Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4th International Conference on Clinical & Experimental Cardiology Hilton San Antonio Airport, USA.

Day 2 :

  • Track 1: Heart Diseases
Speaker

Chair

Anastasia Susie Mihailidou

Royal North Shore Hospital, Australia

Speaker

Co-Chair

Anthony W Ashton

The University of Sydney at Royal North Shore Hospital, Australia

Session Introduction

Svetlana Gorokhova

I.M. Sechenov First Moscow State Medical University, Russia

Title: Association of circadian genes polymorphisms with coronary heart disease
Speaker
Biography:

Svetlana Gorokhova graduated from the Faculty of Medicine at N.I. Pirogov 2nd Moscow Medical Institute, Russia and received Ph.D. degree in 1986. Since 2002 she is a Full Professor at I.M. Sechenov First Moscow State Medical University, Russia and she is also the Head of Laboratory of Experimental Cardiology in Clinical Research Center of JSC Russian Railways. Her work is dedicated to problems of cardiology, health care organization, and implementation of new technologies into 'real-life' clinical practice. She organizes and participates in interdisciplinary projects on environmental and genetic risk factors of cardiovascular diseases.

Abstract:

There is strong evidence that coronary heart disease (CHD) is associated with polymorphisms in several genes connected with dyslipidemia, impaired blood coagulation, inflammation and other factors of the CHD. This suggests the existence of genes that coordinate the activity of risk alleles. Circadian genes are of special interest in this respect; however, the extent of their relationship with coronary atherosclerosis is not known. Our study on polymorphisms of PER, CRY1, CLOCK and NPAS2 circadian genes in patients with CHD revealed the connection between CRY1 polymorphism and coronary atherosclerosis, and between other circadian genes and risk factors of CHD. In particular, polymorphism in CLOCK gene is associated with cholesterol, in PER1 with hemostasis (e.g. fibrinogen) etc. Because circadian genes are also responsible for synchronization of metabolic processes including lipid metabolism, they may be involved into CHD development in a direct (biorhythmicity disturbances such as time shifts or disruption in cycles of atherogenic mechanisms) and indirect way (by affecting various components of atherosclerotic process). We present our data on the association of circadian genes with CHD from this perspective.

Speaker
Biography:

Reto Asmis received his Ph.D. in Biochemistry for the University of Fribourg in Switzerland. He completed postdoctoral fellowships at the University of California in San Diego and the University of Berne in Switzerland. He is a tenured Professor in the Departments of Clinical Laboratory Sciences and Biochemistry and the Associate Dean of the Graduate School of Biomedical Sciences at the University of Texas Health Science Center at San Antonio. He is well-funded both by NIH and private foundations, and has published more than 60 papers. He is currently serving as associate editor of Atherosclerosis.

Abstract:

We reported that metabolic stress primes blood monocytes for chemokine-induced adhesion and migration. This gain-of function phenotype is observed in both dyslipidemic and diabetic mice and is associated with increased Nox4 expression and protein-S-glutathionylation, and results in increased macrophage recruitment and accelerated atherogenesis, but the underlying mechanism was not known. The goal of this study was to determine the role of Nox4 in monocyte priming and to identify the molecular targets of Nox4-derived H2O2 induced by metabolic stress. Prolonged exposure of monocytes to human low density lipoprotein (LDL), high glucose concentrations (HG) or LDL plus HG (LDL+HG) induced Nox4 expression, increased intracellular H2O2 formation, promoted protein S-glutathionylation, and increased chemotaxis in response to MCP-1, PDGF-B and RANTES. Overexpression of Nox4 sensitized monocytes to MCP-1-induced chemotaxis, whereas Nox4 knockdown or overexpression of glutaredoxin 1 (Grx1) protected against both metabolic stress-induced protein-S-glutathionylation and increased chemotaxis. We identified MKP-1 and actin as targets of Nox4-mediated S-glutathionylation and showed that S-glutathionylation of these two proteins accelerates monocyte chemotaxis by hyper-activating ERK and p38MAPK signaling and increasing actin remodeling. We also show that MKP-1 deficiency in monocytes of dyslipidemic LDL-R-null mice mimics monocyte priming and accelerates both MCP-1-induced macrophage recruitment and atherosclerotic lesion formation. In conclusion, monocyte priming for chemokine activation induced by metabolic stress requires the induction of Nox4 and is mediated by the S-glutathionylation of actin and MKP-1. We identified a novel, proatherogenic mechanism through which metabolic disorders promote macrophage recruitment to sites of vascular injury.

Scott R Willoughby

University of Adelaide, Australia

Title: Effect of atrial fibrillation on thrombogenesis
Speaker
Biography:

Scott Willoughby is a Head of the Thrombosis and Vascular Biology Laboratory, Centre for Heart Rhythm Disorders, School of Medicine, University of Adelaide, Australia. Willoughby graduated from the University of Adelaide in 1995 and obtained Ph.D. degree in 1999. He completed his post-doctoral fellowships at the Whitaker Cardiovascular Institute, Boston University, USA under the mentorship of Prof. Joseph Loscalzo and the Cardiology Unit, Queen Elizabeth Hospital, Australia under the mentorship of Prof. John Horowitz. Willoughby was appointed to his current position in 2006. Willoughby's research focus is to understand the integrative physiological mechanisms controlling inappropriate thrombus formation in conditions of increased cardiovascular risk. Current studies focus on two diverse groups of individuals: (1) young subjects exposed to potentially novel high risk environments (paedriatric sleep disordered breathing or following the consumption of energy drinks) and (2) patients at high risk for thromboembolic events (atrial fibrillation). Willoughby has published widely in high impact peer-reviewed journals regarding platelet function and cardiovascular disease and regularly presents at international meetings. Willoughby is a previous recipient of the Young Investigator Award in Thrombosis (2006) from the World Congress of Cardiology.

Abstract:

Atrial fibrillation is the most common sustained cardiac rhythm disturbance to affect humans and causes one-third of strokes in patients over 60 years. The frequency of atrial fibrillation rises rapidly after the sixth decade with a prevalence of approximately 5% in the general population over the age of 65 years and 10% in subjects over 75 years of age. In the absence of rheumatic heart disease the risk of stroke in patients with atrial fibrillation is 5-fold greater after adjusting for other stroke risk factors, while in patients with rheumatic heart disease there is a 17.5-fold increased risk. There is also an increased incidence of silent cerebral infarction. Furthermore, evidence suggests that strokes complicating atrial fibrillation results in increased severity of neurological deficit and are twice as likely to be fatal. Ischaemic strokes are thought to be largely embolic in nature, derived from thrombus in the left atrium or more specifically from the left atrial appendage. Trans-esophageal studies have observed thrombus within the left but not the right atrium, suggesting that local factors specific to the left atrium may be associated with an increased risk of thrombus formation. The exact mechanism by which thromboembolic events, derived from the left atrium, are increased in patients with atrial fibrillation has not yet been determined but haemostatic abnormalities such as platelet activation and endothelial damage/dysfunction, may contribute to thrombus formation in this condition, in keeping with a prothrombotic or hypercoagulable state. This talk is designed to explore the pathophysiological mechanisms that contribute to thrombus formation in patient with atrial fibrillation.

Speaker
Biography:

Khaled Sayed Mahmoud El Maghraby has completed his M.D. at the age of 34 years from AL Minia University. He is the associate professor of cardiology. He has published more than 26 papers in reputed journals.

Abstract:

Background: In patients with acute ST-segment elevation myocardial infarction identifying the culprit artery is either due to right coronary artery or left circumflex artery. The electrocardiogram can lead to earlier risk stratification and better guidance of therapy for reperfusion.
Patients and methods: 50 patients with acute inferior myocardial infarction were divided into two groups; Group A: Patients with ST segment depression in lead aVR ≥1 mv. Group B: Patients with isoelectric ST segment or with ST segment depression in lead aVR <1 mv. All patients were subjected to coronary angiography and echocardiograghy.
Results: Fifty patients with acute inferior myocardial infarction were included in the present study. They were 35 males (70%) and 15 females (30%), with a mean age 55.6 ± 8.8. In group A, left circumflex artery was the culprit artery in 8 (47%) and right coronary artery was the culprit artery in 9 (53%). In group B, left circumflex artery was the culprit artery in 4 (12%) and right coronary artery was the culprit artery in 29 (88%). Patients with aVR depression had significantly larger infarctions, (estimated by peak creatine phosphokinase (CPK-MB) levels and transthoracic echocardiography) than patients without aVR depression.
Conclusion: In patients with inferior wall STEMI, ST-segment depression in aVR was more common in LCX infarcts than RCA infarcts. Patients with aVR depression had significantly larger infarctions, (estimated by peak creatine phosphokinase (CPK-MB) levels and transthoracic echocardiography) than patients without aVR depression.

Speaker
Biography:

Hongxin Zhu is an Associate Professor in Bio-X Institutes, Shanghai Jiao Tong University. He has completed his Ph.D. degree at the age of 29 from Fudan University and postdoctoral studies in UT Southwestern Medical Center at Dallas. He has been serving as an editorial board member of International Journal of Clinical Therapeutics and Diagnosis, and Journal of Biochemical and Pharmacological Research. He is a guest editor for the Journal of Medical Imaging and Health Informatics.

