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

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:

Pampee P. Young is a tenured Associate Professor in the Department of Pathology, Microbiology and Immunology at Vanderbilt University Medical Center. She completed her undergraduate at Rice University in Houston, Tx and obtained her M.D/Ph.D. degrees at UT Southwestern in Dallas, Tx. Her basic science research program in regenerative medicine addresses the role of stem cells and our endogenous repair mechanisms to drive wound healing. Our work is funded by the Veterans Affairs, pharmaceuticals and NIH. Dr. Young also serves as the Medical Director of Transfusion Medicine and Stem Cell Laboratory at Vanderbilt University Hospital and the Veterans Affairs in Nashville.

Abstract:

The Wnt/β-catenin pathway is temporarily activated in the heart following myocardial infarct. The effect of therapeutic inhibition of Wnt pathway on post injury outcome are unknown. Using a newly available, small molecule, GNF6231, which averts Wnt pathway activation by inhibiting Wnt secretion, we sought to investigate whether therapeutic inhibition of the Wnt pathway temporarily after infarct can mitigate post injury cardiac dysfunction and fibrosis, hence reconciling discordant observations from genetic studies. Pharmacologic inhibition of the Wnt pathway by GNF-6231 significantly reduced the decline in cardiac function (∆Fractional Shortening%: 1.4±2.312 in GNF-6231 treated vs. -1.713±3.59 in vehicle-treated), prevented adverse cardiac remodeling, and reduced infarct size (9.07±3.98% vs. 17.18±4.97%). Histologically, Wnt inhibition augmented proliferation of interstitial cells, particularly in the distal myocardium, inhibited cell death, including apoptosis of cardiomyocytes, and reduced myofibroblast proliferation in the peri-infarct region. In vitro studies showed that Wnt inhibition increased proliferation of Sca1+ cardiac progenitors, improved survival of cardiomyocytes, and inhibited collagen I synthesis by cardiac myofibroblasts. Systemic, temporary pharmacologic inhibition of the Wnt pathway following MI resulted in improved function, reduced adverse remodeling and reduced infarct size in mice. Therapeutic Wnt inhibition affected multiple aspects of infarct repair: it promoted proliferation of cardiac progenitors and other interstitial cells, inhibited myofibroblast proliferation, improved cardiomyocyte survival, and reduced collagen I synthesis by myofibroblasts. Our data point to a promising role for Wnt inhibitory therapeutics as a new class of drugs to drive post MI repair and prevent heart failure.

Biography:

Dr Sibel Catirli Enar has completed her MD degree from Istanbul University in 1981.She has become Anestesiology specialist in 1985 and Cardiology specialist in 1992 after completing her education in Ä°stanbul University and Institute of Cardiology (Istanbul University).  She is Associate  Prof.of Cardiology,FESC and FASE.She is working at Turkiye Hospital and Ä°stanbul Memorial Hospital.She is a member of cardiac societies,involved in multicenter trials,and served as speakeror moderator or abstract grader in national and international conferences.She has published more than 25 papers and,contributed to book chapters .She is also serving as associate member at the board of Turkish Society of Cardiology (for 2016-2018).

Abstract:

Systemic hypertension causes hypertensive heart disease.Chronic systemic pressure loading results in left ventricular hypertrophy in order to maintain normal wall stress.In earlier stages of hypertension systolic function is preserved.But in later stages or with concomittant coronary artery disease,systolic function is also impaired.  The echocardiographic findings related with hypertension are as follows:Left ventricular hypertrophy(LVH),leftatrial(LA)dilatation,diastolic dysfunction,systolic dysfunction,mitral anular calcification,aortic sclerosis,aortic root dilatation. LVH is symmetrical in hypertension.   ASE/EAE guidelines and cut off limits for LVH:   LV septal wall thickness>0.9 cm for women and >1.0 cm for men.Mild LVH:LV septal thickness 1.-1.2 cm/1.1-1.3cm.Moderate LVH:1.3-1.5/1.4-1.5cm.Severe LVH:>1.6/>1.7 cm.Left ventricular hypertrophy causes different changes  in longutidunal,radial and circumferential mechanics in patients with hypertensive patients.Longitudinal strain is significantly decreased,while radial strain is increased. Left atrial dilatation is commonly seen in hypertensive patients. Left atrial dilation is related to diastolic dysfunction. Left atrial size is also a predictor of paroxysismal atrial fibrillation in hypertensive patients. Recent studies have shown that measurement of left atrial strain with speckle tracking may be useful in determining left atrial function in hypertensive patients.According to the studies,it has been shown that LA strain  values are lower in hypertensive patients when compared to normals, irrespective to the presence of LA enlargement or LVH.Decrease in SR values are present in all three phases of LA function. Reason for LA dysfunction in hypertensive patients is explained by the chronic pressure exposure of the LA,LA pressure rise and reduction of reservoir and conduit functions. In the earliest stages of the disease,systolic function is preserved unless coronary artery disease accompanies.Small,hypertrophic left ventricule is typical for this form of the disease.    However, recent studies using 2D speckle tracking strain demonstrate that impaired myocardial systolic deformation occurs in hypertensive patients.Therefore,systolic left ventricular longitudinal strain decreases  in the early stages of left ventricular remodelling.     Mitral anular calcification is frequently seen in  chronic hypertensive patients.It is the reason for mild or moderate mitral regurgitation in these patients.  Measures of right ventricular deformation are reduced in patients with LVH secondary to hypertension.So,LVH may cause early sub clinical RV dysfunctionaswell. According to the most recent guidelines,it is stated that initiation or monitoring the response to antihypertensive response is based on clinical parameters. However,periodic evaluation of cardiac function and morphology by echocardiography are necessary because of the progressive charasterstics of hypertensive cardiomyopathy.

Biography:

Dr. Maass joined NYU School of Medicine in 2008 after completing her PhD at the Rheinische Friedrich-Wilhelms-Universität in Bonn, Germany and a postdoctoral fellowship in experimental electrophysiology at Upstate Medical University in Syracuse, NY. She is research assistant professor of medicine at the NYU Leon H. Harney Divison of Cardiology, and specializes in mouse molecular genetics, embryonic stem cell biology and experimental models of cardiovascular development and disease, evidenced by numerous publications. Dr. Maass serves as associate F1000 faculty member for cardiovascular pharmacology and as scientific peer-reviewer, including the American Heart Association’s regenerative cell biology Peer Review Committee.

Abstract:

The majority of cardiac fatalities occur due to cardiac arrhythmias. Clinical data implicate distal parts of the specialized cardiac conduction system, the Purkinje fiber network, as main trigger of ventricular tachyarrhythmia. Owing to the rareness of this cell type, deficiencies in understanding processes governing Purkinje cell differentiation and physiology remain. The discovery of induced cell reprogramming has made generation of target cells from somatic human tissue practical. We recently published a reporter gene based embryonic stem cell model of murine Purkinje cells. Using this cell model, we could perform high throughput transcriptional profiling and compare the expression profile to previous published data obtained from adult hearts. We detected high expression of described Purkinje cell transcription factors, including Tbx3, Tbx5, Irx3, Irx5, Etv1, Hopx, and Nkx2.5. Ongoing work characterizes the top-enriched transcription factors towards their transdifferentiation potential, namely generation of Purkinje cells from pluripotent stem cells or fibroblasts. Towards translational applications, we extended our research to human induced pluripotent stem cells (hiPS). We identified cardiomyocyte subpopulations expressing Purkinje cell markers, including Etv1 and Cntn2 (2.9% Cntn2+TroponinT+; 2.7% Cntn2+Etv1+) and detected increased Cntn2 expression over time. Additionally, we have developed a human iPS Purkinje cell reporter line by targeting the Cntn2 locus with a fluorescent reporter gene using CRISPR/Cas9 technology. Using these complementary approaches, we seek to optimize the generation of cardiac conduction system cells for downstream applications, including screening platforms for urgently needed anti-arrhythmic drugs, as clinical tools in personalized medicine approaches or for regenerative cell replacement therapies.

