Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 3rd International Conference on Clinical & Experimental Cardiology Hilton Chicago/Northbrook, USA.

Day 1 :

  • Track 1: Heart Diseases
Location: Willow
Speaker

Chair

James D Fett

University of Pittsburgh Medical Center, USA

Speaker

Co-Chair

Xiaoping Ren

University of Cincinnati,USA

Session Introduction

James D Fett

University of Pittsburgh Medical Center, USA

Title: Remarkable progress in understanding, treatment and outcomes in peripartum cardiomyopathy since 2000

Time : 11:25-11:45

Speaker
Biography:

James D Fett, MD, MPH, has worked on peripartum cardiomyopathy (PPCM) issues for over 25 years, having been introduced to the condition in Haiti, in 1984. He has authored numerous peer-reviewed articles in numerous medical journals. He has presented PPCM-related abstracts at several Scientific Sessions of the American Heart Association, and made PPCM-related presentations as well as chairing sections at the 2009 Annual International Congress of Cardiology in Shanghai, China, in 2009; at the 1st International Congress on Cardiac Problems in Pregnancy in Valencia, Spain, in 2010; as well as at the 2nd International Congress on Cardiac Problems in Pregnancy in Berlin, Germany, in 2012. He currently serves as Consultant, Peripartum Cardiomyopathy Network of North America (PCN) and as Co-Chairman, Investigations in Pregnancy Associated Cardiomyopathy (IPAC) Study, University of Pittsburgh Medical Center. Early Biographical Data: Born in Campbell, Minnesota, USA 26 August 1934 Campbell Public School, 1-12. Education/Training: University of Sioux Falls, Sioux Falls, SD, BA Chemistry, 1952-55. University of Minnesota/University of Minnesota Medical School, MD, 1955-60. University Minnesota School Public Health, MPH, 1962/63. Institute Tropical Medicine, Antwerpen, Belgium, 1963/64. Kansas City General Hospital, Rotating Internship 1960/61. Lafayette Charity Hospital, Family Practice Residency 1961/62. Abbott Northwestern Hospital, U MN, Internal Medicine Residency, 1968-/70/72. Certifi cation: American Board Internal Medicine, 1970/1973/1980 (lifetime). Professional Experience: Staff Physician, Vanga Hospital, Democratic Republic Congo, 1963-68. Staff Internist, Director School Public Health, Vanga Hospital, Zaire, 1970-72. Staff Internist, Medical Associates Clinic, Pierre, SD, 1973-75. Staff Internist, Clinical Director, Indian Health Service, Rapid City, SD, 1975-80. Chief Medical Officer, Bemidji Area Indian Health Service, 1980-83. Staff Internist, Clinical Director, Indian Health Service, White Earth, MN 1983-84. Medical Director, Hospital Albert Schweitzer, Deschapelles, Haiti, 1984-86. Staff Internist, Clinical Director, Indian Health Service, White Earth, MN 1986-93.

Abstract:

Peripartum cardiomyopathy (PPCM), heart failure from pregnancy-associated cardiomyopathy, entered the modern era in the USA in 2000, with the report from the Workshop on Peripartum Cardiomyopathy from the National Institutes of Health. Since then, there has been a great reduction in mortality in the USA (from a range of 18-56% down to a range of 1-5 % ) and an increasing number of women who have experienced recovery of heart function in the USA (from less than one-third to over onehalf). PPCM may be the non-ischemic cardiomyopathy that has the greatest potential of all cardiomyopathies for full recovery. Despite these impressive changes, from one-third to one-half of PPCM patients still go on to chronic heart failure; and experience other life-threatening complications. An essential key to a better path is to make an earlier diagnosis. Time-of-diagnosis left ventricular systolic function (LVEF) greater than 30-35% is associated with high survival and recovery rates. Increased mortality, chronic cardiomyopathy, thromboembolic complications, serious ventricular tachyarrhythmias, left ventricular assist devices and transplantation are more likely to be associated with diagnostic LVEF below 30-35%. An earlier diagnosis may be associated with the more favorable diagnostic levels, while any delay in diagnosis is more likely to be associated with lower LVEF. Earlier diagnosis can be greatly facilitated when there is an awareness of the possibility of heart failure in a peripartum patient, who ordinarily would be expected to have a healthy heart. This awareness must importantly be present not only in the mother herself, but in all those health professionals with whom she comes in contact, including nurses, mid-wives, obstetricians, emergency room physicians, and primary care providers. A new tool has been developed to help distinguish heart failure signs and symptoms from those of normal pregnancy. There are 3 areas of newer investigations that may help both with earlier diagnosis and more eff ective treatment: Immune system activation, role of cardiotoxic prolactin metabolites, and soluble FLT1 with angiogenic imbalance.

Speaker
Biography:

Xiaoping Ren received his MD in Harbin Medical University in 1984. He performed his Clinical and Research Hand Fellowship training in University of Louisville in Kentucky (1996-2000). During the period, Ren created a feasibility large animal CTA model for limb transplantation to allow modulation of the immune reaction and to investigate immunosuppressant. The Nation's First Hand Transplantation in US was successfully conducted as a direct result of the preclinical swine composite tissue allotransplantation model (CTA). He joined the University of Cincinnati, College of Medicine as faculty member in 2001, then appointed Assistant Professor and Associate Professor and holding position as Professor/Director in HMU since 2012. As well as CTA, another focus of his research program is to understand molecular and neuronal basis of non-ischemic nociceptor-induced cardioprotection. These studies were published in the Journal of Surgical Research and in Circulation. Ren has had over 40 publications in peer-reviewed journals. Currently, he is holding active Memberships of the American Association for Hand Surgery and the American Heart Association.

Abstract:

Our previous studies have identified a novel cardioprotective phenomenon that occurs subsequent to remote trauma (abdominal skin incision), termed RPCT and initiated by a neurogenic ganglionic mechanism. Reasoning that low-trauma non-ischemic remote cardioprotection could have important clinical application, we tested the hypothesis that remote electrical stimulation (ES) of skin nociceptors can reproduce this effect similar to that of RPCT methods, an in vivo mouse I/R model were used. ES was performed 15 minutes prior to I/R or at the beginning of reperfusion. Infarct size was used to evaluate the results of I/R injury (45 min coronary occlusion, 24h reperfusion) with or without prior ES treatments. Histological, functional and biochemical studies were determined at appropriate time points. The results of our studies demonstrate that nociceptor stimulation at specific points does indeed induce a powerful 85% (P<0.01) reduction in infarct size and reduces post-ischemic ventricular dysfunction. Both the number of TUNEL-positive nuclei and DNA fragmentation were significantly reduced in the ES treated group. Cardioprotective effect of ES was abolished by both beta-AR antagonism and in BK2RKO mice. Western blot results show PKC isoform translocation is altered aft er ES and pharmacologic blockade of PKC prevented cardioprotection due to ES. In conclusion, our results support 1) ES elicited a powerful cardioprotection via a neural mechanism, 2) the protective effect of ES against MI involves -AR, BK2R signaling and PKC modulation.