Abstract:

Autophagy is required to maintain cardiac myocyte homeostasis. Cardiac autophagy is up-regulated in response to a variety of factors and enhanced autophagy in the heart can be either adaptive or maladaptive depending upon the context. Previous in vitro studies has shown that rubicon, a component of PI3KC3 complex, suppresses autophagosome/endosome maturation by sequestering UVRAG, which prevents Rab7 activation. We have recently demonstrated that UVRAG deficiency causes impairment of autophagic flux in the heart, leading to age-related cardiomyopathy and cardiac dysfunction accompanied by enhanced inflammation. In this study, we hypothesize that loss of rubicon increased autophagic flux in the heart and protected against sepsis-induced cardiac injury. Rubicon knockout mice were generated by insertion of PiggyBac construct into intron 1 of rubicon gene and loss of rubicon in various tissues were demonstrated by reverse transcription polymerase chain reaction (RT-PCR) and western blot. Rubicon deficiency increased autophagic flux without altering transcript expression of autophagy-related genes in the heart. At baseline, cardiac morphology and function were preserved in rubicon-deficient mice. To determine the effect of rubicon deficiency on inflammatory heart disease, we treated rubicon-deficient mice and corresponding wild type (WT) controls with lipopolysaccharide (LPS). Rubicon deficiency prolonged survival of LPS-treated mice. Quantitative RT-PCR revealed that LPS-induced expression of inflammatory cytokines was attenuated in rubicon-deficient hearts. Autophagy was further enhanced in the heart from rubicon-deficient mice compared with WT controls in response to LPS. In conclusion, Rubicon deficiency enhances cardiac autophagy and attenuates sepsis-induced cardiac injury.

Speaker
Biography:

Salah A. Mohamed is Laboratory and Group Leader in Department of Cardio and Thoracic Vascular Surgery, University Clinic of Schleswig-Holstein Campus Luebeck, the group is dedicated to research on 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:

MicroRNAs (miRNAs) are critical regulators of most major cellular processes. miRNAs appear to play a vital role in the pathogenesis of numerous diseases including atrial fibrillation, the most commonly encountered cardiac rhythm disorder. Among the several miRNAs that appear to be involved in pathogenesis of atrial fibrillation, miRNA 208a is linked to fibrosis and proper cardiac conduction.
We quantified the expression levels of miRNA 208a in left atrial tissue of patients with paroxysmal, persistent, long-standing persistent and permanent arrhythmia using quantitative PCR. In paroxysmal atrial fibrillation, miRNA 208a was expressed moderately, whereas the expression was enhanced in persistent atrial fibrillation and significantly reduced in long-standing persistent atrial fibrillation. The difference between persistent and long-standing persistent atrial fibrillation was significant at p=0.018. The patient with permanent atrial fibrillation displayed the lowest miRNA 208a expression. The findings from our study suggest a decline in miRNA 208a expression with ongoing arrhythmia, possibly preceded by a rise in expression from paroxysmal to persistent atrial fibrillation. The significant changes in miRNA 208a expression over the course of the disease may be used as a diagnostic tool to monitor the progression of atrial fibrillation.

Speaker
Biography:

Peifeng Li has completed his MD and Ph.D. at the age of 30 years from Chinese Academy of Medical Science and postdoctoral studies from Max-Delbruck Center for Molecular Medicine, Germany. He is an Associate Professor at Nebraska Medical Center. He has published more than 62 papers in reputed journals and has been serving as an editorial board member for many journals such as Dataset Papers in Biology, Journal of Clinical and Experimental Cardiology.

Abstract:

MicroRNAs (miRNAs) are a class of small non-coding RNAs that mediate post-transcriptional gene silencing. Mitochondrial fission participates in the induction of apoptosis. It is poorly understood as to how mitochondrial fission program is regulated in cardiomyocytes. In particular, it remains largely unknown whether miRNAs can regulate mitochondrial fission. Reactive oxygen species and doxorubicin could induce mitochondrial fission and apoptosis in cardiomyocytes. Concomitantly, mitofusin 1 (Mfn 1) was downregulated, whereas miR-140 was upregulated upon apoptotic stimulation. We investigated whether Mfn1 and miR-140 play a function role in mitochondrial fission and apoptosis. Ectopic expression of Mfn1 attenuated mitochondrial fission and apoptosis. Knockdown of miR-140 inhibited mitochondrial fission. Our results further revealed that knockdown of miR-140 was able to reduce myocardial infarct sizes in the animal model. We explored the relationship between Mfn1 and miR-140, and observed that miR-140 could suppress the expression of Mfn1, and it exerted its effect on mitochondrial fission and apoptosis through targeting Mfn1. Our data revealed that mitochondrial fission occurs in the cardiomyocytes and can be counteracted by Mfn1. However, the function of Mfn1 is negatively regulated by miR-140. Our present work suggests that Mfn1 and miR-140 are integrated into the program of cardiomyocyte apoptosis.

Speaker
Biography:

Muge N. Kuyumcu-Martinez received her Ph.D. at Baylor College of Medicine where she also pursued her post-doctoral training. She was promoted to an Instructor position at Baylor College of Medicine. In 2010, she was recruited as a tenure track Assistant Professor to the University of Texas Medical Branch. Since then, she has received the prestigious March of Dimes Basil O'Connor Starter Scholar Award. Her senior author publication has made the cover of the Journal of Biological Chemistry. Her research interests are to understand the signals that regulate alternative splicing decisions in the heart and how splicing dysregulation contributes to diabetic heart disease.

Abstract:

Introduction: Diabetic cardiomyopathy can lead to heart failure and death among diabetics independent of effects from hypertension and coronary heart disease. Chronic activation of Protein Kinase C (PKC) signaling promotes diabetic cardiomyopathy by mechanisms that are not well understood. PKC has been implicated in alternative splicing (AS) regulation in the heart.
Aim: Our goal is to determine whether prolonged PKC activity induces alternative splicing abnormalities in diabetic hearts.
Methods: We performed RNA sequencing followed by computational analysis using MISO algorithm to distinguish AS patterns in diabetic versus normal mouse hearts. We used two Type 1 diabetes mouse models (non-obese diabetic and Streptozotocin induced) as well as Type 2 human heart tissues to validate alternative splicing changes by quantitative RT-PCR. Using PKC inhibitors or PKC alpha/beta specific shRNAs, we identified which AS changes in diabetic hearts are controlled by PKC. Splicing changes that are altered in diabetic hearts were targets of a splicing regulator called CELF1. Therefore, we mutated PKC phosphorylation sites on CELF1 to determine the effect of phosphorylation on CELF1 regulated genes that are mis-spliced in diabetes.
Results: We found genome wide alternative splicing changes in diabetic hearts and identified a set of 22 AS events that reverse to a fetal splicing pattern in adult diabetic hearts. GO analysis indicates that the genes that undergo a developmental AS switch in diabetic hearts have important functions in embryonic development and RNA metabolism. Importantly, PKC isozymes alpha and beta control alternative splicing of these genes in fetal hearts via phosphorylation of splicing regulator CELF1. A mutant of CELF1 that is non-phosphorylatable by PKC can no longer regulate splicing events altered in diabetic hearts.
Conclusion: PKC contributes to diabetic cardiomyopathy by activating embryonic splicing programs in adult hearts.

Mladen Jukic

Sunce Clinic, Zagreb, Croatia

Title: CCTA in real not-so-developed world
Speaker
Biography:

Mladen Jukic, MD, FSCCT, FESC, is practicing cardiologist with more than 10 yrs of experience in invasive cardiology and more than 6 yrs experience in CCTA, which he has introduced in Croatia. He's also board member of Croatian Cardiac Society, and managing director of Sunce Clinics, Croatia, the largest private medical business in Croatia. He has a number of presentations on Croatian and international conferences, as well as scientific publications.

Abstract:

During the War in Croatia, from 1991-1995, the majority of patients with CAD were treated conservatively. Revascularization was performed only rarely for ACS patients. In the “Ere of stentomania, 1995-2005”, which due to the limited resources “flamed” in Croatia in smaller intensity than possibly elsewhere, and before the COURAGE-Ere, I performed over 8000 diagnostical procedures and over 1200 PCI-procedures.
The fundamental clinical problem with CAD is in its unpredictability. For that reason my primary professional interest in the last decade has been focused on its early (non-invasive, and in near future probably genetically-based) detection, where nowadays I believe CCTA can prove very usable. To evaluate how CCTA altered the management of patients with suspected CAD we studied 792 patients.
After CCTA, obstructive CAD was excluded in 666 patients. During 12-month follow-up, 98.6% of these patients were free of major adverse cardiac events. Also, indication for ICA was revoked in 77.2% of patients. It was also revoked in all patients with low pre-test risk, 80.7% with intermediate and 72.6% with high risk. Medical therapy was changed in 54.7% of patients.
Based on our 6-year experience and published evidence-based data, I believe that CCTA can help not only in reliable detection of CAD, but also to choose the most appropriate management for the vast majority of CAD-patients. CCTA also can allow for faster, easier and simpler evaluation, and replace ICA in the majority of patients, together with its complications, but also direct and indirect costs it is coupled with.

Speaker
Biography:

Fan Yang has graduated from DongNan University School of Medicine. He is the Deputy Director of Clinic Laboratory in TongJi Hospital which belongs to TongJi University School of Medicine. He has published more than 20 papers in reputed journals and has been studying for over 15 years in clinical immunology.
QiangLin Duan has graduated from TongJi University School of Medicine. He is a doctor of department of cardiology in TongJi Hospital which belongs to TongJi University School of Medicine. He has published more than 20 papers in reputed journals and has been studying for more than 5 years in the project of new strategies in prevention and treatment of venous thromboembolism.

