Dr. James Fallavollita Medicine Veterans Hospital 3495 Bailey Ave Buffalo NY, 14215 View map

OFFICE LOCATIONS

UBMD Internal Medicine 3980 Sheridan Drive 6th Floor Amherst NY, 14226 Phone: 716-882-6544 Fax: 716-882-6833 Contact: Jill Balbuzoski Hours: 8am-4:30pm View map	Insurance Accepted Aetna U.S. Healthcare Blue Cross & Blue Shield of WNY Inc CIGNA HealthCare Community Blue (HMO) Empire Fidelis GHI Independent Health Association (HMO) Medicare NYS Medicaid North American Administrators Nova Preferred Care Railroad Medicare Univera Health Care (HMO)
VA Medical Center 3495 Bailey Ave Buffalo NY, 14215 Phone: 862-8641 View map	Insurance Accepted Aetna U.S. Healthcare Better Health Plan, Inc. (HMO) Community Blue (HMO) Empire Fidelis Independent Health Association (HMO) United Healthcare Univera Health Care (HMO)

DESCRIPTION OF INTERESTS

-My research interests primarily involve the myocardial responses and adaptations to chronic ischemia. This research includes both basic and clinical aspects, with the majority of my efforts involved in basic projects at this time. Our laboratory has developed a porcine model of chronic hibernating myocardium and our initial work has focused on flow and function with particular attention to inotropic and vasodilatory reserve. In addition to standard physiological measurements and correlations, we are interested in the metabolic and molecular adaptations to ischemia. Our preliminary results have confirmed alterations in glucose uptake and sarcoplasmic reticulum calcium regulatory gene expression in our chronic model, similar to that seen in patients with ischemic cardiomyopathy. Most recently we have shown that hibernating myocardium is characterized by apoptotic cell loss with compensatory hypertrophy. Our experiments in chronically hibernating myocardium have been complemented by a series of acute experiments following a period of prolonged moderate ischemia or "short-term hibernation", and other studies in animals with "chronically stunned myocardium" prior to the development of hibernating myocardium. These studies have evaluated alterations in flow, function, oxygen consumption, glucose uptake, sarcoplasmic reticulum calcium regulatory gene expression, glucose transporter expression and troponin degradation. Future studies will extend our understanding of chronically dysfunctional myocardium by evaluating the effects of different modes of ischemia on subsequent dysfunction, the effects of recurrent episodes of ischemia, and detailed evaluation of inotropic reserve in hibernating myocardium. One aspect of my clinical research parallels the basic studies and involves the study of collateral-dependent dysfunctional myocardium and serial changes in regional function with and without revascularization. The second aspect involves the use of electron beam computed tomography to detect coronary artery calcifications as a marker of coronary artery disease with particular attention to young patients with recent hospital admissions for the evaluation of chest pain. My research interests primarily involve the myocardial responses and adaptations to chronic ischemia. This research includes both basic and clinical aspects, with the majority of my efforts involved in basic projects at this time. Our laboratory has developed a porcine model of chronic hibernating myocardium and our initial work has focused on flow and function with particular attention to inotropic and vasodilatory reserve. In addition to standard physiological measurements and correlations, we are interested in the metabolic and molecular adaptations to ischemia. Our preliminary results have confirmed alterations in glucose uptake and sarcoplasmic reticulum calcium regulatory gene expression in our chronic model, similar to that seen in patients with ischemic cardiomyopathy. Most recently we have shown that hibernating myocardium is characterized by apoptotic cell loss with compensatory hypertrophy. Our experiments in chronically hibernating myocardium have been complemented by a series of acute experiments following a period of prolonged moderate ischemia or "short-term hibernation", and other studies in animals with "chronically stunned myocardium" prior to the development of hibernating myocardium. These studies have evaluated alterations in flow, function, oxygen consumption, glucose uptake, sarcoplasmic reticulum calcium regulatory gene expression, glucose transporter expression and troponin degradation. Future studies will extend our understanding of chronically dysfunctional myocardium by evaluating the effects of different modes of ischemia on subsequent dysfunction, the effects of recurrent episodes of ischemia, and detailed evaluation of inotropic reserve in hibernating myocardium. One aspect of my clinical research parallels the basic studies and involves the study of collateral-dependent dysfunctional myocardium and serial changes in regional function with and without revascularization. The second aspect involves the use of electron beam computed tomography to detect coronary artery calcifications as a marker of coronary artery disease with particular attention to young patients with recent hospital admissions for the evaluation of chest pain. My research interests primarily involve the myocardial responses and adaptations to chronic ischemia. This research includes both basic and clinical aspects, with the majority of my efforts involved in basic projects at this time. Our laboratory has developed a porcine model of chronic hibernating myocardium and our initial work has focused on flow and function with particular attention to inotropic and vasodilatory reserve. In addition to standard physiological measurements and correlations, we are interested in the metabolic and molecular adaptations to ischemia. Our preliminary results have confirmed alterations in glucose uptake and sarcoplasmic reticulum calcium regulatory gene expression in our chronic model, similar to that seen in patients with ischemic cardiomyopathy. Most recently we have shown that hibernating myocardium is characterized by apoptotic cell loss with compensatory hypertrophy. Our experiments in chronically hibernating myocardium have been complemented by a series of acute experiments following a period of prolonged moderate ischemia or "short-term hibernation", and other studies in animals with "chronically stunned myocardium" prior to the development of hibernating myocardium. These studies have evaluated alterations in flow, function, oxygen consumption, glucose uptake, sarcoplasmic reticulum calcium regulatory gene expression, glucose transporter expression and troponin degradation. Future studies will extend our understanding of chronically dysfunctional myocardium by evaluating the effects of different modes of ischemia on subsequent dysfunction, the effects of recurrent episodes of ischemia, and detailed evaluation of inotropic reserve in hibernating myocardium. One aspect of my clinical research parallels the basic studies and involves the study of collateral-dependent dysfunctional myocardium and serial changes in regional function with and without revascularization. The second aspect involves the use of electron beam computed tomography to detect coronary artery calcifications as a marker of coronary artery disease with particular attention to young patients with recent hospital admissions for the evaluation of chest pain.

