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Canadian Cardiovascular Society (CCS) CCS540 Oral: Cancer and the Heart Monday, October 25, 2010
Abstracts
289
FACTORS ASSOCIATED WITH HIGH RESIDUAL PLATELET AGGREGATION DURING CHRONIC CLOPIDOGREL THERAPY: ROLE OF BODY MASS INDEX AND DRUG INTERACTIONS G Roberge, J Déry, U Déry, P Lachance, S Rinfret, É Larose, J Rodés-Cabau, G Barbeau, CM Nguyen, O Gleeton, G Proulx, B Noël, L Roy, R De Larochellière, J Després, OF Bertrand Québec, Québec Clopidogrel resistance has been associated with adverse outcomes in acute coronary syndrome (ACS) patients and in patients undergoing percutaneous coronary intervention (PCI). While most studies evaluated resistance early after a loading dose of clopidogrel, few data exist on factors associated with high on-treatment residual platelet aggregation (RPA) during chronic clopidogrel therapy following an ACS. We sought to evaluate the role of concomitant therapy with proton pump inhibitors (PPI), CYP 3A4-metabolyzed statins and other clinical factors on the modulation of platelet aggregation in ACS patients receiving clopidogrel therapy. The use of PPI other than pantoprazole, older age and a BMI>30kg/m2 have an adverse impact on 6-month RPA in ACS patients treated with clopidogrel. Although the clinical correlates of these findings remains unknown, it is reasonable to favor the use of pantoprazole in ACS patients for whom a PPI is indicated. Further studies are needed to determine whether the increased RPA seen in obese patients is a result of lower clopidogrel bioavailability or higher baseline platelet reactivity. Strategies to improve platelet inhibition in obese patients should be developed. Fondation de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec
Canadian Cardiovascular Society (CCS) CCS540 Oral CANCER AND THE HEART Monday, October 25, 2010 292
VITAMIN C MODULATES DOXORUBICIN-INDUCED CARDIOTOXICITY BY REDUCING OXIDATIVE STRESS AND P53 ACTIVATION A Ludke, AK Sharma, PK Singal Winnipeg, Manitoba BACKGROUND: Doxorubicin (Dox) is frequently used as a frontline chemotherapeutic agent against a variety of cancers. However, cardiotoxicity still remains a major concern. The molecular mechanism that plays the major role in this dose-dependent cardiotoxicity is still unknown. It has been suggested that oxidative stress and tumor suppressor p53 activation may participate in the apoptotic cell death in cardiomyocytes exposed to Dox. Improving antioxidant defenses of cardiomyocytes against anthracycline-induced oxidative stress is one strategy for cardiac protection. We tested the hypothesis that Vitamin C, a potent antioxidant, could mitigate dox-induced cardiotoxicity by reducing oxidative stress and interfering with downstream pathways. CONCLUSION: the present study shows that Dox-induced apoptotic cell death involves oxidative stress and p53 activation. Vitamin C blunted these Dox-induced changes, and improved cell survival. The data provide a new insight about the underlying mechanisms for Vitamin C cardioprotection via prevention of oxidative stress, inhibition of p53 activation, and decrease in apoptosis. These findings may suggest an important alternate nutritional approach for preventing Dox-induced cardiotoxicity and better management of cancer patients. Heart and Stroke Foundation Manitoba
Can J Cardiol Vol 26 Suppl D October 2010
293
THE CARDIOPROTECTIVE EFFECTS OF PROBUCOL AGAINST TRASTUZUMAB AND ANTHRACYCLINE-MEDIATED CARDIOTOXICITY JR Walker, A Sharma, T Fang, S Bohonis, PK Singal, DS Jassal Winnipeg, Manitoba BACKGROUND: In breast cancer patients, the administration of Trastuzumab and Doxorubicin is associated with an increased risk of cardiotoxicity. Increased oxidative stress has been suggested as a potential mechanism for this drug-induced cardiomyopathy. The aim of the present study was to determine if the antioxidant probucol would be useful in attenuating chemotherapy-induced cardiac dysfunction. CONCLUSION: The synergistic cardiotoxicity of trastuzumab plus doxorubicin is partially attenuated by the antioxidant probucol.