Abstract:

To investigate localization and distribution of integrin subunit beta1, beta2 and beta3 and morphological changes of ligand-recepter binding in thrombi of acute pulmonary embolism (PE) patients and explore activation of circulated immune cells, inflammatory immune adherence and coagulation response in acute venous thrombosis. In this study, we found: 1) Acute venous thrombi were red thrombi composed of skeletons and filamentous mesh containing large amounts of red blood cells and white blood cells; 2) Integrin subunit beta1, beta2 and beta3 were expressed on lymphocytes, neutrophils and platelets; 3) No expression of integrin beta1 ligands: Laminin, Fibronectin, Collagen I or Collagen-II on lymphocytes; integrin beta2 ligands including ICAM, factor X and iC3b are distributed on neutrophils, and ligand fibrinogen bound to neutrophils; integrin beta3 was expressed on platelets which form the skeleton of thrombi and bound to fibrinogen to construct mesh structure; 4) Factor Xa was expressed on the filamentous mesh; 5) Filamentous mesh was fully filled with red blood cell dominant blood cells. So we can conclude that acute venous thrombosis is an activation process of circulated lymphocytes, neutrophils and platelets mainly, and a whole process including integrin subunit beta2 and beta3 binding with their ligands. Activation of immune cells, inflammatory immune adherence and coagulation response are involved in the acute venous thrombosis.

Speaker
Biography:

Harsha Kumar H N completed his MBBS in 2001 from Government Medical College, Karnataka State and Pursued MD (Community Medicine) from Manipal University, India. He is currently Associate Professor, Department of Community Medicine at Kasturba Medical College. He has about 32 research publications in reputed journals. He is a resource person for training in Research Methodology and Bio-statistics. He has authored and obtained Indian Council of Medical Research (ICMR) Projects. He teaches preventive medicine, conducts outreach health clinics in rural areas and is in charge of research in Non-Communicable diseases. He is in-charge of implementing public health programs in Mangalore City, India.

Abstract:

Background: The prevalence of coronary artery disease in India increased from 1% in 1960 to 9.7% in 1995. Most of them present late. A clinical profile would enable us to better understand severity and Co-Morbidities at the time of presentation. So this study was undertaken.
Objective 1: To know the clinical profile of IHD cases admitted and treated at tertiary care hospital affiliated to KMC Mangalore, Manipal University.
Material & Methods: This retrospective study included diagnosed cases of IHD that were admitted and treated over a period of 2 years (years 2010-12). Relevant clinical information was noted down on a semi-structured proforma. Permission was obtained from Institutional Ethics committee to access the patient files form the Medical Records Department. The details were noted down in the proforma and data entered in SPSS version 12 and analyzed.
Results: out of the 118 cases 55(46.6) presented with features of congestive cardiac failure, 41 (36%) with chest pain, 14 (12.3%) epigastric pain and vomiting & 8 (6.8%) were brought unconscious. The following risk factors were identified for the first time after admission to hospital (%): Hypertension (72.9), Diabetes Mellitus (55.1), Dyslipedaemias (45.3). There were 14.4% Smokers. There was no prior history contact with doctors / voluntary check-ups.
Conclusion: There is a need to raise public awareness to facilitate early diagnosis. Screening camps for identifying diabetics and hypertensive would also be helpful.

Speaker
Biography:

Bhanu Duggal is an Associate Professor of Cardiology, at Grant Medical College and Sir JJ group of Hospitals, India. She has many publications in National and International Journals. And also done a fellowship in structural heart disease at Royal Brompton Hospital, UK and training in Intravascular Ultrasound at Cleveland Clinic, USA

Abstract:

Introduction: Isolated left main coronary stenosis (LMCA) is a rare entity and occurs in 0.7 to 1% patients of coronary artery disease (CAD).
Patients & Methods: Two women with mean age of 31.6 years presented with PR severe exertional angina and dyspnea short duration of (3 ± 1.5 months) while another woman presented with anterior wall myocardial infarction (AWMI). The two women had stress test positive in stage 1 with ST depression in several leads. The echo was normal in these two patients and depressed (LVEF-30%) in one patient with acute MI (30%). All three were non-smokers and did not have any diabetes or elevated cholesterol levels. The inflammatory markers (ESR, CRP) as well as ANA and DNA were negative in these patients.
Coronary angiography in the two women revealed left main coronary artery ostial stenosis. There was additional mild ostial stenosis of the right coronary artery in one patient. The two patients underwent PCI to the left main ostium with short 4mm drug eluting stents. The third patient with AWMI had ostial left main disease with severe thrombotic plaque burden and underwent primary angioplasty after thrombectomy with a drug eluting stent (3.5x12mm) and further dilatation with a non-compliant 4mm balloon. IVUS revealed optimal stent apposition.
Conclusion: We present 3 premenopausal South Asian women with isolated left main stenosis, without the traditional risk factors of CAD and evidence of other non-atherosclerotic causes of left main stenosis. This rare entity has been reported previously, mainly in young oriental and Western women, and histopathological findings in surgical series have revealed early ostial atheromatous involvement, in the absence of atherosclerotic changes in rest of the coronary tree.

Speaker
Biography:

S M Tajdit Rahman is a 5th year medical student studying in Sir Salimullah Medical College, Bangladesh. He is doing his MBBS under renowned cardiologist of Bangladesh and has a fascination for research in cardiology since his early classes. He is well known in his campus as a student researcher. He is doing some researches under renowned professor and has a great achievement in extracurricular activities since his childhood. He is the President of Undergraduate Research Society in Bangladesh and has been serving as an ambassador of different student research conferences. He has attended more than 10 undergraduate research conferences.

Abstract:

ECG is the mainstream investigation in the diagnosis of acute posterior myocardial infarction. It is based on the presence of ST segment depression on pericardial chest leads. However, the absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis and thus may result in inadequate treatment. Many literatures suggest ST segment elevation in V7- V9 in 15-lead ECG can help in early diagnosis of acute posterior myocardial infarction. This study was done to determine the value of 15-lead ECG (including V7-V9) over 12-lead traditional ECG to establish the diagnosis of acute posterior infarction in patients with ischemic chest pain, and to describe the clinical and echocardiographic characteristics of these patients. Total of 140 patients was evaluated by Electrocardiography in standard 12 lead and 15 lead. The patients were categorized into group I having posterior and or associated changes and group II having without posterior changes in ECG. Echocardiography was done to evaluate the posterior wall involvement. We found 12-lead ECG is 42.5% sensitive and 93.8% specific for diagnosis of posterior myocardial infarction, whereas in case of 15-lead ECG it was 82.5% sensitive and 96.3% specific. On echocardiography, posterior wall-motion abnormality was visible in 86.4% of the patients, and 2.8% had evidence of mitral regurgitation. We can conclude 15- lead ECG is more sensitive than 12-lead ECG in diagnosis of acute posterior myocardial infarction. So, we can use it routinely to evaluate a patient with ischemic chest pain.

  • Track 3: Congenital Heart Diseases
Speaker

Chair

Nassir Azimi

La Mesa Cardiovascular, USA

Speaker

Co-Chair

Bhanu Duggal

Sir JJ group of Hospitals, India

Speaker
Biography:

Nassir Azimi is a graduate of Columbia University in New York City. Then, he transitioned to medical school at Dartmouth in New Hampshire. After completing an internal medicine internship in residency at University Colorado, he went on to Yale University to train in cardiology, nuclear cardiology and interventional cardiology and vascular medicine. Currently, he is practicing cardiology at La Mesa Cardiac Center with a focus on the patient rather than any one organ system.

Abstract:

Clinically, Platypnea Orthodeoxia Syndrome (POD) is rarely diagnosed and associated with various cardiac and non-cardiac conditions. Yet there are increasing case reports in the medical literature as awareness of the entity increases amongst clinicians. In this series, we will focus on cardiac etiologies of POD. We will review the clinical course of four patients affected by this syndrome between March 2008 and September 2013. Additionally, we will explore the potential mechanisms for positional shunting in such patients. The (three females and 1 male) patients were average aged 63+/- 12. All had a Patent Foramen Ovale (PFO). The main complaint was dyspnea and dyspnea on exertion. Two patients were already committed to long term oxygen therapy. All improved after percutaneous closure of the PFO with complete resolution of all symptoms. Post PFO closure, none required oxygen supplementation. We postulate that POD is under diagnosed and there are more patients out there yet to be diagnosed with this entity. We will provide an algorithm for correctly diagnosing potential patients. Continued education of our colleagues to raise awareness of this condition is needed to allow proper identification and treatment of POD patients.

Speaker
Biography:

Nian Qing Shi has completed her Ph.D. in Microbiology in 2000 from The University of Wisconsin-Madison. After she finished an industrial post-doctoral training in mitochondrial redox regulation with Tate and Lyle, she returned to academia to investigate the molecular composition and structure/function of a mitochondrial ATP-sensitive potassium (mitoKATP) channel in cardioprotection. Her team identified and cloned the cardiac mitoKATP channel, which had been pursuing by the field since 1991. In her recent studies, Dr. Shi started exploring the roles of HCN2 channels in congenital heart diseases. She serves as editorial members for 3 journals and reviewers for several major cardiac journals.

Abstract:

Congenital heart diseases (CHDs) affect 80,000-120,000 newborns in US annually. CHDs encompass a wide spectrum of cardiovascular malformations, and remain the major cause of infant mortality among all types of birth defects. To date, molecular mechanisms underlying CHDs remain elusive, largely owning to the complexity of the diseases and lack of animal models that can reproduce the disease conditions in a laboratory setting.
The hyperpolarization-activated, cyclic nucleotide-gated cation channels (HCN) are responsible for generating spontaneous pacemaker activities in both cardiac and central nervous systems. These channels are present in other tissue or cell types to perform multiple essential biological functions. We recently characterized two HCN2 knockout (HCN2KO) mouse lines, in which the full-length HCN2 is disrupted. The first line died at approximately 6-weeks of age while the second line could live beyond adulthood with a special diet. Maternal echocardiography data on the KO hearts revealed a markedly underdeveloped left side since embryogenesis, suggesting that HCN2KO mice developed hypoplastic left heart syndrome (HLHS) and subsequent fetal arrhythmia. The survived line remodeled their hearts to permit harder blood pumping, leading to improved survival%. The average size of the survived line was half of WT control at birth; they exhibited a significantly retarded growth rate and were "arrested" at 5-weeks of age. Other additional data further indicates that the hcn locus is a hot spot for HLHS onset. Our novel findings suggest that the HCN2 gene is indispensable in cardiogenesis and these new KO models are therefore innovative platforms for CHD studies.

