clinical approach to multi valvular heart disease
TRANSCRIPT
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APPROACH TO
MULTIVALVULAR HEART DISEASE
Satyam Rajvanshi
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HOW TO DEFINE MVHD
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• Clinically significant MVHD?
• Pathological MVHD?
• VHD without organic valve ds?
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• Clinically significant MVHD?
• Pathological MVHD?
• VHD without organic valve ds?
NO STANDARD DEFINITION
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PRACTICAL DEFINITION
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• Involvement of more than one heart valve
• Clinically significant – alters natural history, management
• Valve may or may not be pathological but must be grossly dysfunctional
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WHY IS MVHD RELEVANT
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• Presentation
• Natural history
• Management
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• Presentation• Symptoms• Physical signs
• Natural history
• Management
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• Presentation• Symptoms• Physical signs
• Natural history
• Management
Relative severity of separate lesions
Order of development of separate lesions
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WHAT CAUSES MVHD
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• Rheumatic Heart Disease• Infective endocarditis• Myocardial Dysfunction (Remodelled heart – MR, PR, TR)• Aging, Degenerative (calcific)• Disorders of other Organs – ESRD, Carcinoid• Myxomatous diseases – Marfan, EDS• CTDs – SLE, APLA, RA• Congenital diseases – Discrete Subaortic stenosis, HOCM,
Shone’s complex, Trisomy (13-15-18), Alkaptonuria• Endocardial Disorders• Thoracic/Mediastinal radiation therapy• Drugs – Ergotamine/Fen-Phen/Methysergide
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• Significant stenosis at multiple valves are usually Rheumatic
• Significant regurgitation at multiple valves are likely Non Rheumatic
• Significant stenosis and regurgitation together are usually Rheumatic
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• Quadrivalvular disease is most likely due to combination of causes – Rheumatic, infective, congenital, inflammatory or degenerative disease
• A unitary cause for quadrivalvular disease is either rheumatic or myxomatous degeneration
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STATISTICS
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ARF with carditis
MV 70-75%MV+AV 20-25%AV 5-8%TV 1-2%PV Rare
Ann Indian Acad Med Sci 1972;8:47-52
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ARF with carditis
CLINICAL
MV 70-75%MV+AV 20-25%AV 5-8%TV 1-2%PV Rare
Ann Indian Acad Med Sci 1972;8:47-52
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ARF with carditis
CLINICAL
MV 70-75%MV+AV 20-25%AV 5-8% HISTOPATHOLOGICAL
TV 1-2% 30-35%PV Rare 15-20%
Ann Indian Acad Med Sci 1972;8:47-52
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ARF with carditis
MV 70-75% MC is MR
MV+AV 20-25% 90-95%
AV 5-8%TV 1-2%PV Rare
Ann Indian Acad Med Sci 1972;8:47-52
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ARF with carditis
MV 70-75%MV+AV 20-25% 2nd MC is AR
AV 5-8% 20-40%
TV 1-2%PV Rare
Ann Indian Acad Med Sci 1972;8:47-52
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Frequency of RHD%
of p
atien
ts w
ith R
HD a
t 5-y
ears
Prognosis – Severity of carditis & Recurrences
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RHD• 378 cases of juvenile RHD (<19 yr), Orrissa
MS 34.9%MR 14.8%AR 6.1%MS+MR 11.9%MS+AR 21.1%MS+MR+TS 4.8%MS+MR+TS+TR 6.4%
Indian Heart J 1999;51:653
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RHD• 378 cases of juvenile RHD (<19 yr), Orrissa
MS 34.9%MR 14.8%AR 6.1%
MS+MR 11.9%MS+AR 21.1% >40% MVHDMS+MR+TS 4.8%MS+MR+TS+TR 6.4%
Indian Heart J 1999;51:653
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RHD• >9000 RHD cases, Orrissa
MS 35%MR 10%AR or AS 3%MS+MR 15%MV+AV 25%MV+TV 12%
Indian Heart J 2003;55:152-157
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RHD• >9000 RHD cases, Orrissa
MS 35%MR 10%AR or AS 3%
