Is It Dead or Alive?
Eric J. Frischhertz,
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
He did not have CP but did c/o
decreased exercise tolerance.
He could walk about 2 blocks before
fatigue limited his activity.
He also reported LE swelling and
He did not have PND.
PMH: HTN, hyperlipidemia, DM2, prostate
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
Medical History (contin):
2ppd for 40 yrs but stopped 6
weeks ago; no alcohol or illicit
VS: BP 147/67 HR 73 RR 16 T
Alert and oriented x3
Carotid pulses 2+ bilat without bruits
No Jugular venous distention
Regular heart rhythm, normal s1/s2,
Distant heart sounds
Both lungs clear but had scant bilat
end expiratory wheezing
Abdomen non-tender with no
Skin dry, no edema, femoral pulses
2+ bilat without bruits, DP/PT pulses
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
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
Cardiac Angiogram (3/30/04):
1. Multivessel CAD.
2. Severely reduced LVEF.
3. Recommend CT surgery consult
and optimization of medical
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.
It was determined after these
results that patient should undergo
a viability study to determine if he
would benefit from
Is It Dead or Alive?
An Overview of
Testing Stunned vs.
Concept was developed in the late
1970’s based on 2 observations:
1. That myocardial dysfunction present
before bypass surgery often reversed
2. And that inotropic stimulation with
epinephrine caused transient
improvement in regional and global LV
dysfunction in patients with CAD.
Diamond, et al. noted in 1978,
“ischemic noninfarcted myocardium
can exist in a state of function
This later led to the proposal by
Rahimtoola of “hibernating
Why This Is Important
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.
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
Evaluation and treatment
Myocardial Perfusion Imaging
(nulcear imaging with thallium,
sestamibi, or PET)
Tissue Doppler Echocardiography
(TDE)/strain rate imaging
Asses wall motion by
ventriculography then dtermine if
there is improvement with NTG (to
improve blood flow) or positive
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
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
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
Images are obtained at rest and 4 hours
In normal myocardium, intial uptake is
high but decreases rapidly within hours
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
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
Both protocols have better
sensitivity that the intial protocol
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
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
Ischemic cells use more glucose
Flourine-18 labeled deoxyglucose
differentiates normal, hibernating
and necrotic myocardium
Back to Our Patient
He underwent thallium delayed
Images were obtained at rest, 10
minutes post injection, and at 24
hours post injection.
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.