SPECIALTIES

Cardiology

PUBLICATIONS

Banas, M.D. Young, H. Fallavollita, J.A. Canty, J.M., Jr.; Persistent reductions in flow and function after revascularization of swine with hibernating myocardium.; Journal of the American College of Cardiology; 2006;

Fallavollita JA Luisi, Jr., A.J. Michalek, S.M. Valverde, A.M. deKemp, R.A. Haka, M.S. Hutson, A.D. Canty, Jr., J.M.; Prediction of Arrhythmic Events with Positron Emission Tomography: PAREPET study design and methods; Contemp Clin Trials; 2006;

Suzuki, G. Lee, T.C. Fallavollita, J.A. Canty, J.M., Jr.; Adenoviral gene transfer of FGF-5 to hibernating myocardium improves function and stimulates myocytes to hypertrophy and reenter the cell cycle.; Circulation Research; 2005; 96; 767-775

Gangasani, A. Sidhu, S. Fallavollita, J.A. Korotchkina, L. G. Suzuki, G. Patel, M.S. Canty, J.M., Jr.; Cardiac pyruvate dehydrogenase complex (PDC) deficiency in mice leads to myocardial hypertrophy and cardiomyopathy.; Circulation; 2005; 112(II); II-21-II-22

Luisi AJ Fallavollita, J.A. Luisi, A.J. Valverde, A.M. Michalek, S.M. Heavey, B.M. Canty, J.M.; Electrocardiographic risk stratification of sudden cardiac death.; J Electrocardiol; 2005; 35(4S); 140-140

Canty, J. M. Fallavollita, J. A.; Hibernating myocardium; J Nucl Cardiol; 2005; 12(1); 104-119

Fallavollita, J.A. Riegel, B.J. Suzuki, G. Valeti, U. Canty, J.M., Jr.; Mechanism of sudden cardiac death in pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy; American Journal of Physiology - Heart & Circulatory Physiology; 2005; 289; H2688-H2696

Luisi AJ Canty, J.M., Jr. deKemp, R.A. Haka, M.S. Toorongian, S.A. Fallavollita, J.A.; Patients with ischemic cardiomyopathy eligible for ICD therapy demonstrate extensive sympathetic denervation out of proportion to previous infarction.; Circulation; 2005; 112; 472-472

Canty JM, Suzuki G, Banas MD, Verheyen F, Borgers M, Fallavollita JA; Hibernating Myocardium. Chronically Adapted to Ischemia but Vulnerable to Sudden Death.; Circ Res; 2004 Mar;

Canty JM Jr, Suzuki G, Banas MD, Verheyen F, Borgers M, Fallavollita JA; Hibernating myocardium: Chronically adapted to ischemia but vulnerable to sudden death; Circulation Research; 2004; 194(8); 1142-1149

Thijssen VL, Borgers M, Lenders MH, Ramaekers FC, Suzuki G, Palka B, Fallavollita JA, Thomas SA, Canty JM Jr; Temporal and Spatial Variations in Structural Protein Expression During the Progression From Stunned to Hibernating Myocardium; Circulation; 2004; 110(21); 2213-2221

Canty JM, Fallavollita JA; Sympathetic nerves and myocyte necrosis: more than meets the eye.; Circ Res; 2003 Oct; 93(9); 796-798

Bett GC, Kathuria S, Szigeti GP, Rasmusson RL, Fallavollita JA, Canty JM; Contractile properties of normal and hibernating pig cardiac myocytes; Proceedings Biomedical Engineering in NY, Alfred University; 2003;

Fallavollita JA, Malm BJ, Canty JM; Hibernating myocardium retains metabolic and contractile reserve despite regional reductions in flow, function, and oxygen consumption at rest.; Circ Res; 2003 Jan; 92(1); 48-55

Malm BJ, Suzuki G, Canty JM, Fallavollita JA; Variability of contractile reserve in hibernating myocardium: dependence on the method of inotropic stimulation.; Cardiovasc Res; 2002 Dec; 56(3); 422-432