Student Presentation Award Finalist – Basic Science Featured Research 294
ROLE OF SURVIVIN AND APOPTOSIS IN DOXORUBICININDUCED CARDIOMYOPATHY: IMPLICATIONS FOR ANTI-APOPTOTIC THERAPIES FOR HEART FAILURE PJ Lee, MA Kuliszewski, H Fujii, D Rudenko, C Liao, H Leong-Poi Toronto, Ontario Apoptosis is one of the key mechanisms by which primary injury or insult leads to cardiomyopathies and end-stage heart failure. Clinical studies indicate apoptosis in failing hearts of different etiologies, persisting up to several of years after the initial insult. Preventing apoptosis may reduce the progression to end-stage heart failure. Survivin, an anti-apoptotic gene, is a candidate for preventing cardiac cell death. Thus, we sought to determine the endogenous expression of survivin after cardiac insult and its relationship to apoptosis and left ventricular (LV) systolic function, in a model of doxorubicin-induced cardiomyopathy. In conclusion, after doxorubicin administration, apoptosis follows a biphasic pattern with an early peak at week 1 post-dox, and a later peak at week 6, corresponding to a persistent reduction in endogenous survivin gene expression and a significant drop in LV fractional shortening at week 6. In this heart failure model, survivin gene therapy may represent a novel therapy to restore survivin gene expression and levels, reduce apoptosis and improve LV systolic function.
295
RECOMBINANT HUMAN ACE2 ATTENUATES PRESSURE OVERLOAD-INDUCED PATHOLOGICAL MYOCARDIAL REMODELING J Zhong, GY Oudit, R Basu, FL Chow, M Shuster, H Loibner, X Wang, JM Penninger, Z Kassiri Shanghai, China BACKGROUND: Pressure overload triggers the renin-angiotensin system (RAS) in association with myocardial oxidative stress, dysfunction and cardiac failure. Angiotensin converting enzyme 2 (ACE2) is the first known homolog of human ACE and functions as a pleiotropic monocarboxypeptidase responsible for the degradation of angiotensin (Ang) II with a high catalytic efficiency. In this study, we evaluated the effects of recombinant human ACE2 (rhACE2) on the pathological hypertrophy and functional response to pressure overload. CONCLUSION: Treatment with rhACE2 significantly attenuates the pressure overload-induced cardiac hypertrophy and resulted in a partial improvement in ventricular dysfunction in banded mice associated with reduced expression of BNP, β-MHC, pro-collagen type Iα1 and pro-collagen type IIIα1. These results clearly demonstrate that rhACE2 can provide therapeutic benefits against pathological myocardial remodeling in a
71D
Abstracts model of heart failure, suggesting that ACE2 can provide a novel therapeutic approach for patients with cardiovascular diseases. Supported by Canadian Institute for Health Research, National Natural Science Foundation of China (30973522;30700328), Alberta Heritage Foundation for Medical Research, and Science and Technology Foundation of Zhejiang Province (2009C33080)
296
PREVENTION OF PATHOLOGICAL HYPERTROPHY, MYOCARDIAL FIBROSIS AND CARDIAC DYSFUNCTION BY ANGIOTENSIN-CONVERTING ENZYME 2 J Zhong, R Basu, D Guo, FL Chow, S Bryns, M Shuster, H Loibner, X Wang, JM Penninger, Z Kassiri, GY Oudit Edmonton, Alberta BACKGROUND: Activation of the renin-angiotensin system (RAS) and the subsequent generation of angiotensin (Ang) II is an important mediator of myocardial fibrosis, pathological hypertrophy and heart failure. Drugs that target Ang II and the AT1 receptor are widely used for the treatment of cardiovascular diseases, such as hypertension, myocardial infarction and heart failure. Angiotensin-converting enzyme 2 (ACE2) is a pleitropic monocarboxypeptidase capable of metabolizing a range of peptide substrates including angiotensin peptides. We hypothesized that ACE2 is a negative regulator of Ang II-mediated signaling and its adverse effects on the cardiovascular system. CONCLUSION: Ang II-mediated oxidative stress, hypertension, myocardial hypertrophy and fibrosis are exacerbated in ACE2-deficient mice resulting in worsening of diastolic dysfunction. Recombinant human ACE2 (rhACE2) attenuates Ang II-mediated hypertension, ventricular hypertrophy and fibrosis and improves diastolic dysfunction in WT mice infused with Ang II. These beneficial effects of rhACE2 correlated with a marked reduction in myocardial and plasma Ang II levels and an enhancement of plasma Ang (1-7) levels. We conclude that ACE2 plays a pivotal role in the inhibition of myocardial hypertrophy, fibrosis and cardiac dysfunction and ACE2 represents a novel therapeutic strategy for cardiovascular disorders. This work was supported by the Canadian Institute for Health Research (G.Y.O. and Z.K.), the Alberta Heritage Foundation for Medical Research (G.Y.O. and J.C.Z.), and National Natural Science Foundation of China (J.C.Z)
297
TARGETING DNA REPAIR TO PREVENT ATHRACYCLINEINDUCED CARDIAC FAILURE PC Shukla, KK Singh, A Quan, Y Pan, M Al-Omran, F Lovren, H Leong-Poi, H Teoh, S Verma Toronto, Ontario BACKGROUND: Anthracycline-based treatment approaches are associated with cardiac dysfunction and remain a significant unmet clinical problem. We hypothesized that strategies aimed at improving DNA repair will promote survival of existing cardiomyocytes, and limit apoptosis in response to doxorubicin. CONCLUSION: We report a novel therapeutic approach to limit anthracycline-based cardiac dysfunction in vitro and in vivo by targeting BRCA1, a gene involved in DNA repair. In addition to the immediate implications for cardiovascular repair, these data may have pharmacogenomic implications for the BRCA1 mutation carriers receiving anthracycline-based chemotherapy.
