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P OSTER<br />

A BSTRACTS<br />

and its sum of boxes. DLB patients without Capgras were able to tolerate<br />

and continue taking cholinesterase inhibitors (p=0.03) without<br />

other significant differences in medication management.<br />

Conclusions<br />

We found that DLB-C patients had more visual hallucinations,<br />

and that caregivers of DLB-C patients endorse greater caregiver burden.<br />

We were unable to discern specific patient characteristics or psychometric<br />

performance data to help us predict who may be at greater<br />

risk of developing Capgras syndrome. Future research is needed to<br />

evaluate management and treatment options for the clinically challenging<br />

behavioral sequelae of DLB and Capgras syndrome.<br />

A140<br />

Computational Modeling of Aging in Cardiac Myocytes.<br />

P. Dalal, E. Sobie. Pharmacology and Systems Therapeutics, Mt. Sinai<br />

School of Medicine, New York, NY.<br />

Supported By: This research is supported by the Medical Student<br />

Training in Aging Research (MSTAR) at Mount Sinai School of<br />

Medicine.<br />

BACKGROUND: The risk of susceptibility to more serious<br />

forms of cardiac arrhythmia rises significantly with normal aging.<br />

These forms of arrhythmia can manifest as palpitations, fibrillation,<br />

and even sudden death. One indicator of arrhythmia risk is action potential<br />

duration in cardiac myocytes. Specifically, the prolongation of<br />

action potential leads to a larger vulnerability period towards after<br />

depolarization. Such rogue depolarization can result in dangerous,<br />

self-sustaining circular currents. Animal studies in the past have<br />

shown that age associated molecular changes in cardiac myocytes include:<br />

a 40% reduction in SERCA pump protein, a 20% reduction in<br />

the transient outward current, a 59% increase in the peak L-Type calcium<br />

channel current, and a 142% increase in the inactivation time<br />

constant of the L-Type calcium channel. Additionally, the action potential<br />

is prolonged by 92% in older rats when compared with<br />

younger rats and the calcium transient decay is slower in aged rats<br />

while its amplitude remains the same.<br />

HYPOTHESIS: Implementing the molecular changes in rat myocytes<br />

into the computational models of Hund (2004), et al and Ten<br />

Tusscher (2004), et al will prolong the action potentials and slow the<br />

calcium transient decay of these models, creating a computational<br />

tool to study age associated arrhythmia risk.<br />

RESULTS: After implementing the four major molecular<br />

changes associated with cardiac aging, the action potential was prolonged<br />

by 4% in the Hund (2004) model and by 77% in the Ten Tusscher<br />

(2004) model. The calcium transient decay was slower in both<br />

models while the calcium transient amplitude was only unchanged in<br />

the Ten Tusscher (2004) model. In the Hund (2004) model, the amplitude<br />

was increased.<br />

CONCLUSIONS: It is possible to generate a computational<br />

model that replicates the age associated changes seen in cardiac myocytes.<br />

The Ten Tusscher (2004) model more accurately replicates<br />

these changes than the Hund (2004) model.<br />

A141<br />

Isolated CNS Post-transplant Lymphoproliferative Disorder in a<br />

Kidney Transplant Recipient.<br />

S. Dahiya, W. Ooi, A. Asik. Internal Medicine/Division of Hematology<br />

and Oncology, Baystate Medical Center, Springfield, MA.<br />

Introduction<br />

Post-transplantation lymphoproliferative disorder(PTLD)is a<br />

very well recognized complication of solid organ transplantation. Its<br />

incidence varies, depending on the graft recipient’s age,the type and<br />

intensity of immunosuppression, and the organ type transplanted.<br />

Extranodal involvement is common in PTLD, although the central<br />

nervous system (CNS) is an uncommon site of disease, especially in<br />

isolation. Literature review suggests less than handful of cases in geriatric<br />

