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VALVULAR HEART DISEASE

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OverviewAortic StenosisMitral StenosisAortic RegurgitationAcute and ChronicMitral RegurgitationAcute and Chronic

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Слайд 1VALVULAR HEART DISEASE
Internal Medicine Didactics
August 12, 2009
Steven R. Bruhl MD,

VALVULAR HEART DISEASEInternal Medicine DidacticsAugust 12, 2009Steven R. Bruhl MD, MS

Слайд 2Overview
Aortic Stenosis
Mitral Stenosis
Aortic Regurgitation
Acute and Chronic
Mitral Regurgitation
Acute and Chronic

OverviewAortic StenosisMitral StenosisAortic RegurgitationAcute and ChronicMitral RegurgitationAcute and Chronic

Слайд 3Etiology
Pathophysiology
Physical Exam
Natural History
Testing
Treatment

EtiologyPathophysiologyPhysical ExamNatural HistoryTestingTreatment

Слайд 4Aortic Stenosis

Aortic Stenosis

Слайд 6Aortic Stenosis Overview:
Normal Aortic Valve Area: 3-4 cm2

Symptoms: Occur when

valve area is 1/4th of normal area.
Types:
Supravalvular
Subvalvular
Valvular

Aortic Stenosis Overview:Normal Aortic Valve Area: 3-4 cm2Symptoms: Occur when valve area is 1/4th of normal area.Types:

Слайд 7Etiology of Aortic Stenosis
Congenital
Rheumatic
Degenerative/Calcific

Patients under 70: >50% have a congenital

cause
Patients over 70: 50% due to degenerative

Etiology of Aortic StenosisCongenitalRheumaticDegenerative/CalcificPatients under 70: >50% have a congenital causePatients over 70: 50% due to degenerative

Слайд 12Pathophysiology of Aortic Stenosis
A pressure gradient develops between the left

ventricle and the aorta. (increased afterload)
LV function initially maintained by

compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines.
Pathophysiology of Aortic StenosisA pressure gradient develops between the left ventricle and the aorta. (increased afterload)LV function

Слайд 13Presentation of Aortic Stenosis
Syncope: (exertional)
Angina: (increased myocardial oxygen demand; demand/supply

mismatch)
Dyspnea: on exertion due to heart failure (systolic and diastolic)
Sudden

death
Presentation of Aortic StenosisSyncope: (exertional)Angina: (increased myocardial oxygen demand; demand/supply mismatch)Dyspnea: on exertion due to heart failure

Слайд 14Physical Findings in Aortic Stenosis
Slow rising carotid pulse (pulsus tardus)

& decreased pulse amplitude (pulsus parvus)

Heart sounds- soft and split

second heart sound, S4 gallop due to LVH.

Systolic ejection murmur- cresendo-decrescendo character. This peaks later as the severity of the stenosis increases.
Loudness does NOT tell you anything about severity
Physical Findings in Aortic StenosisSlow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)Heart sounds-

Слайд 15Natural History
Mild AS to Severe AS:
8% in 10 years
22% in

22 years
38% in 25 years

The onset of symptoms is a

poor prognostic indicator.
Natural HistoryMild AS to Severe AS:8% in 10 years22% in 22 years38% in 25 yearsThe onset of

Слайд 17Evaluation of AS
Echocardiography is the most valuable test for diagnosis,

quantification and follow-up of patients with AS.
Two measurements obtained are:
Left

ventricular size and function: LVH, Dilation, and EF
Doppler derived gradient and valve area (AVA)
Evaluation of ASEchocardiography is the most valuable test for diagnosis, quantification and follow-up of patients with AS.Two

Слайд 18Evaluation of AS
Cardiac catheterization: Should only be done for a

direct measurement if symptom severity and echo severity don’t match

OR prior to replacement when replacement is planned.
Evaluation of ASCardiac catheterization: Should only be done for a direct measurement if symptom severity and echo

Слайд 19Management of AS
General- IE prophylaxis in dental procedures with a

prosthetic AV or history of endocarditis.
Medical - limited role

since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS
Aortic Balloon Valvotomy- shows little benefit.
Surgical Replacement: Definitive treatment
Management of ASGeneral- IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. Medical

Слайд 20Echo Surveillance
Mild: Every 5 years
Moderate: Every 2 years
Severe: Every 6

months to 1 year

Echo SurveillanceMild: Every 5 yearsModerate: Every 2 yearsSevere: Every 6 months to 1 year

