MITRAL STENOSIS, NICVD

7/27/2019 MITRAL STENOSIS, NICVD

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MS (Mitral Stenosis)

Dr. Abu Azam

Associate Professor

Head of Nuclear Cardiology


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Definition of MS:

-Mitral stenosis is the obstruction of the flow of

blood from the left atrium to the left ventriclethrough the narrow mitral valve during diastole.

Area of normal mitral valve orifice and area in

MS.

a) 4-6 cm2 normal.b) If it is narrowed < 3.5cm2 then consider as MS.

< 0.5-1 cm2 = Severe or Critical MS

1-1.5cm2 = Moderate MS

1.5-3.5 cm2 = Mild Ms.* Critical MS vs. Critical AS.

- Severe AS:


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3. Causes of MS.

a) Rheumatic fever (viz. recurrent rheumatic endocarditis).

b) Congenital, specific in infant and children ,rare in adult.- Dysplasia of mitral valve.

- Parachute mitral valve.

- Supravalvar ring in left atrium.

c) Rarely calcification of valve as well as annulus.

Simulating MS but not actual cause.

d) LA thrombus.

e) Left atrial myxoma.

f) Bacterial vegetation in LA.

g) Congenital association e.g. Lutembachers syndrome.4. Incidence of MS.

-Female: Male = 3:2 i.e. 2/3rd of MS takes place in female.

-Less then 1% (< 1%) streptococcal sore throat leads to Rheumatic

fever.


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* Some statistical information about MS.

i).Rheumatic origin: 90-95%

ii).Others: only 5%

-Congenital.-Calcification.

-Malignant Carcinoid.

-Methysergide therapy.

iii). 25 % of rheumatic heart disease is pure MS.

iv).40 % of RHD is combined lesion of with AR/MR/AS.

v). 50 % of MS gives +ve history of rheumatic fever.

*Percentage of severe MS.

- About 10% of MS are severe.

* MS vs. AF.-50% of MS present with AF.

-Age for AF in MS is 30-35 yrs, even 20-25 years in

Bangladesh.


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* Some statistical information about MS.

i).Rheumatic origin: 90-95%

ii).Others: only 5%

-Congenital.-Calcification.

-Malignant Carcinoid.

-Methysergide therapy.

iii). 25 % of rheumatic heart disease is pure MS.

iv).40 % of RHD is combined lesion of with AR/MR/AS.

v). 50 % of MS gives +ve history of rheumatic fever.

*Percentage of severe MS.

- About 10% of MS are severe.

* MS vs. AF.-50% of MS present with AF.

-Age for AF in MS is 30-35 yrs, even 20-25 years in

Bangladesh.


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Important incidences to be remembered for MS.

i). M: F = 1: 2-3

ii).Rheumatic origin: 50%.

iii).MV alone: 40 50% (i.e. either pure MS or pure MR or both).

iv).Aortic valve alone: 15 20%

v).Combined: 35 40%

vi).Total MV involvement: 90 95%

vii).25% all RF: Pure MS.

viii).50 % of MS associated with MR.

ix).75 % of all MS in female are Rheumatic Origin.

x).3 % of Total streptococcal infection cause RF. Again

xi). 1 % of total RF will involve heart.


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Primary and secondary changes (Pathology) in MS.

i).Primary changes of MS:

- Cusps: Thickening and fibrosis of cusps and later calcification.

- Commissures: Fusion of cusps at commissure.

-Chordae: Thickening, fibrosis and shortening of chordae resulting contracture of

leaflets.-Above three lesion combinely produces funnel shaped or fish mouth appearance of

mitral valve orifice.

ii).Secondary affects or changes of MS:

- Calcification of leaflet tissue.

-LA enlargement.

-PH with its signs.

-RV enlargement.

-TR.

-Fibrosis and disorganization of atrial muscle causes AF.

* Pathology in MR.

- Cusps are fibrosed, thickened and deformed.

- Chordae fused and shortened.

- Calcification of commissure/s.

- Sometimes dilatation of MV ring.

* AF vs. MS.

-Increased LA pressure and chronic process of rheumatic fever leading to LA dilation,

fibrosis and disorganization of LA muscle, there by conduction disturbance and AF.