Canadian Society of Cardiac Surgeons (CSCS) CSCS320 Oral ISSUES IN VALVE SURGERY Monday, October 25, 2010 300
MID-TERM CLINICAL OUTCOMES FOLLOWING TRANSAPICAL AORTIC VALVE IMPLANTATION J Higgins, J Ye, A Cheung, L Ding, DA Wood, JG Webb, SV Lichtenstein Vancouver, British Columbia BACKGROUND: Catheter-based approaches have emerged over the past few years as a treatment option for non-surgical candidates with severe symptomatic aortic stenosis (AS). At our center, transapical aortic valve implantation (AVI) is reserved for individuals with poor peripheral arterial access or previous mitral valve surgery. According to the literature, survival is extremely poor for elderly patients with symptomatic severe AS who are declined for aortic valve replacement; 3-year survival is 10-21%. The objective of our study is to describe mid-term clinical outcomes following transapical AVI in this population. CONCLUSION: In comparison to the literature, transapical aortic valve implantation appears to provide great midterm survival benefit to the cohort of patients with symptomatic severe AS who are declined for conventional aortic valve replacement. A randomized clinical trial will further determine the survival benefit of transapical AVI in this challenging group of patients.
301
OUTCOME OF PATIENTS WITH PARADOXICAL LOW FLOW, LOW GRADIENT SEVERE AORTIC STENOSIS WITH PRESERVED LV EJECTION FRACTION FOLLOWING AORTIC VALVE REPLACEMENT M Clavel, JG Dumesnil, P Mathieu, P Pibarot Québec, Québec BACKGROUND: Discordant findings between aortic valve area (AVA<1.0cm2) and mean gradient (MG<40mmHg) may raise uncertainty regarding the actual severity of the aortic stenosis. Some investigators reported that this clinical presentation often reflects the presence of a severe AS with concomitant “paradoxical” low flow. Others suggested that this discordance may also be related to an inconsistency in the cut-off values of AVA and gradient and they proposed an adjustment of the AVA cut-off value to 0.8cm2. Our objective was thus to analyze the impact of aortic valve replacement (AVR) as a function of flow and gradient. CONCLUSION: In patients with paradoxical low flow and severe AS on the basis of AVA, AVR is associated with a powerful protective effect, regardless of the level of gradient. These findings confirm that the present AVA cut-off values for severe stenosis appear to be adequate regardless of gradients. CIHR
302
EARLY CLINICAL AND HEMODYNAMIC OUTCOMES OF A NEW AORTIC BIOPROSTHESIS (TRIFECTA): A MULTICENTRE STUDY A Cheung, E Carbonneau, G Fradet, R MacArthur, M Pellerin, V Rao, J Wood Vancouver, British Columbia BACKGROUND: The St Jude Medical TrifectaTM valve is a newly designed stented pericardial bioprosthesis, intended for implantation in the aortic position. Its unique design maximizes hemodynamic and valve performance. We report the early Canadian multicentre clinical and hemodynamic outcomes. CONCLUSION: The SJM TrifectaTM aortic valve demonstrates excellent early clinical and hemodynamic results. Further follow-up is required to assess its long-term durability and performance.
