Insufficient Evidence

1
Insufficient Evidence?

• Jimmy Klemis, MD
• Cardiology/CT Surgery Conference

2
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
  1-2hrs 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

3
Case Presentation

• PMHx
• Chronic LBP
• Obesity
• OSA/ CPAP
• Depression/Anxiety
• Basal Cell Carcinoma
• Social
• no alcohol, cocaine, tobacco or drugs married
  with 1 teenage son
• Meds (at presentation)
• Carvedilol 50 bid, Celebrex, Lasix, ASA,
  anxiolytic, hydrocodone, Combivent MDI

4
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

5
Case Presentation

• Lab
• Chem 142 \ 110 / 14 H/H 16.6/ 46
• 4.4 / 27 \ 1.4
• TSH, LFT, FLP, WBC/PPC, Coags nl
• ECG NSR, PRWP, nl axis, no ischemia

6
Previous workup

• April 2001
• ETT-Sesta 9.2 METS, (-) ischemia, EF 24
• ECHO dilated LV, conc LVH, EF 40
• sclerotic AV, AVA 1.7, minimal AI
• June 2001
• 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
• Carvedilol refilled, sent back to
  PCP/Cardiologist.

7
Clinical Course

• July 2001
• Cardiologist recommends transplant for
  idiopathic dilated CMP
• September 2001
• 2nd opinion referral to VAMC
• NYHA Class IV, exam with AI admitted
• carvedilol, cox-2 d/ced ACEI/diuresis
  initiated
• November 2001
• NYHA Class II, symptomatic improvement
• January 2001
• NYHA Class III despite maximal med Rx
• Cath nl coronaries, Ao Root 3 AI

8
Serial ECHO/clinical findings
9
Chronic Aortic Insufficiency

• Etiology
• Pathophysiology
• History / Physical Findings
• Natural History
• Diagnosis
• Management

10
Etiology

• Aortic Root
• 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
• Rheumatic
• Calcific degeneration
• Congenital (Bicuspid, VSD)
• Myxomatous degeneration
• Endocarditis
• Structural degeneration of Bioprosthetic valve
• Other (SLE, AS, Takayasu, Whipple, Crohns)

11
Anatomy / Pathology
Braunwauld 6th ed
12
Chronic AI - Pathophysiology

• 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

13
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
14
Hemodynamics
Braunwauld 6th ed
15
Hemodynamic/ Auscultory
Braunwauld 6th ed
16
History

• DOE, Orthopnea, PND
• usually after 4th / 5th decade and significant
  cardiomegaly and LV dysfxn
• Angina pectoris
• develops later, nocturnal sxs prominent often
  with diaphoresis due to HR slowing with arterial
  DBP falling to low levels
• Palpitations / Head pounding
• 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.
17
Physical Findings

• de Musset sign head bobbing with heartbeat
• Corrigan pulse water hammer pulse
• Bisferiens pulse brach/ fem arteries
• Hill sign popliteal gt brachial by 60mmHg
• Traube sign pistol shot sounds over fem
  artery
• Duroziez sign sys m when femoral artery
  compressed proximally and diastolic m when
  compressed distally
• Quincke sign capillary pulsations
• Apical impulse - diffuse, hyperdynamic and
  displaced inf/lat
• systolic thrill base/suprasternal notch /
  carotid arteries

18
Physical Findings

• Diastolic murmur
• high frequency, sitting up, leaning forward
• duration gt 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
• Austin Flint murmur
• mid-late diastolic apical rumble severe AR
• Wide Pulse Pressure
• Systolic flow murmur (/thrill)

19
Natural History
Mortality rate for severe AICHF sxs gt 20-50/yr2
2Aronow , et a. Am J Cardiol 1994 74 286. l
Bonow, et al. JACC Nov 1988
20
CXR
21
ECHO

• 2D/ M-Mode
• AV/ Ao Root anatomic abnormalities
• LV dimension / sphericity
• AMVL fluttering, reverse doming
• increased EPSS
• Doppler
• Color Flow Mapping
• Continuous Wave
• Flow reversal in desc Ao (100 sens 97 spec for
  severe AI)
• Limitations What is severe AI?

22
AMVL fluttering
Color Flow top mild, bottom moderate
23

Continuous Wave Doppler
Chronic AI
Acute AI
24
Cardiac Catheterization
25
Medical Management

• Vasodilators
• goal is to reduce SBP, improve forward SV,
  reduce regurgitant volume
• Uses
• 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
• Nifedipine, Hydralizine, ACEI, Nipride, Prazosin
• Children/ severe AR ACEI reversed LV
  dilatation/wall stress
• avoid (-) inotrope in LV dysfxn

26
Effect of Nifedipine in pt with severe
asymptomatic AR and nl LV fxn
Scognamiglio, et al. NEJM 1994331689-694
27
Medical Management

• Rx CHF diuretics, aldactone, dig
• avoid vigorous exertion if symptomatic AI
• control diastolic BP (increases regurg)
• avoid BB - prolong diastole, increase AR

28
Paradigm Shifts
29
Timing of Surgery

• Goal is to intervene before irreversible LV
  systolic dysfxn ensues
• initially reversible, mainly due to afterload
  excess full recovery in LV size/fxn possible
• with progressive chamber dilatation, decreased
  myocardial contractility gtgt afterload excess as
  cause of LV dysfxn.
• associated with worse recovery of LV fxn and
  increased mortality

30
Surgical Therapy

• Indications for AVR (Severe AR)1
• Sxs (NYHA III-IV) regardless of LV fxn
• Sxs (NYHA II) with evidence of progressing LV
  dysfxn ( LV ESD 55, LV EF lt50-55)
• 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
• Predictors of Postoperative Prognosis
• LV systolic function
• LV End Systolic Size ( LV ESD)

1 Bonow, et al. Circulation 1998981949-84
31
Bonow, et al. JACC Nov 1998
32
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
33
Summary of Surgical Timing

• Asymptomatic, nl LV size/fxn
• Asymptomatic, ESD gt55 EF lt 50-55
• serial exam/ measurements q 2-4 mos
• Symptomatic, mild-mod LV dysfxn
• Symptomatic, severe LV dysfxn
• Hi surgical risk, but worse with med Rx
  (mortality 20-50)
• individualize

34
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

35
Surgical Options

• Ao Root disease
• annuloplasty or other valve sparing surgery
  possible if pure Ao Root dz
• Primary AV disease
• valve replacement

36
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 109345,
1995.)
Braunwauld 6th ed
37
Figure 29-16 A. Carpentier-Edwards Supra- annular
porcine bioprosthesis. B. Hancock II porcine
bioprosthesis. C. Hancock modified orifice
porcine bioprosthesis. D. St. Jude Medical
Bioimplant porcine bioprosthesis.
Figure 29-15 A. Björk-Shiley Monostrut
mechanical prosthesis. B. Sorin Allcarbon
monoleaflet mechanical prosthesis. C.
Medtronic-Hall mechanical prosthesis. D.
Omnicarbon mechanical prosthesis.
Edmunds. Cardiac Surgery in the Adult. Ch 29
38
Key Points

• Severe AR is clinical dx
• murmur, pulse pressure, etc
• 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
• LV ESD gt55mm
• LV EF lt 50-55
• Mortality HF/Severe AR 20-50 1yr
• Individualize therapy and tailor to pt
  presentation

39
55 Saves Lives