Post on 21-Jul-2015
Is It Dead or Alive?Eric J. Frischhertz, M.D.
History of Present Illness:History of Present Illness: 73 yo man with PMH of HTN, DM2, 73 yo man with PMH of HTN, DM2,
hyperlipidemia, and CAD presented on hyperlipidemia, and CAD presented on 5/12/04 with cc of fatigue and dyspnea.5/12/04 with cc of fatigue and dyspnea.
He was dx’d with CAD by angiogram on He was dx’d with CAD by angiogram on 3/30/04 and was also found to have 3/30/04 and was also found to have severe LV dysfxn at that time (LVEF severe LV dysfxn at that time (LVEF 20%).20%).
He did not have CP but did c/o He did not have CP but did c/o decreased exercise tolerance.decreased exercise tolerance.
HPI (continued)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:Medical History: PMH: HTN, hyperlipidemia, DM2, prostate PMH: HTN, hyperlipidemia, DM2, prostate
cancer, CADcancer, CAD
PSH: umbilical hernia repairPSH: umbilical hernia repair
Meds: zocor 40mg qd, asa 325mg qd, Meds: zocor 40mg qd, asa 325mg qd, toprol xl 50mg qd, hyzaar 50/12.5mg qd, toprol xl 50mg qd, hyzaar 50/12.5mg qd, aldactone 25mg qd, glipizide 5mg qd, aldactone 25mg qd, glipizide 5mg qd, carnitine 330mg tid, prevacid 15mg qdcarnitine 330mg tid, prevacid 15mg qd
Allergies: noneAllergies: none
Medical History (contin):Medical History (contin):
Social Hx: +Tobacco—smoked 2ppd for 40 yrs but stopped 6 weeks ago; no alcohol or illicit drug use.
Physical Exam:Physical Exam: VS: BP 147/67 HR 73 RR 16 T VS: BP 147/67 HR 73 RR 16 T
97.697.6
Alert and oriented x3Alert and oriented x3
Carotid pulses 2+ bilat without bruits Carotid pulses 2+ bilat without bruits
No Jugular venous distentionNo Jugular venous distention
Regular heart rhythm, normal s1/s2, Regular heart rhythm, normal s1/s2, Distant heart soundsDistant heart sounds
Physical Exam:Physical Exam: Both lungs clear but had scant bilat Both lungs clear but had scant bilat
end expiratory wheezingend expiratory wheezing
Abdomen non-tender with no Abdomen non-tender with no organomegalyorganomegaly
Skin dry, no edema, femoral pulses Skin dry, no edema, femoral pulses 2+ bilat without bruits, DP/PT pulses 2+ bilat without bruits, DP/PT pulses 2+ bilat2+ bilat
139
4.2
104 19
26 0.9121 8.6
11.1
34.1266
Hb A1c 5.9%
T Cholesterol 167
Triglycerides 73
HDL 41
LDL 107
BNP 394
Laboratory Data:Laboratory Data:
Laboratory Data:Laboratory Data:
12-Lead EKG—nsr, left axis deviation, 12-Lead EKG—nsr, left axis deviation, incomplete LBBB, LVH, when compared to incomplete LBBB, LVH, when compared to EKG from 3/24/04 there was now T wave EKG from 3/24/04 there was now T wave inversion in the lateral leadsinversion in the lateral leads
Chest X-ray—no acute pulmonary processChest X-ray—no acute pulmonary process
Results:Results:
Cardiac Angiogram (3/30/04):Cardiac Angiogram (3/30/04):2.2. Multivessel CAD.Multivessel CAD.3.3. Severely reduced LVEF.Severely reduced LVEF.4.4. Recommend CT surgery consult Recommend CT surgery consult
and optimization of medical and optimization of medical management.management.
Results: Echocardiogram (5/7/04):2. LAE, LVE.3. AK of inferior, apical, anterior, and
inferoseptal segments with severe HK of remaining segments.
4. LVEF ~ 15%.5. Eccentric LVH6. 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:2. That myocardial dysfunction present
before bypass surgery often reversed after surgery.
3. 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.