Patient is a 59 yrs old asian male, active smoker, without any significant past medical history, presented with dysnea and chest pain. He was evaluated for coronary artery disease with treadmill exercise stress test. He underwent one day rest – stress myocardial perfusion imaging with Tc-99m Sestamibi.

The SPECT images do not show any reversible myocardial perfusion defects to suggest presence of exercise induced myocardial ischemia. The gated images showed normal left ventricular wall motion with an ejection fraction of 50%.

Incidentally seen is a large intensely active mediastinal mass. This finding was further evaluated by a CT scan which showed a large anterior mediastinal mass.

This was removed by mini sternotomy and pathology revealed a thymoma, measuring 8.0 x 7.5 x 5.5 cms. No morphological features suggestive of malignancy were found in any sections.

Increased tc-99m tetrofosmin uptake in a mediastinal tumor during myocardial perfusion imaging. Vijayakumar V, Soloff E, Rahman AM. Clin Nucl Med. 2004 Jun;29(6):390-1.

Focal uptake of radioactive tracer in the mediastinum during SPECT myocardial perfusion imaging. Chadika S, Kokkirala AR, Giedd KN, Johnson LL, Giardina EG, Bokhari S. J Nucl Cardiol. 2005 May-Jun;12(3):359-61.

Patient is a 42 yrs old Asian woman who presented with chest pain and dysnea. Myocardial perfusion imaging was performed using a one day protocol and exercise stress. She exercised on treadmill following Bruce protocol for 3:46 minutes. Resting heart rate of 66 beats per minute rose to 158 beats per minute, 87 % predicted maximum heart rate. She received 0.37 GBq (10.0 mCi) Tc-99m Sestamibi IV at rest and 1.11 GBq (30.0 mCi) Tc-99m Sestamibi IV at stress.

The images do not show any reversible perfusion defects to suggest exercise induced myocardial ischemia. There is a moderately severe, fixed, myocardial perfusion defect involving the anterior wall of the left ventricle, worse at rest. These findings are characteristic of a breast implant attenuation artifact. The MIP images show a photopenic implant in the left breast, in the left anterior oblique projection.

Recognition of artifact is important for the accurate interpretation of myocardial perfusion images. Breast implants are one of the known causes of attenuation artifacts in myocardial perfusion scintigraphy studies in women. By attenuating the counts from the anterior wall of the left ventricle, the implants cause a fixed perfusion defect, which may lead to misinterpretation of the study (1-3).

References:

1. Curtiss T. Stinis, Paul E. Lizotte, Mohammad-Reza Movahed. Impaired myocardial SPECT imaging secondary to silicon- and saline-containing breast implants. The International Journal of Cardiovascular Imaging (2006) 22: 449–455.

2. Movahed MR. Attenuation artifact during myocardial SPECT imaging secondary to saline and silicone breast implants. Am Heart Hosp J. 2007 Summer; 5(3):195-6.

3. Meine TJ, Patel MR, Heitner J, Fortin TA, Pagnanelli RA, Gehrig TR, Kim R, Borges-Neto S. Cardiac imaging impaired by a silicone breast implant. Clin Nucl Med. 2005 Apr; 30(4):262-4.

This case was compiled by Dr. Amin Samarghandi (Excel Diagnostics)

A 62 year-old man with non-ischemic cardiomyopathy was admitted for worsening shortness of breath and lower extremity swelling. DVT was ruled out on bilateral duplex ultrasound. The transthoracic echocardiogram showed a large heteroechogenic mass in the left ventricle, raising the possibility of intra-cardiac tumor. MRI was contraindicated due to AICD.

FDG PET-CT was performed and demonstrated a large photopenic defect corresponding to the relatively homogenous hypodensity in the left ventricle, consistent with an intracardiac thrombus. The patient was treated for his CHF exacerbation and referred for heart transplant evaluation.