Laurentiu M. Popescu

Carol Davila University of Medicine and Pharmacy, Romania

Title: Telocytesand stem cells in myocardial regeneration

Time : 12:05-12:25

Speaker
Biography:

L M Popescu, MD, Ph.D. Dr. h.c.mult., is currently Professor of Cellular and Molecular Medicine, University of Medicine and Pharmacy, Bucharest, and Head of the National Institute of Pathology, Bucharest, Romania. With over 140 scientific articles in peer-reviewed journals, he is cited about 3000 times (Hirsch index above 30). He is Editor-in-Chief (and founder) of the Journal of Cellular and Molecular Medicine (Wiley/Blackwell), 5-year IF: 5.8. In 2012, Popescu was awarded the ‘Medal of Merit’ of the International Academy of Cardiovascular Sciences for his outstanding achievements in cardiovascular research. He is credited with the discovery of telocytes.

Abstract:

Telocytes (TCs) are a newly described (2010) distinct type of interstitial cells. TCs are defined by their very long prolongations (hundreds of micrometers) called telopodes (Tps); see www.telocytes.com and Wikipedia. Patch voltage-clamp data shows that TCs are unexcitable cells. TCs were found in many organs where they form a 3D network among the organ-specific cells and blood capillaries, nerve endings and immunoreactive cells. Beyond the ultrastructural portrait of TCs, the immuno-phenotype, gene profile and the microRNA imprint were also described.Unlike other interstitial cells, TCs are key-players in intercellular signaling. Tps establish direct contacts (junctions) with neighboring cells (long distancesignaling). Short distance (local) signaling of TCs is achieved by extracellular vesicles, mainly by shed vesicles (in situ electron microscopy indicated an average diameter of 180 nm; n= 6,094). Cardiac TCs have been identified in epi-, myo-and endo-cardium. Of particular interest are the junctions (nanocontacts) between stem and/or progenitor cells and TCs in myocardium stem niche in situ, as found by electron tomography. Cultured cardiac TCs release growth factors (VEGF), cytokines (IL6) and chemokines (CXCL-1), presumably through shed vesicles (SELDI-TOF-MS and xMAP Technology). Using the membrane impermeable calcein and RNA oligoswe found in vitro that cardiac TCs can shuttle microRNAs to other cells through vesicles. Cardiac TCs co-cultured with cardiac stem cells in a transwell system (400 nm pores) enhances stem cell differentiation to cardiac myocytes. This makes the tandem TCs-Stem cells a valuable candidate for myocardial regeneration.

Emad Aziz

Columbia University College of Physicians & Surgeons, USA

Title: Improving health care quality in an insolvent system: Who will lead?

Time : 12:25-12:45

Speaker
Biography:

Emad Aziz have been working at St. Lukes since 2004 as an intern, resident and fellow and now he is an EP fellow. During his residency, after program he assisted Eyal Herzog in creating many of our novel pathways for the management of cardiac patients. In 2006, he started the ACAP Advanced Cardiac Admission Program, which included 6 state of the art novel pathways for the management of chest pain, heart failure, atrial fi brillation, hyperglycemia in the CCU, syncope and hypertension, including developing a hospital wide database, with patient follow-ups. These databases served as a cornerstone for research, resulting in more than 82-presented abstracts and 25 published manuscripts. In conjunction with the ACAP databases, Emad Aziz also started an ACAP Volunteer group comprising of multiple internal medicine residents, pre-medical and medical students from Columbia University, New York College of Osteopathic Medicine, Touro College, and Hunter College as well as FMG's who are seeking residencies in the United States about 60 members. All were instrumental in implementing, managing and data collection. Recently, he has published Two new pathways- ESCAPE Pathway for Sudden Cardiac Death Prevention and MOCHA Pathway for the Management of Survivors of Out of the Hospital Cardiac Arrest; both were contributory in increasing awareness of sudden cardiac death, referral for ICD implantation and favorable outcome for out-of-hospital cardiac arrest.

Abstract:

Introduction: Variation in quality and outcomes is substantial and is driven (at least somewhat) by provider behavior Suboptimal health care quality and outcomes contribute to excess costs Higher quality is not generally associated with higher overall costs, but improving quality oft en reduces provider revenue under current payment systems. Care Gap exists due failure to, translate, transfer and utilize medical knowledge effectively.
Problem: Despite overwhelming clinical trial evidence, expert opinion, national guidelines, and a vast array of educational conferences, evidence-based, life-saving therapies continue to be underutilized New approaches to improving the use of proven, guideline-recommended, life-saving therapies are clearly needed Implementation of critical pathways and management plans for hospitalized patients is becoming a mainstream in achieving the goal of optimal quality of care.
Methods and Implementation: In 2004, a new program "Advanced Cardiac Admission Program" (ACAP) was developed and implemented at St. Luke's-Roosevelt Hospital Center, New York, NY. ACAP consisted of tools and strategies for implementing ACC/AHA guidelines. Up-to-date the ACAP program includes 8 state of the ART Pathways in management. We identified 5 main areas for implementation: Development group, Hospital administration, Residents/fellows, Nursing and Quality management. Th e successful utilization and integration of these five main target areas, we believe are integral in the institution wide acceptance of the ACAP program and eventually our positive outcome data.
Conclusion: Cardiovascular diseases pose a huge clinical and economic burden. Prevention is sub-optimal/proven therapies are underutilized-there remains a huge Care Gap. Comprehensive primary & secondary prevention strategies are required. Multiple interventions are required to Bridge the Care Gap. Educational resources and management tools are necessary at point of care. Development of critical pathways can ensure that patients are more likely to receive the recommended therapeutics. Cardiac performance measures might be the basis for payment in the future. Our physicians & our profession must lead in improving our health care system.

Break: Lunch Break 12:45-13:30 @ Hickory

Anastasia Susie Mihailidou

Royal North Shore Hospital & University of Sydney, Australia

Title: Sex differences during myocardial infarction: Role of autophagy

Time : 13:30-13:50

Speaker
Biography:

Anastasia Susie Mihailidou is a cardiovascular clinical scientist, graduating with a Ph.D. in Pharmacology from University of Sydney in 1988. She is currently Clinical Senior Lecturer for Sydney Medical School, University of Sydney and Senior Hospital Scientist at Royal North Shore Hospital. Anastasia has both clinical and basic research interests as Director of the Ambulatory Blood Pressure Monitoring Service for a major Tertiary Referral Centre and Head of the Cardiovascular & Hormonal Research Laboratory. Her research focus is regulation of aldosterone/mineralocorticoid receptors in the heart and has made a signifi cant contribution to understanding the role of corticosteroid hormones (and antagonists). She was the fi rst to show aldosterone has both rapid and sustained effects on regulation of sodium transport in the heart, with increased levels of intracellular sodium. These fi ndings have generated great interest, leading to award of the Pfi zer Prize for best research at the International Society of Hypertension (2002). Her current research focus is to determine the role of aldosterone and mineralocorticoid receptors in diabetes.