Amballur D John

Johns Hopkins Bayview Medical Center, USA

Title: 2014 update on cardio pulmonary resuscitation
Speaker
Biography:

Amballur D John is currently an Assistant Professor of Anesthesiology and Critical Care Medicine, Director of Student Education, Department of Anesthesia at Johns Hopkins Bayview Medical Center, Baltimore, USA. He did his B.A. from Harvard University and his M.D. from New York Medical College, USA. He has trained in Internal Medicine Residency at Metro West Medical Center, Anesthesiology and Critical Care Medicine Residency at Johns Hopkins Hospital and his Fellowship in Cardiac Anesthesiology from Johns Hopkins Hospital, Cardiac Anesthesiology from Massachusetts General Hospital.

Abstract:

It is well over 50 years since the modern era of Cardio-Pulmonary Resuscitation began with Dr. Peter Safar's successful resuscitations of people who had suffered cardiac arrest. These successful resuscitations by Dr. Safar were performed at the former Baltimore City Hospital (now known as the Johns Hopkins Bayview Medical Center). Laboratory work on cardio- pulmonary resuscitation began in earnest in the late 1950's and early 1960's. By the late 1960's the first set of national guidelines were promulgated. Leadership in the field of cardio pulmonary resuscitation has changed from Anesthesiologists and Critical Care Physicians to cardiologists and the American Heart Association.
Despite many advances in the field of medicine and our increased knowledge and understanding of resuscitation, success rates as defined by intact neurological outcome in those surviving to hospital discharge will remain low 15%-20%. Is there a difference between in hospital and out of hospital arrests? Does the patient's underlying medical condition matter? Have newer in-hospital Rapid Response Teams and Code Teams helped? Is it possible to quantify factors that lead to worse outcomes or improved outcomes? What are the novel therapies and when is it appropriate to use such treatments? These questions remain to be answered.

Speaker
Biography:

Bhanu Duggal is an Associate Professor of Cardiology, at Grant Medical College and Sir JJ group of Hospitals, India. She has many publications in National and International Journals. And also done a fellowship in structural heart disease at Royal Brompton Hospital, UK and training in Intravascular Ultrasound at Cleveland Clinic, USA

Abstract:

Background: Congenital pulmonary valve stenosis (PS) and secundum atrial septal defect (ASD) are relatively common forms of congenital heart diseases but combination of these two conditions is rare. Dual intervention in patients with congenital heart defect have been reported and few cases of combined of transcatheter valvuloplasty for PS and percutaneous ASD closure have been reported.
Objective: To study the effectiveness and safety of simultaneous transcatheter valvuloplasty and atrial septal occlusion in cases of Trilogy of Fallout.
Methods: 4 patients with Triology of Fallot with mean age of 11.25 years presented, between April 2009 and Oct 2013. The diagnosis was established by clinical examination & echocardiography. They underwent cardiac catheterization and as there was a significant gradient across the pulmonary valve, successful balloon pulmonary valvotomy (BPV) was done. This was followed by ASD device closure under TEE guidance. The mean procedural time was 90 minutes (60-120 mts). One patient (patient 2) went into transient pulmonary edema post-BPVwhich settled after diuretics, nitroglycerine and morphine.
Conclusion: In our 4 patients, percutaneous treatment was effective with successful ASD occlusion and right ventricular pressure relief. It is feasible to do BPV followed by ASD device closure as this prevents an increased left to right shunt and at the same time the device placement is not disturbed by arrhythmias and ectopics as we pre-dilate the PV.
It is also convenient for the patient to undergo BPV and ASD device closure concurrently and avoid open heart surgery with quicker recovery, less morbidity and shorter hospital stay. The series also highlights the need to monitor patients closely in the post-operative period, especially those with long standing pulmonary stenosis for sudden onset of acute pulmonary edema/hemorrhage.

Speaker
Biography:

Christine Burgmeier is an Assistant Physician in the Department of General and Pediatric Surgery at Ulm, Germany. Her special interest and research topic is minimally-invasive surgery in term and preterm infants. Recently, she evaluated the hemodynamic effects of laparoscopy and thoracoscopy in babies with congenital heart defects. She completed medical school at the Ludwigs-Maximilians-University Munich, Germany in 2005. After that she started her surgical training in the Department of Cardiothoracic Surgery in Stuttgart. Since 2010, she is doing her special training for pediatric surgery.

Abstract:

Aim: Laparoscopic surgery is progressively performed in pediatric surgery, even in small infants and premature babies. From the technical point of view size and weight of the child are no longer limiting factors. Additionally, more complex and long-lasting laparoscopic procedures can be performed and enable nearly scar less surgery as well as quicker recovery. Nevertheless, there is a lack of knowledge about the influence of insufflation and pneumoperitoneum on the cardiovascular system, especially in infants with cardiac anomalies. The aim of this study was to evaluate the hemodynamic effects of laparoscopic surgery in term and preterm infants with cardiac anomalies.
Methods: In this retrospective, single institution study all term and preterm infants with cardiac anomalies undergoing laparoscopic surgery within the first six months of life were included. Between January 2004 until January 2013, 131 term and preterm infants were identified. We evaluated the type of cardiac anomaly, performed operative procedure, operative time, intra-abdominal pressure and hemodynamic changes in the postoperative course. .
Results: Altogether, 80 preterm and 51 term infants underwent different complex and even long-lasting laparoscopic procedures. The most common procedure was laparoscopic hernia repair. Median operative time was 67 minutes with a median intra-abdominal pressure of 13 mm Hg. Cardiac anomalies ranged from persistent foramen ovale (PFO), atrium septal defect (ASD) to ventricular septal defect (VSD) and tetralogy of Fallot. 33.6 % of patients had combinations of cardiac anomalies. 8.4% of the patients had hemodynamically relevant shunting preoperatively. In the postoperative course hemodynamic impairment was noted in three infants (2.3%). Only one of them presented cardiorespiratory instability in the postoperative course.
Conclusion: In this retrospective study, different laparoscopic procedures could be performed in numerous infants with cardiac anomalies. Preoperative evaluation by a firm pediatric cardiologist is crucial and decides about the operative approach. In the future, prospective studies are necessary to further clarify indications and contraindications of laparoscopic surgery in this distinct group of patients.

Speaker
Biography:

Natasa Chrysodonta is currently a final year medical student at the University of Bristol, and has a BSc in Medical Sciences with Management from Imperial College London. She has been awarded the Elizabeth Williams MBChB year 3 Psychiatry, Ethics & Law Prize in 2012.

Abstract:

Introduction: Coarctation of the Aorta (CoA) accounts for approximately 5-10% of congenital heart disease and if it remains unrepaired the median age of death is 31 years. This highlights the necessity for an early diagnosis and treatment. Despite the method of repair the outcome is highly dependent on a number of risk factors and complications. The literature lacks evidence surrounding the description in the relationship between CoA-repair and Pulmonary Hypertension (PH), with the later significantly decreasing survival. Thus it was aimed to investigate the relationship between paediatric CoA-repair and the presence of PH prior or following CoA-repair.
Methodology: A retrospective Case series was conducted at Bristol's Royal Hospital for Children (BHC). The sample was filtered through the paediatric population at BHC using specific criteria. The information required was gathered from the patients’ electronic records and the results were analysed using Microsoft Excel 2010.
Results: In total 578 records were reviewed with only 8 matching the inclusion criteria. All patients were found to have associated heart lesions and 63% underwent an additional cardiac surgical procedure, out of which 39% were associated with treating PH. Patients with pre-existing PH were found to develop more short-term complications than the post-operative PH group. The later presented with arterial PH of which early onset worsened the outcome. PH developing in adult life seemed to cause a degree of re-coarctation.
Conclusion: Despite the small size, this Case series lays the ground for future research. Further work is required to enrich our understanding and improve the health-care we provide.

Speaker
Biography:

Md Sazid Rezwan is a 5th year medical student studying in Sir Salimullah Medical College, Bangladesh. He is doing his MBBS under renowned cardiologist of Bangladesh and has a fascination for research in Cardiology as well as Neuro-surgery since his early classes. He is doing some researches under renowned professor and has a great achievement in extracurricular activities. He has been serving as an ambassador of different student research conferences. He is the session winner of 23rd ESC of Public Health. He has attended more than 10 undergraduate research conferences both locally and internationally.

Abstract:

Congenital cardiac disease is a common problem experienced in medical practice. Many studies have been carried out worldwide, showing incidence variation in different parts of the world as 5-10/1000 live birth. In Bangladesh, a mere study was done in this respect. This retrospective study was conducted from the records preserved in hospital register, compiled by the author from pediatric cardiology and obstetric department over a period of 4 years extends from 2010-2013 in Sir Salimullah Medical College Hospital. 6520 cases of live births weighing more than 1500 gm and age over 28th weeks of gestational period were recorded by clinical examination and echocardiography with color Doppler. This study showed that 196 babies out of 6520 live births had CHD as 30/1000 live births. Study also expressed that higher incidence of CHD in preterm baby than full term baby. Amongst the congenital Heart lesions, Atrial Septal Defect, Ventricular Septal Defect, Patent Ductus Arteriosus, Tetralogy of Fallot`s, TGA were commonest having 20.41%, 13.78%, 10.71%, 8.67% and 4.59% respectively. 15.81% of the patients had other associated somatic anomalies among which down syndrome was the commonest (7.14%). CHD of various patterns deserves crucial challenge among the newborns for management in Bangladesh. Various factors like high maternal age, drugs intake, antenatal infection, family history, gestational DM, down's syndrome, mother having SLE are related to these diseases. Further, appropriate research can be accomplished taking large relevant sample gathering from different tertiary medical college hospitals to reveal actual scenario to prevent and treat the diseases.

