Mitral Stenosis for beginners

Pratap Sagar Tiwari

Pic ref: http://int-prop.lf2.cuni.cz/foto/016/pic00026.jpg

Uptodate 20.3

Mitral stenosis

• MS is characterized by obstruction to leftventricular inflow at the level of MV due tostructural abnormality of the MV apparatus.1

• MS is due to thickening and immobility of themitral valve leaflets.

• The normal MVO has a CSA of 4-6 cm2.1. Carabello, B. A. (2005). "Modern Management of Mitral Stenosis". Circulation 112 (3): 432–7

Etiology

• Rheumatic heart disease• Congenital MS• Mitral annular calcification (particularly in

patients with ESRD).• Conditions that simulate MS: IE with large

vegetation, LA myxoma, ball valve thrombus, andcor triatriatum.

• Less common causes: malignant carcinoiddisease, SLE, RA, mucopolysaccharidoses, Fabrydisease, Whipple disease, and methysergidetherapy.

Rheumatic mitral stenosis

• In RMS, the MVO is slowly diminished by progressivefibrosis, calcification of the valve leaflets.

• The flow of blood from LA to LV is restricted and LAPrises, leading to pulmonary venous congestion andbreathlessness.

• There is dilatation and hypertrophy of the LA, and leftventricular filling becomes more dependent on leftatrial contraction.

• Note: The association of atrial septal defect withrheumatic mitral stenosis is called Lutembachersyndrome.

Pathophysiology

LAE

Atrial Fibrillation

↑LAP precipitate pul

edema Acute dyspnea

↓Ventricular fillingThromboembolism Palpitation

Stroke

Hoarseness :due to compression of the LRLN by a dilated LA or pulmonary artery (Ortner syndrome)

High pressure ruptures

Pulmonary vessels :hemoptysis

Pulmonary HypertensionBackward transmission of the elevated left atrial pressure

↑ Pulmonary artery pressure

↑RAP & development of right sided heart failure

RV hypertrophy &

enlargement

Hepatomegaly & Pulsatile liver

Tricuspid regurgitation

JVD

Parasternal heave

Prominent v wave

Prominent a wave

TR

Peripheral edema

Loud P2, later becomes palpable

Pathophysiology: MS

Fatigue/Dyspnea/↓Functional capacity

↓ MVA

Pul congestionAFib

↑ LAP

↑ LAP transmitted to pulmonary venous system

LA enlargement (compensation to attempt to

lower LAP)

↑ LAP, LAE LA remodelling

LA clotExertional Dyspnea

/Pul edema

↑PVR ,PHTN RV pressure overload RVH

RV dilates & fails

With significant obstruction

to flow from PVR & MS

CO ↓ (first

with exercise

then at rest)

History

• Generally asymptomatic at rest during the early stage. However,factors that ↑ HR such as fever, severe anemia, thyrotoxicosis,exercise, and Afibdyspnea.

• Systemic embolization may lead to stroke, renal failure, or MI.• Hoarseness :compression of the LRLN against the pulmonary artery

by the enlarged LA. Also, compression of bronchi by the enlarged LAcan cause persistent cough. Cough also occurs due to pulcongestion

• Hemoptysis may occur.• Palpitation• Chest pain (due to pul hypertension)• Oedema / Ascites (Right heart failure)• Pregnant women with mild MS may become symptomatic during

their 2nd trim (↑in blood vol ).

Physical examination

• Presence of mitral facies (pinkish-purplepatches on the cheeks) indicate chronic severeMS (reduced CO & vasoconstriction).

JVD may be seen.

• In pt with sinus rhythm, a prominent a wave:↑ RA pressure from pul HTN & RVfailure.

• A prominent v wave :is seen with TR.

Palpation

• The arterial pulses are reduced in volume dueto the decreased SV.

• Pulses may be irregular in Afib.

• Tapping apex beat that is not displaced.

• Left parasternal heave - presence of RVH dueto pulmonary HTN

• A P2 may be palpable in the 2LICS.

