when it reaches its maximum excursion.

• Systolic clicks may be multiple and may be followed by a high-pitched, latesystolic crescendo-decrescendo murmur, which occasionally is "whooping"or "honking" and is heard best at the apex.

• The click and murmur occur earlier with standing, during the strain phaseof the Valsalva maneuver, and with any intervention that ↓ LV volume,exaggerating the propensity of mitral leaflet prolapse.

• Conversely, squatting and isometric exercises, which ↑LV volume, diminishMVP; the click-murmur complex is delayed, moves away from S1, and mayeven disappear.

• Some patients have a mid-systolic click without a murmur; others have amurmur without a click. Still others have both sounds at different times.

Acute vs Chronic MR