11^th Annual Cardiology Summit September 12-13, 2016 Philadelphia, Pennsylvania, USA

Biography:

Dr. Antzelevitch is Professor and Executive Director of Cardiovascular Research at the Lankenau Institute for Medical Research and Director of Research at Lankenau Heart Institute in Wynnewood, PA. Awards include the Distinguished Scientist Award from the North American Society of Pacing and Electrophysiology (Heart Rhythm Society), Carl J. Wiggers Award of the American Physiological Society, the Distinguished Scientist Award of the American College of Cardiology and the Distinguished Service Award of the Cardiac Electrophysiology Society. He has published over 500 original papers and reviews and six books. He is currently Associate Editor of the Heart Rhythm journal and Secretary-Treasurer of the Cardiac Electrophysiology Society

Abstract:

A prominent J wave is encountered in a number of life-threatening cardiac arrhythmia syndromes, including the Brugada (BrS) and early repolarization (ERS) syndromes. BrS and ERS differ with respect to the magnitude and lead location of abnormal J waves in the ECG and are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. Both are associated with vulnerability to polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death (SCD) in young adults. J wave syndromes are characterized by J-point and ST-elevation in distinct ECG-leads. The region most affected by BrS is the anterior right ventricular outflow tract, accounting for why J-point and ST-segment elevation are generally limited to the right precordial leads. The region most affected in ERS is the inferior wall of the left ventricle, accounting for why the appearance of J waves or early repolarization in the inferior ECG leads is associated with the highest risk for development of arrhythmias and SCD. Despite two decades of intensive research, risk stratification and the approach to therapy of these two inherited cardiac arrhythmia syndromes are still undergoing rapid evolution. Considerable controversy exists as to risk stratification, approach to therapy as well as mechanisms underlying these two syndromes. My objective in this presentation is to provide an integrated review of the clinical characteristics, risk stratifiers, as well as the molecular, ionic, cellular and genetic mechanisms underlying these two interesting syndromes, which have captured the interest and attention of the cardiology community worldwide in recent years.

Biography:

Guy H Fontaine has made 16 original contributions in the design and the use of the first cardiac pacemakers in the early 60s. He has serendipitously identified ARVD during his contributions to antiarrhythmic surgery in the early 70s. He has developed the technique of Fulguration to replace surgery in the early 80s. He has been one of the “216 individuals who have made a significant contribution to the study of cardiovascular disease since the 14^th century”, one of the “500 greatest geniuses of the 21th century” (USA Books), one of the “100 life time of achievement” (UK Book). He has 900+ publications including 201 book chapters. Reviewer of 23 scientific journals both in basic and clinical science. He has served as a member of the Editorial Board of Circulation during 5 years after reviewing during decades papers for this Journal. He has given 11 master lectures of 90’ each in inland China in 2014. He has developed new techniques of hypothermia for neurologic brain protection in OHCA, stroke and spinal cord injury. He is the first to have resuscitated his wife at home with an external defibrillator (Schiller) still working after 30 years. He has also invented a high-tech device which can be considered as the ultimate in palliative care

Abstract:

ARVCs is covering a spectrum of mostly inherited cardiomyopathies of increasing interest because od a relatively small number of mututions have been identified in 60% of patients (Fressart Europace 2014). The mechanisms of EGS anomalies are btter understood as well as their long term prognosis leading to CHF (Hulot Circulation 2004)

Arrhythmogenic Right Ventricular Dysplasia (ARVD) is mostly due to PKP2 desmosomal mutation with increased RV size with apoptotic thinness of the free wall and segmental anomalies of contraction. This is also due to the presence of fat and interstitial fibrosis mostly observed in the RV free wall and LV apex. This disease is frequent in the general population 3.7% but become clinically apparent in a small number of cases (Fontaine AJC 2014). Clinical presentation is mostly ventricular arrhythmias which can lead to unexpected sudden cardiac death especially in young people and during endurance sports. Some of these patients seen at a late stage of the disease can be misclassified as IDCM. However, in some rare patients, the disease can stop completely its progression.

Brugada syndrome (BrS) has a unique ECG pattern of coved type observed only in lead V1.  Structural changes are sometimes producing a Phenotype suggesting ARVD. However, these dkiseases are two different entities with some degree overlap both phenotypically and genotypically in a small number of cases.

Right Ventricular Outflow Tract Ventricular Tachycardia (ROVT VT) is generally benign but one personal case of SD with pathologic documentation demonstrated a localised infundibular anomaly suggesting localised ARVD.

Naxos disease has been identified in the Greek eponym disease is the homozygous form with associated palmoplantar keratosis. This led to the identification of the first mutation Plakoglobin leading to the discovery of multiple candidate genes and finally other mutations.