Abstract:

Ischemic heart disease continues to be the leading cause of mortality, morbidity and burden of disease, with gender differences reported in presentation and clinical outcomes; the incidence in men is almost twice that in women, although more women than men die suddenly without any previous symptoms. Th ere is increased interest in defining the mechanisms for the sex related differences in cardiac damage following myocardial infarction, however, conflicting reports continue. Myocardial ischemia reduces blood fl ow and triggers programmed cell death (apoptosis), with progressive loss of cardiomyocytes resulting in tissue damage. Primary clinical strategy is to restore blood fl ow although this may further increase tissue damage, myocardial reperfusion injury (I/R). Autophagy, a cell survival pathway which is induced during I/R. We examined the role of androgens and estrogens during myocardial infarction (MI) in male and female animals, and how autophagy and apoptosis may contribute to the sex differences in cardiac damage. Mature age-matched male and female Sprague Dawley rats were used intact or surgically gonadectomized. Animals were anesthetised and hearts isolated and subjected to regional ischemia-reperfusion (I-R). In males, regional myocardial I-R in hearts from intact male rats produced significantly larger infarct size than those from female rats. Aggravated reperfusion injury correlated with increased apoptosis in the area at risk, consistent with the smaller infarct size in female hearts there was signifi cantly less apoptosis. We also found a gender dependent shift in the balance between autophagy and apoptosis, which has not been previously reported.

Speaker
Biography:

Anthony Ashton has completed his Ph.D. in 1998 at the University of New South Wales, Australia. His postdoctoral studies at the Albert Einstein College of Medicine focused on novel mechanisms of treatment for the heart post-infarction. He is currently the Director of Basic Research, in the Division of Perinatal Research at the Kolling Institute for Medical Research in Sydney. He has published more than 51 papers in reputed journals, serves on the editorial board and as a reviewer for multiple biomedical journals and for multiple funding bodies.

Abstract:

Apoptosis is an important mechanism of cardiac myocyte loss during ischemia-reperfusion injury and heart failure. We have identified that the endogenous inhibitor of apoptosis ARC (Apoptosis Repressor with Caspase recruitment domain) is essential for minimizing cardiac damage post-infarction. ARC is degraded quickly, via ubiquitination and proteosomal targeting, upon reperfusion injury which is then permissive for the onset of the apoptosis associated with reperfusion injury. However, the mechanism by which ARC protects the myocardium basally are incompletely understood. We have previously found that ARC prevents activation of both the extrinsic and intrinsic apoptosis pathways. However, what has been unappreciated until now is that ARC directly blocks DNA degradation induced by a variety of apoptotic stimuli. Using antibody arrays, we discovered ARC interacts with the key facilitators of apoptotic nuclear remodeling (ICAD, acinus and helicard) and prevents their activation by executioner caspases. The functional importance of these interactions were demonstrated by the ability of ARC to prevent nuclear remodeling in vivo as the ARC null mice were highly sensitive to the effects of ischemia on processing of ICAD/acinus/ helicard. Thus, targeting ARC degradation during reperfusion injury would salvage the myocardium and prevent progression to failure. To this end we have recently identified mineralocorticoid activation as a novel regulator of ARC degradation that is readily antagonized and results in promising reduction of mortality post-infarction. In conclusion, salvage of ARC expression and activity is a novel and readily achievable mechanism by which the after effects of infarction can be targeted therapeutically for patient benefit.

Speaker
Biography:

Stenina-Adognravi has acquired her Ph.D. at the National Cardiology Center in Moscow, Russia. The regulation of vascular gene expression, mechanisms of atherogenesis and functions of the vascular extracellular matrix are her long-standing interests. Her professional activities include more than 30 publications related to vascular biology problems, most of them in high impact journals; peer review of manuscripts for reputable journals and participation in vascular biology grant review groups. She is currently an Associate Staff (Associate Professor) at the Cleveland Clinic, Department of Molecular Cardiology. Stenina is currently working on the molecular mechanisms of association between diabetes and cardiovascular disorders.

Abstract:

Remodeling of the vascular wall initiates and defines the development of cardiovascular disease, diabetic complications, tumor growth, and many other devastating chronic diseases. Remodeling and growth of the blood vessels is guided and regulated by the extracellular matrix (ECM), which signals through the cell surface receptors, controls adhesion, migration, survival and proliferation of the vascular cells. Composition of ECM and its interactions with cells are cell-type-specific and local. Hyperglycemia causes profound changes in composition of vascular ECM, and these changes are hallmark of diabetic vascular complications (the primary cause of the mortality and the morbidity of diabetics). We have been exploring the cell and tissue-specific molecular mechanisms that regulate the production of ECM in response to glucose and can explain the tissue and organ-specific effects of hyperglycemia on vasculature. We have described molecular details of a cell-type-specific transcriptional mechanism controlling production of thrombospondin-1 (TSP-1)(one of the most potent anti-angiogenic ECM proteins implicated in cancer development, diabetic complications and atherogenesis) in endothelial cells (EC) and vascular smooth muscle cells (SMC). In addition to cell-specific transcriptional pathways activated by hyperglycemia, we have discovered a novel tissue-specific post-transcriptional microRNA-dependent mechanism inhibiting the production of TSP-1 to increase angiogenesis in selected tissues in response to hyperglycemia. This novel pathway offers a breakthrough explanation for the tissue-and organ-specific vascular complications of diabetes and for the well documented but poorly understood association between hyperglycemia and several cancers. It also suggests a new target for the prevention and treatment of vascular diabetic complications and cancers in diabetic patients. A combination of cell-and tissue-specific transcriptional and post-transcriptional pathways maintains the spatial and temporal regulation of production of the ECM proteins in response to hyperglycemia.

Sitratullah Olawunmi Maiyegun

Texas Tech University Health Science Center, USA

Title: Mid aortic syndrome: A rare cause of hypertension in children

Time : 14:30-14:50

Speaker
Biography:

Sitratullah Olawunmi Maiyegun is an Assistant Professor of Pediatrics, TTUHSC, SOM, El Paso.Medical education at College of Medicine, of the University of Lagos, Nigeria. She completed Pediatrics Residency at Lagos University Teaching Hospital, Nigeria. In the USA, Pediatric Residency at TTUHSC El Paso Texas. She had a Mini fellowship / Elective Course in Child Maltreatment, University of Texas, San Antonio, Child Abuse Division in Center for Miracles. Board certified in General Pediatrics. Her Bachelor of Medicine and Bachelor of Surgery (MBBS) Lagos. Fellowship of the Nigerian Postgraduate Medical College in Pediatrics (FMCPead) Nigeria. Membership of the Royal College of Physicians (MRCP) United Kingdom. Fellow of the American Academy of Pediatrics.