Intra-cardiac mass is a rare and serious condition. Imaging has an essential role in identifying the etiology. MRI has been successfully used to evaluate intra-cardiac masses including thrombi (1). FDG PET-CT has also been used to evaluate benign and malignant cardiac tumors presenting as an intracardiac mass (2-5). Compared to MRI, PET-CT is not limited by the presence of AICDs or metallic prosthesis. In addition, a negative PET-CT exam carries a very high negative predictive value to rule out primary or metastatic cardiac tumor.

1: Barkhausen J, Hunold P, Eggebrecht H, Schüler WO, Sabin GV, Erbel R, Debatin JF. Detection and characterization of intracardiac thrombi on MR imaging. AJR Am J Roentgenol. 2002 Dec;179(6):1539-44.

2: Gates GF, Aronsky A, Ozgur H. Intracardiac extension of lung cancer demonstrated on PET scanning. Clin Nucl Med. 2006 Feb;31(2):68-70.

3: Kim JH, Jung JY, Park Y, Hwang SI, Jung CS, Lee SH, Yoo CW. Non-small cell lung cancer initially presenting with intracardiac metastasis. Korean J Intern Med. 2005 Mar;20(1):86-9.

4: Bittner HB, Sharma AD, Landolfo KP. Surgical resection of an intracardiac rhabdomyoma. Ann Thorac Surg. 2000 Dec;70(6):2156-8.

5: Agostini D, Babatasi G, Galateau F, Grollier G, Potier JC, Bouvard G. Detection of cardiac myxoma by F-18 FDG PET. Clin Nucl Med. 1999 Mar;24(3):159-60.

This case was prepared by Dr. David He BCM

A 73 years old male with past medical history of HTN, DM, CVA, COPD, and CHF was admitted for worsening CHF. Echocardiogram showed low EF and severe pulmonary hypertension. One day stress (dipyridamole) / rest myocardial perfusion imaging was performed with Tl-201 (thallium chloride).

The images show a large and severe, minimally reversible perfusion defect in the infero-lateral wall, suggesting presence of dipyridamole induced myocardial ischemia in the RCA territory. The gated images show severe global hypokinesis with an ejection fraction of 24%. The 24 hr delayed SPECT images show more reversibility in the infero-lateral wall, suggesting viable hibernating myocardium.

Subsequent coronary angiography identified diffuse three vessel disease and a 100% occluded right sided PDA with collaterals from the LAD septal branches, low output cardiac failure with high filling pressures, and severe pulmonary hypertension. Due to lack of good targets with his diffuse disease, as well as multiple co morbidities, he was not deemed a good surgical candidate for CABG, and was instead managed with maximal medical therapy.

Pathophysiology of myocardial ischemic syndromes varies with the severity of coronary artery disease and time. With sudden, severe, and prolonged ischemia, myocyte death with tissue infarction and loss of contractile function is the end result. In cases of significant but less severe ischemia occurring over protracted time, down regulation of myocyte metabolism can occur, with myocytes maintaining viability in the setting of depressed contractile function, a state described as hibernating myocardium. Rahimtoola (1) described hibernating myocardium as a state of persistently impaired myocardial function at rest due to reduced coronary blood flow, that can partially or completely be restored by either increasing supply (restore blood flow) or reducing demand (reduce O2 requirements of the hibernating cardiac tissue). One of the limitations of myocardial perfusion SPECT is in differentiating ischemic but viable (hibernating) myocardium from infarcted/scar tissue (2). Delayed SPECT with Tl-201 and PET imaging with F-18 FDG are valuable tools in the assessment of hibernating myocardium (3).

1) Rahimtoola, Circulation Feb 1982; 65(2): 225-41
2) Bonow et al, Circulation 1991; 83: 26-37
3) Ramos et al, Rev Cardiovasc Med. 2008; 9(4):225-31

This case was compiled by Joseph Vollink PA and Dr. David He (BCM)

52 yrs old male with past medical history of Afib and HTN (non compliant with β blocker for rate control) presented to the Emergency Room with a 3 day history of chest pain. He was admitted for cardiovascular evaluation, including nuclear stress testing, echocardiography, and cardiac catheterization.

