Eric Arnold Brody

Interests

No activities entered.

Courses

No activities entered.

Scholarly Contributions

Journals/Publications

• Brody, E. (2016). An Unusual Case of Giant Pulmonary Artery Aneurysm. Texas Heart Institute Journal.
• Brody, E. (2016). Time-to-Treatment for Myocardial Infarction: Barriers and Facilitators Perceived by American Indians in Three Regions. Journal of Community Health, 1-10.
• Wilson, D., Kalra, N., Brody, E. A., Van Dyk, H., & Sorrell, V. L. (2009). Left atrial appendage aneurysm-a rare anomaly with an atypical presentation. Congenital heart disease, 4(6), 489-93.
  More info

  Left atrial appendage aneurysm (LAAA) is a rare condition caused by congenital dysplasia of the atrial muscles. Patients usually present with atrial tachyarrhythmias as a result of ectopic foci of atrial rhythm generation or systemic thromboembolism. We report a case of a 38-year-old Native American female presenting with 1-month history of cough, in sinus rhythm, and found to have a large cyst-like structure next to the left ventricular lateral wall on transthoracic echocardiography. This structure was later confirmed as a LAAA on cardiac magnetic resonance imaging. Patient underwent aneurysmectomy without any complications.
• Sewell, J. L., Malasky, B. R., Gedney, C. L., Gerber, T. M., Brody, E. A., Pacheco, E. A., Yost, D., Masden, B. R., & Galloway, J. M. (2002). The increasing incidence of coronary artery disease and cardiovascular risk factors among a Southwest Native American tribe: the White Mountain Apache Heart Study. Archives of internal medicine, 162(12), 1368-72.
  More info

  Rates of cardiovascular disease and its risk factors seem to be increasing in American Indian populations, yet these changes have received little documentation.
• Bizjak, E. D., Nolan, P. E., Brody, E. A., & Galloway, J. M. (1999). Procainamide-induced psychosis: a case report and review of the literature. The Annals of pharmacotherapy, 33(9), 948-51.
  More info

  To describe a case of procainamide-induced psychosis in an adult treated for atrial fibrillation.
• Marshall, E. S., Raichlen, J. S., Kim, S. M., Intenzo, C. M., Sawyer, D. T., Brody, E. A., Tighe, D. A., & Park, C. H. (1995). Prognostic significance of ST-segment depression during adenosine perfusion imaging. American heart journal, 130(1), 58-66.
  More info

  To determine the significance of ST-segment depression during adenosine perfusion imaging for predicting future cardiac events, 188 patients with interpretable electrocardiograms were assessed 1 to 3 years (mean 21.5 +/- 6.6 months) after adenosine testing. At least 1 mm of ST-segment depression was observed in 32 (17%) patients, with > or = 2 mm of ST-segment depression in 10 (5.3%). Thirty-seven cardiac events occurred during the study period: 2 cardiac deaths, 5 nonfatal myocardial infarctions, 6 admissions for unstable angina, and 24 revascularizations. Univariate predictors of events were a history of congestive heart failure, previous non-Q-wave myocardial infarction, previous coronary angioplasty, use of antianginal medication, ST-segment depression during adenosine infusion (particularly > or = 2 mm), any reversible perfusion defect, transient left ventricular cavity dilation, and the severity of perfusion defects. Multivariate analysis identified > or = 2 mm ST-segment depression as the most significant predictor of cardiac events (relative risk [RR] = 6.5; p = 0.0001). Other independent predictors of events were left ventricular dilation (RR = 3.8; p = 0.002), previous coronary angioplasty (RR = 3.3; p = 0.001), a history of non-Q-wave myocardial infarction (RR = 2.3; p = 0.01), and the presence of any reversible defect (RR = 2.0; p = 0.05). We conclude that ST-segment depression occurs uncommonly during adenosine infusion, but the presence of > or = 2 mm of ST-segment depression is an independent predictor of future cardiac events and provides information in addition to that obtained from clinical variables and the results of adenosine perfusion imaging.
• Lauva, I. K., Brody, E., Tiger, E., Kent, R. L., Copper, G., & Marino, T. A. (1986). Control of myocardial tissue components and cardiocyte organelles in pressure-overload hypertrophy of the cat right ventricle. The American journal of anatomy, 177(1), 71-80.
  More info

  Previous studies have demonstrated that there is a disproportionate increase in connective tissue in right ventricular myocardium subjected to pressure-overload hypertrophy associated with depressed cardiac contractility. While the myocardium is primarily responsive to load, the aim of the present study was to determine whether catecholamines also modulate the response of myocardial tissue components and cardiocyte organelles in pressure-overload-induced cardiac hypertrophy. Four experimental groups of cats were examined: a sham-operated control group, a group which had their pulmonary arteries banded in order to induce a pressure overload, a group which had been subjected to the same pressure overload, but in addition had beta-adrenoceptor blockade produced prior to and during the pressure overloading, and a group which had been subjected to the same pressure overload, but in addition had alpha-adrenoceptor blockade produced prior to and maintained during the pressure overloading. As in our previous study, there was a significant and equivalent degree of right ventricular hypertrophy in all experimental groups with pressure overload when assessed either as the ratio of right ventricular weight to body weight or as cardiocyte cross-sectional area. At the light microscopic level, the disproportionate increase in the volume density of myocardial connective tissue seen in banded animals was completely prevented by either alpha- or beta-adrenoceptor blockade. At the electron microscopic level, there was a reduction in the mitochondrial and myofibrillar volume fractions following beta-adrenoceptor blockade. The results of this study provide evidence for a modulatory role of catecholamines in the control of myocardial connective-tissue proliferation in pressure-overload-induced cardiac hypertrophy. There is also evidence to support the role of the adrenergic nervous system in regulating cardiocyte subcellular organelles, independent of the regulation of cardiocyte size.
• Marino, T. A., Brody, E., Lauva, I. K., Kent, R. L., & Cooper, G. (1986). Reversibility of the structural effects of pressure overload hypertrophy of cat right ventricular myocardium. The Anatomical record, 214(2), 141-7.
  More info