72D
Can J Cardiol Vol 26 Suppl D October 2010
289
FACTORS ASSOCIATED WITH HIGH RESIDUAL PLATELET AGGREGATION DURING CHRONIC CLOPIDOGREL THERAPY: ROLE OF BODY MASS INDEX AND DRUG INTERACTIONS G Roberge, J Déry, U Déry, P Lachance, S Rinfret, É Larose, J Rodés-Cabau, G Barbeau, CM Nguyen, O Gleeton, G Proulx, B Noël, L Roy, R De Larochellière, J Després, OF Bertrand Québec, Québec Clopidogrel resistance has been associated with adverse outcomes in acute coronary syndrome (ACS) patients and in patients undergoing percutaneous coronary intervention (PCI). While most studies evaluated resistance early after a loading dose of clopidogrel, few data exist on factors associated with high on-treatment residual platelet aggregation (RPA) during chronic clopidogrel therapy following an ACS. We sought to evaluate the role of concomitant therapy with proton pump inhibitors (PPI), CYP 3A4-metabolyzed statins and other clinical factors on the modulation of platelet aggregation in ACS patients receiving clopidogrel therapy. The use of PPI other than pantoprazole, older age and a BMI>30kg/m2 have an adverse impact on 6-month RPA in ACS patients treated with clopidogrel. Although the clinical correlates of these findings remains unknown, it is reasonable to favor the use of pantoprazole in ACS patients for whom a PPI is indicated. Further studies are needed to determine whether the increased RPA seen in obese patients is a result of lower clopidogrel bioavailability or higher baseline platelet reactivity. Strategies to improve platelet inhibition in obese patients should be developed. Fondation de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec
Canadian Cardiovascular Society (CCS) CCS540 Oral CANCER AND THE HEART Monday, October 25, 2010 292
VITAMIN C MODULATES DOXORUBICIN-INDUCED CARDIOTOXICITY BY REDUCING OXIDATIVE STRESS AND P53 ACTIVATION A Ludke, AK Sharma, PK Singal Winnipeg, Manitoba BACKGROUND: Doxorubicin (Dox) is frequently used as a frontline chemotherapeutic agent against a variety of cancers. However, cardiotoxicity still remains a major concern. The molecular mechanism that plays the major role in this dose-dependent cardiotoxicity is still unknown. It has been suggested that oxidative stress and tumor suppressor p53 activation may participate in the apoptotic cell death in cardiomyocytes exposed to Dox. Improving antioxidant defenses of cardiomyocytes against anthracycline-induced oxidative stress is one strategy for cardiac protection. We tested the hypothesis that Vitamin C, a potent antioxidant, could mitigate dox-induced cardiotoxicity by reducing oxidative stress and interfering with downstream pathways. CONCLUSION: the present study shows that Dox-induced apoptotic cell death involves oxidative stress and p53 activation. Vitamin C blunted these Dox-induced changes, and improved cell survival. The data provide a new insight about the underlying mechanisms for Vitamin C cardioprotection via prevention of oxidative stress, inhibition of p53 activation, and decrease in apoptosis. These findings may suggest an important alternate nutritional approach for preventing Dox-induced cardiotoxicity and better management of cancer patients. Heart and Stroke Foundation Manitoba
Can J Cardiol Vol 26 Suppl D October 2010
293
THE CARDIOPROTECTIVE EFFECTS OF PROBUCOL AGAINST TRASTUZUMAB AND ANTHRACYCLINE-MEDIATED CARDIOTOXICITY JR Walker, A Sharma, T Fang, S Bohonis, PK Singal, DS Jassal Winnipeg, Manitoba BACKGROUND: In breast cancer patients, the administration of Trastuzumab and Doxorubicin is associated with an increased risk of cardiotoxicity. Increased oxidative stress has been suggested as a potential mechanism for this drug-induced cardiomyopathy. The aim of the present study was to determine if the antioxidant probucol would be useful in attenuating chemotherapy-induced cardiac dysfunction. CONCLUSION: The synergistic cardiotoxicity of trastuzumab plus doxorubicin is partially attenuated by the antioxidant probucol.
