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Is It Dead or Alive

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He was dx'd with CAD by angiogram on 3/30/04 and was also found to have severe ... Cardiac Angiogram (3/30/04): Multivessel CAD. Severely reduced LVEF. ... – PowerPoint PPT presentation

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Title: Is It Dead or Alive


1
Is It Dead or Alive?
  • Eric J. Frischhertz, M.D.

2
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 dxd 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.

3
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.

4
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

5
Medical History (contin)
  • Social Hx Tobaccosmoked 2ppd for 40 yrs but
    stopped 6 weeks ago no alcohol or illicit drug
    use.

6
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

7
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

8
Laboratory Data
11.1
19
139
104
266
8.6
121
34.1
4.2
26
0.9
Hb A1c 5.9 T Cholesterol 167 Triglycerides
73 HDL 41 LDL 107
BNP 394
9
Laboratory Data
  • 12-Lead EKGnsr, 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-rayno acute pulmonary process

10
Results
  • Cardiac Angiogram (3/30/04)
  • Multivessel CAD.
  • Severely reduced LVEF.
  • Recommend CT surgery consult and optimization of
    medical management.

11
Results
  • Echocardiogram (5/7/04)
  • LAE, LVE.
  • AK of inferior, apical, anterior, and
    inferoseptal segments with severe HK of remaining
    segments.
  • LVEF 15.
  • Eccentric LVH
  • Severe MR, mild TR.


12
Management
  • It was determined after these results that
    patient should undergo a viability study to
    determine if he would benefit from
    revascularization.

13
Is It Dead or Alive?
  • An Overview of Myocardial Viability Testing
    Stunned vs. Hibernating Myocardium

14
Hibernating myocardium
  • Concept was developed in the late 1970s based on
    2 observations
  • That myocardial dysfunction present before bypass
    surgery often reversed after surgery.
  • And that inotropic stimulation with epinephrine
    caused transient improvement in regional and
    global LV dysfunction in patients with CAD.

15
Ventriculogram with Epinephrine
16
  • 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.

17
Why This Is Important
18
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.

19
Support for Stunning as a Cause of Hibernation
  • In animal studies, repetitive stunning led to
    persistent LV dysfunction despite return of
    normal blood flow.
  • 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.

20
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.

21
Evaluation and treatment
  • Ventriculography
  • Dobutamine Echocardiography
  • Myocardial Perfusion Imaging (nulcear imaging
    with thallium, sestamibi, or PET)
  • MRI

22
Other Modalities
  • Tissue Doppler Echocardiography (TDE)/strain rate
    imaging
  • Electroanatomic mapping
  • Myocardial contrast echocardiography

23
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

24
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

25
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)

26
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

27
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.

28
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

29
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

30
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

31
Positron Emission Tomography
  • Ischemic cells use more glucose than normal.
  • Flourine-18 labeled deoxyglucose differentiates
    normal, hibernating and necrotic myocardium

32
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33
Back to Our Patient
  • He underwent thallium delayed imaging.
  • Images were obtained at rest, 10 minutes post
    injection, and at 24 hours post injection.

34
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35
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36
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.
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