  • Track 4: Cardiac Therapeutic Agents
Speaker

Chair

Nisha Jain Garg

University of Texas Medical Branch, USA

Speaker

Co-Chair

Mark D. Rekhter

Eli Lilly & Co, USA

Speaker
Biography:

Nisha Jain Garg, Ph.D. is currently a Professor in the Departments of Microbiology & Immunology and Pathology in School of Medicine, and serves as Robert E. Shope, MD and John S. Dunn Distinguished Chair in Global Health, Director, Global Health Policy, Epidemics, International Organization and Associate Director, Center for Tropical Diseases at the University of Texas Medical Branch at Galveston. She also serves as a member of the NIH study sections and the American Society of Microbiology International Education Board; Associate editor of the American Journal of Pathology and the Journal of Neuroparasitology; and on the Editorial Boards of several journals. Recently she served as Senior Scientific Advisor at the US Agency for International Development USAID. She has developed a strong and successful research program in the field of tropical infectious cardiomyopathy.

Abstract:

Chagas disease is endemic in Latin America and an emerging infectious disease in the US. No effective treatments are available. TcG1, TcG2 and TcG4 antigens are highly conserved in clinically-relevant Trypanosoma cruzi (Tc) isolates, and recognized by B and T cells in infected host. Delivery of these antigens as a DNA-prime/protein-boost vaccine (TcVac2) elicited lytic antibodies and type 1 CD8+T cells that expanded upon challenge infection, and provided >90% control of parasite burden and myocarditis in chagasic mice and dogs. Here in, we determined if peripheral blood can be utilized to capture the TcVac2-induced protection from Chagas disease. We evaluated the sera levels of TckDNA/Tc18SrDNA and murine mitochondrial DNA (mtDNA) as indicators of parasite persistence and tissue damage; and effect of sera on macrophage phenotype. Circulating TckDNA/Tc18SrDNA and mtDNA were decreased by >3-5-fold and 2-fold, respectively, in vaccinated/infected mice as compared to non-vaccinated/infected mice. Macrophages incubated with sera from vaccinated/infected mice exhibited M2 surface markers (CD16, CD32, CD200 and CD206), moderate proliferation, low oxidative/nitrosative burst, and regulatory/anti-inflammatory cytokine (IL-4+IL-10>TNF-alpha) response. In comparison, macrophages incubated with sera from non-vaccinated/infected mice exhibited M1 surface markers, vigorous proliferation, substantial oxidative/nitrosative burst, and proinflammatory cytokine (TNF-alpha>>IL-4+IL-10) response. Cardiac infiltration of macrophages and TNF-alpha and oxidant levels were significantly reduced in TcVac2-immunized chagasic mice.
Conclusion: Circulating TcDNA and mtDNA levels and macrophage phenotype mediated by sera constituents reflects in vivo levels of parasite persistence, tissue damage and inflammatory/anti-inflammatory state; and have potential utility in evaluating disease severity and efficacy of vaccines and drug therapies.

Speaker
Biography:

Mark D. Rekhter received his Ph.D. in 1987 at the 2nd Moscow Medical Institute (Russia) and followed up with a postdoctoral training at the University of Washington and University of Michigan (USA). Currently, he is a Senior Research Advisor at the Lilly Research Laboratories, Eli Lilly and Co. Dr. Rekhter leads pre-clinical drug discovery teams in the area of cardiorenal complications of diabetes. Recently, he received Lilly Research Laboratories President's Scientific Award (the highest recognition given at Eli Lilly and Co for scientific achievements).

Abstract:

During the last decade, approval of new drugs decreased in spite of significant increase in R&D spending. The reasons for compound attrition will be discussed. A part of potential solution is the focus on “reverse translation” when clinical data are translated back to the pre-clinical drug discovery space. I will provide specific examples of learning from failed clinical trials (CETP inhibitor), from human genetics (PCSK9) and from human pathophysiology. The latter is exemplified by the importance of local blood flow patterns making certain areas of human arterial tree prone to development of atherosclerosis. In collaboration with a biotech company HemoShear, we have applied these fluid dynamics patterns in a co-culture of primary human endothelial and smooth muscle cells to test vascular effects of GLP-1 (7-36) and its degradation products. Local hydrodynamics combined with high glucose and inflammatory stimuli affected expression of GLP-1 receptor in vitro. DPP4-induced degradation product GLP-1(9-36) prevented smooth muscle cell apoptosis in the pro-atherogenic environment. These effects were missed in the static cell culture conditions. Thus, learning from the clinical studies (“reverse translation”) provides value for drug discovery and improves potential for the “forward translation” from bench to the bedside.

Renuka R. Nair

Sree Chitra Tirunal Institute for Medical Sciences and Technology, India

Title: Relationship between oxidative stress and energy metabolism in hypertension induced cardiac remodeling
Speaker
Biography:

Renuka R Nair received her Ph.D. from Osmania University (India) in 1979 and joined as a Postdoctoral Fellow at the Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India. She was appointed as a faculty at the Institute in 1984, and is currently the Head of the Division of Cellular and Molecular Cardiology. Her research interest is focused on prevention of adverse cardiac remodeling in chronic pressure overload. She is also working on the role of cardiac stem cells in myocardial regeneration. She is a fellow of the National Academy of Medical Sciences, India.

Abstract:

Hypertension induced left ventricular hypertrophy is an independent risk factor for cardiac failure. Hence, strategies that promote reverse remodeling forms an important component in the treatment of hypertension. Cardiomyocytes incubated with human serum samples showed a direct correlation of oxidative stress with cellular hypertrophy. In vitro experiments using cardiac myocytes and fibroblasts; and studies in spontaneously hypertensive rat (SHR) have established the role of oxidative stress in the initiation and progression of hypertrophy. Hypertrophy is accompanied by a shift in energy substrate preference from fatty acids to glucose. Though initially adaptive, chronic dependence on glucose can be maladaptive. Stimulation of fatty acid oxidation in SHR using the peroxisome proliferator activated receptor- alpha agonist fenofibrate showed an age dependent paradoxical effect. Association between oxidative stress and hypertrophy was apparent, as young SHR (2-month-old) showed regression of hypertrophy and oxidative stress; whereas the converse was observed in older rats (6-month-old). The fatty acid transporter CD36 is defective in hypertensives. Medium chain triglycerides (MCT) bypass CD36. Significant reduction of oxidative stress and hypertrophy was observed in older SHR on supplementation of MCT (5%) in the diet. Blood pressure was maintained, thereby delinking blood pressure reduction from cardiac remodeling. In SHR, an inverse relation was observed between NFκB and MCAD establishing the relation between oxidative stress and metabolic shift and is possibly intimately linked with regulation by PGC-1alpha. The concept that hypertrophy is an essential compensation for increased wall stress needs reconsideration; and treatment should be directed at prevention of transition from adaptive cardiac remodeling to cardiac failure.

Speaker
Biography:

Jean C. Bopassa is currently working as an Assistant Professor in the department of Physiology, School of Medicine, University of Texas Health Science Center at San Antonio, USA

Abstract:

Introduction: Estrogen effect can be mediated by three receptors: Classical estrogen receptors: alpha (ERalpha) and beta (ERbeta), and recently identified G protein-coupled estrogen receptor1 (GPER1).
Hypothesis: We investigated the role of ERalpha, ERbeta and GPER1 in mediating rapid estrogen-induced cardioprotection in male mice hearts subjected to ischemia/reperfusion using wild type (WT) and gene specific knockout animals.
Methods: Isolated hearts from wild type (WT: C57BL/6NCrL), ERalpha-/-, ERbeta-/- and GPER1-/- were perfused using Langendorff apparatus with Krebs Henseleit buffer (control) or with the addition of estrogen (40 nM). Hearts were subjected to 18 min global ischemia followed by 60 min reperfusion. Cardiac function was recorded during the entire experiment and myocardial infarct size was measured by TTC staining at the end of the reperfusion. Mitochondria calcium retention capacity (CRC) required to induce the mitochondrial permeability transition pore (mPTP) opening were assessed after 10 min reperfusion. Protein levels were measured by Western Blot in whole heart lysates after 5 min treatment just before ischemia, and after 10 min reperfusion. LY294002 and U0126 were used as inhibitor of PI-3K/Akt, and MAPK/ERK translocation, respectively.
Results: In WT, ERalpha-/- and ERbeta-/-, estrogen treatment significantly improved cardiac functional recovery, reduced infarct size and improved mitochondrial CRC. However, estrogen effects were completely absent in GPER1-/-. Estrogen treatment during 5 min before ischemia induced up-regulation of Akt, GSK-3beta, and ERK1/2 phosphorylation in WT mouse as compared with control but not in GPER1-/-. U126 abolished estrogen effect on mitochondrial CRC while LY294002 could not prevent estrogen effect on GSK-3beta observed in WT. P<0.05 and n=3-6.
Conclusion: Rapid activation of GPER1 induces cardioprotection effect against ischemia/reperfusion injury. Estrogen effects through GPER1 are associated with phosphorylation of GSK-3beta and ERK1/2, and inhibition of the mPTP opening.