  The purpose of the present quantitative structural study was to determine whether the histological alterations seen in pressure overloaded myocardium return to normal, as in vitro contractile function does, upon removal of the pressure overload stimulus. Three experimental groups of four cats each were studied: a group with pulmonary artery banding to create a pressure overload, a group that had been subjected to an equivalent duration of pressure overload and then had that pressure overload removed, and a group of sham-operated controls. Seven to 10 weeks after each operative procedure, the right ventricular pressure was elevated only in the pulmonary artery-banded group. The right ventricle/body weight ratio was significantly increased in the pressure overloaded group only. The body weight at sacrifice, the left ventricle/body weight ratio, and the right ventricular end-diastolic pressure did not differ significantly in the three groups. The striking histological changes in the right ventricular myocardium hypertrophing in response to a pressure overload were the decrease in the volume density of cardiocytes and the increase in connective tissue in papillary muscles. These were reversed when the pressure overload was removed. This study demonstrates that when a pressure overload is removed, myocardial structure returns to normal as the function returns to normal. Given the critical importance of the proportion of cardiocytes and connective tissue components to both systolic and diastolic cardiac function, these data support the hypothesis that the abnormal proportions of these structures provide a potential morphological basis for at least some of the functional abnormalities observed in pressure overload hypertrophy of the cat right ventricle.

Presentations

• Brody, E., Malasky, B. R., Freund, N. S., Koepke, L., Painter, B., Sanderson, P., & Galloway, J. M. (2004, May). Excellence in Quality of Care Indicators for Native American Patients with Acute Myocardial Infarction. AHA 5th Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke. Washington, D.C..
• Malasky, B. R., Sewell, J., Sethi, G., Brody, E., & Galloway, J. M. (2004, May). Coronary Artery Bypass Grafting in Native Americans: Risk Factors and Outcomes. AHA 5th Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke. Washington, D.C..

Poster Presentations

• Meltzer, N., Gormally, J., & Brody, E. (1998, April). Homocysteine levels among Native American patients evaluated for coronary artery disease by the Native American Cardiology Program from 1995- 1998. IHS Research Conference. Albuquerque, NM: Indian Health Services.

Others

• Brody, E., Brownstein, J. N., Nesoff, E., & O'Leary, M. (2012, October). Ml time to treatment in rural American Indian country: Qualitative insight into delays. American Public Health Association Annual Meeting..
• Brody, E., Brownstein, J. N., O'Leary, M., & O'Leary, M. (2013, November). Beliefs and behavioral intentions regarding myocardial infarction among American Indians. American Public Health Association Annual Meeting.
• Brody, E., Duarte, A. C., June-Tsosie, A., Sewell, J. L., Malasky, B. R., Ranger-Moore, J., Cudilo, E., Sanderson, P., Freund, N. S., & Galloway, J. M. (2008, March). Dramatic Time to Treatment Delay in Acute Myocardial Infarction in Rural Native Americans. JACC.
• Duarte, A. C., June-Tsosie, A., Sewell, J. L., Malasky, B. R., Ranger-Moore, J., Cudilo, E., Sanderson, P., Freund, N. S., Galloway, J. M., & Brody, E. A. (2007, JAN). Excessive time to treatment delay in rural native americans presenting with acute myocardial infarction: Temporal trends 1999-2006. JOURNAL OF INVESTIGATIVE MEDICINE.
• Brody, E., Galloway, J. M., Malasky, B., & Freund, N. S. (2003, Spring). B-type Natriuretic Peptide (BNP): A New Tool in the Diagnosis of Congestive Heart Failur. The IHS Primary Care Provider.
• Brody, E., Galloway, J. M., Malasky, B. R., & Freund, N. S. (2002, Spring). The Diagnosis of Myocardial Infarction and Cardiac Troponins: An Expanding Role in IHS Facilities. The IHS Primary Care Provider newsletter.
• Malasky, B. R., Galloway, J. M., Freund, N. S., & Brody, E. (2002, Spring). Management of St Segment Elevation Myocardial Infarction: Thrombolytic Guidelines. The IHS Care Provider newsletter.
• Brody, E., Sewell, J., Malasky, B. R., Koepke, L., Painter, B., Marez, P., & Galloway, J. (2001, Fall). Time-to-treatment delay in Native American patients with acute myocardial infarction. Circulation.
• Brody, E., Sewell, J., Koepke, L., Painter, B., Marez, P., & Galloway, J. (2000, Spring). Marked presentation delay in Native American Patients with acute myocardial infarction.. JACC.
• Brody, E., Fiora-Gormally, J., & Meltzer, N. (1998, April). Lipoprotein (a) and coronary artery disease among Native American patients evaluated by the Native American Cardiology Program from 1995-1997. IHS Research Conference.
• Brody, E., Galloway, J. M., Pacheco, E., & Koepke, L. (1997, Spring). Guidelines for Chronic Anticoagulation Therapy: Addressing the Special Needs of Native American Patients. The IHS Primary Care Provider.
• Raichlen, J. S., Brody, E., Tighe, D. A., & McDonald, M. E. (1996, Spring). Effect of cardiac surgery on septal function: An intraoperative transesophageal study using acoustic quantification.. Journal of the American Society of Echocardiography.
• Brody, E., & Chung, E. K. (1998, Fall). Predictive value of less stringent ECG criteria for inferior myocardial defects in thallium-201 imaging. Clinical Research.