Myocardial perfusion imaging was performed with Dipyridamole stress test using one day Tc-99m-Tetrofosmin rest-stress protocol. There were no symptoms or ECG changes to suggest dipyridamole induced myocardial ischemia. The images do not show any reversible perfusion defects to suggest presence of dipyridamole induced myocardial ischemia. Left ventricle is dilated (EDV 176 ccs) and hypertrophied. Gated images show global hypokinesis with an ejection fraction of 34%. These findings suggest non ischemic cardiomyopathy. Echocardiography showed left ventricular hypertrophy and dilatation with a globally reduced ejection fraction of 30-40%.

Subsequent coronary angiography confirmed no significant occlusive disease in coronary arteries. Pt was discharged with continued medical management and follow up with his cardiologist for Afib and newly diagnosed non ischemic cardiomyopathy. ACE inhibitor and diuretic were added to his medical regime for afterload reduction and fluid control.

Although there are many potential causes of non ischemic CMP (1), a possibility may be related to his Afib history and being off his rate control meds for some unknown length of time. One known cause of CMP is tachycardia induced CMP (2), resulting from Afib with poor HR control; the resulting tachycardia puts a large workload on the heart with a resulting deterioration in LV function over time. Although the pt was not tachycardic on evaluation in the ER, he had been off his rate control meds for some unknown time, and could quite possibly be tachycardic for frequent unknown lengths of time, that could eventually have contribute to deterioration of LV function over time.

1) Taylor, G., Primary Care Cardiology, 2nd edition, Blackwell pub, 2005
2) Khasnis et al, PACE July 2005; 28 (7): 710-21

This case was compiled by Dr. David He and Joseph Vollink PA, MEDVAMC

A 55 yrs old male was admitted with a 3 week history of acute onset anasarca. Past medical history was significant for COPD and HTN. Medications included lisinopril and lasix. Admission EKG showed right atrial enlargement and right ventricular hypertrophy. Myocardial perfusion imaging with stress testing was ordered to rule out myocardial ischemia.

Images at rest and stress did not show any reversible defects to suggest presence of dipyridamole induced ischemia. Flat interventricular septum and a D shaped left ventricle were noted, along with dilated and hypertrophied right ventricle. Normal left ventricular wall motion was seen along with ejection fraction of 70%. The gated images also show right ventricular hypokinesis.

Patient subsequently underwent agitated saline echocardiogram, which was negative for intracardiac shunt, and catheterization showed pulmonary HTN with a PASP of 58mm Hg.

This case demonstrates findings with myocardial perfusion imaging – RV hypertrophy, D shaped left ventricle / septal flattening with a fixed defect mimicking scar – that suggest the presence of Pulmonary HTN. The finding of abnormal tracer uptake in the septum, at both rest and stress (fixed defect), typically would be defined as scar. However, this same finding was recently described in a single case report (1) in association with pulmonary hypertension; although the mechanism is not defined, it may be related to acute RV pressure overload compromising septal blood flow throughout the cardiac cycle, resulting in a “fixed” defect, which has been described in a canine model previously (2).

1) Maeder et al, Kard Medizin 2007;10: 113-14
2) Gibbons et al, Am J Physiol Heart Circ Physiol 2006; 290: H2432-8

This case was compiled by Joseph Vollink PA, MEDVAMC

This case was compiled by Joseph Vollink PA, MEDVAMC
A 60 yrs old african american male with PMH of HTN, hypercholesterolemia, smoking (1 PPD x 40 yrs, quit about 5 months ago secondary to episodes of chest pain), family history significant for father with CAD and death from cardiac event at age 67, presented with chest pain. He was admitted to the hospital 4 months ago and was recommended to undergo MPI with stress testing.

Before starting the stress test, baseline HR was 65 bpm, BP was 145/76, baseline EKG showed NSR, normal axis, LAD, QTC 433 ms, and biphasic T waves in lead V2, as well as inverted T waves in leads V3 – V5. The EKG changes noted at the time of stress testing, as well as at hospital discharge, were consistent with Wellens syndrome, which suggests significant proximal LAD disease.

At peak dipyridamole stress (55.7 mg administered IV over 4 min), HR was 85, BP was 131/75. Patient reported mild (3/10) chest tightness and EKG showed >1 mm downsloping ST depression in the anterior leads. These resolved after the administration of 100 mg Aminophylline IV, during the recovery

The SPECT myocardial perfusion images at rest and stress showed a large, moderately severe, reversible distal anterior, anteroseptal, and apical perfusion defect suggestive of dipyridamole induced myocardial ischemia. Mild transient ischemia dilation of the left ventricle was noted with EDV = 170cc. The gated images showed normal left ventricular wall motion with an ejection fraction of 55%. Given the constellation of symtoms, EKG changes during stress testing at low double product, imaging findings, and resting EKG findings suggestive of proximal LAD disease, he was taken to the ER for admission and cardiology evaluation. Pt was taken to cardiac cath lab, where he was found to have a very tight 99% obstruction in the proximal LAD, as well as a 50% circumflex lesion. Cardiothoracic surgery was consulted, and patient underwent CABG.

Wellens syndrome is a constellation of clinical and EKG findings strongly suggestive of proximal LAD disease. Wellens syndrome was originally described by Wellens in his 1982 paper with DeZwaan and Bar(1).
The criteria for Wellens syndrome are(2):

1) Biphasic and/or inverted T waves in leads V2, V3, with similar changes occasionally in leads V1, V4, V5, V6.
2) No /minimal elevation of cardiac troponin.
3) No/minimal ST elevation.
4) No loss of R wave progression.
5) No Q wave.
6) Hx of CP/angina.

Patients with Wellens syndrome are at high risk of significant anterior MI and extensive myocardial damage and/or death. There are two basic types described, according to the EKG pattern noted: (findings of both types may be present simultaneously as well)

1) Type 1, with primarily the biphasic T wave pattern.
2) Type 2, with the deeply inverted T wave pattern.

Current AHA/ACCF/HRS recommendations for the standardization and interpretation of the EKG(3) state that the specific EKG pattern (type 2) consistent with Wellens syndrome should be interpreted as consistent with severe stenosis of the proximal LAD ( and/or recent hemorrhagic CVA).

Early revascularization is recommended in patients presenting with Wellens syndrome, as the they have poor prognosis with medical therapy alone(4). Exercise/Dobutamine stress testing is not NOT recommended, as there is significant risk of a cardiac event, and possibly death, with the significant stress load on the heart and a significant proximal LAD lesion present.(5, 6) If dipyridamole stress testing is considered, it should be done very cautiously; contrary to what many physicians believe, dipyridamole can also actually induce ischemia in the presence of coronary stenosis (7,8,9) , with an increase in the double product, ST segment changes, and chest pain, as was seen in this patient; a low threshold should be present for test termination if the patient exhibits significant chest pain or has significant ST changes in multiple leads.

The findings of Wellens syndrome on EKG before a stress test should alert clinicians to the strong possibility of a significant proximal LAD lesion; stress testing, if done at all, should only be done cautiously with dipyridamole, with a low threshold for early test termination should signs or symptoms of significant ischemia present themselves; strong consideration should be given to proceed directly with cardiac catheterization with pt’s presenting with the Wellens syndrome, rather then stress testing of any kind.

1) DeZwaan et al Am Heart J 1989; 117: 657-65
2) Tatli et al Cardiology J 2009; 16: 73-75
3) Wagner et al JACC 2009; 53, 11: 1003-11
4) Nisbet et a l J Emergency Med 2008; 20, 10: 1-4
5) Rhinehardt et al AM J Emerg Med 2002; 20(7): 638-43
6) Tandy et al Ann Emerg Med 1999; 33: 347-351
7) Picano et al Amer Heart J 1989; 118: 314-319
8) Lucarini et al Chest 1992: 102; 444-47
9) Picano et al Circulation 1991; 83(suppl III): III-19 – III-26