Abstract:

Case report: A 6-year-old Hispanic female, with no dysmorphic features. She was on treatment for Lichen sclerosis etatrophicus and was found to have episodic symptomatic hypertension. She had multiple episodes of severe headache; vomiting and vision disturbance that required ER visits. No significant PMH or inflammatory symptoms and signs. FSH was significant for migraine in siblings and mother. Father was deported to Mexico after the initial clinic visits. Physical examination was within normal limit. Peripheral pulses were well felt and no differential blood pressure between the limbs. Investigations: CXR did not show abnormalities. EKG showed multiple wide complexes. Holter monitoring showed ventricularectopy. Labs showed high renin activity: 6.41 ng/mL/h (0.25-5.82). CMP, ESR, ANA, cortisol, thyroid function test (TFT), Angiotensin converting enzyme (ACE), total cathecolamines, vanillylmandelic acid (VMA), homovanillic acid (HVA) and were all within normal limits. Scleroderma and SLE screen were negative. Renal Doppler US was within normal limit. Echocardiography showed no evidence of coarctation of the aorta. Cardiologist and nephrologist were consulted and she was cleared as situational hypertension. Subsequent follow-up chest auscultation revealed paravertebral continuous bruit in the inter-scapular region. Chest and abdominal CT angiogram showed abnormal tapered stenosis of the subdiaphragmatic descending thoracic aorta with distal kinking. There is greater than 50% luminal narrowing. No definitive evidence of arteritis. There was significant decrease in luminal diameter which maybe resulting in bilateral renal hypoperfusion and renin dependent hypertension. Treatment: Cardiologist re-consulted and she was started on Labetalol. Angiography and catheterization were done to determine the extent of abnormalities and calculate the gradient prior to surgery. She is awaiting surgery to be done in San Antonio. Conclusion: Mid Aortic Syndrome (Coarctation) is a rare (0.5 to 2%) cause of hypertension in children. Th e diagnosis requires high index of suspicion. Inter-scapular auscultation should always be part of routine cardiac examination in children.

Tatsuya Shimizu

Tokyo Womens Medical University, Japan

Title: Cell sheet based tissue engineering for myocardial tissue repair

Time : 14:50-15:10

Speaker
Biography:

Tatsuya Shimizu is the Professor of Department of Tissue Regeneration, Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University. He graduated from Faculty of Medicine, the University of Tokyo and got medical doctor (MD) in 1992. After two-year clinical training, he made a specialty of cardiovascular medicine including catheterization and got Ph.D. in 1999. After that, he moved to ABMES of TWMU and have developed myocardial tissue engineering research based on "cell sheet technology". His recent work is especially concentrated on neovascularization in myocardial tissue graft to reconstruct more functional tissue.

Abstract:

Recently, regenerative medicine has rapidly progressed as a new approach to treat various types of diseases that can't be cured with conventional drugs or surgical techniques. Although isolated cell injection therapy is clinically performed, its application is limited due to significant cell loss and difficulties for controlling graft size and shape. Therefore, tissue engineering technology has been expected to complement the efficacy of cell therapy. We have developed novel technology "cell sheet-based tissue engineering", which has realized cell-dense tissue fabrication without any scaffolds. Confluently cultured cells are harvested as contiguous cell sheets from temperature-responsive culture surfaces only by lowering temperature. Cell sheets are directly transplanted onto damaged tissues or stacked into multi-layer constructs. Autologous myoblast cell sheet transplantation has been clinically applied for the patients suffering from severe heart failure. Some patients have recovered and clinical study is now on going. For industrializing cell sheet-based therapy, we have now started to develop safe and automated tissue fabrication systems including the units for cell isolation, mass subculture, cell sheet harvest and stacking. As next step, the technology development for fabricating pulsatile cardiac tissue and scaling-up the construct has been requested to treat more severe heart diseases and, in future, to replace donor organ implantation. Mass culture of ES/iPS cells, sorting of cardiac cells and sufficient vascularization within multiple layers of cell sheets are key technologies to be broken through. We are now challenging to fabricate functionally pulsatile human heart tissues for future transplantation.

Speaker
Biography:

Jodi Tinkel completed her medical training at the University of Toledo Medical center and is currently an Assistant Professor and invasive cardiologist at UT. She is the Medical Director of cardiac rehabilitation and has research interests in ischemic preconditioning, platelet activation, cardiac imaging and plaque stability.

Abstract:

Remote ischemic preconditioning has been shown to reduce the extent of myocardial infarction during an ischemic event as well as prior to a planned cardiac intervention. Vigorous exercise has been shown to have similar cardiovascular benefits to remote ischemic preconditioning in healthy individuals. Despite this effect, many individuals who exercise regularly present with cardiovascular disease. Those individuals who participate in cardiac rehabilitation programs provide a unique opportunity to determine whether the effects of more vigorous exercise prior to a cardiac event result in improved outcomes. We analyzed our cardiac rehabilitation database and compared individuals with the highest and the lowest exercise capacity as determined by their peak oxygen consumption on a CPX test prior to initiating a cardiac rehabilitation program to compare baseline characteristics and outcomes. Group 1 (VigEx) includes individuals with higher MVO2 (mean MVO2 33 and METS 9) and Group 2 (LowEx) includes those with lower MVO2 (mean MVO2 11 and METS 3). Men accounted for 95% of the total in the VigEx group. Women made up 31% of our total population but only accounted for 5% of those in VigEx. VigEx had lower mean BMI than LowEx (26 v. 34). Smokers comprised only 19% of the total in VigEx but 30% in LowEx. Only 5% of VigEx subjects had diabetes, whereas 60% of LowEx had diabetes. VigEx had 17% of its subjects with 0-1 CV risk factors compared to none of the subjects in LowEx. LowEx had 36% with >5 CV risk factors but only 7% of VigEx had >5 CV risk factors. Only 12% of VigEx subjects required coronary artery bypass graft ing and 41% underwent percutaneous coronary intervention. In LowEx, 27% required CABG and 12% underwent PCI. 72% of the subjects in VigEx had a preserved ejection fraction but only 50% of subjects in LowEx. None of the subjects in VigEx had severely reduced ejection fraction, while 28% of LowEx had an EF <30%. In conclusion, individuals with cardiovascular disease who participate in more vigorous exercise prior to their cardiac event have improved EF and decreased need for CABG, and may obtain a protective benefit similar to RIPC. Also, given the safety of vigorous exercise in the cardiac rehabilitation population and its similar effects to RIPC, cardiac rehabilitation programs should promote vigorous exercise capable individuals. Further studies could be considered in cardiac rehabilitation patients who cannot perform more vigorous exercise to determine if a program of RIPC would provide further benefit.