MS+MR 15%MV+AV 25% >50% MVHD
MV+TV 12%
Indian Heart J 2003;55:152-157
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RHD• 518 RHD cases, JIPMER Pondicherry
MS+AS+TS 2.5%(Triple stenosis)
Indian Heart J 1999;51:667
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RHD• NIMS, Hyderabad 2002
MS+MR 12.9%AS+AR 4.4%
MS+AR 13.9%MS+MR+AR 2.0%MS+MR+TR 8%MS+AR+TR 8%
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RHD• 434 RHD AUTOPSY cases, Mumbai
MV 21%AV 2%
MV+AV 21%MV+AV+TV 27%MV+TV 5%MV+TV+PV 2%MV+AV+TV+PV 19%
Indian Heart J 2002;54:676-80
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WHEN DO WE SUSPECT A MVHD
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• Patient does not fit in single valve picture• By history/examination/ECG/CXR
• Presentation time frame different from usual natural history
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• Know the classical markers of significant lesions
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HISTORY-WISE
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MS
• Exertional dyspnoea – 1st and MC symptom– PND– Orthopnea– 5-10 yrs from ARF to symptoms (15-20 yrs in
western population) – Progresses over 3-5 yrs from NYHA II to IV
(5-10 yrs in western population)• Hemoptysis• Systemic embolism• RVF – but after NYHA IV state
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MR
• History– Long asymptomatic period – 10-20 yrs from ARF to
symptoms (a decade longer than MS)– Once severe MR – Symptomatic within 6-10 yrs– Symptoms herald LVSD or AF – Rapid decline in
survival• Chronic weakness/Fatigue/Exercise Intolerance
– MC • Dyspnoea – less common and late
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AS
• History– Long asymptomatic period – 10-20 yrs from ARF to
symptoms (a decade longer than MS)– 10-15 yrs from Mild to Severe AS– Once severe AS – Symptomatic within 2 yrs– Symptoms – Rapid decline in survival
– 2 HF/3 Syncope/5 Angina• Exercise intolerance and dyspnoea – MC• Exertional Angina• Exertional Presyncope (> than Syncope)
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AR
• Long (perhaps longest!) asymptomatic period – After ARF– After development of AR– Once symptomatic – course similar to AS
• Exercise intolerance and dyspnoea - MC• Palpitations – exertional and resting – even
painful! – may precede other symptoms by months-yrs
• Nocturnal (and exertional) angina
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TS
• Never solitary• RVF – (Tender hepatomegaly, ascites,
anasarca) – without disabling dyspnoea• Fatigue/Exercise intolerance more prominent
than dyspnoea – d/t low CO
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EXAMINATION-WISE
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Severe MS
• Prolonged diastolic murmur• Thrill• A2 OS gap• Pulmonary hypertension• Cardiomegaly• Congestive Heart failure
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A2-OS Gap
• Inversely proportional to severity• 40 – 120 msec• HR, LAP, LV EDP, LV compliance, mobility• Narrow always tight MS• Widened (falsely)– Bradycardia– AR– Low output (Sev PAH, TR, CHF)– Inc LV EDP (LV dysfunction)
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Severe MR
• Cardiomegaly• LV S3/diastolic murmur• Wide split S2• ? Thrill• LV dysfunction• Pulmonary hypertension• Congestive Heart failure
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Severe AS• Pulsus parvus et tardus• Peaking of systolic murmur• Paradoxical split S2• LV S4• Apico-carotid delay (often neglected)• Thrill• Cardiomegaly• LV dysfunction (S3)• Pulmonary hypertension• Congestive Heart failure
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Severe AR
• Hill’s Sign• Duration of diastolic murmur• Austin Flint murmur• Thrill (rare)• Cardiomegaly• LV S3• LV dysfunction• Pulmonary hypertension• Congestive Heart failure
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Things that Stand are
• AV disease– Pulse– Hill’s sign
• Murmur characteristic (except MR)• Diastolic thrill• S2– Paradoxical spilt – AS– Wide split – MR
• A2 OS gap - mostly
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HOW TO APPROACH
MS/MR/AS/AR SEVERE?
MVHD SUSPECTED?
EXAMINEECG/ECHO/CATH
WHICH ONE IS DOMINANT?
