Biography
Perry Fisher is an Internal Medicine resident at the Mount Sinai Beth Israel Medical Center in New York. Born and raised in Queens, New York, Fisher attended an accelerated B.S./ M.D. program at the Sophie Davis School of Biomedical Education. He completed his clinical medical school training at Albany Medical College. Along the way, Fisher performed clinical research, presented at multiple conferences and lectures, published works, and amassed several awards honoring his work. Fisher now practices inpatient medicine at Beth Israel Hospital, and maintains outpatient privileges at the Ryan NENA Community Health Center – serving the underserved population of New York City’s Lower East Side. He has a passion for the art of Cardiology, and aspires to specialize in Cardiovascular Medicine.
Abstract
Angioimmunoblastic T-Cell Lymphoma (AITL) is an uncommon lymphoma with rare cardiac manifestations. We present a clinical example where non-contrast and contrast enhanced echocardiograms demonstrated remarkably different myocardial compositions, particularly in our patient identifying infiltrating lymphoma in the myocardium. Case: A 68-year-old African American man with past medical history of AITL presented with weakness and fatigue for 2 weeks. Transthoracic echocardiogram (TTE) without contrast was performed that showed a pericardial effusion and an echolucency of the left ventricle concerning for pseudoaneurysm. Repeat TTE was performed using IV contrast revealed the presence of multiple non-communicating hypodensities within the myocardium. Pericardial fluid analysis did not reveal evidence of lymphoma, however pleural fluid cytology exhibited abnormal cells consistent with T-cell lymphoma. Discussion: In our patient, contrast enhanced echocardiography identified infiltrating lymphoma in the myocardium that was not seen with standard 2D imaging. Echocardiographic contrast agents are excellent tools for the evaluation of the LV endocardium especially in the detection and classification of intracardiac masses, including thrombi and tumors. Most malignant tumors, secondary to neovascularization, have an abnormally concentrated and dilated vasculature and concordantly, will display increased contrast enhancement compared to the adjacent myocardium. Contrary to the norm, we found metastatic lesions in our patient with deceased pixel intensity. The use of contrast agents should be considered when evaluating patients with non-cardiac diseases that have the potential for infiltrating the myocardium, but the level of contrast enhancement may be variable with certain types of tumors.: Angioimmunoblastic T-Cell Lymphoma (AITL) is an uncommon lymphoma with rare cardiac manifestations. We present a clinical example where non-contrast and contrast enhanced echocardiograms demonstrated remarkably different myocardial compositions, particularly in our patient identifying infiltrating lymphoma in the myocardium.
Biography
To be updated soon..
Abstract
Oxygen free radicals associated with ischemia-reperfusion (IR) injury in cardiomyocytes is known to cause mitochondrial damage. However, the exact mechanism of how the oxygen free radicals develop in the mitochondria due to IR stress is currently unclear. In the current study, we focus upon understanding the role of frataxin (FXN) in regulating mitochondrial damage associated with IR injury. FXN, a nuclear encoded mitochondrial matrix protein, has been observed to regulate mitochondrial iron homeostasis and thus mitochondrial energy regulation. Loss of FXN, in Friedreich’s ataxia, is associated with mitochondrial iron overload and increased ROS formation and cellular damage. In this study, we hypothesized that FXN protects cardiomyocytes against IR injury by preventing the dysregulation of myocardial bioenergetics. We identified that FXN expression is increased in response to IR injury and that increase is mediated by hypoxia inducible factor (HIF-1ï¡) which results in regulation of mitochondrial iron homeostasis and the ensuing mitochondrial ROS formation. Most surprisingly, we observed that enhanced FXN expression displayed elevated levels of glutathione (GSH) and superoxide dismutase (SOD). Furthermore, these findings were supported in our FXN over-expressing and knock down cells under the same IR condition. Together, these results demonstrate that increased expression of FXN is cardio-protective against IR injury through its anti-oxidant effect and by improving mitochondrial energetics.