Speaker
Biography:

Anita A. Mehta is a Principal in charge, Professor & Head, Department of Pharmacology, L. M. College of Pharmacy and Dean Zone-I, Gujarat Technological University. She has vast research experience in area of cardiovascular diseases and diabetes with over 150 publications. Her contributions to research have been recognized with 21 awards. She has been associated with numerous prestigious research projects of USIEF-Fulbright, UGC, DST and GUJCOST as principal investigator. She is reviewer of numerous national & international journals. She has organized national conference on Pharmacology and World Congress of the international Academy of Cardiovascular Sciences as joint organizing secretary. She has visited Canada for six week under Global International Experience Program. She has delivered scientific talk at Memphis, Minneapolis, Detroit, New York, New Jersey (US) and Glasgow, (UK).

Abstract:

Introduction: Vascular endothelial growth factor (VEGF) mediated therapeutic angiogenesis has been failed to improve cardiac functioning in heart failure patients that may be related to endothelial dysfunctioning. Telmisartan and atorvastatin improves endothelial cell functioning and widely suggested for treatment of cardiovascular diseases.
Objectives: To study effects of telmisartan and atorvastatin treatment on VEGF induced angiogenic responsiveness in coronary endothelial cells (VEGF-ang-res-cEC).
Methods: Male wistar rats were divided into nine groups, normal rats, diabetic rats 30 ds., diabetic rats 60 ds., telmisartan treated normal rats-diabetic rats 30ds.-diabetic rats 60 ds. and atorvastatin treated normal rats-diabetic rats 30ds.-diabetic rats 60 ds. Each group was further divided into two subgroups; sham heart and IR heart. Coronary endothelial cells (cEC) were isolated from each subgroup for study of ang-res-cEC and NO bioactivity.
Results: Telmisartan and atorvastatin treated groups significantly increased VEGF-ang-res-cEC as compared to their respective non treated groups except atorvastatin treated IR heart-diabetic rats 60 ds. Similarly, telmisartan and atorvastatin showed significant increase in VEGF induced NO release from cEC of treated groups as compared to their respective non treated groups except atorvastatin treated IR heart-diabetic rats 60 ds. The effects of telmisartan and atorvastatin were significantly inhibited by pretreatment of cECs with eNOS inhibitor, NG-nitro-l-arginine methylester (l-NAME) and PI3K inhibitor, wortmannin whereas PKC inhibitor, chelerythrine, attenuated effects of atorvastatin only.
Conclusion: Our data suggest that telmisartan improves coronary angiogenic activity in normal, early and late phase diabetic rats via stimulating VEGF/PI3K/eNOS/NO pathway whereas effect of atorvastatin depend on stimulation of VEGF/PI3K/eNOS/NO and VEGF/PKC/eNOS/NO pathway.

Speaker
Biography:

Galya Naydenova Atanasova completed her Ph.D. training in Cardiology from Department of Cardiology, Pulmonology and Endocrinology at Pleven Medical University, Bulgaria. She is a General Practitioner and Cardiologist in Trainee at Pleven Medical University, Bulgaria. She specialized in General Medicine from Pleven Medical University, Bulgaria during 1993. She has attended to many International Events and presented her research work. She did many researches on metabolic syndrome and myocardial infarction of heart.

Abstract:

Various studies have shown relation between increase of arterial stiffness and metabolic syndrome (MS). Some researches have demonstrated that apolipoprotein B/Apolipoprotein A1 (Apo B/Apo A1) and pulse pressure (PP) are associated with MS. Objectives of this study are to evaluate influence of the metabolic syndrome and its components on PP and apolipoprotein B/Apolipoprotein A1.
A total of 107 persons without any apparent disease were selected. Among these subjects MS was found in 36. One way ANOVA test, multiple comparison test of means and multiple logistic regression analyses are used.
The four groups used in ANOVA are men and women with and without MS. The ANOVA F-statistic is 3.683 with p-value 0.0145. The multiple comparison test showed differences between subjects with and without MS. The first logistic regression includes gender, PPand Apo B/Apo A1. The results showed that for simultaneously increase of PP with 5 mm Hg and increase of Apo B/Apo A1 with 0.05045 it was expected about 1.5787 times increase in the odds ratio (OR) of MS. In the second logistic regression the PP and all other components of MS are included. The result showed that for increase of PP with 5 mm Hg it was expected about 1.5787 times increase in the OR of MS.
The results indicated relation between wide PP and increase of OR of MS. The increase of OR of MS with parallel increase of PP and Apo B/Apo A1 is obtained. Increase of PP and Apo B/Apo A1 influence on cardio metabolic risk.

  • Track 5: Biophysics and Systems Biology
    Track 6: Cancer and Heart
Speaker

Chair

Anthony Martin Gerdes

New York Institute of Technology-College of Osteopathic Medicine, USA

Speaker

Co-Chair

Yoshiaki Omura

New York Medical College & Heart Disease Research Foundation, USA

Session Introduction

A Martin Gerdes

New York Institute of Technology-College of Osteopathic Medicine, USA

Title: Wrong about Beta Blockers! Wrong about positive inotropes! Wrong about thyroid hormone treatment of heart failure?
Speaker
Biography:

A Martin Gerdes completed his Ph.D. at the University of Texas Medical Branch at Galveston in 1978 and was recently recognized as the 2013 Distinguished Alumnus of the Graduate School of Biomedical Sciences. Throughout his career, work has focused on understanding the cellular and molecular mechanisms of maladaptive ventricular remodeling in heart failure and potential treatments. He has published over 100 peer reviewed journal articles and has been the PI on ~$30M in NIH funding during his career. He has identified key cellular mechanisms involved in dilated heart failure, including a maladaptive change in myocyte shape.

Abstract:

Medical opinion currently opposes thyroid hormone (TH) treatment of heart failure (HF), largely due to fear that overdosing may lead to increased arrhythmias and death. Yet, overwhelming evidence suggests that TH treatment of HF offers great promise. Importantly, recent clinical studies have shown increased HF mortality as TH function declines. A rat study showed that hypothyroidism eventually evolves into dilated HF with chamber dilatation from myocyte lengthening and impaired coronary blood flow. Cardiac diseases typically lead to re-expression of fetal genes, which also occurs in hypothyroidism. New studies show that heart diseases may trigger cardiac tissue hypothyroidism by upregulation of the D3 deiodinase, which converts T4 to inactive rT3. We showed that dilated HF results in excessive myocyte lengthening from series addition of new sarcomeres in the absence of a compensatory change in cell diameter. Indeed, this cellular change may largely account for the hallmark change in HF, increased chamber diameter/wall thickness ratio. THs not only induce a physiological, proportional growth of myocyte length and width, they promote a beneficial change in myocyte shape in the background of diseases leading to dilated HF. A new study shows that both hypo- and hyperthyroidism promotes arrhythmias. A major impediment to clinical trials is lack of a protocol that restores cardiac tissue T3 levels safely and improves cardiac function without inducing hyperthyroidism. We will present new data documenting a safe treatment/monitoring protocol in various animal models of HF that should easily translate to patients.

Speaker
Biography:

Yoshiaki Omura received Oncology Residency Training and a Doctor of Science Degree through research on Pharmaco-Electro Physiology of Single Cardiac Cells in vivo and in vitro from Columbia University. He published over 250 articles and 7 books. He is currently Adjunct Professor, New York Medical College; Director of Medical Research, Heart Disease Research Foundation; Executive Editor, Integrative Oncology etc. Using his new diagnostic, U.S.-patented method, he can non-invasively and rapidly measure many neurotransmitters, chemicals, asbestos, viruses and bacteria. He developed a non-invasive, quick diagnostic method of malignancies, as well as a method of evaluating the effects of any treatment.

Abstract:

Some cancer patients receiving chemotherapy complain about heaviness or dull pain in their heart area. ECGs of these patients often do not show any significant abnormalities, and Cardiac Troponin I in blood is often not increased. However, these patients feel worse after subsequent chemotherapy sessions. When the patient dies, cancer is blamed. However, using our new, non-invasive diagnostic method which uses Electromagnetic Field Resonance Phenomenon between 2 identical molecules, which received a US patent, we can find invisible biochemical abnormalities, which are missed by standard diagnostic methods of ECG inspection based on visible wave forms and voltage. By analyzing the ECGs of chemotherapy patients before and after chemotherapy, we found on normal-appearing ECGs there are often significant abnormalities in the "Vulnerable Period for Ventricular Fibrillation" part of the rising T-Wave. Our previous studies from not only recorded ECGs but also EEGs, EMGs, & "Mouth, Hand and Foot Writing" indicated that invisible biochemical changes between a known exact amount of specific molecules and identical molecules information around involved area exist in recorded ECGs, EEGs etc. Although the ECGs may look normal, this rising portion of the T-Wave of ECGs with or without abnormalities in other parts of recorded ECGs often shows significant increase in Cardiac Troponin I. In the same location of ECGs, we can also detect abnormally increased concentration for calcium with or without additional information on viral, bacterial or fungal infections. By using such a method, we can save many lives by preventing potential death by cardiotoxic chemotherapy agents.

Speaker
Biography:

Nisha Jain Garg, Ph.D. is currently a Professor in the Departments of Microbiology & Immunology and Pathology in School of Medicine, and serves as Robert E. Shope, MD and John S. Dunn Distinguished Chair in Global Health, Director, Global Health Policy, Epidemics, International Organization and Associate Director, Center for Tropical Diseases at the University of Texas Medical Branch at Galveston. She also serves as a member of the NIH study sections and the American Society of Microbiology International Education Board; Associate editor of the American Journal of Pathology and the Journal of Neuroparasitology; and on the Editorial Boards of several journals. Recently she served as Senior Scientific Advisor at the US Agency for International Development (USAID. She has developed a strong and successful research program in the field of tropical infectious cardiomyopathy.