Break: Coffee Break 15:30-15:45 @ Hickory
Speaker
Biography:

Anush Oganesian is a Research Assistant Professor in the Department of Anesthesiology at the University of Washington. She received her BS/ MS in Molecular Biology/Chemistry from the Yerevan University in Armenia and her Ph.D. in Biochemistry/Organic Chemistry from the Institute of Element Organic Compounds, Academy of Sciences in Moscow, Russia. Anush did her post-doctorial training at the University of Washington with Linda Sandell in the Department of Orthopedics studying the extracellular matrix proteins including the N-propeptide of type IIA procollagen and its interaction with TGFbeta1 and BMP-2 proteins. She continued her postdoctoral training in the laboratory of Daniel Bowen-Pope in the Department of Pathology focusing on biochemical characterization, functional studies and signal transduction pathways regulated by PTPRQ and Phogrin, novel transmembrane protein tyrosine phosphatases with PTEN-like lipid-phosphatase activities.

Abstract:

Various cardiovascular disorders, such as hypertension and heart failure, are associated with polymorphisms in genes involved in the regulation of adrenergic system, mostly beta-Adrenergic Receptors (AR) and alpha2ARs. Three alpha1AR (alpha1AR) subtypes have been characterized and are expressed in human heart and vessels (alpha1a, alpha1b, alpha1d), mediating actions of the sympathetic nervous system through binding of the endogenous catecholamines epinephrine and norepinephrine. The predominant subtype in human vessels and heart is alpha1aAR. A few studies have reported an association between alpha1aAR polymorphisms with hypertension and heart failure in humans. Previously 9 naturally occurring human SNPs in the alpha1aAR coding region have been identified and pharmacologically characterized. The alpha1aAR-G247R (alpha1a-247R) SNP present in the third intracellular loop of the alpha1aAR was identified in a patient with severe hypertension. Several reports also suggest that specific alpha1aAR genetic variants are associated with human hypertension. We therefore explored whether there are unique molecular mechanisms that might account for this association. We recently reported that alpha1a-247R confers proliferative advantage to fi broblasts cultured under serum-deprived conditions and importantly, in the absence of agonist stimulation. Our results suggest that increased cell proliferation triggered by the naturally occurring human genetic variant alpha1aAR-G247R is due to intrinsic MMP-7 and ADAM- 12 dependent activation of an autocrine loop leading to constitutive production of HB-EGF and transactivation of EGFR in the absence of agonist. These findings provide the first evidence for a novel mechanism of sympathetically-mediated human hypertension triggered by a naturally occurring human genetic variant, alpha1a-247R activated signal transduction pathway. We also study the constitutive and agonist-induced biological effects of this SNP and the signaling pathways activated in cardiomyoblasts. We show that cardiomyoblasts expressing alpha1a-247R exhibit increased proliferation without agonist stimulation, undergo hypertrophy upon agonist stimulation, and change the cell morphology and phenotype to highly proliferative, fibroblast-like cells. These data confirm our previous findings that agonist-and serum-independent EGFR transactivation leading to enhanced proliferation of fibroblasts expressing alpha1a-247R is not cell type dependent but generalizable phenomena. Our observations also suggest that this SNP may lead to changes of vessel and heart structure, and lead to cardiovascular disease. These findings also raise the tantalizing hypothesis that a naturally occurring alpha1aAR genetic variant may be mechanistically involved in some forms of human hypertension, and that MMP/ADAM-specific inhibitors may be effective therapeutic agents for treatment of some forms of sympathetically-mediated human hypertension.

Speaker
Biography:

Khalid S Al-Numair is working as a Professor of Nutrition Science in the College of Applied Medical Sciences, King Saud University. He got his Bachelor degree in Food and Nutrition and MS in Human Nutrition from the King Saud University, Riyadh, Saudi Arabia. He obtained his Ph.D. in Community and Applied Nutrition, from University of Nebraska, USA in April, 2004. In addition he performed many Administrative responsibilities being the Vice-President Assistant for graduate studies and scientific research, 2009-Present; Consultant, Vice President for Knowledge Exchange and Technology Transfer, 2008-Present; and Deputy director of Prince Sultan Bin Abdulaziz International Program for Distinguished Research 2008- 2009. Khalid and along his university career excelled himself as a distinguished fellow for instance he got the Publication Quality Awards, KSU,2009; Prince Bandar Ben Sultan Al-Saud's Academic Excellence Award for doctoral degree, USA, 2004; Outstanding Student, Intensive English Program, University of Nebraska-Lincoln, USA, 1999; The Ideal Student's Award-College of Food Sciences and Agriculture, King Saud University, 1995; and the Social Activities Excellence Award, College of Food Sciences and Agriculture, KSU, 1995. He has published a good number of papers in reputed journals and serving as an editorial board member in various journals.

Abstract:

The present study was designed to investigate the preventive effect of morin on lysosomal enzymes in isoproterenol (ISO) treated myocardial infarcted rats. Myocardial ischemia was induced by subcutaneous injection of ISO hydrochloride (85mg/kg BW, twice at an interval of 24 hrs) for two consecutive days. The morin (40 mg/kg BW) was administered daily for 30 days and subsequently two doses of ISO administered on 29th and 30th days. The activities of lysosomal enzymes beta-glucuronidase,beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and D were increased significantly (P<0.05) in the serum and heart of ISO-induced cardiotoxic rats. The pretreatment of morin and two doses ISO treated rats exhibited significant (P<0.05) reduction of these lysosomal enzymes activities. Morin protects the lysosomal membrane damage against ISO-induced cardiac damage as evidenced by reduced activities of these lysosomal enzymes.

Speaker
Biography:

Mohammed Alsaif graduated from King Saud University Riyadh and in August 1989 to July 1990: Worked as a Rotating Intern in King Khalid University hospital and affiliated hospitals with an overall “excellent” evaluation. The internship year included: three months of Internal medicine, three months of surgery, three months of obstetrics and gynecology, and three months of pediatrics. From August 1990 to october 1992 he worked as a resident in the department of dermatology at Prince Salman Hospital . He has done training for diploma in dermatology and veneriology at the Department of dermatology, King Saudi University. He worked as assistant professor of dermatology Department of dermatology, King Saud University. He worked as director at King Saud University Fellowship for (postgraduate)training program in dermatology.