Слайд 22Simplified Indications for Surgery in Aortic Stenosis
Any SYMPTOMATIC patient with

severe AS (includes symptoms with exercise)
Any patient with decreasing EF
Any

patient undergoing CABG with moderate or severe AS
Simplified Indications for Surgery in Aortic StenosisAny SYMPTOMATIC patient with severe AS (includes symptoms with exercise)Any patient

Слайд 23Summary
Disease of aging
Look for the signs on physical exam
Echocardiogram to

assess severity
Asymptomatic: Medical management and surveillance
Symptomatic: AoV replacement (even in

elderly and CHF)
SummaryDisease of agingLook for the signs on physical examEchocardiogram to assess severityAsymptomatic: Medical management and surveillanceSymptomatic: AoV

Слайд 24Mitral Stenosis

Mitral Stenosis

Слайд 25Mitral Stenosis Overview
Definition: Obstruction of LV inflow that prevents proper

filling during diastole
Normal MV Area: 4-6 cm2
Transmitral gradients and symptoms

begin at areas less than 2 cm2
Rheumatic carditis is the predominant cause
Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.
Mitral Stenosis OverviewDefinition: Obstruction of LV inflow that prevents proper filling during diastoleNormal MV Area: 4-6 cm2Transmitral

Слайд 26Etiology of Mitral Stenosis
Rheumatic heart disease: 77-99% of all cases
Infective

endocarditis: 3.3%
Mitral annular calcification: 2.7%

Etiology of Mitral StenosisRheumatic heart disease: 77-99% of all casesInfective endocarditis: 3.3%Mitral annular calcification: 2.7%

Слайд 31MS Pathophysiology
Progressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced

emptying)
worse with exercise, fever, tachycardia, and pregnancy
Increased Transmitral Pressures: Leads

to left atrial enlargement and atrial fibrillation.
Right heart failure symptoms: due to Pulmonary venous HTN
Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure
MS PathophysiologyProgressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced emptying)worse with exercise, fever, tachycardia, and pregnancyIncreased

Слайд 32Natural History of MS
Disease of plateaus:
Mild MS: 10 years

after initial RHD insult
Moderate: 10 years later
Severe: 10 years later

Mortality:

Due to progressive pulmonary congestion, infection, and thromboembolism.
Natural History of MSDisease of plateaus: Mild MS: 10 years after initial RHD insultModerate: 10 years laterSevere:

Слайд 33Physical Exam Findings of MS
prominent "a" wave in jugular venous

pulsations: Due to pulmonary hypertension and right ventricular hypertrophy

Signs

of right-sided heart failure: in advanced disease

Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks
Physical Exam Findings of MSprominent

Слайд 34Diastolic murmur:
Low-pitched diastolic rumble most prominent at the apex.


Heard best with the patient lying on the left side

in held expiration
Intensity of the diastolic murmur does not correlate with the severity of the stenosis

Heart Sounds in MS

Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex. Heard best with the patient lying on

Слайд 35Loud Opening S1 snap: heard at the apex when leaflets

are still mobile 
Due to the abrupt halt in leaflet motion

in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips.
A shorter S2 to opening snap interval indicates more severe disease.

Heart Sounds in MS

Loud Opening S1 snap: heard at the apex when leaflets are still mobile Due to the abrupt halt

Слайд 36Evaluation of MS
ECG: may show atrial fibrillation and LA enlargement
CXR:

LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD

STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

Evaluation of MSECG: may show atrial fibrillation and LA enlargementCXR: LA enlargement and pulmonary congestion. Occasionally calcified

Слайд 38Management of MS
Serial echocardiography:
Mild: 3-5 years
Moderate:1-2 years
Severe: yearly

Medications: MS

like AS is a mechanical problem and medical therapy does

not prevent progression
-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Duiretics for fluid overload
Management of MSSerial echocardiography: Mild: 3-5 yearsModerate:1-2 yearsSevere: yearlyMedications: MS like AS is a mechanical problem and

Слайд 39Management of MS
Identify patient early who might benefit from percutaneous

mitral balloon valvotomy.

