Aurora Cardiovascular Services Case of the Month

ACS Editorial Board

Jasbir S. Sra, MD
Andrew Boyle, MD
Tanvir Bajwa, MD
David C. Kress, MD
Bijoy K. Khandheria, MD
A. Jamil Tajik, MD
Steven Port, MD
Masood Akhtar, MD

View past cases

November - 2010:
The Thick Heart

September - 2010:
Microreentrant Atrial Tachycardia Five Years Following Left Atrial Ablation of Atrial Fibrillation

August - 2010
Percutaneous Repair of Clinically Significant Mitral Regurgitation

The Role of Myocardial Viability Imaging in the Management of Complex Coronary Artery Disease

Keyoor Patel, DO; Steven Port, MD

January 2011

Case Description

A 79-year-old man presented to the Aurora West Allis Memorial Hospital emergency department on Aug. 1, 2010, with progressive chest discomfort that had been occurring for two weeks. The patient initially attributed the discomfort to reflux, although there was an exertional component to it. On the day of admission, the discomfort occurred without provocation and was unremitting. He was taking metoprolol, glyburide, benazepril, simvastatin, insulin and omeprazole. On evaluation in the emergency department, the patient had a sinus tachycardia (120 beats/min), a blood pressure of 94/62 mmHg, and no evidence of congestive heart failure (CHF) by physical examination or X-ray. An electrocardiogram (ECG) showed an intraventricular conduction delay and marked horizontal ST-segment depression (Figure 1), and the patient had an elevated troponin level of 0.42 ng/mL. His complete blood count (CBC) showed a hemoglobin of 8.2 g/dL. White blood cell (WBC) and platelet counts were normal. His creatinine was 3.8 mg/dL with a blood urea nitrogen (BUN) of 78 mg/dL. The patient had a history of stable myelodysplastic syndrome requiring monthly transfusion and had stable chronic renal insufficiency with an estimated glomerular filtration rate (eGFR) less than 20 ml/min.

Figure 1: Patient's emergency department electrocardiogram showing intraventricular conduction delay and marked ST-segment depression.


Aurora Cardiovascular Services medical group was asked to accept the patient in transfer for cardiac catheterization. After the patient was informed of his high risk for acute on chronic renal insufficiency and potential need for dialysis, he consented to transfer to Aurora St. Luke's Medical Center. That same day, Dr. Steven Port performed cardiac catheterization, which revealed the following hemodynamic data: pulmonary artery pressure 56/26 (mean 41); pulmonary capillary wedge pressure 33/43 (mean 33); aortic pressure 94/52. His coronary angiography showed: mild diffuse disease of the left main artery; a severe ulcerated plaque in the left anterior descending (LAD) artery just distal to the first septal perforator and proximal to the major diagonal branch with a reasonably normal distal LAD; 90% stenosis of the ostial circumflex as well as a severe lesion in the proximal portion of one of the major marginal branches; and 100% occlusion of the proximal right coronary artery with limited left-right collateral filling (Figure 2). A low-contrast-volume ventriculogram showed a dilated and diffusely hypocontractile left ventricle with an estimated left ventricular ejection fraction of 20%. An intra-aortic balloon pump was inserted and set to 1:2 augmentation due to the tachycardia, and the patient was sent to the Cardiac Intensive Care Unit (CICU) for diuresis and consultations with nephrology, hematology, cardiovascular (CV) surgery and interventional cardiology. The patient's chest pain had resolved.

Figure 2: Angiography showing mild diffuse disease of the left main artery: a severe ulcerated plaque in the left anterior descending (LAD) artery just distal to the first septal perforator and proximal to the major diagonal branch (arrowhead) with a reasonably normal distal LAD (Panel A); 90% stenosis of the ostial circumflex (arrowhead) (Panel B); and 100% occlusion of the proximal right coronary artery with limited left-right collateral filling (Panel C).

Dr. Daniel O'Hair of CV surgery felt that the patient's comorbidities and catheterization findings put him at extremely high risk for an adverse outcome with bypass surgery. The patient was offered high-risk percutaneous coronary intervention (PCI) and, after all parties weighed in on the case, he returned to the catheterization lab on Aug. 2 for attempted PCI of the LAD lesion, which was felt to be the culprit vessel causing the patient's myocardial infarction (heart attack), due to its ulcerated appearance and the diffuse precordial ST-segment changes. Dr. Joaquin Solis successfully stented the LAD with a 3.024-mm drug-eluting stent. Because the LAD was successfully treated without complication, several attempts were made to cross the ostial circumflex lesion as well, but these attempts were unsuccessful, and the patient was returned to the CICU in stable condition.