UHL’s anomaly is rare form which suggests major early apoptosis creating an arrhythmogenic substrate which proved importaznt to demonstrate the re-entrant mechanism of ventricular arrhythmias.

These cardiomyopathies can be affected by a genetically superimposed myocarditis which is frequently the determinant of prognosis (Lopez-Ayala HR 2016).

Experimental ablation of the disease has been demonstrated on the Zebra fish and the mouse opening new vistas for its treatment and prevention (Saffitz Science 2015).

Biography:

Yiu-Fai Chen has completed his PhD in 1982 from Department of Physiology and Biophysics, University of Illinois (Urbana-Champaign) and postdoctoral training at the University of Alabama at Birmingham (UAB) School of Medicine. He is currently a Professor of Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine at UAB. He has been actively involved in cardiovascular research for more than 30 years and have been continuously funded by NIH and AHA, and pharmaceutical and biotechnology companies since 1985, upon completion of his postdoctoral training. He has published 176 peer-reviewed articles published in high impact journals.

Abstract:

Interleukin-8 receptors A/B (IL8RA/B) are homing device for neutrophils to target injured tissues. We developed an innovative targeted cell therapy using ECs that overexpress IL8RA/B to repair the cardiovascular injury. We transduced rat aortic ECs (RAECs), induced-pluripotent ECs (rat-iPS-ECs), or porcine coronary artery ECs (PCAECs) with adenoviruses carrying IL8RA/B genes. We hypothesize that healthy IL8RA/B-ECs can target injured arteries, thus inhibiting infiltration of neutrophils/macrophages and inflammatory responses, and accelerating re-endothelialization and suppressing the injury-induced neointima formation. In rat model, young male SD rats received balloon injury of the carotid artery and were immediately i.v.transfused with 1) vehicle, 2) 1.5x106 control RAECs or rat-iPS-ECs, or 3) 1.5x106 IL8RA/B-RAECs or rat-iPS-IL8RA/B-ECs. One group of rats were sacrificed 24 hr post injury to measure infiltration of neutrophils/macrophages and pro-inflammatory cytokines expression. Another group was sacrificed 2 wks post injury to measure neointima formation. In pig model, young Yorkshire pigs received stent implantation in the LAD and circumflex coronary arteries and were immediately i.v. transfused with 15x106 IL8RA/B-PCAECs or vehicle. Pigs were sacrificed 4 wks after stenting to measure restenosis. Rats transfused with IL8RA/B-RAECs or rat-iPS-IL8RA/B-ECs had significantly decreased neutrophils/macrophages infiltration, inflammatory cytokines expression, and neointima formation in injured arteries. Pigs transduced with IL8RA/B-PCAECs had reduced injury-induced arterial restenosis. Results indicate that transfused adult ECs or iPS-ECs with overexpression of IL8RA/B mimic the behavior of neutrophils that target to injured vessels, preventing inflammation and restenosis. Targeted delivery of ECs to arteries with endoluminal injury provides a novel strategy for the treatment of cardiovascular diseases.

Biography:

With over 35 years of non-profit management experience, Mary McGowan currently serves as Chief Executive Officer of WomenHeart: The National Coalition for Women with Heart Disease to ensure the successful implementation of the organization’s strategic direction and increase its visibility and brand recognition nationally. Prior to joining WomenHeart in 2010, McGowan served as Executive Director of the Allergy & Asthma Network. She held various positions with the American Academy of Pediatrics during her service of 18 years. McGowan earned a Masters Degree in Human Resources Development from the George Washington University and a B.A. from Trinity University.

Abstract:

WomenHeart is the only patient-centered organization solely devoted to improving the healthy and quality of life of the 42.7 million American women living with and at risk for heart disease. We have thousands of members, including women heart patients and their families, health care providers, advocates and consumers committed to helping women live longer, healthier lives. We provide an array of support programs for women nationwide, including our 110 local Support Networks in 40 states, each led by trained women heart patient volunteers – WomenHeart Champions. Support Networks meet monthly at National Hospital Alliance (NHA) member hospitals. rnrnThe NHA, comprised of 40 hospitals, is the nation’s only partnership program between WomenHeart and progressive hospitals across the country committed to advancing women’s heart health and gender specific cardiovascular care in their communities. This valuable alliance gives women heart patients leverage to improve their own lives, which results in better patient outcomes and lower readmission rates. Through the NHA, WomenHeart supports the trained WomenHeart Champions and provides an educational curriculum for their Support Network meetings. Additionally, we work with the hospitals' clinicians to improve their continuing education with quarterly webinars and media and co-branding opportunities. In 2015, WomenHeart launched its NHA Capacity Building Program, giving grants to hospitals who could otherwise not afford the membership in order to reach women heart patients in underserved communities. Our next step is to further expand the NHA by using predictive analysis to target hospitals that show high rates of readmission for specific heart conditions. rn