Abstract:

To investigate the antihyperlipidemic effect of crude ethanolic extract of Melothria maderaspatana (M. maderaspatana) leaf (CEEM) on deoxycorticosterone acetate (DOCA)-salt hypertensive rats. A midscapular incision was made on each rat and the left kidney was excised after ligation of the renal artery. The surgical wound was closed using an absorbable suture. After one week recovery period, hypertension was induced by subcutaneous injection of DOCA-salt solution, twice a week, and the rats received a 1% sodium chloride solution as drinking water throughout the experimental period. CEEM or nifedipine was administered orally once a day for 6 weeks. In DOCA-salt hypertensive rats, the level of plasma and tissues of total cholesterol (TC), triglycerides (TG), free fatty acids (FFA) and phospholipids (PL) significantly increased and administration of CEEM significantly reduced these parameters towards normality. Further, the levels of low density lipoprotein-cholesterol (LDL-C) and very low density lipoprotein-cholesterol (VLDL-C) significantly increased while high density lipoproteincholesterol (HDL-C) decreased in hypertensive rats and administration of CEEM brought these parameters to normality which proved their antihyperlipidemic action. Histopathology of liver, kidney and heart on DOCA-salt induced rats treated with CEEM showed reduced the damages towards normal histology. These findings provided evidence that CEEM was found to be protecting the liver, kidney and heart against DOCA-salt administration and the protective effect could attribute to its antihyperlipidemic activities.

Speaker
Biography:

Vidosava B Djordjevic has completed her Clinical Biochemistry specialization at the age of 30, and Ph.D. at the age of 36 at the Faculty of Medicine, Nis University. She is the Director of the Centre for Medical Biochemistry, Clinical Centre Nis, and the Chief of the Institute of Biochemistry, Faculty of Medicine, Nis University. She has published more than 40 papers in reputable journals and four chapters in international books. She is a reviewer for a few respectable journals, and a member of the Editorial Board of The Journal of Medical Biochemistry.

Abstract:

Nitric oxide (NO) is an important signalling molecule in a variety of physiological processes. It is synthesized from L-arginine by different isoforms of the nitric oxide synthase (neuronal-nNOS, inducible-iNOS and endothelial-eNOS). Blood vessel cells and cardiomiocytes express all three isoforms. NO produced by vascular endothelium regulates a number of healthy endothelium functions. NO produced in cardiac smooth cells regulates cardiac contractility. Due to its importance for vascular function, an abnormal production of NO can adversely affect blood flow and other vascular functions. The free radical activity of NO can cause cellular damage by the induction of nitrosative stress leading to protein modification by nitrosylation and nitro-tyrosination. It has been suggested that alterations in NO generation are a critical cause of injury in coronary heart disease. A biological link between the endothelial damage and atherosclerotic coronary arterial disease has been presumably related to an decreased arterial bioavailability of NO. However, there is a considerable controversy regarding whether myocardial ischemia results in increased or decreased NO formation. Beside NO synthesis, L-arginine may be transformed by the methylation in monomethylarginine and two forms of dimethylarginine: symmetrical dimethylarginine (SDMA) and asymmetric dimethylarginine (ADMA). ADMA is a natural, competitive inhibitor controlling NOS activity. ADMA has been found to be elevated in different conditions associated with the endothelial dysfunction, but it is also suggested as a predictor of future coronary events in patients with the elevated cardiovascular risk, and in acute coronary events as an independent cardiovascular risk factor.

Break: Panel Discussions
17:30-18:30 Cocktails sponsored by Journal of Clinical & Experimental Cardiology @ Hickory
  • Track 2: Congenital Heart Diseases
Location: Aspen II
Speaker

Chair

Ming K. Heng

University of California Los Angeles, USA

Speaker

Co-Chair

Emad F Aziz

Columbia University College of Physicians & Surgeons, USA

Session Introduction

Shiyou Chen

University of Georgia, USA

Title: Response gene to complement 32 in cardiovascular diseases

Time : 11:50-12:10

Speaker
Biography:

Shiyou Chen has completed his Ph.D. from Nanjing Agricultural University in China and postdoctoral studies from University of Iowa School of Medicine and National Institutes of Health. He is an Associate Professor in the department of Physiology and Pharmacology, University of Georgia. He has published more than 40 papers in reputed journals and serving as a reviewer for several reputed scientific journals and grant agencies including American Heart Association and National Institutes of Health.

Abstract:

Abnormal smooth muscle cell (SMC) differentiation and phenotypic modulation play important roles in the development of several prominent cardiovascular diseases such as atherosclerosis, intimal hyperplasia, vein graft stenosis, restenosis following angioplasty, and aortic aneurysm. SMC phenotypic modulation is an important process in vascular remodeling following injury. Response gene to complement 32 (RGC-32) is originally identified as a cell cycle regulator in SMC, endothelial, and various cancer cells. We find that RGC-32 is an important regulator of smooth muscle differentiation and phenotypic modulation. RGC- 32 promotes injury-induced lesion formation through stimulation of SMC proliferation and migration. In addition, RGC-32 is involved in epithelial-mesenchymal transition (EMT) and fibroblast activation, two important processes implicated in organ fibrosis. Knockout of RGC-32 in mice reduces the infarcted area in heart and decreases collagen expression in the infarcted area aft er ischemia-induced myocardial infarction. It appears that RGC-32 plays a critical role in cardiac fibroblast activation, leading to an enhanced collagen deposition, which eventually causes cardiac fibrosis.

Alan W Nugent

University of Texas Southwestern Medical Center, USA

Title: Biodegradable stents in congenital heart disease

Time : 12:10-12:30

Speaker
Biography:

Alan Nugent completed medical school at the University of Melbourne in Australia and pediatric training at the Royal Children's Hospital. He moved to Children's Hospital Boston to complete training in Pediatric Cardiology and commenced his faculty career as interventional cardiologist in Boston. In 2008, he was recruited by the University of Texas Southwestern (UTSW) Medical Center as an Associate Professor of Pediatrics and Children's Medical Center Dallas as Director of Cardiac Catheterization. Research interests in the past have included trans-catheter valve replacement and present research is focused on biodegradable stents applicable to congenital heart disease. This effort involves collaboration with the Department of Cardiovascular and Thoracic Surgery at UTSW Medical Center and the Biomedical Engineering Program at UTSW Graduate School of Biomedical Science.

Abstract:

Background: Much research has been accomplished on biodegradable stents for adult coronary artery disease. The recent impetus for renewed interest is due to late complications arising from permanent scaffolds in the circulation. Another clinical group that would derive substantial benefit from biodegradable stent technology is growing children.
Methods: PLLA stents have been designed to larger diameters suitable for infants and young children with congenital heart disease. The design incorporates a novel coil straightening mechanism enabling larger diameters. Bench and pre-clinical testing has been performed.
Results: Characteristics of the PLLA fiber are improved with annealing. A dual helical stent design has consistent stent mechanics over a wide range of diameters in bench testing. Preclinical testing of diameters 3 to 8mm has been performed with promising results in regards to deliverability and inflammatory profile.
Conclusion: Initial bench and pre-clinical testing of a biodegradable stent suitable for congenital heart disease applications is promising. Further studies are planned.