In the CICU, the patient did well physically and emotionally. As activity advanced, overt CHF did not become a problem. His renal insufficiency did progress, however, and dialysis was initiated on Aug. 6 by Dr. Ahmed Malik, a nephrologist. The patient was able to transfer out of the CICU and continued to show overall clinical improvement, to the point that we asked CV surgery to consider surgical revascularization of the circumflex coronary artery. It was agreed that if we could demonstrate substantial viability of the myocardium in the circumflex distribution, surgical revascularization could be considered.

Assessing Myocardial Viability

There are several approaches currently in use for the assessment of myocardial viability. They include assessments of myocardial perfusion, myocardial metabolism, myocardial thickening and motion, and myocardial necrosis. Single photon emission computed tomography (SPECT) myocardial perfusion imaging may be performed with either thallium-201 or a technetium-based perfusion agent. Segments of myocardium where the uptake of the radionuclide is less than 50% of the peak uptake in the entire ventricle are considered nonviable. Conversely, segments with uptake greater than 50% of peak uptake are generally considered viable. Delayed imaging in the case of thallium-201 or nitroglycerin-enhanced imaging with either thallium or technetium agents may increase the uptake of the tracer, thus demonstrating viability. Myocardial perfusion and metabolism may be assessed using positron emission tomography (PET) imaging. Perfusion is typically evaluated with rubidium or N-13 ammonia, while glucose metabolism is assessed with F-18 deoxyglucose (FDG). The combined demonstration of reduced perfusion (ischemia) and increased FDG uptake (increased anaerobic metabolism) in the same myocardial territory suggests myocardial viability. Echocardiography may be used to demonstrate myocardial thickening at rest and during inotropic stimulation, typically using low-dose (approx. 5 mcg/kg/min) intravenous dobutamine. Myocardial segments with adequate wall thickness at rest (typically 7 mm) that show an increase in wall thickening with low-dose dobutamine are considered viable. The dobutamine dose may then be increased progressively to see if myocardial thickening subsequently deteriorates such that it becomes worse than it was at rest. That dual-phase response denotes both viability and, importantly, ischemia analogous to myocardial perfusion/metabolism imaging. Delayed-enhancement magnetic resonance imaging (MRI) has recently emerged as a sensitive and reproducible technique for distinguishing necrotic/fibrotic nonviable myocardium from viable myocardium. Gadolinium is injected intravenously and, after its initial first pass through the ventricle, repeat imaging at 10-15 minutes will show retention of the gadolinium in necrotic/fibrotic myocardium. The millimeter resolution of MRI allows identification of transmural viability as well. MRI cannot, as yet, be performed in patients with pacemakers or defibrillators.

In our patient's case, a myocardial perfusion/metabolism study was performed. Figure 3 shows the PET FDG metabolism study and the corresponding SPECT perfusion scan. The SPECT images demonstrate markedly reduced uptake of technetium (99 mTc) sestamibi (Cardiolite) throughout the circumflex territory, indicating low blood flow (ischemia), while the PET images show markedly increased uptake of FDG in the circumflex territory, indicating active anaerobic metabolism despite low blood flow. Hence, the entire circumflex territory was felt to be viable. Note the reduction in uptake at the apex (Figure 4) on both the perfusion and metabolism images at the apex, indicating infarction.

Figure 3: PET FDG metabolism study (rows 1 and 3) and the corresponding SPECT perfusion scan (rows 2 and 4). SPECT images demonstrate markedly reduced uptake of technetium (99 mTc) sestamibi (Cardiolite) throughout the circumflex territory (white arrows), indicating low blood flow (ischemia), while the PET images show markedly increased uptake of FDG (yellow arrows) in the circumflex territory, indicating active anaerobic metabolism despite low blood flow.

Figure 4: FDG metabolism (left) and SPECT perfusion (right) images showing matched reductions in flow and metabolism at the apex (arrows), indicating infarction.


On the basis of this study and the continued clinical stability of the patient, Dr. Paul Werner performed coronary artery bypass graft (CABG) surgery, which included saphenous vein grafts to the two large marginal branches of the circumflex coronary artery, on Aug. 14. The patient easily weaned from bypass and did well subsequently. He was transferred to telemetry on Aug. 18 and then transferred to subacute rehabilitation on Aug. 20. On Sept. 1, he was seen as an outpatient in our cardiology clinic in stable condition on carvedilol, lisinopril, simvastatin, digoxin and aspirin along with other noncardiac medications.

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Contact information

Aurora Cardiovascular Services: Phone: (414) 649-3370 or (800) 649-1989.