Biography:

2007: Graduate of Faculty of Medicine, School of Heath Sciences, University of Thessaly, Larissa, Greece. 2011-2012: Performance specialty of pathology in the general hospital of Kozani, Greece.2013-2016: Performance specialty of cardiology in the general hospital of Kilkis, Greece. 2010- The present: Scientific collaborator of the Respiratory Medicine Department and Sleep Laboratory, University Hospital of Larissa, Greece.2013: European Resuscitation Council ALS PROVIDER COURSE2/2016: Doctor of Philosophy degree (PhD) of the University of Thessaly, Larissa, Greece. Doctoral thesis: ‘‘Cardiovascular risk in mild-moderate Obstructive Sleep Apnea Syndrome (OSAS)’’. Oral Presentation of clinical cases (‘‘Ebstein’s anomaly’’) in the Cardiology Symposium entitled ‘Advancements in Cardiology 2015’ held in Veroia, Greece, 24 January 2015.Speech at the 22th National Pulmonology Conference (5-7 December 2013, Athens) entitled: ‘‘Identifying phenotypes of Obstructive Sleep Apnea Syndrome via Hierarchical Cluster Analysis.’’Speech at the 21th National Pulmonology Conference (18-21 October 2012, Athens) entitled: ‘‘The DJ-1 protein as a biomarker in Obstructive Sleep Apnea Syndrome’.’Poster at the 4th Congress of Pathology of Central Greece (29-31 March 2012, Larissa) entitled ‘‘Stevens-Johnson Syndrome -Toxic Epidermal Necrolysis (or Lyell) - Retrospective Study.’’

Abstract:

It is estimated that 30% to 40% of hypertensive patients have OSA, and 50% to 56% of OSA patients have hypertension. Scientific data about the interaction between OSA and hypertension are continuously increasing. However, it had been difficult to clarify the cause-effect relationship between the two disorders. Data from some studies support a dose-response relationship of OSA at baseline and the cumulative incidence of hypertension. In contrast, other studies have reported that the unadjusted risk of hypertension increases in concert with AHI (apnea-hypopnea index), but this association was not significant after adjustment for potential confounding variables. Latest data from a retrospective study published in the ‘‘Journal of Clinical Hypertension’’ have revealed that age, BMI, comorbidity (CCI), daytime oxygen saturation, and indices of hypoxia during sleep are the most precise predictors for hypertension. In contrast, AHI and DI (desaturation index) participated weakly in the statistical model. Therefore, although AHI and DI were independent predictive factors for hypertension, both were not included in the most accurate predictors for development of hypertension. It seems that AHI and DI are more complex measures reflecting the degree of intermittent hypoxia, and therefore are susceptible to variability in the clinical setting. It is suggested that daytime and nocturnal hypoxemia as consequences of chronic intermittent hypoxia play a central role in OSA-related hypertension. In particular, the shift from chronic intermittent hypoxia to daytime and nocturnal hypoxia may represent a direct prelude to the development of hypertension.

Biography:

Dr. Wellnhofer has completed his MD in 1984 at Technical University in Munich and his PhD 2010 at Charité University Medicine Berlin on the field of “modelling and simulation in cardiac imaging”. He has done studies in informatics and statistics as well as health economy. He is clinical cardiologist, scientist and university teacher. His current fields of work are cardiac imaging in particular of coronary atherosclerosis, biomedical informatics and statistics, regulatory issues regarding software as medical device and health technology assessment. He published more than 90 papers in reputed journals and holds several patents. His h-index is 23

Abstract:

Dobutamine stress CMR (DCMR) is an accurate and safe non-invasive test for coronary artery disease (CAD) with high negative predictive value. Direct catheterization (CA) is still an alternative approach that is incentivized by the current reimbursement policy in many countries. Since long-term outcome and cost data from randomized controlled prospective trials are rarely available when new health technologies emerge, evidence based reimbursement policy requires retrospective data mining and lags behind medical and technical evolution. This paper presents level five HTA data on DCMR based on a long term follow-up of patients with suspected stable CAD (sCAD) who underwent DCMR and controls with direct CA. We expected that a DCMR guided approach would be at least as effective as direct CA with respect to survival and more patient friendly in terms of fewer hospitalizations during follow-up by avoiding direct CA. Generally, we suggest data mining digital documentation of early adoption phases of new technologies as source of evidence. This study was a single center retrospective cohort trial that compares two different pathways for managing patients with sCAD and intermediate event risk. Groups (CMR: 209 pts. CA: 293 pts) were matched by propensity scores. Clinical data were collected from institutional quality assurance and research databases. Median patient follow-up was 7.9 years. Primary clinical endpoints were death and cardiac re-hospitalizations. The cost data were calculated per patient and hospital stay from original resource utilization data provided to the German federal InEK/G-DRG database. We chose cost contribution accounting as method to compare both approaches.

