Insufficient Evidence?
Jimmy Klemis, MD
Cardiology/CT Surgery
Conference
Case Presentation
49 WM sent for “transplant” evaluation from local
cardiologist
 HPI – DOE x 6mos-1year, insidious onset, also
with L sided Chest tightness when tired/stressed
and occasionally awakens him at night, last 12hrs and relieved with anxiolytics. Occasional
lightheadedness after taking Coreg. Denies
PND, Orthopnea, cough, pre/syncope. Former
maintenance worker, now on medical leave. Pt
states trying to remain active (walking/
swimming) but limited by dyspnea
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Case Presentation
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PMHx:
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Social:
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Chronic LBP
Obesity
OSA/ CPAP
Depression/Anxiety
Basal Cell Carcinoma
no alcohol, cocaine, tobacco or drugs; married with 1
teenage son
Meds (at presentation)
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Carvedilol 50 bid, Celebrex, Lasix, ASA, anxiolytic,
hydrocodone, Combivent MDI
Case Presentation
PE: HR 65 BP 170/67
 HNT: jvp est 10cm,
 CV: nl S1/2, + S3, no S4; PMI displaced
laterally to ant ax; 3/6 diastolic
decrescendo m USB
 Resp: basilar rales
 Abd: obese, no ascites/masses
 Ext: tr edema, distal pulses brisk
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Case Presentation
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Lab:
Chem 142 \ 110 / 14
H/H 16.6/ 46
4.4 / 27 \ 1.4
TSH, LFT, FLP, WBC/PPC, Coags nl
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ECG: NSR, PRWP, nl axis, no ischemia
Previous workup
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April 2001
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June 2001
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ETT-Sesta: 9.2 METS, (-) ischemia, EF 24%
ECHO: dilated LV, conc LVH, EF 40%
“sclerotic” AV, AVA 1.7, minimal AI
R/L Cath: nl coronaries
CI 1.9 L/min
RA 21/15 RV 76/27 PA 67/25 PCWP 32
PVR 1.0 Wood Units SVR 2812
Nipride: PA systolic 674740
July 2001 – VA consult NP clinic
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Carvedilol refilled, sent back to PCP/Cardiologist.
Clinical Course
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July 2001
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September 2001
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2nd opinion referral to VAMC
NYHA Class IV, exam with AI – admitted
carvedilol, cox-2 d/c’ed; ACEI/diuresis initiated
November 2001
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Cardiologist recommends transplant for “idiopathic dilated CMP”
NYHA Class II, symptomatic improvement
January 2001
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NYHA Class III despite maximal med Rx
Cath : nl coronaries, Ao Root 3+ AI
Serial ECHO/clinical findings
Date
LVESD EF
AI
Clinical
1995
35 mm
normal
moderate No sxs
1997
46 mm
normal
moderate No sxs
9/01
65
40%
severe
11/01
56
55%
moderate NYHA II
1/02
57
43%
moderate NYHA III
NYHA IV
Chronic Aortic Insufficiency
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Etiology
Pathophysiology
History / Physical Findings
Natural History
Diagnosis
Management
Etiology
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Aortic Root
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Age related dilatation
Medial degeneration/ Marfans
Dissection
HTN
Other ( osteogenesis imperfecta, Reiters, syphilitic aortitis, Bechet,
psoriatic arthritis, relapsing polychondritis, UC arthritis, AS, giant cell
arteritis
Aortic Valve
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Rheumatic
Calcific degeneration
Congenital (Bicuspid, VSD)
Myxomatous degeneration
Endocarditis
Structural degeneration of Bioprosthetic valve
Other (SLE, AS, Takayasu, Whipple, Crohns)
Anatomy / Pathology
Braunwauld 6th ed
Chronic AI - Pathophysiology
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increased LV EDV
addition of new sarcomeres in series/ elongation of
myocytes and myocardial fibers (Eccentric Hypertrophy)
enlarged chamber/ increased wall stress is stimulus for
concentric hypertrophy
dilatation and hypertrophy with resultant recruitment of
preload reserve allow compensation and maintenance of
LV systolic function
may be asymptomatic for decades until
decompensated state develops, wall thickening unable
to keep pace with hemodynamic load, increased
interstitial fibrosis and decreased compliance 
symptoms of CHF ensue
Pressure Volume Relationships in Chronic AI
CO at rest may approach 25 L/min in severe AI with little increase in EDP
very large EDV (Cor Bovinum)
Braunwald 6th ed
Hemodynamics
Braunwauld 6th ed
Hemodynamic/ Auscultory
Braunwauld 6th ed
History
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DOE, Orthopnea, PND
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Angina pectoris
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usually after 4th / 5th decade and significant
cardiomegaly and LV dysfxn
develops later, nocturnal sxs prominent; often with
diaphoresis due to HR slowing with arterial DBP
falling to low levels
Palpitations / Head pounding
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especially in supine position, pounding of heart
against chest wall
tachycardia from stress/exertion may precipitate and
cause extreme discomfort for pt
From Braunwauld. Cardiovascular Dz, 6th ed.