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Symptoms (possible presentation) of MS:

- 50% of patient gives history of Rheumatic fever.

- Usually gives symptom when MV area is less than 2 cm2

.- Symptoms can be described as follows:

i). Fatigue

ii). SOB: on exertion or rest, Orthopnea or PND.

iii). Palpitation

iv). Acute pulmonary edema.v). Hemoptysis.

vi).Repeated RTI.

vii). CCF.

viii). Chest pain.

ix). Metabolic manifestation.

x). Systematic embolism.

xi). IE.

xii). Ortners system.


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Signs in MS on physical examination:

- Malar flush.

- Dusky discoloration of cheek.

- May be orthopnic.

Pulse:

i. May be normal.

ii. May be normal with law volume, due to low cardiac output or due to failure.

iii. May be tachycardia due to impending failure.

iv. In AF pulse may be irregularly irregular and also Pulsus deficit of unequal volume.

v). If atrial flutter, the pulse rate is high but regular/irregular.

Blood Pressure:

-Usually normal.

-Blood pressure can be high if thrombo embolism in renal artery.

JPV:

-May be normal.

-Raised JVP if heart failure.

-Prominent a wave may be found in patient with sinus rhythm having pulmonary hypertension. It is due to forceful contraction of RA

against noncompliant (hypertrophy) RV in RVH, but normal v wave.

-Prominent v wave if TR.

-Absent a wave in AF, but prominent v wave with slow Y descent.

Precordium:

-Tapping apex: A palpable 1st heart sound producing tapping apex at normal position.

-Diastolic thrill is a classical finding at apex.

-A para sternal lift on left side.

-Palpable P2.

-Loud 1st heart sound.

-Opening snap medial to apex.

-MDM with presystolic accentuation at apex.

-S4 possible in failure of RV.

-May be murmur of TR/ PR.

-S3 not possible in MS.

* Role of exercise to elicit MDM and exaggeration of HF.

-Flow rate along mitral valve is an important contributing factor for pressure gradient in mitral valve. Actually flow rate (FR) through the

mitral valve is equal to 4 (four) multiple of pressure gradient between LA to LV.

- So small variation in FR as found in exercise will produces a marked increase in pressure gradient. So clear MDM.

-Similarly exercise exaggerates heart failure.


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Consequences of MS on different chambers of heart.

-Due to obstruction, LA pressure rises. The rise of LA pressure depends, on severity of MS and flow across it. In

mild MS LA pressure remain within normal limit at rest but rises during exertion. In critical MS the LA pressure

raises up to 25mmHg.

-LA pressure is parallel with pressure in pulmonary vein and pulmonary capillary wedge pressure

(PCW).[Normal PCW: 5-14 mmHg, mean: 10 mmHg].

-As there is increased pulmonary capillary pressure, there is also concomitant rise of pulmonary arterial

pressure.

[Normal values:

i). PA(S): 15-30mmHg, mean: 25mmHg].

ii).PA (EDP): 5-15 mmHg, mean: 10 mmHg.

-LV (EDP) and LV filling pressure is normal in pure MS. But it is increased in MS with MR/IHD/HCM

-PA pressure normal at rest in mild MS but rise during exercise. In severe MS the PA pressure raised even at

rest.

-RV function maintains up to pressure 70 mmHg. If exceed 70mmHg RV dysfunction develops followed byincrease RA pressure

*Acute pulmonary edema (i.e. acute LHF) in severe MS of early vs. late.

If PCW rapidly rise to 30mmHg it will crosses the hydrostatic pressure, so there may be pulmonary edema. If

the process takes place slowly, fluid exudes into alveolar wall and a physical barrier eventually develops

between alveoli and capillaries consisting of thickened capillary basemen membrane. This will limit pulmonary

edema. So in late case of MS there is less acute LHF.

* Kerleys B line vs. MS.

As there is more fluid in interstitial tissue, lymphatic channel try to remove it. So there is dilation of lymph

channel giving Kerleys B line.

*Importance of pulmonary capillary pressure in X-ray of MS.

i). 15-25 mmHg: upper lobe diversion.

