Is It Dead or Alive

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					Is It Dead or Alive?
    Eric J. Frischhertz,
    M.D.
History of Present Illness:
   73 yo man with PMH of HTN, DM2,
    hyperlipidemia, and CAD presented on
    5/12/04 with cc of fatigue and dyspnea.
   He was dx’d with CAD by angiogram on
    3/30/04 and was also found to have
    severe LV dysfxn at that time (LVEF
    20%).
   He did not have CP but did c/o
    decreased exercise tolerance.
HPI (continued)
 He could walk about 2 blocks before
  fatigue limited his activity.
 He also reported LE swelling and
  orthopnea.
 He did not have PND.
Medical History:
   PMH: HTN, hyperlipidemia, DM2, prostate
    cancer, CAD
   PSH: umbilical hernia repair
   Meds: zocor 40mg qd, asa 325mg qd,
    toprol xl 50mg qd, hyzaar 50/12.5mg qd,
    aldactone 25mg qd, glipizide 5mg qd,
    carnitine 330mg tid, prevacid 15mg qd
   Allergies: none
Medical History (contin):
       Hx: +Tobacco—smoked
 Social
 2ppd for 40 yrs but stopped 6
 weeks ago; no alcohol or illicit
 drug use.
Physical Exam:
   VS: BP 147/67      HR 73     RR 16       T
    97.6
   Alert and oriented x3
   Carotid pulses 2+ bilat without bruits
   No Jugular venous distention
   Regular heart rhythm, normal s1/s2,
    Distant heart sounds
Physical Exam:
   Both lungs clear but had scant bilat
    end expiratory wheezing
   Abdomen non-tender with no
    organomegaly
   Skin dry, no edema, femoral pulses
    2+ bilat without bruits, DP/PT pulses
    2+ bilat
 Laboratory Data:


139 104 19                      11.1
                    121   8.6          266
4.2   26    0.9                 34.1