Physical Findings
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de Musset sign –
head bobbing with heartbeat
– “water hammer” pulse
Bisferiens pulse – brach/ fem arteries
Hill sign – popliteal > brachial by 60mmHg
Traube sign – “pistol shot sounds” over fem artery
Duroziez sign – sys m when femoral artery compressed proximally
 Corrigan pulse
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and diastolic m when compressed distally
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Quincke sign – capillary pulsations
 Apical impulse - diffuse, hyperdynamic and displaced inf/lat
 systolic thrill
– base/suprasternal notch / carotid arteries
Physical Findings
 Diastolic murmur
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Austin Flint murmur
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high frequency, sitting up, leaning forward
duration > intensity correlates with severity
mild AR – early diastole, hi pitched blowing
severe AR – holodiastolic, rough
musical (“cooing dove”) – eversion/perforation of Ao cusp
Primary valve dz – heard best LSB 3-4 intercostal
Ao Root dz – heard best RSB
mid-late diastolic apical rumble – severe AR
Wide Pulse Pressure
Systolic flow murmur (/thrill)
Natural History
Mortality rate for severe AI+CHF sxs > 20-50%/yr2
Bonow, et al. JACC Nov 1988
2Aronow
, et a. Am J Cardiol 1994; 74: 286. l
CXR
ECHO
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2D/ M-Mode
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Doppler
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AV/ Ao Root anatomic abnormalities
LV dimension / sphericity
AMVL – fluttering, reverse doming
increased EPSS
Color Flow Mapping
Continuous Wave
Flow reversal in desc Ao (100% sens 97% spec for
severe AI)
Limitations – What is severe AI?
AMVL fluttering
Color Flow – top mild, bottom moderate
Continuous Wave Doppler
Chronic AI
Acute AI
Cardiac Catheterization
Medical Management
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Vasodilators
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Uses
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goal is to reduce SBP, improve forward SV, reduce regurgitant
volume
severe AR + sxs/ LV dysfxn
short term hemodynamic improvement in pt with symptomatic
AR before AVR
prolong compensated phase of asymptomatic patients
No indication for asymptomatic pt with mild AI and normal LV
fxn
Studied in AI
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Nifedipine, Hydralizine, ACEI, Nipride, Prazosin
Children/ severe AR – ACEI reversed LV dilatation/wall stress
avoid (-) inotrope in LV dysfxn
Effect of Nifedipine in pt with severe
asymptomatic AR and nl LV fxn
Scognamiglio, et al. NEJM 1994;331:689-694
Medical Management
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Rx CHF – diuretics, aldactone, dig
avoid vigorous exertion if symptomatic AI
control diastolic BP (increases regurg)
avoid BB - prolong diastole, increase AR
Paradigm Shifts…
Timing of Surgery
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Goal is to intervene before irreversible LV
systolic dysfxn ensues
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initially reversible, mainly due to afterload
excess – full recovery in LV size/fxn possible
with progressive chamber dilatation,
decreased myocardial contractility >>
afterload excess as cause of LV dysfxn.
associated with worse recovery of LV fxn and
increased mortality
Surgical Therapy
 Indications for AVR (Severe AR)1
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Predictors of Postoperative Prognosis
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1
Sxs (NYHA III-IV) regardless of LV fxn
Sxs (NYHA II) with evidence of progressing LV
dysfxn ( LV ESD ~ 55, LV EF <50-55%)
Angina (CHA Class II or higher) w or w/o CAD
mild-mod LV dysfxn (EF 25-49%) regardless of sxs
mod-sev AR and undergoing CABG or other valvular
surgery
LV systolic function
LV End Systolic Size ( LV ESD)
Bonow, et al. Circulation 1998;98:1949-84
Bonow, et al. JACC Nov 1998
Postoperative Mortality
- Operative Mortality Rate 3-8%
- Late Mortality 5-10%/yr in survivors with preop marked cardiomegaly and /or
prolonged preop LV dysfxn
Braunwauld 6th ed
Summary of Surgical Timing
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Asymptomatic, nl LV size/fxn
Asymptomatic, ESD >55 EF < 50-55%
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serial exam/ measurements q 2-4 mos
Symptomatic, mild-mod LV dysfxn
Symptomatic, severe LV dysfxn
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Hi surgical risk, but worse with med Rx
(mortality 20-50%)
individualize
Post Operative Considerations
Preload kept high immediate postop
period to fill dilated LV
 temporary IABP use may be necessary
until LV fxn improves early post op
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Surgical Options
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Ao Root disease
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annuloplasty or other valve sparing surgery
possible if pure Ao Root dz
Primary AV disease
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valve replacement
AV sparing conduit
Figure 46-42 Repair of the aortic valve in patient with severe AR. Conduit tailoring in the
supravalvular position. The conduit is cut to replace three (left), two (middle), or one (right)
individual sinuses. The aortic aneurysm is replaced and the valve is spared.
(From David TE, Feindel CM, Bos J: Repair of the aortic valve in patients with aortic
insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg 109:345, 1995.)
Braunwauld 6th ed
Figure 29-15 A. Björk-Shiley Monostrut
mechanical prosthesis. B. Sorin Allcarbon
monoleaflet mechanical prosthesis.
C. Medtronic-Hall mechanical prosthesis.
D. Omnicarbon mechanical prosthesis.
Figure 29-16 A. Carpentier-Edwards Supraannular porcine bioprosthesis. B. Hancock II
porcine bioprosthesis. C. Hancock modified
orifice porcine bioprosthesis. D. St. Jude
Medical Bioimplant porcine bioprosthesis.
Edmunds. Cardiac Surgery in the Adult. Ch 29
Key Points
 Severe AR is clinical dx
murmur, pulse pressure, etc
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ECHO – flow reversal desc Ao
 Serial clinical/ noninvasive followup
 Med Rx: ACEI/Vasodilator; avoid exertion/BB
 Predictors of worse prognosis in Severe AR “55” rule
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LV ESD >55mm
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LV EF < 50-55%
 Mortality HF/Severe AR 20-50% 1yr
 Individualize therapy and tailor to pt presentation
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55
Saves
Lives