Docstoc

Insufficient Evidence

Document Sample
Insufficient Evidence Powered By Docstoc
					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 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
               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
         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
           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
                  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.
                    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/c’ed; 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
   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   NYHA IV

11/01   56      55%      moderate NYHA II

1/02    57      43%      moderate NYHA III
     Chronic Aortic Insufficiency
   Etiology
   Pathophysiology
   History / Physical Findings
   Natural History
   Diagnosis
   Management
                                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)
Anatomy / Pathology




  Braunwauld 6th ed
     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
      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
     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.
                  Physical Findings
   de Musset sign –       head bobbing with heartbeat

 Corrigan pulse       – “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
    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
                 Physical Findings
 Diastolic murmur
       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
   Austin Flint murmur
       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

                               2Aronow   , et a. Am J Cardiol 1994; 74: 286. l
Bonow, et al. JACC Nov 1988
CXR
                         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?
AMVL fluttering



                  Color Flow – top mild, bottom moderate
Continuous Wave Doppler



               Chronic AI




                Acute AI
Cardiac Catheterization
             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
         Effect of Nifedipine in pt with severe
           asymptomatic AR and nl LV fxn




Scognamiglio, et al. NEJM 1994;331:689-694
        Medical Management
   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
    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 >>
        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
             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
       Predictors of Postoperative Prognosis
            LV systolic function
            LV End Systolic Size ( LV ESD)
1   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
   Asymptomatic, nl LV size/fxn
   Asymptomatic, ESD >55 EF < 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
 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
               Surgical Options
   Ao Root disease
       annuloplasty or other valve sparing surgery
        possible if pure Ao Root dz
   Primary AV disease
       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      Figure 29-16 A. Carpentier-Edwards Supra-
mechanical prosthesis. B. Sorin Allcarbon   annular porcine bioprosthesis. B. Hancock II
monoleaflet mechanical prosthesis.          porcine bioprosthesis. C. Hancock modified
C. Medtronic-Hall mechanical prosthesis.    orifice porcine bioprosthesis. D. St. Jude
D. Omnicarbon mechanical prosthesis.        Medical Bioimplant porcine bioprosthesis.




   Edmunds. Cardiac Surgery in the Adult. Ch 29
                   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 >55mm
    LV EF < 50-55%
 Mortality HF/Severe AR 20-50% 1yr
 Individualize therapy and tailor to pt presentation
55
Saves
Lives

				
DOCUMENT INFO
Shared By:
Categories:
Tags:
Stats:
views:0
posted:2/23/2013
language:Unknown
pages:39