Parasternal Heave

• Grade 1 : visible but not palpable

• Grade 2 : Visible & palpable and obliterable

• Grade 3: Visible & palpable but not obliterable

Cardiac auscultation: Heart sounds

• The S1 is accentuated because of a wideclosing excursion of the mitral leaflets.

• The degree of loudness of the S1 depends onthe pliability of the MV.

• The intensity of the S1 ↓ as the valve becomesmore fibrotic, calcified, and thickened.

• The S2 is initially normal but, with thedevelopment of PHTN, P2 becomes ↑ inintensity .

Cardiac auscultation: Opening snap

• An OS of the MV is heard at the apex whenthe leaflets are still mobile .

• The OS is due to the abrupt halt in leafletmotion in early diastole.

• Note: The OS following S2 may be mistaken for a split S2(OS is best appreciated at the apex, not the base. )

• As the MS progresses and LAP is ↑, the OSoccurs earlier after S2 or A2. Thus, the shorterthe A2-OS interval, the more severe the MS.

Cardiac auscultation: murmur

• low-pitched diastolic rumble that is mostprominent at the apex.

• Although the intensity of the diastolic murmurdoes not correlate with the severity of thestenosis, the duration of the murmur is helpfulsince it reflects the transvalvular gradient and theduration of blood flow across the valve.

• The ↑ in atrial pressure after atrial contraction,results in an increase in the loudness of themurmur, termed "presystolic accentuation" .

MS:

• The diastolic murmur and OS are diminished withinspiration, but augmented with expiration (in contrastto TS). With inspiration, the A2-OS interval widens .

• Increasing venous return, eg, by lying the patient downand lifting the legs, augments the gradient; as a result,the diastolic murmur lengthens while the A2-OSintervals shorten. (Similar changes are seen inresponse to exercise.)

• In contrast, reducing venous return with amyl nitrate,the Valsalva maneuver, or standing after squattingshortens the murmur and lengthens the A2-OSinterval.

MS: murmur

• On auscultation of mitral area of the heart, s1 isshort ,sharp and accentuated and s2 is normal.

• Opening snap is heard just after s2.

• There is low pitched, mid –diastolic, rumblingmurmur with presystolic accentuation of Grade 4intensity in the mitral area without any radiation.

• The murmur is best heard at cardiac apex withbell of steths ,in left lateral position ,at the heightof expiration and after doing mild exercise.

MDM: D/D

• It is not Carey coombs murmur (occurs in active rheumaticvulvulitis and oedema of MV cusps gives rise to soft MDM)because there is absence of loud s1, OS and diastolic thrill.

• It is not Austin flint murmur (which is a functional low pitchmid diastolic murmur in pt with AI in which murmur isproduced as the regurgitant jet flow hits the anterior mitralleaflets) because in AFM, the presystolic component is absent,there is no thrill, and S1 is not loud. And there is no OS.Moreover in AFM of AI ,there are features of LVH andperipheral signs of AI which is not present in this case.

• It is not MDM of TS ,because the murmur of TS would be bestheard in LSB and increases at the height of inspiration.

CXR

CXR

• Backward displacement of esophagus by enlarged LA(in latview)

• Enlarged LA , Double shadow due to enlarged LA

• Straightening of left heart border

• Splaying of carina (The left main bronchus is lifted up by theenlarged LA)

• Prominent upper zone pulmonary veins (Inverted moustachesign / Antler’s horn sign / Cephalisation pulmonary of bloodflow)

• Kerley B lines (indicating fluid collection in the interlobularsepta)

Management

• Patients with minor symptoms should be treatedmedically.

• Intervention by balloon valvuloplasty, mitral valvotomyor MVR should be considered if the patient remainssymptomatic despite medical Rx or if PHTN develops.

• Anticoagulation :to reduce the risk of systemicembolism,

• Ventricular rate control (digoxin, β-blockers CCB) inAFib

• Diuretic therapy to control pulmonary congestion.• Antibiotic prophylaxis against infective endocarditis is

no longer routinely recommended.

End of slides