Thomas SA, Fallavollita JA, Suzuki G, Borgers M, Canty JM; Dissociation of regional adaptations to ischemia and global myolysis in an accelerated Swine model of chronic hibernating myocardium.; Circ Res; 2002 Nov; 91(10); 970-977

Luisi AJ, Fallavollita JA, Suzuki G, Canty JM; Spatial inhomogeneity of sympathetic nerve function in hibernating myocardium.; Circulation; 2002 Aug; 106(7); 779-781

Fallavollita JA, Logue M, Canty JM; Coronary patency and its relation to contractile reserve in hibernating myocardium.; Cardiovasc Res; 2002 Jul; 55(1); 131-140

Fallavollita JA, Canty JM; Ischemic cardiomyopathy in pigs with two-vessel occlusion and viable, chronically dysfunctional myocardium.; Am J Physiol Heart Circ Physiol; 2002 Apr; 282(4); 1370-1379

Luisi AJ Fallavollita,J.A. Suzuki,G. Canty,J.M.,Jr.; Spatial inhomogeneity of sympathetic nerve function in hibernating myocardium; Circulation; 2002; 106(7); 779-781

Fallavollita JA, Lim H, Canty JM; Myocyte apoptosis and reduced SR gene expression precede the transition from chronically stunned to hibernating myocardium.; J Mol Cell Cardiol; 2001 Nov; 33(11); 1937-1944

Canty JM, Fallavollita JA; Lessons from experimental models of hibernating myocardium.; Coron Artery Dis; 2001 Aug; 12(5); 371-380

Fallavollita JA, Logue M, Canty JM; Stability of hibernating myocardium in pigs with a chronic left anterior descending coronary artery stenosis: absence of progressive fibrosis in the setting of stable reductions in flow, function and coronary flow reserve.; J Am Coll Cardiol; 2001 Jun; 37(7); 1989-1995

Feng J, Schaus BJ, Fallavollita JA, Lee TC, Canty JM; Preload induces troponin I degradation independently of myocardial ischemia.; Circulation; 2001 Apr; 103(16); 2035-2037

Feng J, Schaus BJ, Fallavollita JA, Lee TC & Canty JM Jr; Preload induces troponin degradation independently of myocardial ischemia; Circ. Res.; 2001 Jan; 103; 2035-2037

Fallavollita JA, Trojan C, Canty JM; Transmural distribution of FDG uptake in stunned myocardium.; Am J Physiol Heart Circ Physiol; 2000 Jul; 279(1); 102-109

Canty JM, Fallavollita JA; Chronic hibernation and chronic stunning: a continuum.; J Nucl Cardiol; 2000; 7(5); 509-527

Lim H, Fallavollita JA, Hard R, Kerr CW, Canty JM; Profound apoptosis-mediated regional myocyte loss and compensatory hypertrophy in pigs with hibernating myocardium.; Circulation; 1999 Dec; 100(23); 2380-2386

Fallavollita JA, Jacob S, Young RF, Canty JM; Regional alterations in SR Ca(2+)-ATPase, phospholamban, and HSP-70 expression in chronic hibernating myocardium.; Am J Physiol; 1999 Oct; 277(4 Pt); 1418-1428

Thomas SA, Fallavollita JA, Lee TC, Feng J, Canty JM; Absence of troponin I degradation or altered sarcoplasmic reticulum uptake protein expression after reversible ischemia in swine.; Circ Res; 1999 Sep; 85(5); 446-456

Canty JM, Fallavollita JA; Resting myocardial flow in hibernating myocardium: validating animal models of human pathophysiology.; Am J Physiol; 1999 Jul; 277(1 Pt); 417-422

Fallavollita JA, Canty JM; Differential 18F-2-deoxyglucose uptake in viable dysfunctional myocardium with normal resting perfusion: evidence for chronic stunning in pigs.; Circulation; 1999 Jun; 99(21); 2798-2805

Thomas SA, Fallavollita JA, Lee TC, Feng J & Canty JM Jr; Absence of troponin I degradation or altered sarcoplasmic reticulum uptake protein expression following reversible ischemia in swine; Circ. Res.; 1999 Jan; 85; 446-456

Fallavollita JA, Perry BJ, Canty JM; 18F-2-deoxyglucose deposition and regional flow in pigs with chronically dysfunctional myocardium. Evidence for transmural variations in chronic hibernating myocardium.; Circulation; 1997 Apr; 95(7); 1900-1909

Fallavollita JA, Kumar K, Brody AS, Bunnell IL, Canty JM; Detection of coronary artery calcium to differentiate patients with early coronary atherosclerosis from luminally normal arteries.; Am J Cardiol; 1996 Dec; 78(11); 1281-1284

Canty JM, Fallavollita JA; Hibernating myocardium represents a primary downregulation of regional myocardial oxygen consumption distal to a critical coronary stenosis.; Basic Res Cardiol; 1995 Jan; 90(1); 5-8

Fallavollita JA, Brody AS, Bunnell IL, Kumar K, Canty JM; Fast computed tomography detection of coronary calcification in the diagnosis of coronary artery disease. Comparison with angiography in patients < 50 years old.; Circulation; 1994 Jan; 89(1); 285-290