MODIFYING / PRECIPITATING
FACTORS?
DIAGNOSISPROGNOSTICATE
MANAGEMENTGDM
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Non valvular Factors
Modify/Precipitate presentation– Arrhythmias– Infective endocarditis– RF recurrence – valvulitis and myocarditis– Volume overload states – Anemia, worsening
Renal failure, Dietary non-compliance– Pressure overload states – Uncontrolled HTN– Ischemia – CAD/ACS, Respiratory illness, altitude– SIRS – Infection, MC Pneumonia
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Non valvular Factors
Modify/Precipitate presentation– Arrhythmias– Infective endocarditis– RF recurrence – valvulitis and myocarditis– Volume overload states – Anemia, worsening
Renal failure, Dietary non-compliance– Pressure overload states – Uncontrolled HTN– Ischemia – CAD/ACS, Respiratory illness, altitude– SIRS – Systemic Infection, MC Pneumonia
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Some Rules of Combined Valve Lesions
Severe lesions
dominate
Proximal lesions
dominate
Multivalvular disease – 1+1 may not be 2• Ability to
compensate
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MS/MR
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Severe MR – Is there MS?
• Thrill
• Prolonged MDM
• Opening Snap
• Loud S1
• Severe PAH
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Pulmonary symptoms: Cough, Hemoptysis, Pulmonary Edema
S2 Variable Wide splitS1 Loud (mostly) VariablePAH Severe Variable
OS +
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AS/AR
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Severe AR - is there AS?
• Pulse
• Systolic decapitation
• Late peaking, harsher, louder murmur
• Heaving apical impulse
• Thrill
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S2 Paradoxical Normal/NarrowS4 + -Apex Heaving, Not shifted Hyperkinetic, shifted
Hill’s Sign
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MS/AR
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MS Vs. Austin Flint
Characteristic MS Austin Flint
Diastolic Murmur Prolonged with thrill Soft/shorterApex RV
TappingLV
Hyperkinetic
Added sounds OS S3
PAH Severe mild
S1 Loud (mostly) -
AF Suggestive -
Hand grip
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MS/AS
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In severe AS – presence of loud S1, absence of S4 - indicates MS
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MR/AR
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• Exception to proximal distal rule – AR usually predominates in physical signs
• In Severe MR, mild-mod AR well tolerated• In Severe AR, even mild-mod MR worsens
symptoms as LV dilates further
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MR/AS
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+ TS
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TS• Easily escapes detection• More fatigue, CHF/RVF - Less PND orthopnea• Distal lesions SYMPTOMS masked, signs may remain
prominent• JVP is the key
– Giant a waves– Slow Y descent
• Pulsatile liver• Murmur of TS
– Location– Pre systolic or mid diastolic– Inspiratory augmentation
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TR
Characteristic High pressure Low pressure
Murmur PSM Early systolic with
variable duration
Pitch High low
Shape PSM Decrescendo
P2 Loud Normal
JVP CV waves Variable
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INVESTIGATIONAL CAVEATS
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• Doppler-echocardiographic methods have been validated in single valve disease but not in multivalve disease
• Interactions between different valve lesions.• Methods that depend less on loading
conditions are preferred, such as direct planimetry of the stenotic valves
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Diagnostic caveats in MVHD
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MANAGEMENT
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• In the EuroHeart Survey, the operative risk ranged from 0.9% to 3.9% for single valve interventions and rose to 6.5% in cases of multiple valve disease
Ann Thorac Surg 1999;67:943-51
• In the Society of Thoracic Surgeons National Database, mortality was 4.3% and 6.4% for isolated aortic and mitral valve replacement, respectively, to 9.6% for multiple valve replacement (Doubles)
Eur Heart J 2003;24:1231-43
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• TVR: overall operative mortality was 22 %
Ann Thorac Surg 2005;80:845-850
• Operative mortality was similar for TVR 13% vs. repair 18% p = 0.64.
• Higher mortality for higher NYHA class
Ann Thorac Surg 2009;87:83-89
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CONCLUSION
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MVHD
• Widely prevalent• Alters natural history and presentation• Requires careful evaluation• Management guidelines differ
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La Clairvoyance, 1936 By Rene Magritte