2. >25mmHg: Kerleys B line.

So without catheter study we can say the PCW roughly.


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* PH is a protective phenomenon in MS: short discussion.

-As the pulmonary capillary pressure increase by passive backward transmission of elevated

LA pressure to pulmonary capillaries. So there is reactive vasoconstriction of pulmonary

arterioles and small pulmonary arteries leading to reactive pulmonary arterial hypertension.

This is largely reversible if MS is corrected. But in long standing MS organic obliterative

changes (e.g. arterial hypertrophy and atheroma) in vascular bed develops which is

irreversible, In time severe pulmonary hypertension leading to RVF, TR, and PR. This

process of pulmonary vascular changes is a protective phenomenon. Such as -

-Vasoconstriction prevents development pulmonary congestion by preventing blood surging

into pulmonary vasculatures from abrupt rise in RV output.

- Prevent damping up blood behind the stenotic valve.- So interstitial edema reduces, engorgement of pulmonary vein reduce with redistribution

of blood from base to apex of lung (i.e. Upper lobe diversion).

- Drawback of this protective mechanism is the reduced CO.

[Normal:

i).PA(S): 15 mmHg, mean 25: mmHg.

ii).PA (D):5-15 mmHg, mean: 10 mmHg].

*Long standing MS patient suffer from dyspnea at rest even- explain.In severe long standing MS chronic pulmonary vascular congestion leads to increased

rigidity i.e. decreased lung compliance. So there is increase work of breathing. There by

patient of long standing MS remain dyspnic, even with out any failure.

*PVR- what it imply?

Pulmonary vascular resistance (PVR) implies pulmonary arteriolar constriction.


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Conditions simulating MS both clinically and radiologically

- LA myxoma.

- Ball valve thrombus in LA.

- Bacterial vegetation in LA

- Cor tri atrium biventricularies.- Calcification of mitral valve annuals.

*Presentation of LA myxoma:

-Like MS, due to obstruction of mitral valve orifice.

-Like PH, due to obstruction of pulmonary venous opening.

* D/D of LA myxoma in echo:- LA myxoma.

- Ball valve thrombus.

* D/D of mass in LA in Echo:

i).Ball valve thrombus: Mass remain free in chamber. It will move up anddown through mitral valve in echo.

ii). Myxoma: usually remains attached on IAS.

iii).LA thrombus: Remains confined and attached into LA appendages in earof hair


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Complications of MS.i). Acute pulmonary edema (Acute LHF).ii). Fatal massive hemoptysis.iii). AF usually with rapid ventricular rate.

iv).CCF.v). Thromboembolic manifestation.vi). PH.vi). Acute and chronic bronchitis.vii).Cardiac cirrhosisviii).Very rarely IE.*Common sites of thromboembolic manifestation in MS.-Systemic embolism from LA thrombus.-Pulmonary embolism from DVT leading to pulmonary infarction.* Common sites of systemic embolism:- Brain e.g. CVA in 50% cases.-Heart e.g. IHD-Kidney leading to systemic hypertension.- Mesentery.-Bifurcation of aorta.-Eyes.*DVT and MS:-It is due to prolonged immobilization.


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Type of congenital MS.

- Supra valvar.

- Valvar.

- Sub valvar.

*Parachute mitral valve:- short discussion.

- It is a special type of congenital MS.

-In Parachute mitral valve there is one papillary muscle.

-Chordae arises from one papillary muscle and inserted into two commissuresgiving a parachute appearance.

-That single chordae is hypertrophied.

-It is diagnosed by findings of signs of MS in children.

-Usually no H/O RF.

-In echo cross section at the papillary muscle level will show single echogenicand hypertrophied papillary muscle.


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Changes of sings of MS if it develops AF.

- Irregularly irregular pulse.

- Pulsus deficit.

- Absent a wave in JVP.

- Disappeared of presystolic accentuation, because no atrial click in AF.

- S1: Intensity is variable.

- S2 : Intensity is normal or variable.

- OS: Present.

*Opening Snap(OS) in AF, HF , Calcification and IE.

-In AF: OS present.

-In HF: OS persist.

-In Calcification: OS absent.-In IE: present if no damage of cusps.