population.<br />

Case<br />

65 year old female presented with complaints of intermittent expressive<br />

aphasia. Her medical history was remarkable for polycystic<br />

kidney disease leading to kidney failure and thus requiring transplant.<br />

Her transplant history includes, failed first transplant in 1995<br />

from a deceased donor and subsequent living-related donor transplant<br />

in 2005 from her son with unrelated blood type requiring heavy<br />

immunosuppresion. She was on mycophenolate, tacrolimus and prednisone<br />

for immunosuppressive regimen. Her neurological exam was<br />

significant for word finding difficulty and left eye ptosis. Rest of the<br />

physical exam was within normal limits. A spinal tap showed slight elevation<br />

of proteins to 149mg/dl and decreased glucose to 36mg/dl,<br />

raising a question of ongoing infectious process. An urgent MRI was<br />

obtained which showed multiple discrete enhancing lesions throughout<br />

the supratentorial and infratentorial white matter with leptomeningeal<br />

involvement. An extensive infectious workup looking<br />

for various causes of enhancing lesion in this severely immunosuppressed<br />

patient was negative. A brain biopsy was eventually performed,<br />

which showed monomorphic PTLD, categorized as EBV-associated<br />

diffuse large B-cell lymphoma. Given her kidney disease, she<br />

was started on a rather unconventional regimen with weekly rituximab<br />

for 8 weeks and 4 cycles of monthly intrathecal cytarabine. Her<br />

immunosuppresive regimen was changed to sirolimus only. She has<br />

been in remission since last 1 year, but unfortunately developed allograft<br />

rejection because of reduction in immunosuppressive regimen.<br />

Discussion<br />

Isolated CNS-PTLD following kidney transplant is exceedingly<br />

rare. However, it must be considered as a differential in transplant patients<br />

with CNS symptoms to avoid delay in diagnosis. Advanced age<br />

is considered as a poor prognostic factor, but this elderly patient did<br />

rather well with the unconventional regimen as outlined above.<br />

A142<br />

Deep Vein Thrombosis and Pulmonary Embolism (DVT/PE) with<br />

JAK2 positive Polycythemia Vera (PCV) and mild hematologic<br />

findings.<br />

R. Lands, S. Kelley. Department of Medicine, University of Tennessee,<br />

Knoxville, TN.<br />

An 81-year-old man came to the emergency room after becoming<br />

suddenly short of breath while taking a shower. Any exertion<br />

after that exacerbated his dyspnea but was relieved by lying down. He<br />

did not have chest pain, pleuritic or otherwise. He had no preceding<br />

illness, immobilization or prolonged travel. He was previously<br />

healthy with a history of hypertension and gout, but he was on no<br />

meds at the time of admission. Physical examination showed him to<br />

be in no distress at rest while wearing oxygen. Lungs were without<br />

rales or rhonci and his respiratory effort was normal. There was no<br />

edema of either lower extremity. High sensitivity D-Dimer was<br />

greater than 5000 ng/ml. EKG demonstrated right heart strain. Chest<br />

x-ray demonstrated elevation of the hemidiaphragm. Creatinine was<br />

1.9 mg/dl. Ventilation perfusion scan of the lungs was interpreted as<br />

high probability for left and right lower lobe pulmonary emboli.<br />

Doppler venous studies demonstrated bilateral deep vein thromboses<br />

of the lower extremities.<br />

Hgb was 17 g/dl and Hct 53%. WBC was 32,000 without basophilia<br />

or eosinophilia. Cells containing JAK-2 V617F mutation<br />

were present. BCR/ABL was absent. Erythropoietin was 1 mIU/ml.<br />

No further imaging was performed given his marginal renal function.<br />

Review of his old records demonstrated a very mild leukocytosis and<br />

upper normal hemoglobin levels for several years prior to this admission.<br />

One month after discharge, he followed up in the hematology<br />

clinic where his WBC was 15x103 and his hemoglobin 15.8mg/dL.<br />

Discussion: JAK2 is a gain of function mutation with tyrosine kinase<br />

activity that is present in 90% of patients with PCV. While it is<br />

primarily a diagnostic marker now, there is evidence that it might<br />

S64<br />

AGS 2012 ANNUAL MEETING

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