Biography:

Dr.Omer ISIK has completed his MD degree at the age of 25 years in 1981 from Hacettepe University and gained his speciality in Thoracic and Cardiovascular Surgery from Kosuyolu Heart and Research Center (Istanbul, Turkey) at 1987 . He became, first vice chief, and than Chief of the Surgery department in the same center in in 1991, and 1992 respectively, until 1997. He gained the “Associate Professor of Thoracic and Cardiovascular Surgery” degree in 1991, and the “Professor of Thoracic and Cardiovascular Surgery” in 1997. He studied as the Staff surgeon, Head of the dept.of Cardiovascular Surgery, Dean, Vice Dean in various University Hospitals, and private hospitals. He is the Director of Cardiovascular Department of the Pendik Regional Hospital in Istanbul. He has more than 100 International publications, and more than 200 speaks in International meetings; 4 Book Chapters. He had been chairman, vice chairman in more than 10 national, and international organizations, and editorial board of more than 15 national and international journals.

Abstract:

Prosthetic graft replacement has been almost the most standard surgical therapy of the aortic aneurysms and/or the dissections. Bleeding from the suture lines is one of the most serious complications in early postoperative period which may lead to re-establishing the cardiopulmonary bypass. At late postoperative period, the ‘pseudoaneurysm’ formation may occur due to this operative procedure. Some preventive techniques have been reported to overcome to those complications such as using strips, pledgeds, inclusion of the prosthetic graft into the aorta or applying of tissue adhesives, etc. But, almost all of them are not free of adverse effects, such as inflammation, infection, and dense adhesions, etc.We have described a new an a novel technique, named “eversion technique” to minimizing the complications of aortic graft replacement. The technique is described simply as everything the native aortic tissue during the anastomosis and so reinforcing the suture line by a fresh and living tissue.We have applied this technique in 42 patients who undergone to ascending aortic replacement for the ascending aortic aneurysm and dissection in a period of 2 years. Those group have been analyzed retrospectively, and the derived data reported. We haven’t seen any complication due to the operation in-general and due to the described technique itself.The “Eversion Technique” in aortic surgery is a simple, reliable, and reproducible technique to reduce the complications of the aortic prosthetic graft replacement.

Biography:

Dr. Susmita Chakrabarti has completed her PhD from Jadavpur University, Kolkata, India and currently pursuing her studies at the Cleveland Clinic Foundation, Cleveland, Ohio. She has published her research work in many reputed journals including Cell. Because of enormous promise of this study in cardiovascular research, MOG1 article was selected by the Editors as one of the most important manuscripts in Circulation’s Topic Review series published in Circulation and the Circulation subspecialty journals in the year of 2013.

Abstract:

Despite tremendous improvements in its prevention and treatment, cardiac-arrhythmias are themajor cause of morbidity and mortality worldwide accounting for >1.2 million hospitalizations and 400,000 sudden-deaths each year in the United States.The cardiac voltage gated sodium channel, Nav1.5, is crucial for maintaining normal cardiac rhythm. Loss-of-function mutations in the Nav1.5-encoding gene SCN5A cause a vast array of cardiac disorders including Brugada Syndrome (BrS), Sick Sinus Syndrome (SSS), Dilated Cardiomyopathy (DCM), Cardiac Conduction Disease (CCD) and Atrial Fibrillation (AF). However, no effective treatment is available for these syndromes, except for invasive implantation of defibrillators or pacemakers in some cases. Defects in cell-surface-trafficking of ion-channels have been demonstrated to be a unique molecular mechanism underlying a variety of arrhythmic disorders. As SCN5A-mutations causing BrS, DCM and SSS act by loss-of-function; agents increasing cardiac-sodium-current (INa) may aid towards safe, effective treatment. In 2008, we reported that a 20kD protein MOG1 is a novel cofactor modulating Nav1.5-function. In 2013, we demonstrated the therapeutic potential of MOG1 in vitro to rescue the Nav1.5-trafficking-defects and reduced INa associated with BrS, DCM and SSS. We are currently evaluating the therapeutic potential of MOG1 in vivo. Reduced INa has also been associated with inherited cardiovascular disorders like myocardial infarctions/ ischemia and heart-failure. Thus, the MOG1-therapy to facilitate membrane-trafficking of Nav1.5 may be utilized for the trafficking-defective subset of cardiac channelopathies.