Abstract:

Objectives: Determine the pathological importance of oxidative stress-induced injurious processes in chagasic heart dysfunction.
Background: Trypanosoma cruzi-induced inflammatory pathology and a feedback cycle of mitochondrial dysfunction and oxidative stress may contribute to Chagas disease.
Methods: Sprague Dawley rats and C57BL6 mice (wt and MnSODtg) were infected with T. cruzi. Infected rats were treated with phenyl-alpha-tert-butylnitrone (PBN-antioxidant) and/or benzonidazole (BZ-anti-parasite). We monitored myocardial parasite burden, oxidative adducts, mitochondrial complex activities, respiration and ATP synthesis rates, and inflammatory and cardiac remodeling responses during disease development. Cardiac hemodynamics was determined for all rats.
Results: BZ (not PBN) decreased the parasite persistence and immune adverse events (proinflammatory cytokine expression, NADPH oxidase and myeloperoxidase activities, and inflammatory infiltrate) in chronic hearts. PBN and BZ (not BZ alone) decreased the mtROS level, oxidative adducts (malonyldialdehyde, 4-hydroxynonenal, carbonyls), hypertrophic gene expression (ANP, BNP, αsk-Actin), and collagen deposition, and preserved the respiratory chain efficiency and energy status in chronic hearts. Subsequently, left-ventricular dysfunction was prevented in PBN/BZ-treated chagasic rats. MnSODtg mice controlled cardiac oxidative and inflammatory stress, mitochondrial damage, and collagen remodeling during chronic Chagas disease.
Conclusions: BZ treatment after acute stage decreased the parasite persistence and inflammatory pathology. Yet, oxidative adducts, mitochondrial dysfunction and remodeling responses persisted and contributed to declining cardiac function in chagasic rats and mice. Combinatorial treatment (PBN/BZ) or control of mitochondrial oxidative stress was beneficial in arresting the T. cruzi-induced inflammatory and oxidative pathology and chronic heart failure in chagasic rats.

David E. Dostal

Texas A&M Health Science Center, USA

Title: Mechanosensing and regulation of cardiac function
Speaker
Biography:

David E. Dostal received his Ph.D. in 1986 at the University of Missouri-Columbia followed by postdoctoral training at the University of Virgina, Charlottesville. Currently, he is a Professor at Texas A&M Health Science Center and Research Biologist at the Central Texas Veterans Health Care System in which his laboratory, funded by the NIH and the Veterans Affairs, conducts research in the area of heart failure and cellular signaling mechanisms. He also serves as a member of the NIH Cardiac Contractility, Hypertrophy, and Failure Study Section, chair of an American Heart Association Signaling Study Section, an International Expert Panel member for the Singapore Ministry of Health and several scientific journal editorial boards. He has recently received the prestigious Research Career Scientist Award from the Department of Veterans Affairs for his scientific achievements.

Abstract:

Heart failure is the leading cause of morbidity and mortality in developed countries. Cardiac dysfunction in patients with hypertension-induced heart failure is characterized by reduced left systolic and diastolic ventricular function, which is associated with myocyte hypertrophy and ventricular remodeling. Although the pathophysiological mechanisms associated with pressure overload-induced cardiac hypertrophy have the focus of intense scientific investigation for over 3 decades, the cellular mechanisms remain poorly understood. There is abundant evidence that regulation of protein phosphorylation through intracellular kinases and phosphatases is a key mechanism by which cells respond to extracellular stimuli, Within this area of research, the stress activated protein kinases (SAPKs), which include c-jun N-terminal kinases (JNKs) and p38 MAP kinase, have been shown to be activated by a number of cellular stresses including mechanical stretch. Recent studies by our laboratory and others suggest that p38 is responsible for causing many of the pathological aspects of heart failure, whereas JNK may be cardioprotective. Using in vivo and in vitro models, we have demonstrated that both beta1-integrin and the angiotensin type I receptor (AT1) serve as mechanosensors, which can temporally regulate contractile function in cardiac myocytes through regulation of p38 and JNK. These studies also revealed that JNK plays a major role in maintaining cardiac diastolic function by regulating intracellular calcium through phosphorylation of phospholamban. The demonstration that JNK has an important role in the regulation of contractile function and diastolic function may provide a new therapeutic approach for the treatment of diastolic heart disease.

Speaker
Biography:

Nadia Jahroudi completed her Ph.D. from University of Calgary and Postdoctoral studies from Harvard Medical School. She is currently an associate professor at the Department of Medicine, University of Alberta.

Abstract:

Despite common lineage, endothelial cells of distinct vascular beds exhibit significant heterogeneity in structure, function and gene expression pattern. This heterogeneity is mainly observed in vivo; however some organ-specific attributes specifically those that relate to endothelial-cells’ response to external stimuli are exhibited in cultured endothelial cells. The molecular basis of endothelial cell heterogeneity and its response to external stimuli is not understood. We have extensively studied transcriptional regulation of a highly endothelial restricted gene, namely von Willebrand factor in vitro, in vivo, and in response to external stimuli such as hypoxia. We have demonstrated that distinct regions and specific transacting factors participate in regulation of VWF transcription in endothelial cells of distinct organs; and based on these results generated targeting vectors that can express desired genes specifically in endothelial cells of distinct organs. Additionally we have demonstrated that VWF transcription in response to hypoxia is differentially regulated in endothelial cells of lung compared to those in other organs in vivo. We have also evidence that VWF response to hypoxia is differentially regulated in endothelial cells of heart compared to lung when these cells are grown in culture. Determining the molecular basis of differential response of endothelial cells to external stimuli, in combination with the ability to target the expression of desired molecules in endothelial cells of specific organs, will provide an opportunity for development of effective therapeutic interventions based on specific and targeted manipulation of endothelial cells of desired organs.

Speaker
Biography:

Il-man Kim is an assistant professor at Georgia Regents University. He completed his Ph.D. at the University of Illinois and postdoctoral training at Duke University. He is working on multi-disciplinary research projects related to cardiac disease. Particularly he is studying G protein-coupled receptor-mediated signaling pathways. He was selected as a finalist for the American Heart Association (AHA) Katz Basic Research Prize. He has been awarded three AHA grants. He has served on the grant review committee of AHA and NIH as well as Medical Research Council in UK. He has served on the editorial board member of several cardiovascular journals.

Abstract:

MicroRNAs (miRs) are small, non-coding RNAs that function to post-transcriptionally regulate gene expression. First transcribed as long primary miR transcripts (pri-miRs), they are enzymatically processed in the nucleus by Drosha into hairpin intermediate miRs (pre-miRs) and further processed in the cytoplasm by Dicer into mature miRs where they regulate cellular processes following activation by a variety of signals such as those stimulated by beta-adrenergic receptors (betaARs). Initially discovered to desensitize betaAR signaling, beta-arrestins are now appreciated to transduce multiple effector pathways independent of G protein-mediated second messenger accumulation, a concept known as biased signaling. We previously showed that the beta-arrestin-biased beta-blocker carvedilol activates cellular pathways in the heart. Our recent data demonstrated in human cells and mouse hearts that carvedilol upregulates a subset of mature and pre-miRs but not their pri-miRs in beta1AR-, G protein-coupled receptor kinase 5/6- and beta-arrestin1-dependent manner. Mechanistically, beta-arrestin1 regulates miR processing by forming a nuclear complex with hnRNPA1 and Drosha on pri-miRs. Loss- and gain-of-function approaches in cardiomyocytes (CMs) and in vivo mouse hearts also uncovered that beta-arrestin1-regulated miRs increased CM survival by repressing apoptotic genes. Our findings indicate a novel function for beta1AR-mediated beta-arrestin1 signaling activated by carvedilol in miR biogenesis, which may be linked, in part, to its mechanism for cell survival. These results also suggest that miR-target pairs regulated by beta-arrestin1 may exert cardio protective effects.

Speaker
Biography:

Mohamed M. Sayed-Ahmed is a Professor of Pharmacology, King Saud University, Saudi Arabia and he graduated from College of Pharmacy, Egypt in 1985. After that he joined the National Cancer Institute, Cairo University, Egypt and completed his master thesis. In 1994, he started his Ph.D. at College of Medicine, Duke University Medical Centre, North Carolina, USA. He spent three years investigating the mechanisms where by anti-cancer drugs interfere with carnitine system and how carnitine supplementation prevents chemotherapy-induced multiple organ failure. In 1997, he received his Ph.D. in Pharmacology from National Cancer Institute, Cairo University, Egypt. From 2004, he is working as the Professor in the Department of Pharmacology, College of Pharmacy, King Saud University.