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Grading of MS depending on cross sectional area of mitral

valve.

i).Mild MS: 1: 5 2.5 cm2.

ii).Moderate MS: 1.0 1.5 cm2.

iii).Severe MS: < 1 cm2 (0.5 1 cm2).

39. Steps of PH in MS.

i).Initial reversible PH caused by.

-Backward pressure of LA. It is passively causing PH.

-Reactive vasoconstriction of precapillary arteriolar sphincter.

ii).Late irreversible PH caused by.-Obliterative change in arterioles and venules.


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Importance of transvalvular pressure gradient in MS.

-Transmitral pressure gradient at early diastole is an important determinant of S/S of MS and its complication.

-Any factor which increases transmitral gradient cause HF.

-Definition: It is the pressure gradient between LA and LV (i.e. transmitral) at the early diastole.

-What not? It is not the end diastolic pressure gradient. Because at the end of the diastole virtually no pressure

gradient exists at mitral valve level i.e. it is O (zero) at end of the diastole.

-For practical purposes early diastolic pressure gradient can be measured by simultaneously recording the PCW

and LV pressure during early diastole.

[Normal:

i).Transmitral pressure gradient at early diastole: 6 -10 mmHg.

ii).LVEDP:4-12 mmHg, mean: 7mmHg.iii).LA pressure: 4-12 mmHg, mean: 7 mmHg].

-When transmitral pressure gradient > 10 mmHg at early diastole, then that MS will give S/S.

-If it is >20 mmHg, then it is either tight MS or severe MS.

-Normally LA mean pressure is always higher than the early diastolic pressure of LV. Usually 6 10 mmHg

higher in normal person.

-If LA pressure high up, then:

i). OS come early. ii).MDM prolonged, and indicates iii). Tight MS.

* Reverse trans mitral gradient, what does it imply?

-In AR/AS the transmitral pressure gradient is opposite to MS.

-Normally pressure difference is existed between LA to LV.

- In AR/AS the pressure difference existed between LV to LA.


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Mechanism of PND in MS.

- Redistribution of fluid to centre and withdrawal of gravity. During the day, patient is

usually remaining in standing up or on walking, so fluid accumulate at depended

part. But at night fluid accumulate in the lung due to withdrawal of gravity, causing

increase venous return. Heart cannot expel this extra load, there by congestion inLungs.

- During sleep cough reflex is working less. So when patient awoke from sleep then

fluid accumulates to a critical level.

- During sleep respiratory center work less. So when he/she awoke from sleep he/she

becomes very dyspnoeic.

-Daring sleep respiratory drive reduces. So threshold for reparatory distress reduce. So

when patient awoke from sleep pulmonary congestion reach a critical level.

- During sleep diaphragm raises. Vital capacity reduces.

-During sleep high intra abdominal press compresses the liver. More blood goes to

lungs and more venous return.

42. When pulmonary edema in MS occur.

-If capillary hydrostatic pressure more than colloid osmotic pressure then there will be

pulmonary edema.


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Causes of loud 1st heart sound.

-MS

-Tachycardia.

-TS.

-Ebsteins anomaly.

-Ball valve thrombus.

-LA myxoma.

-Cor tri atrium.

-Pericardial constriction in AV grove.

* Short PR interval vs. loud 1st heart sound.

- Short PR interval causes loud 1st heart sound, but if PR interval


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Investigation of MS.

- Blood for R/E if infection.

- Urine for R/E if infection. .- Blood for C/S, if infection e.g. IE.

- X-ray.

- ECG.

- Echo.

- Catheter if associated with other valvular involvement or age of

patient is above 40 years.

*Indication of CAG in MS.

-If age of the MS patient is above 40 years.


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Prophylaxis in MS.

A).Secondary prophylaxis for Rheumatic fever.

-Age below 6 years. or

- Body weight bathos 27 Kg.

- Inj. Benzathine Penicillin.

.6 lakhs deep im in gluteus at 3 wk interval. Or- Oracin K tab (125 mg) 1 tab BD.

-Age above 6 years. or

- Body weight 27 Kg.

- Inj. Benzathine Penicillin.

.12 lakhs deep im in gluteus at 3 wk interval. Or

- Oracin K tab (250 mg) 1 tab BD.

B).Prophylaxis for IE:

-Rare in pure MS, Still not immune.

-So give prophylaxis for IE when indicated, such as tooth extraction, delivery, urethral catheter.

i) Before delivery give single dose of:-

- Cap amoxicillin, 3 gm by mouth in single dose.

+

Inj. Gentamicin 1.5 mg/ kg in single dose

ii).Dental procedure under LA.

-1ST Dose 1 hr before:

Cap amoxicillin 3 gm (12 caps) by mouth in single dose.

-2nd dose 8 hr after operation:

cap amoxicillin 3 gm by mouth in single dose.

Or

-Erythromycin: 1st dose 1 hr before procedure,1 gm orally followed by 500 mg 6 hourly for 2 days.


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MS female becomes pregnant. How to manage?

-Routine follows up in collaboration with a gynecologist.

-If there is heart failure, control the failure with digoxine, vasodilators. It is better to avoid diuretic, which may cause reduction of

amniotic fluid.

-If heart failure not controlled with medicine, emergency PTMC or surgery is indicated.

-If severe MS, at early pregnancy, failure not controlled with optimum medications termination of pregnancy is preferable.- If moderate to severe MS at 2nd or 3rd trimester of pregnancy elective CMC or PTMC is preferable.

* Some adverse situation faced in pregnancy with MS.

i).1st trimester: Chance of abortion.

ii).2nd trimester: stable fetus

iii).3rd trimester: chance of premature delivery.

*Preferable time for elective CMC or PTMC in case of symptomatic pregnant MS patient.

- 2nd trimester of pregnancy, at that time is in stable condition in womb.

*Married female with MS, attends in your chamber for contraceptive. What is your advice to couple?

i). Advice to wife to avoid contraceptive pill.

ii). Advice her husband to use condom.

* What is the problem to use contraceptive pill in MS (and MR) patient?

-Pills precipitate in formation of thrombus as well as thrombo embolism.

- It also causes salt and water retention, there by precipitate heart failure.

* Female patient, known case of MS, recently married, or diagnosed just after marriage. Attend in your chamber for advice. What

is your suggestion?-At the beginning thoroughly examines the patient.

-Investigation should do according to necessity.

- Then decision takes as follows:

i). If tight MS: PTMC or Operation should do before conception.

ii).If moderate: Pregnancy is allowed, but follows up along with a gynecologist.

iii).Mild MS: In this condition pregnancy can be allowed with out any hazard.


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Follow up before operation in MS.

- Patient should live with in his/her cardiac reserve.

If not symptomatic defer operation.Antibiotic prophylaxis for RF and IE.

Normal diet to fit for operation.

Mild diuretic to avoid overload.

Control anemia with iron and vitamin.

Follow up.

i).Sign of PH e.g loud P2.

ii).X-ray.iii).ECG.

iv). Echo.


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Indication of intervention or surgery in MS.

a). Indication of PTMC or CMC.

i). NYHA grade II b onward: Provided

-Pliable, noncontracted and noncalcified mitral valve, with

-Minimum or no sub valvular adhesion or calcification.

ii).Critical or tight or severe MS:

-In this MS, surgery (PTMC or CMC) is indicated without symptom.

iii).Systemic embolism, after 6 month.

iv).MS with repeated AF.

v).MS with repeated thrombo embolism.

vi).IE (though rare in MS); after 3 month.

vii).Prophylactive CMC:

-Tight MS girl recently married, do CMC before conception.

viii).Elective CMC:

-Pregnancy with progressing symptoms, do elective CMC in mid trimester

ix).Emergency CMC:

Pregnancy with uncontrolled heart failure, do emergency CMC at any time.

b).Indication of OMC.- Severe MS with severe sub valvular fibrosis or calcification.

- MS with ASD.

- MS with MR.

- Rigid valve.

- LA thrombus.


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*Criteria of severe MS?


-Opening snap (OS): Present.

-Prolonged MDM.

-In Echo:

i).MVA: 20mmHg in Doppler.

iii). EF SLOPE:


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Name of Intervention or Operation in MS.

i). PTMC

(ii) CMC.

(iii) OMC:

a). mitral valve repair.

b).Mitral valve replacement (MVR).

Pre- requisite in MS for PTMC or CMC?

- Pure MS.- Loud S1.

- OS should present.

- Prolonged MDM.

- Pliable, noncontracted and noncalcified leaflets.

- Noncalcified Commissures.

- No or Minimum sub valvular fibrosis or calcification.

-No associated MR/ LA thrombus or other valve involvement.


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Contraindication of PTMC or CMC?

- Leaflets heavily fibrosed, calcified and distorted.

- Cardiac cirrhosis.

- Presence of Rheumatic activity e.g. High ESR.

- Thrombus in LA.

- MS with MR.

- On IE.-CCF.

Clinical indication of PTMC or CMC?


- OS.

- No systolic murmur at the apex.


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Complication of PTMC?

a). Early complication of PTMC.

-Hemorrhage.

-Hemo pericardium.

-LV perforation.

-Embolism viz. cerebral.

-Iatrogenic MR.-Iatrogenic ASD.

-Low out put syndrome.

-Infection.

-AF.

b). Late complication of PTMC.

-Restenosis at a rate of 10% per year.


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Complication of CMC?

a). Early complication of CMC.

-Hemorrhage.

-LV injury.

-Embolism viz. cerebral.

-Iatrogenic MR. In 25 % cases of CMC there is MR.

-Low out put syndrome.-Infection.

-AF.

-Post cardiotomy syndrome, 1-8 weeks after CMC.

b). Late complication of CMC.

-Restenosis at a rate of 5% per year, i. e. 100% in 20 years.


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Complication of CMC?

a). Early complication of CMC.

-Hemorrhage.

-LV injury.

-Embolism viz. cerebral.-Iatrogenic MR. In 25 % cases of CMC there is MR.

-Low out put syndrome.

-Infection.

-AF.

-Post cardiotomy syndrome, 1-8 weeks after CMC.

b). Late complication of CMC.

-Restenosis at a rate of 5% per year, i. e. 100% in 20 years.

* Post cardiotomy syndrome.

i). 3 P: such as Pericarditis, Pleurisy and Pyrexia, 1-8 weeks after CMC.

ii). Represent autoimmune reaction to heart muscle or to the blood in pericardium.

iii).No need of treatment or may prescribe steroid.* AF after PTMC or CMC or OMC?

- Develops shortly after surgery in about 25% cases.

- Often resolve spontaneously within 3 weeks.

-If not resolve, Correct with DC shock.


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Complication after OMC?

- Complication from prosthetic material,

- Complication from anticoagulant.How many times PTMC and CMC can be repeated on a

patient?

- CMC usually can not repeat, because auricle wasremoved on CMC.

- PTMC can repeat as long as suitable for intervention.

Prognosis after surgery.

- PTMC: 10 years.

- CMC: 10 years.

-OMC: 20 years.


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Advice to a patient on discharge after PTMC or CMC or OMC in patient with

MS with AF with CCF.

- Prophylaxis for IE.

- Secondary prophylaxis of RF.- Continue the diuretics till desired life style can maintain with out any

symptoms. Similarly continue the antiarrhythmic drugs.

- On discharge do ECG, X-ray, Echo and preserves it as document of LA and LV

size. Then repeat after 5 yrs.

- No need of anticoagulant if no AF.

Choice of Valve.

-Female within reproductive age where family is incomplete gives tissue

valve.

-Replacement requires within 6-7 years. During this period family should be

completed.

-Tissue calcified early. Pregnancy may be one of the causes.

-6 wk to 3 month anticoagulant is sufficient for tissue valve.


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Medical Treatment of MS.

Medical treatment can not reduce the obstruction, so supportive

measure is indicative.

- Patient should live within his cardiac reserve.

- Secondary Prophylaxis for Rheumatic fever.

- Prophylaxis of IE.

-Treatment of CCF.-Treatment of AF.

-Treatment of systemic embolism.

-Treatment of CVA.

-Treatment of infection.

-Balloon valvuloplasty (PTMC).

MITRAL STENOSIS, NICVD

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