Biography:

I am a PhD.candidate, 29 years old, male and study in Nanjing medical university, Nanjing, China. My Ph.D. supervisor is Dr. Zhijian Yang who has received your invitation to attend the “11th International Cardiac Conference”to be held during September 12-13, 2016. Dr. Zhijian Yang has published more than 20 papers in reputed journals and has been serving as an editorial board member of repute. As his Ph.D. student, I am now engaged in the study regarding the regeneration of the infarcted heart. Our study results are encouraging and the abstract is shown above. I am very excited now to apply to attend the “11th International Cardiac Conference”. I hope to have the opportunity to listen to the speeches from so many outstanding experts worldwide and communicate with them face to face. I am looking forward to hearing from you. Thanks.

Abstract:

Ischemic heart disease is the leading cause of morbidity and mortality worldwide due to the inability of the heart to replace lost myocytes. While the discovery of c-kit+ cardiac stem cells (CSCs) provides us a new opportunity to repair the damaged heart, the proliferation, differentiation and regulation of the CSCs remains elusive. Therefore, here we investigated whether adenovirus vector containing hepatocyte growth factor gene (Ad-HGF) can promote the proliferation and differentiation of c-kit+ CSCs into cardiomyocytes, smooth muscle cells or endothelial cells. We firstly discovered a positive correlation between the expression levels of HGF and c-kit+ CSCs among neonatal, adult and senior SD rats in vivo. Notably, epicardial injection of Ad-HGF following MI activates c-kit+ CSCs and promotes proliferation and differentiation into cardiomyocyte, endothelial cell and smooth muscle cell in vivo. Ad-HGF treatment promotes angiogenesis, inhibits fibrosis and improves the cardiac function of the rat following MI. The protective role of HGF may be due to the activation of c-Met receptor, and subsequent activation of the p-Akt-p21/p27-cell cycle pathway. Meanwhile, the levels of Bcl-2/Bcl-xL were elevated, while the levels of cleaved caspase 3 and Bax were reduced. Taken together, Ad-HGF promotes heart repair by regulating c-kit+ cardiac stem cell proliferation and differentiation and prevents heart failure following MI. This approach may provide new strategy for the treatment of ischemic heart disease.

Biography:

Yunle Wang is a Ph. D. student in Nanjing Medical University. She is major in cardiology and works for the team of Prof. Zhijian Yang. Her studies focus on the protection effect of hepatocyte growth factor on myocardial infarction, and the function of autophagy in myocardial ischemia disease.

Abstract:

Hepatocyte growth factor (HGF) is widely known as a protective factor in ischemic myocardium, however the mechanism remains unclear. Autophagy at early stage of hypoxia has been demonstrated to play an important role in protecting myocardium both in vivo and vitro. We performed this study to investigate the association between the protective effect of HGF and autophagy. We found that autophagy in neonatal rat ventricular myocytes (NRVMs) increased at early stage after hypoxia and HGF release was consistent with the change of autophagy. Then we added exogenous HGF to the cells and enhanced autophagy was detected, while neutralizing HGF got opposite effects. However, after inhibition of autophagy using 3-methyladenine, apoptosis of myocytes increased, indicated that the protective effect of HGF was autophagy-dependent. This may be associated with clearance of injured mitochondria as the marker of mitochondrial autophagy, Parkin, was induced when HGF was added to cell medium. Our results provided insight into a potential mechanism in which exogenous HGF prevented NRVMs from apoptosis after hyoxia. Upregulation of Parkin through administration of exogenous HGF may be a potential therapeutic strategy for myocytes ischemia.

Biography:

Dr Dileep Rohra graduated with medicine as major from Sindh Medical College, Karachi, