The Essentials of Valvular Heart Disease

Report
Some Essentials of
Valvular Heart Disease
CCU lecture series
Case 1
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56 YO M presents for DOE 6 months
Denies CP, syncope, palpitations
PMH significant for hypercholesterolemia
Had “murmur since I was a child”
Mother died of heart failure in 60s
Non-smoker
Case 1
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HR 66 BP 120/85
Neck: No bruits
Chest: CTA
CVS: RRR, harsh 3/6 SEM radiating to
carotids
Abdomen: Soft, NT
Ext: No c/c/e
Aortic Stenosis
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Obstruction most commonly located at the
level of the aortic valve
May be congenital or acquired (most
common)
Calcific AS is associated with traditional
risk factors for atherosclerosis (smoking,
high LDL, HTN)
Also seen in ESRD, Pagets, SLE,
alkaptonuria
Pathophysiology
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Aortic stenosis generally develops
gradually, leading to LV hypertrophy
As stenosis progresses, LVEDP begins to
increase – LV function usually remains
normal until late in disease process
Diastolic dysfunction may also contribute
to symptom onset
Clinical Features
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3 classic symptoms of severe AS
DOE
Syncope
Angina
Physical Exam
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Pulse
Heart sounds (second heart sound)
Murmur
Other clinical manifestations (bleeding,
embolic events, CAD)
Testing
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EKG
CXR
Echo
Cardiac catheterization
CT/MRI?
Catheterization findings
Cardiac MRI and CT
Grading Severity of AS
Low Gradient AS
Indications for Surgery
Indications for Surgery
Treatment
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No effective medical therapy for what is
primarily a mechanical obstruction
Aortic valve replacement is standard of
care
Mechanical vs. Bioprosthetic valves
The Ross procedure
Aortic root replacement?
Balloon Valvuloplasty
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31 patients >90 years old who underwent
balloon valvuloplasty from 2003-2006
Patients all had severe symptomatic AS
and were deemed high risk for surgery
Mean STS score was 18.5%
Results
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25 patients underwent retrograde BAV, 6
anterograde
Mean AVA increased from 0.52 to 0.92
cm²
Mean NYHA Class increased from 3.4 to
1.8
30 day mortality was 9.7%
CoreValve
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86 patients with symptomatic severe AS,
>80 years old and high risk for cardiac
surgery enrolled
Percutaneous AV replacement attempted
with 18 and 21 French systems
Results
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Acute device success was 88%
Successful implantation led to a significant
reduction in gradient
Aortic regurgitation remained unchanged
Procedural mortality was 6%
30 day mortality was 12%
The SALTIRE Study
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155 patients with moderate to severe AS
enrolled – randomized to 80 mg
atorvastatin or placebo
AV stenosis and calcification assessed by
echocardiography and cardiac CT
Primary endpoints changes in aortic jet
velocity and AV calcium score
SALTIRE
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LDL decreased to 62 mg/dl in the
atorvastatin group, 131 in placebo
No significant change in endpoints
The Critically Ill AS patient
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Remember…
Atrial fibrillation is bad!
Vasopressor agents are preferable to
inotropes for blood pressure support
Think IABP early
Always auscultate before you give NTG
for chest pain!
Management Recommendations
Case Number 2
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72 YO M in the emergency department
has had CP x 5 days
Finally decides to come to the ED
Hypoxic on room air, rales 1/2 way up
Heart sounds difficult to appreciate
Troponin is 44
EKG
Stat Echo performed…
Acute Mitral Regurgitation
Three main mechanisms
• Flail leaflet due to mitral valve prolapse
• Chordae tendinae rupture due to trauma,
infective endocarditis or rheumatic fever
• Papillary muscle dysfunction due to
ischemia/infarction (what kind of infarction
will more often present with acute MR?)
Mitral Valve Anatomy
Pathophysiology
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Hemodynamic changes much more
pronounced than in chronic MR due to
lack of time for adaptation
The abrupt increase in left atrial pressure
is transmitted to the pulmonary circulation
Cardiac output falls and systemic vascular
resistance increases
Clinical Manifestations
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Often present in cardiogenic shock and
acute pulmonary edema
Physical exam may reveal a hyperdynamic
precordium (will the apex be displaced?)
The murmur
Up to 50% of patients will not have an
audible murmur at the time of evaluation
Testing
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Echocardiography mainstay of diagnosis
Cardiac catheterization may be required
for determination of the extent and
severity of concomitant CAD
Hemodynamics are characteristic
Mitral Regurgitation
Treatment
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Definitive treatment is surgical
Supportive measures include nitroprusside
(what is the mechanism?) and possibly
dobutamine for low cardiac output
IABP
Class I Indications for
MV Surgery in Severe MR
Acute symptomatic MR
• Chronic severe MR with NYHA class II, III or IV
in absence of severe LV dysfunction and/or
LVESD>55 mm.
• Symptomatic or asymptomatic patients with
mild/mod LV dysfunction (EF 30-60%) and endsystolic dimension >40 mm
• MV repair recommended over replacement for
majority of pts; pts should be referred to
experienced surgical center.
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Surgery
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Surgical mortality can be as high as 50% however mortality is uniformly worse
without surgical intervention
Valve repair is always preferable to
replacement, if possible
The success rates depend on the etiology
of the valvular dysfunction

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