IE prophylaxis: Patients with prosthetic valves or a

Hx of IE for dental procedures.
Management of MSIdentify patient early who might benefit from percutaneous mitral balloon valvotomy.IE prophylaxis: Patients with prosthetic

Слайд 44Simplified Indications for Mitral valve replacement
ANY SYMPTOMATIC Patient with NYHA

Class III or IV Symptoms

Asymptomatic moderate or Severe MS with

a pliable valve suitable for PMBV
Simplified Indications for Mitral valve replacementANY SYMPTOMATIC Patient with NYHA Class III or IV SymptomsAsymptomatic moderate or

Слайд 45Aortic Regurgitation

Aortic Regurgitation

Слайд 47Aortic Regurgitation Overview
Definition: Leakage of blood into LV during diastole

due to ineffective coaptation of the aortic cusps

Aortic Regurgitation OverviewDefinition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic

Слайд 48Etiology of Acute AR
Endocarditis
Aortic Dissection

Physical Findings:
Wide pulse pressure
Diastolic murmur
Florid pulmonary

edema

Etiology of Acute AREndocarditisAortic DissectionPhysical Findings:Wide pulse pressureDiastolic murmurFlorid pulmonary edema

Слайд 49Treatment of Acute AR
True Surgical Emergency:
Positive inotrope: (eg, dopamine, dobutamine)


Vasodilators: (eg, nitroprusside)
Avoid beta-blockers
Do not even consider a balloon pump

Treatment of Acute ARTrue Surgical Emergency:Positive inotrope: (eg, dopamine, dobutamine) Vasodilators: (eg, nitroprusside)Avoid beta-blockersDo not even consider

Слайд 51Etiology of Chronic AR
Bicuspid aortic valve
Rheumatic
Infective endocarditis

Etiology of Chronic ARBicuspid aortic valveRheumatic Infective endocarditis

Слайд 52Pathophysiology of AR
Combined pressure AND volume overload

Compensatory Mechanisms: LV dilation,

LVH. Progressive dilation leads to heart failure

Pathophysiology of ARCombined pressure AND volume overloadCompensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

Слайд 53Natural History of AR
Asymptomatic until 4th or 5th decade
Rate of

Progression: 4-6% per year
Progressive Symptoms include:
- Dyspnea: exertional, orthopnea, and

paroxsymal nocturnal dyspnea
Nocturnal angina: due to slowing of heart rate and reduction of diastolic blood pressure
Palpitations: due to increased force of contraction
Natural History of ARAsymptomatic until 4th or 5th decadeRate of Progression: 4-6% per yearProgressive Symptoms include:- Dyspnea:

Слайд 54Physical Exam findings of AR
Wide pulse pressure: most sensitive
Hyperdynamic and

displaced apical impulse
Auscultation-
Diastolic blowing murmur at the left sternal

border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve
Physical Exam findings of ARWide pulse pressure: most sensitiveHyperdynamic and displaced apical impulseAuscultation- Diastolic blowing murmur at

Слайд 56MRI of the Heart Revealing a Central, High-Velocity Jet Projecting

into the Left Ventricular Cavity. The jet clearly strikes the anterior

mitral-valve leaflet, causing distortion and premature closure during diastole.
MRI of the Heart Revealing a Central, High-Velocity Jet Projecting into the Left Ventricular Cavity.  The

Слайд 57The Evaluation of AR
CXR: enlarged cardiac silhouette and aortic root

enlargement
ECHO: Evaluation of the AV and aortic root with measurements

of LV dimensions and function (cornerstone for decision making and follow up evaluation)
Aortography: Used to confirm the severity of disease
The Evaluation of ARCXR: enlarged cardiac silhouette and aortic root enlargementECHO: Evaluation of the AV and aortic

Слайд 59Management of AR
General: IE prophylaxis in dental procedures with a

prosthetic AV or history of endocarditis.
Medical: Vasodilators (ACEI’s), Nifedipine

improve stroke volume and reduce regurgitation only if pt symptomatic or HTN.
Serial Echocardiograms: to monitor progression.
Surgical Treatment: Definitive Tx
Management of ARGeneral: IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. Medical:

Слайд 62Simplified Indications for Surgical Treatment of AR
ANY Symptoms at rest

or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes

dilated
Simplified Indications for Surgical Treatment of ARANY Symptoms at rest or exerciseAsymptomatic treatment if:EF drops below 50%

Слайд 63Mitral Regurgitation

Mitral Regurgitation

Слайд 64Definition: Backflow of blood from the LV to the LA

during systole
Mild (physiological) MR is seen in 80% of normal

individuals.

