Raul J. Guzman, MD
Associate Professor of Surgery
Division of Vascular Surgery
Beth Israel Deaconess Medical Center
Harvard Medical School
110 Francis St, Suite 5B
Boston, MA 02215
Office Phone: 617-632-7384
Office Fax: 617-632-9979
After completing his undergraduate studies in Applied Mathematics and Biology at Brown University in Providence, RI, Dr. Guzman attended the Johns Hopkins School of Medicine where he obtained his medical degree. He subsequently obtained training in General Surgery at Lenox Hill Hospital prior to beginning his research fellowship in the Cardiology Branch of the NIH, NHLBI in Bethesda, MD. He continued his research training in the Division of Vascular Surgery, Stanford Medical Center where he stayed to complete clinical training as a Vascular Surgery Fellow. In 1998, Dr. Guzman began his first faculty appointment in the Division of Vascular Surgery at the Vanderbilt University School of Medicine in Nashville, TN. In 2013, he joined the Division of Vascular Surgery at Beth Israel Deaconess Medical Center with an interest in the underlying mechanisms and clinical implications of arterial calcification. His lab is located on the 8th floor of the Dana Building in BIDMC East Campus.
Basic Research - My laboratory focus on the basic mechanisms that control smooth muscle cell (SMC) differentiation during medial artery calcification. We are interested in the role of matrix degrading enzymes and their potential to control SMC phenotypic transformation. Our lab uses several animal models of arterial calcification as well as organ culture systems and primary, cultured SMCs. Using these experimental methods, we hope to develop novel therapeutic strategies aimed and reducing medial artery calcification to prevent amputation in patients with peripheral artery disease.
Clinical Research: My lab group has developed the tools for quantifying arterial calcification in the lower extremity using CT, x-ray, and US based methods. We use this information to study the relationship between tibial artery calcification and outcomes in patients undergoing arterial procedures for limb ischemia. We are interested in studying the physiological effects of calcification on vascular stiffness and pedal ischemia so that we may develop therapeutic strategies to slow its progress and improve outcomes in our patients with limb ischemia.
Dr. Guzman has been named to Boston Magazine’s Best Doctors in Vascular Surgery list for the last 3 years.
New and Noteworthy Publications:
Zettervall SL, Soden PA, Ultee KH, Seldon C, Oh J, McGann K, Schermerhorn ML, Guzman RJ.. Elevated serum phosphate levels are associated with decreased amputation-free survival after interventions for critical limb ischemia. J Vasc Surg. 2016 Sep 22. PMID: 27667151.. In this study, we show that elevated phosphate levels are associated with increased mortality and decreased amputation-free survival after interventions for chronic limb-threatening ischemia. We suggest that poor outcomes may be due to the stimulatory effects of phosphate on medial artery calcification.
Lin T, Wang XL, Zettervall SL, Cai Y, Guzman RJ.. Dorsomorphin homologue 1, a highly selective small-molecule bone morphogenetic protein inhibitor, suppresses medial artery calcification. J Vasc Surg. 2016 Jun 30. pii: S0741-5214(16)30090-8. PMID: 27374065. . In this study, we show that selective BMP inhibition can inhibit calcium accumulation in vascular SMCs and arterial segments exposed to elevated phosphate levels. We propose that such small molecules may have clinical utility in reducing medial artery calcification in our population of vascular patients.
Deas DS Jr, Marshall AP, Bian A, Shintani A, Guzman RJ.. Association of cardiovascular and biochemical risk factors with tibial artery calcification. Vasc Med. 2015 Aug;20(4):326-31. PMID: 25907899. In this clinical study of patients with chronic limb-threatening ischemia, we show that increased preoperative pulse pressure is associated with procedural complications and increased mortality. We suggest that arterial stiffness is a marker of increased risk in vascular patients, and might be a suitable target for interventions aimed at improving outcomes in this high-risk population.
Guzman RJ, Brinkley DM, Schumacher PM, Donahue RM, Beavers H, Qin X. J Am Coll Cardiol. . Tibial artery calcification as a marker of amputation risk in patients with peripheral arterial disease. Vasc Med. 2015 Aug;20(4):326-31. PMID: 25907899. This cross-section study in patients without end-stage renal disease shows that tibial artery calcification has risk factors that are similar but not identical to those for coronary artery calcification and peripheral atherosclerosis.
Guzman RJ, Brinkley DM, Schumacher PM, Donahue RM, Beavers H, Qin X. J Am Coll Cardiol.. Tibial artery calcification as a marker of amputation risk in patients with peripheral arterial disease. 2008 May 20;51(20):1967-74. doi: 10.1016/j.jacc.2007.12.058. PMID: 18482666.. In this study using tibial calcification scoring by CT scan, we show that i patients presenting with PAD, the TAC score is associated with the stage of disease and it identifies those who are at high risk for amputation better than traditional risk factors and an abnormal ABI.
Qin X, Corriere MA, Matrisian LM, Guzman RJ.. Matrix metalloproteinase inhibition attenuates aortic calcification. Arterioscler Thromb Vasc Biol. 2006 Jul;26(7):1510-6. PMID: 16690876. In this translational study involving rat models of arterial calcification, we show that MMPs are involved in aortic calcification, and inhibiting their activity could reduce calcium accumulation in the arterial wall.