Alexander Tuzov

National Center of Forensic Medicine, Israel

Title: Sudden death due to eosinophilic arteritis of a major coronary artery

Time : 12:30-12:50

Speaker
Biography:

Alexander Tuzov has completed hid Ph.D at National Center of Forensic Medicine from Israel and working as assistant professor at National Center of Forensic Medicine, Israel.

Abstract:

Coronary arteritis is the fourth most common cause of fatal cardiac disease, after coronary atherosclerosis, congenital anomalies and coronary dissection. Eosinophilic inflammation of the coronary arteries is extremely rare, involves the major coronaries and occurs as an isolated disease or as part of Churg-Strauss syndrome or Wegener's granulomatos is with involvement of other internal organs. A case of sudden and unexpected death of a healthy young woman is presented. An autopsy revealed eosinophilic inflammation of Left coronary artery with thrombosis of the lumen, causing a fatal cardiac failure. No other pathology was detected. We discuss the importance of performing a full autopsy, including microscopic inspection of the tissues, in order to glean the cause of death and learn about new and rare pathologies.

Break: Lunch Break 12:50-13:30 @ Hickory

Nenad Zlatanovikj

Private Medical Practice Cor-Medico, Republic of Macedonia

Title: Cross influence of homocysteine and other risk factors in development and extent of coronary artery disease

Time : 13:30-13:50

Speaker
Biography:

Nenad Zlatanovikj has graduated at the Faculty of Medicine at the University of Cyril and Methodius in Skopje, Republic of Macedonia. He has fi nished his residency in Internal Medicine in 2003. He completed his residency in Cardiology in 2009 and in the same year he obtained his Masters Degree. He is author and co-author of number of papers dealing with cardiac pacing and markers of coronary heart disease. He has worked at the University Cardiology Clinic from 1998-2010, and he also worked at the Faculty of Medicine in Skopje as Teaching Assistant in Internal Medicine. Since 2010, he works in his own private practice.

Abstract:

Homocysteine and its relation to coronary artery disease (CAD) has been known and thoroughly investigated for decades. And while the influence of its increased levels is undoubted in the development of CAD, the treatment of hyperhomocystinemia as a risk factor in CAD remains at least elusive. Our study was the first one aiming to evaluate homocysteine levels in Macedonian population. 165 patients were evaluated, divided into 3 groups based on their 10 years risk for CAD based on ATP and Framingham criteria. The control group with CAD risk less than 10%, the high risk group with CAD risk more than 20% and the CAD group where patients had diagnosed coronary disease. All patients were evaluated for risk factors and markers:fasting homocysteine, sex, age, smoking status, hypertension, family history of CAD, blood lipids, white blood cells, BUN, creatine and fasting blood sugar.Mean value of homocysteine in the control group was 13.02µmol/l, in the high risk group the level was 16.0µmol/l (p=0.04) and for the CAD group it was 15.03µmol/l (p=0,02) In the high risk group, homocystein was correlated with the total CAD risk (p=0.04) and the white blood cells count (p=0.02). In males from the group homocysteine correlated with the total CAD risk (p=0.001), total cholesterol (p=0.001) and creatinin p=0.001).In the CAD group, homocysteine level correlated only with the high grade coronary occlusion of 95% of arterial lumen (p=0.04).

Salah A. Mohamed

Universitaetsklinikum Schleswig-Holstein, Germany

Title: Studies on aortic and aortic valve diseases

Time : 15:10-15:30

Speaker
Biography:

Salah A Mohamed, Laboratory and Group Leader in Department of Cardio and Thoracic Vascular Surgery, University Clinic of Schleswig-Holstein Campus. The group dedicated research interests to aging, biomarker, aortic and aortic valve diseases. He has published more than 20 papers in reputed journals and serving as an Editorial Board Member of repute.

Abstract:

Bicuspid aortic valve (BAV) is the most common of the congenital cardiac malformations with an estimated incidence of 1-2% in the general population. Patients with BAV are predisposed to early and frequent endocarditis, stenosis, regurgitation, which often accompanied by aneurysm and dissection. A family-based genome-wide analysis found that BAV was linked to chromosomal regions 5q, 13q, and 18q with autosomal dominant inheritance, reduced penetrance, and a non-Mendelian pattern. Mutations have been detected in the transmembrane receptor NOTCH1 (gene map locus 9q) in familial and sporadic BAV cases. Mutations in the vascular smooth muscle cell alpha actin gene (mapped to chromosome 10q) have also been identifi ed in BAV patients. Down regulated expression of ubiquitin fusion degradation 1-like, a gene that is highly expressed in the outflow tract during embryogenesis, was observed in the cusps of BAV patients as compared with those of controls. Heterozygous Nkx2-5- defi cient, Fgf8, Nos3, and Gata5 mice are at higher risks for developing BAV. BAV can also manifest as different types of left ventricular outflow tract abnormalities, including aortic coarctation, arch hypoplasia, and supravalvular and mitral valve stenosis. A male predominance of more than 3:1 has been reported for BAV, and this anomaly is very frequent in X0 Turner's syndrome. This talk will give an overview on our present understanding of aortic and aortic valve pathogenesis, particularly in patients with BAV and other connective tissue disorders. We discuss the genetic basis and the basic pathology underlying these disorders. In addition, we discuss recent insights into pathophysiology and treatment.

A D John

Johns Hopkins Bayview Medical Center, USA

Title: Cardiopulmonary resuscitation- How can we improve?
Speaker
Biography:

Amballur David John is an assistant professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine. He is the director of student education for the department. John received a B.A. from Harvard and an M.D. from New York Medical College. He completed an internship and a residency in internal medicine at Framingham Union Hospital in Framingham, Massachusetts. After a residency in anesthesiology and critical care medicine at Johns Hopkins, he conducted a fellowship in cardiac anesthesiology at Massachusetts General Hospital in Boston.After a year as an instructor at Harvard Medical School, Dr. John came to John Hopkins in 2002 as an instructor and joined the faculty in 2003 as an assistant professor.He is a fellow of the Royal Society of Medicine and has been named among America’s Top Anesthesiologists. He is a member of several professional organizations, including the American Medical Association, the American College of Physicians and the American Society of Anesthesiologists, and he serves on the editorial board of the Journal of Cardiology and Vascular Medicine. He is board certified in anesthesiology and critical care medicine.