Student Presentation Award Finalist – Basic Science Featured Research 294
ROLE OF SURVIVIN AND APOPTOSIS IN DOXORUBICININDUCED CARDIOMYOPATHY: IMPLICATIONS FOR ANTI-APOPTOTIC THERAPIES FOR HEART FAILURE PJ Lee, MA Kuliszewski, H Fujii, D Rudenko, C Liao, H Leong-Poi Toronto, Ontario Apoptosis is one of the key mechanisms by which primary injury or insult leads to cardiomyopathies and end-stage heart failure. Clinical studies indicate apoptosis in failing hearts of different etiologies, persisting up to several of years after the initial insult. Preventing apoptosis may reduce the progression to end-stage heart failure. Survivin, an anti-apoptotic gene, is a candidate for preventing cardiac cell death. Thus, we sought to determine the endogenous expression of survivin after cardiac insult and its relationship to apoptosis and left ventricular (LV) systolic function, in a model of doxorubicin-induced cardiomyopathy. In conclusion, after doxorubicin administration, apoptosis follows a biphasic pattern with an early peak at week 1 post-dox, and a later peak at week 6, corresponding to a persistent reduction in endogenous survivin gene expression and a significant drop in LV fractional shortening at week 6. In this heart failure model, survivin gene therapy may represent a novel therapy to restore survivin gene expression and levels, reduce apoptosis and improve LV systolic function.
295
RECOMBINANT HUMAN ACE2 ATTENUATES PRESSURE OVERLOAD-INDUCED PATHOLOGICAL MYOCARDIAL REMODELING J Zhong, GY Oudit, R Basu, FL Chow, M Shuster, H Loibner, X Wang, JM Penninger, Z Kassiri Shanghai, China BACKGROUND: Pressure overload triggers the renin-angiotensin system (RAS) in association with myocardial oxidative stress, dysfunction and cardiac failure. Angiotensin converting enzyme 2 (ACE2) is the first known homolog of human ACE and functions as a pleiotropic monocarboxypeptidase responsible for the degradation of angiotensin (Ang) II with a high catalytic efficiency. In this study, we evaluated the effects of recombinant human ACE2 (rhACE2) on the pathological hypertrophy and functional response to pressure overload. CONCLUSION: Treatment with rhACE2 significantly attenuates the pressure overload-induced cardiac hypertrophy and resulted in a partial improvement in ventricular dysfunction in banded mice associated with reduced expression of BNP, β-MHC, pro-collagen type Iα1 and pro-collagen type IIIα1. These results clearly demonstrate that rhACE2 can provide therapeutic benefits against pathological myocardial remodeling in a
71D
Abstracts model of heart failure, suggesting that ACE2 can provide a novel therapeutic approach for patients with cardiovascular diseases. Supported by Canadian Institute for Health Research, National Natural Science Foundation of China (30973522;30700328), Alberta Heritage Foundation for Medical Research, and Science and Technology Foundation of Zhejiang Province (2009C33080)
296
PREVENTION OF PATHOLOGICAL HYPERTROPHY, MYOCARDIAL FIBROSIS AND CARDIAC DYSFUNCTION BY ANGIOTENSIN-CONVERTING ENZYME 2 J Zhong, R Basu, D Guo, FL Chow, S Bryns, M Shuster, H Loibner, X Wang, JM Penninger, Z Kassiri, GY Oudit Edmonton, Alberta BACKGROUND: Activation of the renin-angiotensin system (RAS) and the subsequent generation of angiotensin (Ang) II is an important mediator of myocardial fibrosis, pathological hypertrophy and heart failure. Drugs that target Ang II and the AT1 receptor are widely used for the treatment of cardiovascular diseases, such as hypertension, myocardial infarction and heart failure. Angiotensin-converting enzyme 2 (ACE2) is a pleitropic monocarboxypeptidase capable of metabolizing a range of peptide substrates including angiotensin peptides. We hypothesized that ACE2 is a negative regulator of Ang II-mediated signaling and its adverse effects on the cardiovascular system. CONCLUSION: Ang II-mediated oxidative stress, hypertension, myocardial hypertrophy and fibrosis are exacerbated in ACE2-deficient mice resulting in worsening of diastolic dysfunction. Recombinant human ACE2 (rhACE2) attenuates Ang II-mediated hypertension, ventricular hypertrophy and fibrosis and improves diastolic dysfunction in WT mice infused with Ang II. These beneficial effects of rhACE2 correlated with a marked reduction in myocardial and plasma Ang II levels and an enhancement of plasma Ang (1-7) levels. We conclude that ACE2 plays a pivotal role in the inhibition of myocardial hypertrophy, fibrosis and cardiac dysfunction and ACE2 represents a novel therapeutic strategy for cardiovascular disorders. This work was supported by the Canadian Institute for Health Research (G.Y.O. and Z.K.), the Alberta Heritage Foundation for Medical Research (G.Y.O. and J.C.Z.), and National Natural Science Foundation of China (J.C.Z)
297
TARGETING DNA REPAIR TO PREVENT ATHRACYCLINEINDUCED CARDIAC FAILURE PC Shukla, KK Singh, A Quan, Y Pan, M Al-Omran, F Lovren, H Leong-Poi, H Teoh, S Verma Toronto, Ontario BACKGROUND: Anthracycline-based treatment approaches are associated with cardiac dysfunction and remain a significant unmet clinical problem. We hypothesized that strategies aimed at improving DNA repair will promote survival of existing cardiomyocytes, and limit apoptosis in response to doxorubicin. CONCLUSION: We report a novel therapeutic approach to limit anthracycline-based cardiac dysfunction in vitro and in vivo by targeting BRCA1, a gene involved in DNA repair. In addition to the immediate implications for cardiovascular repair, these data may have pharmacogenomic implications for the BRCA1 mutation carriers receiving anthracycline-based chemotherapy.