Chronic Mitral Regurgitation Overview

Definition: Backflow of blood from the LV to the LA during systoleMild (physiological) MR is seen in

Слайд 65Acute MR
Endocarditis
Acute MI:
Malfunction or disruption of prosthetic valve

Acute MREndocarditisAcute MI:Malfunction or disruption of prosthetic valve

Слайд 66Management of Acute MR
Myocardial infarction: Cardiac cath or thrombolytics

Most other

cases of mitral regurgitation is afterload reduction:
Diuretics and nitrates
nitroprusside,

even in the setting of a normal blood pressure.
Management of Acute MRMyocardial infarction: Cardiac cath or thrombolyticsMost other cases of mitral regurgitation is afterload reduction:Diuretics

Слайд 67Management of Acute MR
Do not attempt to alleviate tachycardia with

beta-blockers. Mild-to-moderate tachycardia is beneficial in these patients because it

allows less time for the heart to have backfill, which lowers regurgitant volume.

Management of Acute MRDo not attempt to alleviate tachycardia with beta-blockers. Mild-to-moderate tachycardia is beneficial in these

Слайд 68Treatment of Acute MR
Balloon Pump
Nitroprusside even if hypotensive
Emergent Surgery

Treatment of Acute MRBalloon PumpNitroprusside even if hypotensiveEmergent Surgery

Слайд 69Myxomatous degeneration (MVP)
Ischemic MR
Rheumatic heart disease
Infective Endocarditis
Etiologies of Chronic Mitral

Regurgitation

Myxomatous degeneration (MVP)	Ischemic MRRheumatic heart diseaseInfective EndocarditisEtiologies of Chronic Mitral Regurgitation

Слайд 70Pathophysiology of MR
Pure Volume Overload
Compensatory Mechanisms: Left atrial enlargement, LVH

and increased contractility
Progressive left atrial dilation and right ventricular dysfunction

due to pulmonary hypertension.
Progressive left ventricular volume overload leads to dilation and progressive heart failure.
Pathophysiology of MRPure Volume OverloadCompensatory Mechanisms: Left atrial enlargement, LVH and increased contractilityProgressive left atrial dilation and

Слайд 71Physical Exam findings in MR
Auscultation: soft S1 and a holosystolic

murmur at the apex radiating to the axilla
S3 (CHF/LA overload)
In

chronic MR, the intensity of the murmur does correlate with the severity.
Exertion Dyspnea: ( exercise intolerance)
Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation
Physical Exam findings in MRAuscultation: soft S1 and a holosystolic murmur at the apex radiating to the

Слайд 72The Natural History of MR
Compensatory phase: 10-15 years
Patients with asymptomatic

severe MR have a 5%/year mortality rate
Once the patient’s EF

becomes <60% and/or becomes symptomatic, mortality rises sharply
Mortality: From progressive dyspnea and heart failure

The Natural History of MRCompensatory phase: 10-15 yearsPatients with asymptomatic severe MR have a 5%/year mortality rateOnce

Слайд 73Imaging studies in MR
ECG: May show, LA enlargement, atrial fibrillation

and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary

artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment
TEE if transthoracic echo is inconclusive
Imaging studies in MRECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MRCXR: LA

Слайд 75Management of MR
Medications
Vasodilator such as hydralazine
Rate control for atrial fibrillation

with -blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Diuretics for

fluid overload
Management of MRMedicationsVasodilator such as hydralazineRate control for atrial fibrillation with -blockers, CCB, digoxinAnticoagulation in atrial fibrillation

Слайд 76Management of MR
Serial Echocardiography:
Mild: 2-3 years
Moderate: 1-2 years
Severe: 6-12

months

IE prophylaxis: Patients with prosthetic valves or a Hx of

IE for dental procedures.
Management of MRSerial Echocardiography: Mild: 2-3 yearsModerate: 1-2 yearsSevere: 6-12 monthsIE prophylaxis: Patients with prosthetic valves or

Слайд 79Simplified Indications for MV Replacement in Severe MR
ANY Symptoms at

rest or exercise with (repair if feasible)
Asymptomatic:
If EF

onset atrial fibrillation
Simplified Indications for MV Replacement in Severe MRANY Symptoms at rest or exercise with (repair if feasible)Asymptomatic:If

Слайд 80THANK YOU

THANK YOU

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