Abstract:

Cardiopulmonary resuscitation was first successfully done by Dr. Peter Safar at Baltimore City Hospital (now-Johns Hopkins Bayview Medical Center). Since the 1960's, massive educational efforts have been instituted by a variety of organizations to increase awareness and to define the essential components of basic and advanced life saving skills. Yet, survival rates remain poor for out of hospital cardiopulmonary arrests and are location dependent within hospitals. The field of medicine has advanced markedly over the past five decades, but cardiopulmonary resuscitation appears stagnant. Why? How can we improve survival from cardiopulmonary resuscitation?

Speaker
Biography:

Shaoliang-Chen is a Deputy President of the hospital, Department Director of cardiology. He had done his Doctor of Philosophy in the year 2006 at Suzhou University. He is a Committee member of Interventional Cardiology Professional Group, Chinese Society of Cardiology, Member of Academic Committee of Cardiovascular Interventional Therapy Training Center, Chinese Medical Association, Member of Standing Committee of Cardiovascular Department, Internal Medicine Doctor Association Committee, Chinese Medical Doctor Association, Chief member of Peripheral Vascular Disease Committee, Jiangsu Institute of Integrated Traditional and Western Medicine, Vice director committee member of Jiangsu province society of Cardiology, Vice director member of Cardiovascular Committee, Jiangsu Institute of Integrated Traditional and Western Medicine, Vice chairman of Cardiovascular Disease Management Committee, Chinese Association for International Exchange of Medical Care, Chief member of Jiangsu Province Branch, Working Committee of Cardiovascular Rehabilitation Medicine Professional Committee, Chinese Association of Social Workers, Member of the Fifth Committee of Internal Medicine, Jiangsu Province Branch of Medical Association, The American College of Cardiology (F.A.C.C), The Society for Cardiovascular Angiography and Interventions (FSCAI), American Society of Angiology (FASA).

Abstract:

Background: Previous studies reported that baroreceptors and sympathetical nerves ending in or near bifurcation arear of main pulmonary artery (PA) participated in the modulation of pulmonary arterial pressure (PAP), and surgical denervation was effective in reducing PAP response to unilateral PA occlusion. However, there is no study reported the effect of percutaneous pulmonary artery denervation (PADN) by radiofrequency ablation on PAP.
Methods: Distal basal trunk and interlobar artery of left PA in five Mongolia dogs were sequentially occluded for 10 minutes by a balloon inflation to completely stop the blood flow distal to balloon, respectively. PADN by use of a specifically designed system was underwent at five levels: Level 1 (just at the bifurcation level), Level 2 (at the ostial left branch), Level 3 (at the ostial right branch) and Level 4 (5mm distal to the orifice of right) or 5(5mm distal to left branches). After PADN, balloon inflation was performed at the same sits as before PADN. Systolic, mean and diastolic PAP, cardiac output (CO), right ventricular pressure(RVP), pulmonary vessel resistance (PVR), pulmonary arterial occlusion pressure (PAOP) were measured before and during balloon inflation. Transpulmonary pressure gradient (TPG) was calculated. ECG was monitored through the whole procedure. PADN was performed only in Level 4 and Level 5 in another 4 dogs.
Results: Baseline systolic, mean and diastolic PAP were 29.2±3.8 mmHg, 14.6±1.7 mmHg and 9.2±1.1 mmHg, respectively. Hemodynamic parameters did not change during distal basal trunk occlusion. During occlusion of left interlobar artery, PAP, systolic RVP and PVR gradually increased and reached peak value aft er 5-min(Δ13.4 mmHg, p<0.001; Δ14.8 mmHg, p=0.044 and Δ622.3 dye/s/cm5, p<0.001, respectively), without significant difference in mean and diastolic RVP, PAOP and CO. The average PADN procedural time was 18.6 minutes. After PADN procedure in Level 1-3 but not in Level 4 or 5, the PAP response to left interlobar artery occlusion was completely abolished.
Conclusion: Occlusion of left interlobar artery was associated with significant increase of PAP. Th is pressure response was completely abolished by PADN around the bifurcation area of main PA.

Break: Coffee Break 15:30-15:45 @ Hickory
Speaker
Biography:

Erkin M. Mirrakhimov, MD, Ph.D., Professor. Graduated Kyrgyz State Medical Institute in 1983. In 1983-1989 and 1991-1995 worked at Scientific Research Cardiological Center in Moscow, Russia. From 1995 till now works as head of Internal Chair at Kyrgyz State Medical Academy, Bishkek, Kyrgyzstan, Head of Atherosclerosis and Coronary Heart Disease department at National Center of Cardiology and Internal disease, Bishkek, Kyrgyzstan, professor of Internal Chair ant Kyrgyz-Russian (Slavic) University. The main field of scientific interest is markers of cardiovascular disease and metabolic syndrome including people living at high altitude. Results of scientific work published in different peer-reviewed journals and he is a President of Kyrgyz Society of Cardiology

Abstract:

Speaker
Biography:

Abdulaziz U Joury is 22 years old medical student at King Saud University, Riyadh, Saudi Arabia. He is interested in cardiology and cardiac sciences. Trained at numerous hospitals. He represents his country nationally and internationally on several occasions. Held several classes and workshops covering medical field. Coordinated numerous campaigns and participating in number of researches.

Abstract:

Acute myocardial infarction AMI in the setting of acute coronary syndrome (ACS) carries an ominous prognosis.We sought to assess the incidence, in-hospital outcomes among patients who presented with AMI as first presentation of ACS. The Second Gulf Registry of Acute Coronary Events (Gulf RACE-2) is a multinational observational study of patients with ACS, which enrolled 3,059 patients.Of 3,059 patients with ACS, 22.2% were presented with MI as first presentation, the male gender accounts for the majority of the cases 680 (86.6%).Congestive heart failure (6.7% vs. 0.3%), valvular heart disease (1.4% vs. 0.1%), cerebrovascular accident or transient ischemic attack (6.5% vs. 2.3%) and chronic renal failure (3.1% vs. 0.6%) were determined in both groups with superiority among patients with prior MI vs. no prior MI. Covariates such as smoking and certain chronic diseases (hypertension and hyperlipidemia) were also determined. In-hospital events and short and long-term prognosis was determined in both groups. Infarction or reinfection events were more among prior MI group (6.7% vs. 2.5%), recurrent Ischemia (27.1% vs. 15.7%) and ongestive heart cfailure (20.2% vs. 11.8%). In-hospital mortality rate was significantly higher inpatients with prior MI (9.4% vs. 6.0%) compared to patients with no prior MI (all P<0.001). Comorbidities associated with the ACS were more common among patients with prior MI than patients with no prior MI. In-hospital events were determined in both groups with higher rate among patient with prior MI. Prior MI patients showed significantly higher in-hospital mortality compared to patients with no prior MI.

Break: Panel Discussions
17:30-18:30 Cocktails sponsored by Journal of Clinical & Experimental Cardiology @ Hickory