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Valvular Heart Disease
J.B. Handler, M.D.
Physician Assistant Program
University of New England
Abbreviations
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VHD- valvular heart disease
RF- rheumatic fever
MR- mitral regurgitation
AR- aortic regurgitation
HF- congestive heart failure
MS- mitral stenosis
LAP- left atrial pressure
PuVR- pulmonary vascular
resistance
RV- right ventricle
CO- cardiac output
TR- tricuspid regurgitation
PI- pulmonic insufficiency
NSST-T- non specific ST-T
PAH- pulmonary artery
hypertension
SV- stroke volume
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RVH- right ventricular hypertrophy
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AoV- aortic valve
MVA- mitral valve area
PSVT- paroxysmal
supraventricular tachycardia
MVR- mitral valve replacement
MVP- mitral valve prolapse
AS- aortic stenosis
SEM- systolic ejection murmur
LVEDP- left ventricular end
diastolic pressure
PND- paroxysmal nocturnal
dyspnea
LSB- left sternal border
ACE- angiotensin converting
enzyme
BE- bacterial endocarditis
RF- rheumatic fever
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Etiologies of VHD
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Rheumatic valve disease
Congenital, including bicuspid aortic valve.
Coronary heart disease: MI, papillary muscles
Dilation of the aorta: Aortic root disease
Chronic “wear and tear”: aortic sclerosis/stenosis
Dilation of the LV- from any cause: MR
Endocarditis
MV prolapse
Others
Acute Rheumatic Fever: IO
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2/3 all cases - developing countries
Episodes of RF are quite uncommon in U.S.,
except in immigrants.
Epidemiology - Identical to that of Group A
Streptococcus; children 5-15
Pathogenesis- oropharyngeal infection; RF
follows the sore throat; usually within 2-3 wks.
Mechanism - systemic immune process involving
Group A strep. antigens; abnormal immune
response. Preventable with adequate Rx of
streptococcal pharyngitis.
IO – Interest Only
Diagnosis - Jones Criterion
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Carditis - Pancarditis involving valves,
endocardium, myocardium and pericardium
– Healing of Rheumatic valvulitis - fibrous thickening
resulting in valvular stenosis or insufficiency
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Migratory polyarthritis
Sydenham’s Chorea
Subcutaneous nodules
Erythema marginatum
Treatment
Antistreptoccal Rx until regimen finished;
Penicillin IM or oral (10 day course)
Erythromycin and others are alternatives
 Arthritis/fever - Salicylates
 Severe carditis- Glucocorticoids
 HF, MR, AI - specific Rx.
 Secondary prophylaxis to prevent
recurrences- PCN or alternative until adult.
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Cardiac Pressures
4-12
4-12
4-12
8-15
4-12
4-12
4-12
Images.google.com
Mitral Regurgitation-Etiology
Chronic Rheumatic heart disease- ing
frequency
 LV dilatation from any cause
 Coronary Heart Disease: Papillary muscle
dysfunction with ischemia/infarction
 Mitral Valve Prolapse
 Infective endocarditis
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Mitral Regurgitation
Images.google.com
Pathophysiology of MR
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Blood regurgitates from LV into LA.
LV volume increases progressively as severity of
MR increases.
– Increased blood return to LA: pulmonary veins +
regurgitant volume from previous beat.
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LV function- well preserved initially; often
deteriorates in later stages as does cardiac output
(CO). LV compensates for volume overload via
the Starling mechanism.
Left atrium (and LV) dilates over time - LAP and
LVEDP gradually risepulmonary congestion
– Afib. common.
Symptoms
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Often asymptomatic for years
Fatigue, DOE, orthopnea- symptoms of left sided
heart failure (detailed discussion later in CV
system).
With chronic severe MR –Elevation of pulmonary
venous pressure leads to  PuVR  PAH and
subsequent Rt Heart failure: hepatic congestion,
peripheral edema, etc.
Physical Exam
Palpation: Systolic thrill may be present at
apex depending on turbulence.
 Auscultation: S1 soft or absent; S3 gallop if
significant MR; Systolic Murmur is
hallmark - Gr. II-IV/VI holosystolic in most
cases -radiates to axilla (exception is MVP);
murmur is high pitched and blowing.
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Additional Findings
ECG: LAE; Atrial arrhythmias (Afib).
 Echo/Doppler: LA & LV size; LV
function. Can estimate severity of MR;
LV often dilates with progressive MR.
 CxR: Late findings - Progressive LVE; HF;
pulmonary edema.
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LVE- left ventricular enlargement
CxR- chest x-ray
Treatment of MR
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Medical - Treatment depends on severity.
Once symptomatic: Decreased physical activity
and Na restriction. Drug therapy often
significantly improves symptoms and patients may
do well for many years.
– ACE inhibitors or other vasodilators: decrease
afterload and preload.
– Diuretics: decrease preload, Na and volume overload
– Inotropic agents: digoxin- limited role
Treatment of MR
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Surgical- Indications:
– Severe MR with Sx
– Dilating LV with progressive dysfunction  EF (even
with mild symptoms).
– Timing of surgery is important; needs to be done before
significant deterioration of LV function/EF.
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Surgical result dependent on pre-existing LV
function. Mitral valve repair is preferred to MV
replacement.
Mitral Valve Prolapse
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Very common (3-5% adults) - Excessive
redundant MV tissue from abnormal connective
tissue:
– MVP - most common form involves MV without
major connective tissue disease elsewhere in body.
Familial form also exists- autosomal dominant.
– MVP as part of major CT disease (Marfan’s, Ehler’sDanlos) or variations; these disorders are uncommon.
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Pathology- myxomatous degeneration of MV
leaflet tissue.
Associated deformities: high arched palate; pectus
excavatum.
Mitral Valve Prolapse
Images.google.com
MVP: Pathology
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Mitral regurgitation can develop due to redundant
floppy valve leaflets and/or involvement of the
MV supporting structures – chordae tendineae.
Stress on Papillary muscles or chordae is
presumed reason for localized and atypical chest
pain.
Abnormal valve structure and MR can predispose
to infective endocarditis but incidence is very
low antibiotic prophylaxis no longer indicated.
Clinical Features
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Female > male; Sx, when present, commonly
occur at ages 15-30.
Most are asymptomatic; often detected on PEcharacteristic murmur.
Most common symptoms when present: chest
pain (*atypical) and palpitations.
Arrhythmias common: PAC’s, PVC’s, PSVT,
non-sustained VTach.
Sudden death – exceedingly rare arrhythmias
*Atypical – CP unlike the pain/discomfort that is present with coronary heart disease
Physical Findings
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Auscultation: Mid to late systolic click (tensing
of chordal structures).
High pitched late systolic murmur best heard at
apex.- click and murmur occur earlier and get
louder with maneuvers that decrease LV
volume: standing after squatting, valsalva.
Maneuvers that increase LV volume delay the
click and soften the murmur: isometric hand grip,
squatting.
Additional Findings/Treatment
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ECG: NST-TW changes. Usually in leads II, III,
aVF.
Echo/Doppler: Diagnostic; shows MVP and
identifies MR when present.
Treatment: Reassurance; ß-Blockers for chest
pain or arrhythmias; additional anti-arrhythmics
usually not necessary.
Infrequently, severe MR develops requiring MV
repair (more common in men than women).
Mitral Stenosis
2/3 females, 1/3 males- only cause is RF.
 About 40% of all cases of RF develop MS.
 Valve leaflets thicken and calcify,
commisures fuse; valve orifice narrows;
subvalvular supporting apparatus involved.
 Least common rheumatic valvular lesion.
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Mitral Stenosis
Images.google.com
Images.google.com
Pathophysiology
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Normal MVA - 4-6 cm2. Valve leaflets fuse,
decreasing valve area. Severe MS < 1 cm2.
LA pressure rises in order to propel blood across
the stenotic valve- pressure gradient compared to
LVEDP.
LAP reflected backwards into the pulmonary
circulation results in pulmonary venous
congestionpulm capillary congestion 
interstitial fluid  dyspnea. Pulmonary
arterioles subsequently constrict.
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LV function usually normal. LVEDP normal.
Chronic severe MS - Elevation of pulmonary
vascular resistance (PVR) and subsequent
development of Pulmonary Artery Hypertension
(PAH).
Chronic PAH RVH  RV dysfunction and
failure.
CO at rest- usually normal but does not rise
adequately with exercise. With severe MS and
PAH, CO eventually falls.
Symptoms/Complications
DOE, orthopnea, PND pulmonary edema
 Findings of Rt Ht failure - late
 Atrial arrhythmias: PAC’s, Atrial
Fibrillation and Flutter
 Hemoptysis  ruptured pulmonary
capillaries
 Atrial Thrombi and embolization - (AFib)
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Physical Exam
Palpation: prominent RV impulse
 Auscultation: S1 loud/accentuated; S2 loud
if PAH present
Opening Snap of MV-apex, follows S2.
Diastolic Rumble- Follows OS; low
pitched/apex; length correlates with
severity; MR murmur often audible.
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Additional Findings
ECG: LAE/LAA; RAD, RVH (over time)
 Echo/Doppler: diagnostic-shows abnormal
valve motion, estimates the gradient and
MVA, defines LA size and LV function.
 CxR: Pulmonary congestion; RVE.
 Cardiac Cath: Documents gradient, MVA,
presence or absence of MR and more.
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MS - Treatment
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Sodium restriction, diuretics.
Rate control of Afib or cardioversion.
Surgery -Mitral valvulotomy - marked
symptomatic improvement. MVR only when
repair cannot be done (mortality 3-5 %).
Percutaneous balloon valvuloplasty- alternative to
surgery; if successful, avoids or delays need for
surgery.
Aortic Stenosis-Etiologies
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Common: 20% all valvular disease; 80% males
Bicuspid valve leaflets thicken, fuse
Rheumatic valvulitis leaflets thicken, fuse
Idiopathic – Sclerocalcific: chronic wear and teardevelops in the elderly  leaflets thicken, fuse
Note: Thickening/calcification (without fusing) of
the AoV often occurs with aging (Aortic
Sclerosis) without progressing to significant
aortic stenosis  Gr II/III murmur. Important to
differentiate using history (asymptomatic), PE and
echocardiogram if needed.
Aortic Stenosis
Images.google.com
Pathophysiology
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Obstruction to LV outflow- pressure overload.
Systolic gradient between LV and Ao.
Obstruction gradual - initially well tolerated; LV
hypertrophy is compensatory.
Cardiac Output often normal at rest - does not
adequately rise with activity.
Late in course- LV failure, LVEDP rises, CO falls.
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Myocardial oxygen consumption (MVO2) increases
from LVH and high LV pressures.
Coronary blood flow is impaired from high LV
pressures.
Myocardial ischemia can occur in the absence of
*CHD severe LVH/ high pressures  outstrips
coronary blood flow
– Associated CHD may be present.
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Normal AoV area: 2.5-3.0 cm2
Critical AS: valve area <0.75 cm2
*CHD- coronary heart disease
AS Hemodynamics
Images.google.com
Symptoms of AS
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Exertional dyspnea - elevation of LVEDP
transmitted backward into pulmonary circuit.
Angina Pectoris-Increased MVO2 (pressure
overload and hypertrophy) and decreased coronary
reserve. *CHD may co-exist but does not have to
be present for angina to develop.
Syncope - Peripheral vasodilation with inadequate
forward CO with activity or from arrhythmia.
HF occurs late - very poor prognosis.
CHD – coronary heart disease
Physical Exam
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Carotid pulse rises slowly; sustained peak.
Apex displaced laterally; +/- systolic thrill;
systolic ejection sound (click ) variable.
Aortic valve closure is delayed - fixed or
paradoxical splitting of S2.
S4 gallop common.
Murmur - SEM (crescendo-decrescendo)- peaks
in mid to late systole depending on severity;
harsh, low pitched, best heard at base and
radiates to carotids – Grade II-IV/VI.
Additional Findings
ECG: LVH common; LAA.
 Echo/Doppler: Diagnostic- identifies LVH,
valve calcification and restriction; estimates
gradient and aortic valve area.
 CxR: LV prominence, displaced apex.
 Cardiac Cath: Usually necessary prior to
surgery; identifies gradient, valve area, LV
function and presence or absence of CAD.
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Natural History: Untreated
Angina Pectoris -death within 3 years
 Syncope - death within 3 years
 Dyspnea - death within 2 years
 CHF - death within 1.5 years
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Treatment
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Medical - Mild to moderate AS without
symptoms: Careful F/U; serial echo/doppler
studies. Limited role for meds once symptoms
begin.
Surgical- severe or symptomatic AS. Valve
replacement with tissue or mechanical valve - Op
risk 4%; 60-70% 10 yr. survival; marked
symptomatic improvement.
– Ross procedure an option for young patients with AS.
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Ballon valvuloplasty- palliative
Aortic Regurgitation- Etiology
75% male
 Rheumatic Heart Disease
 Infective endocarditis on previously
deformed valve
 Aortic Root disease and dilatation
 Bicuspic Aortic Valve (AS more common
than AR)
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Aortic Regurgitation
AR: Pathophysiology
Increase in LVEDV (preload): blood
returning from LA + regurgitant blood.
 LV dilates- allows increased SV (stroke
volume) and adequate effective forward SV
(Starling’s law).
 Over time (years) LV function gradually
declines and EF (ejection fraction)
deteriorates.
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Pathophysiology
LV deterioration often precedes symptoms
(reason for serial echo/doppler exams).
 As AR progresses, CO fails to rise
adequately with exercise, LV dysfunction
worsens  Increased LVEDP pulmonary
congestion HF.
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AR: History
Sometimes familial - Connective tissue
disease.
 History of RF or infective endocarditis.
 Patient often asymptomatic for 10-15 yrs.
with significant AI.
 Symptoms: Palpitations, exertional dyspnea,
orthopnea; PND and HF occur later.
 Atypical chest pain common.
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AR: Physical Exam
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Arterial Pulse - Rapid rising “water-hammer
pulse” and collapsing pulse.
“Quinke’s pulse” - alternate flushing and palling
of the skin at the nail root.
“Pistol shot” sound over femoral artery in systole.
Derosiez’ sign - to and fro murmur over femoral
artery.
Arterial pulse pressure widened- elevated
systolic pressure (often greater than 200mm) and
lowered diastolic pressure.
Physical Exam
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Palpation - apex displaced laterally/inferiorly.
Diastolic Thrill may be present along LSB.
Auscultation: S2 soft; S3 common; high pitched
blowing diastolic decreshendo murmur (LSB).
Best heard with diaphragm – patient sitting
upright/leaning forward.
Systolic ejection (increased flow across AoV)
murmur.
Additional Findings
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ECG - Increased voltage/LVH develops over time.
Echo/Doppler: early on LV contractility normal
or increased - later, LV dysfunction; AI jet
detectable and semi quantitated by Doppler.
Cardiac Cath: Identifies severity of AI, degree of
LV dysfunction and intra-cardiac pressures.
Needed to assess coronary arteries in older adults.
Cath may not be needed in younger patients.
Treatment of AR
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Medical - very close follow-up; serial
Echo/Doppler studies.
Same Rx as for CHF: Afterload reduction with
vasodilators (ACEI, hydralazine). Preload
reduction with diuretics; digoxin may be useful in
selected individuals.
Surgical - Timing of surgery is difficult as pts.
with AI do not develop symptoms until after the
development of LV dysfunction.
Surgery indicated for progressive LV dilatation
and dysfunction +/- symptoms.
Surgery
Aortic Valve Replacement with
bioprosthesis (tissue valve) or mechanical
valve. Ross procedure an option if young.
 Op mortality dependent on pre-op LV
function (5% or greater mortality).
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