Hb A1c 5.9%                 BNP 394
T Cholesterol 167
Triglycerides 73
HDL 41
LDL 107
     Laboratory Data:
   12-Lead EKG—nsr, left axis deviation,
    incomplete LBBB, LVH, when compared to
    EKG from 3/24/04 there was now T wave
    inversion in the lateral leads
   Chest X-ray—no acute pulmonary process
Results:
    Cardiac Angiogram (3/30/04):
1.   Multivessel CAD.
2.   Severely reduced LVEF.
3.   Recommend CT surgery consult
     and optimization of medical
     management.
Results:
    Echocardiogram (5/7/04):
1.   LAE, LVE.
2.   AK of inferior, apical, anterior, and
     inferoseptal segments with severe
     HK of remaining segments.
3.   LVEF ~ 15%.
4.   Eccentric LVH
5.   Severe MR, mild TR.
Management:
   It was determined after these
    results that patient should undergo
    a viability study to determine if he
    would benefit from
    revascularization.
Is It Dead or Alive?
    An Overview of
    Myocardial Viability
    Testing Stunned vs.
    Hibernating
    Myocardium
Hibernating myocardium
    Concept was developed in the late
     1970’s based on 2 observations:
1.   That myocardial dysfunction present
     before bypass surgery often reversed
     after surgery.
2.   And that inotropic stimulation with
     epinephrine caused transient
     improvement in regional and global LV
     dysfunction in patients with CAD.
Ventriculogram with
Epinephrine
 Diamond, et al. noted in 1978,
  “ischemic noninfarcted myocardium
  can exist in a state of function
  hibernation.”
 This later led to the proposal by
  Rahimtoola of “hibernating
  myocardium.”
Why This Is Important
Pathophysiology
   May result from repetitive
    myocardial stunning, which is
    different from hibernation in that it
    is caused by short term reduction in
    flow, a re-establishement of that
    flow, and subsequent LV dysfunction
    of limted duration.
Support for Stunning as a
Cause of Hibernation
1.   In animal studies, repetitive stunning
     led to persistent LV dysfunction despite
     return of normal blood flow.
2.   Gradual increase in coronary stenosis in
     animals causes tissue supplied by the
     stenotic vessel to increase uptake of
     fluorine-18 labeled deoxyglucose, a
     glucose analog, which is a characteristic
     of hibernating myocardium.
Histopathologic
Characteristics
   Loss of contractile proteins (sarcomeres)
    without loss of cell volume in a
    substantial number of cells.
   Glycogen-rich perinuclear zones adjacent
    to areas of numerous small mitochondria.
   Nuclear changes with heterochromatin
    distributed evenly over the nucleaplasm
   Substantial loss of sarcoplasmic
    reticulum.
Evaluation and treatment
 Ventriculography
 Dobutamine Echocardiography
 Myocardial Perfusion Imaging
  (nulcear imaging with thallium,
  sestamibi, or PET)
 MRI
Other Modalities
 Tissue Doppler Echocardiography
  (TDE)/strain rate imaging
 Electroanatomic mapping
 Myocardial contrast
  echocardiography
Ventriculography
 Asses wall motion by
  ventriculography then dtermine if
  there is improvement with NTG (to
  improve blood flow) or positive
  inotropic stimulation
 Limited by subjective evaluation
Dobutamint Stress Echo
   Evaluates the “inotropic reserve”
   Viable myocardium shows improved
    global and regional contractile function.
   An improved contractile response requires
    at least 50% viable myocytes in a given
    segment
   The predictive value of the test is best
    when there is a biphasic response, i.e.,
    improved contractile function with low
    dose infusion and worsening function with
    high dose
DSE continued
   This represents an initial recruitment of
    contractile reserve followed by
    inducement of ischemia
   Infusion with low dose dobutamine (2.5
    to 5 mcg/kg/min) and increase
    incrementally while obtaining echo
    images at each dose
   Sensitivity 84% (CI 82-86%)
   Specificity 81% (CI 79-84%)
Nuclear Scan: Thallium
   Thallium-201 is a potassium analog which
    can be detected by single photon
    emission computed tomography (SPECT)
   Uptake by myocardial cells depends on an
    active transport process requiring intact
    sarcolemmal membranes and adequate
    ATP stores
   Images are obtained at rest and 4 hours
    later
   In normal myocardium, intial uptake is
    high but decreases rapidly within hours
Thallium continued
 In hibernating myocardium, initial
  uptake is low but increases over
  time due to thallium redistribution.
 Uptake of greater than 50% of that
  in the normal area is the best
  predictor of functional recovery after
  revascularization.
Thallium Protocols
 In addition to the 4 hour protocol,
  there have been studies with
  reimaging at 24 hours and also with
  reinjection of a smaller dose of
  thallium prior to obtaining
  redistribution images
 Both protocols have better
  sensitivity that the intial protocol
Technetium-99m Sestamibi
 Sestamibi is a lipphilic cationic
  compound. The uptake across
  myocardial mebmranes is passive
  and requires the presence of intact
  electrochemical membrane gradients
 There is limited redistribution after
  initial uptake which would appear to
  limit its usefulness in determining
  viability
Sestamibi Continued
 However, multiple studies
  comparing sestaimibi with thallium
  have shown that sestamibi produces
  results similar to that of thallium
 This would indicate that the kinetics
  of sestamibi are more complex
  under low flow conditions than can
  be explained by a simple flow
  dependent model
Positron Emission
Tomography
 Ischemic cells use more glucose
  than normal.
 Flourine-18 labeled deoxyglucose
  differentiates normal, hibernating
  and necrotic myocardium
Back to Our Patient
 He underwent thallium delayed
  imaging.
 Images were obtained at rest, 10
  minutes post injection, and at 24
  hours post injection.
Findings
   17% of the left ventricular
    myocardium, located in the inferior
    and the inferolateral wall,
    demonstrates viability by thallium
    scintigraphy. 12% of the
    myocardium in the same region has
    no viability and represents scar.