Canadian Society of Cardiac Surgeons (CSCS) CSCS320 Oral ISSUES IN VALVE SURGERY Monday, October 25, 2010 300
MID-TERM CLINICAL OUTCOMES FOLLOWING TRANSAPICAL AORTIC VALVE IMPLANTATION J Higgins, J Ye, A Cheung, L Ding, DA Wood, JG Webb, SV Lichtenstein Vancouver, British Columbia BACKGROUND: Catheter-based approaches have emerged over the past few years as a treatment option for non-surgical candidates with severe symptomatic aortic stenosis (AS). At our center, transapical aortic valve implantation (AVI) is reserved for individuals with poor peripheral arterial access or previous mitral valve surgery. According to the literature, survival is extremely poor for elderly patients with symptomatic severe AS who are declined for aortic valve replacement; 3-year survival is 10-21%. The objective of our study is to describe mid-term clinical outcomes following transapical AVI in this population. CONCLUSION: In comparison to the literature, transapical aortic valve implantation appears to provide great midterm survival benefit to the cohort of patients with symptomatic severe AS who are declined for conventional aortic valve replacement. A randomized clinical trial will further determine the survival benefit of transapical AVI in this challenging group of patients.
301
OUTCOME OF PATIENTS WITH PARADOXICAL LOW FLOW, LOW GRADIENT SEVERE AORTIC STENOSIS WITH PRESERVED LV EJECTION FRACTION FOLLOWING AORTIC VALVE REPLACEMENT M Clavel, JG Dumesnil, P Mathieu, P Pibarot Québec, Québec BACKGROUND: Discordant findings between aortic valve area (AVA<1.0cm2) and mean gradient (MG<40mmHg) may raise uncertainty regarding the actual severity of the aortic stenosis. Some investigators reported that this clinical presentation often reflects the presence of a severe AS with concomitant “paradoxical” low flow. Others suggested that this discordance may also be related to an inconsistency in the cut-off values of AVA and gradient and they proposed an adjustment of the AVA cut-off value to 0.8cm2. Our objective was thus to analyze the impact of aortic valve replacement (AVR) as a function of flow and gradient. CONCLUSION: In patients with paradoxical low flow and severe AS on the basis of AVA, AVR is associated with a powerful protective effect, regardless of the level of gradient. These findings confirm that the present AVA cut-off values for severe stenosis appear to be adequate regardless of gradients. CIHR
302
EARLY CLINICAL AND HEMODYNAMIC OUTCOMES OF A NEW AORTIC BIOPROSTHESIS (TRIFECTA): A MULTICENTRE STUDY A Cheung, E Carbonneau, G Fradet, R MacArthur, M Pellerin, V Rao, J Wood Vancouver, British Columbia BACKGROUND: The St Jude Medical TrifectaTM valve is a newly designed stented pericardial bioprosthesis, intended for implantation in the aortic position. Its unique design maximizes hemodynamic and valve performance. We report the early Canadian multicentre clinical and hemodynamic outcomes. CONCLUSION: The SJM TrifectaTM aortic valve demonstrates excellent early clinical and hemodynamic results. Further follow-up is required to assess its long-term durability and performance.
72D
Can J Cardiol Vol 26 Suppl D October 2010