Abstract:

This study investigated whether cyclophosphamide (CP) and ifosfamide (IFO) therapy alters the expression of the key genes engaged in long-chain fatty acid (LCFA) oxidation outside rat heart mitochondria, and if so, whether these alterations should be viewed as a mechanism during CP and IFO-induced cardiotoxicity. Adult male Wistar albino rats were assigned to one of six treatment groups: Rats in group 1 (control) and group 2 (L-carnitine) were injected intraperitoneal (i.p.) with normal saline and L-carnitine (200 mg/kg/day), respectively, for 10 successive days. Animals in group 3 (CP group) were injected i.p. with normal saline for 5 days before and 5 days after a single dose of CP (200 mg/kg, i.p.). Rats of group 4 (IFO group) were received normal saline for 5 successive days followed by IFO (50 mg/kg/day, i.p.) for 5 successive days. Rats of group 5 (CP-carnitine supplemented) were given the same doses of L-carnitine as group 2 for 5 days before and 5 days after a single dose of CP as group 3. Rats of group 6 (IFO-carnitine supplemented) were given the same doses of L-carnitine as group 2 for 5 days before and 5 days concomitant with IFO as group 4. Immediately, after the last dose of the treatment protocol, blood samples were withdrawn and animals were sacrificed for biochemical and gene expression studies. Treatment with CP and IFO significantly decreased expression of hear fatty acid binding protein (H-FABP) and carnitine palmitoyltransferase I (CPT I) genes in cardiac tissues. Moreover, CP but not IFO significantly increased Acetyl-CoA Carboxylase (ACC) mRNA expression. Conversely, IFO but not CP significantly decreased mRNA expression of Malonyl-CoA Decarboxylase (MCD). Both CP and IFO significantly increased serum lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CK-MB), and malonyl-CoA content in cardiac tissues. Interestingly, carnitine supplementation completely reversed all the biochemical and gene expression changes-induced by CP and IFO to the control values, except CPT I mRNA and protein expression remained inhibited by IFO. Data from the current study suggest that: (1) CP and IFO therapy are associated with the inhibition of the expression of H-FABP and CPT I genes in cardiac tissues with the consequent inhibition of mitochondrial transport and oxidation of LCFA. (2) The progressive increase in cardiotoxicity enzymatic indices and the decrease in H-FABP and CPT I expression may point to the possible contribution of these genes in CP and IFO-induced cardiotoxicity. (3) L-carnitine prevents CP and IFO-induced cardiotoxicity via modulating the expression of genes engaged in fatty acid oxidation in the heart.

Speaker
Biography:

Ahmad M. Slim has completed his MD/MS at the age of 24 years from the America University of the Caribbean and Postgraduate Medical Education at St John's hospital, MI as well as SAUSHEC, San Antonio. He is Assistant Professor of Medicine at University of Texas Health Science Center, San Antonio as well as Uniformed Services University of Health Science. He is the Director of Cardiovascular Research, Preventive Cardiology Clinic and Cardiac Imaging in San Antonio Military Medical Center. He has published more than 25 papers in reputed journals, book chapters and has been serving as an editorial board member of repute.

Abstract:

Patient prognosis has been shown to directly correlate with the severity of coronary artery disease (CAD) diagnosed by coronary computed tomography angiography (CCTA), myocardial perfusion imaging (MPI), as well as cardiac magnetic resonance imaging (CMR). As such multi-modality imaging techniques are becoming more readily available it is prudent to understand the indications, limitations and benefits of each technique and when utilize it. We have reviewed the utilization of these modalities in patients who are low risk with high risk occupations, intermediate risk, as well as high risk when clinically indicated to provide easy to use guidance for clinicians supporting the unique population we serve. This approach resulted in significant cost reduction to the department of defense with associated improve cardiovascular outcomes when downstream utilization was assessed. In addition, we have translated that success and implemented programs in the emergency department where patients disposition to home was decreased to a mean of 3 hours with zero incidence of cardiovascular events in 30 days, further improving the downstream utilization of cardiovascular testing.

Speaker
Biography:

Zorana Vasiljevic-Pokrajcic has completed her Ph.D. at the age of 25 years from Belgrade University School of Medicine and Postdoctoral studies from Belgrade University School of Medicine. She was head Urgent Cardiology Department of Cardiology Clinic Medical Faculty, University of Belgrade, Clinical Centre Serbia 1998-2012. She is Full professor of Internal Medicine/Cardiology, Medical Faculty, University of Belgrade. She was former President of Cardiology Society of Serbia and Coronary Care Association of Serbia. She has published more than 250 papers in reputed journals, 635 citations of Scopus and has been serving as an editorial board member

Abstract:

It is well known that prognosis of ST-segment elevation myocardial infarction (STEMI) patients (pts) is time dependent on applying reperfusion therapy (RT), pPCI or fibrinolysis (FT), standard therapy, PCI centre network, possibility of medical and technical equipment, but also depending of pts age, comorbidity, risk factors and time from symptom onset to RT. There was no data from Serbia as a country in transition and country being under embargo during more than 10 years. In our observational, cross sectional study the data was used from the hospital registry for acute coronary syndrome (HORAKS); we analyzed 15354 consecutive STEMI pts from 2007. to 2009., mean age 63.6±12.0 years, m/f 65/35%. The RT was applied in 55.3% pts: pPCI in 21.9% pts aged 60.0±11.7, m/f 70.5/29.5 and FT in 33.4% pts aged 61.2±11.3, m/f 68.3/32.0. There were 44.6% non reperfused pts which were the oldest, mean age 67.1±11.6 (P) and with the most female with m/f 60.6/39.4. Overall STEMI hospital mortality was 11.8%; in pPCI group 6.2%, in FT group 10.5% and in nonreperfused pts 15.7%. Significant predictors of the fatal in-hospital outcome in reperfused patients were (HL, χ2=13.492, p=0.096, c statistic 0.876, SE 0.007, 95% CI 0.861-0.891) ages ≥75 years, the time from symptoms onset >360 minutes, anterior localization, Killip > I, especially cardiogenic shock, diabetes mellitus, previous stroke, treatment in non-PCI center and the lack of application of the p-PCI. Odds ratio (OR) higher than 2.0 were in variables: HF, age ≥75 years and lack of application of the p-PCI.
Conclusion: Estimated risk level of the patients was the most dependent of ages and comorbidities: heart failure, diabetes and stroke. The time from the symptom onset to arrival to the medical hospital is the important factor, but in Serbia the crucial factors are type of RT -pPCI end estimated risk level of pts.

Speaker
Biography:

Monica V Marquezini is a Scientific Researcher at Pro-Blood Foundation of Blood Center of São Paulo. She is also part of Experimental Air Pollution Laboratory, Medical School of University of São Paulo, Brazil, since 2010. Marquezini is a Expert in Cellular and Molecular Biology with cell surface proteins studies and extracellular matrix research. And she is Teacher of Cell and Molecular Biology themes at different graduation careers, Post-graduation advisor, Coordinator of specialization courses and National and International Projects. She done her Ph.D. in Science from the Federal University of São Paulo-School of Medicine during 1996 and M.Sc. in Molecular Biology. She graduated in Biological Sciences Medical Modality from the University Methodist Piracicaba, Brazil (1983).

Abstract:

The goal of this study was to evaluate the genotoxic potential effects of air pollution (PM2.5) generated by traffic on exposed individuals, during work, from São Paulo City, Brazil. The study involved 58 male workers from São Paulo City: 43 are taxi drivers and traffic controllers, that characterize the downtown's environment and 15 workers from the Forest Institute, that characterize the outskirt of the City, called "city green belt".
Each participant used a Personal Environmental Monitoring Sampler (PEMS) designed by our team, to measure PM 2.5 particles mass. The PEMS were operated continuously at 4-LPM over 24-hour. Particles were collected on a policarbonate membrane filter. The frequency of Micronucleus (MN) in exfoliated oral mucosa cells and peripheral blood lymphocytes of the voluntaries was also determined.
The exposure to PM2.5 was higher in the downtown workers than in the outskirt workers (mean±SE, 39.2±2.1 and 22.9±1.4, respectively; p<0.001, ANOVA). The frequency of MN found in both, downtown and outskirt workers, was high either in lymphocyte (mean±SD, 7.8±0.4 and 4.6±0.5, respectively; p<0.001, ANOVA) as in oral mucosa (mean±SE, 16.1±0.7 and 6.6±0.4, respectively; p<0.001, ANOVA).
In conclusion, the MN has served both as biomarkers of genetic damage, as indicators to monitoring occupational health. These markers may have applicability in assessing genotoxicity in exposed individuals due to their high reliability. Therefore, it should be accepted and used by the government for the benefit of its citizen's occupational health.

Senthil Vadivu Arumugam

Madras ENT Research Foundation, India

Title: Cochlear implantation and cardiac associations
Speaker
Biography:

Senthil Vadivu Arumugam has completed her DNB at the age of 30 years. She is the coordinator of Cochlear Implant program at Madras ENT Research Foundation. She has published 5 papers in reputed International Journals. She has attended various National and International Conferences and presented papers in scientific sessions and won awards for few. She worked as a Joint secretary for 1st National Conference on snoring and Sleep Apnoea, Chennai, February 2013.

Abstract:

Cochlear implantation is a standard surgery for restoration of hearing in profoundly deaf candidates. Profound deafness may at times, manifest as a part of a syndrome associated with cardiac anomalies. Cardiac co-morbidities may influence cochlear implantation in a spectrum of ways from minor intra operative issues to major life threatening complications. Issues related to pre-operative, intra operative and post-operative care needs to be addressed by an efficient in house cardiologist.
Our retrospective study was aimed at analyzing the various cardiac co-morbidities encountered in 500 cochlear implants over the past decade. This study was focused on developing a profile of cardiac complications influencing cochlear implantation and suggests a protocol for management of various cardiac issues related to cochlear implantation. My presentation will reflect the surgeon's perspective of standard pre-operative work up and peri-operative and post-operative care to be given during cochlear implantation. Relevant literature has been reviewed. Case series of 30 profoundly deaf children (below 12 years) who had associated cardiac problems and underwent cochlear implantation in our institution were included in our study. Over all cardiac disease were identified in 30 out of 500 implantees (16.6%) in our experience.
The cardiac disease can be categorized into 3 groups: candidates with isolated Patent Ductus Arteriosus (PDA) as Group A (8/30), Syndromic and non Syndromic candidates with PDA and other associated anomalies as Group B (18/30), and candidates with syndromes without PDA association as Group C (4/30).
The overall incidence of cardiac problems in profoundly deaf candidates is identified. Descriptive profile of the same has been created and appropriate management for the same discussed.
A protocol for management of cardiac co-morbidities influencing cochlear implantation has been designed and detailed insight for the optimal management of these issues has been discussed with surgeon's perspective.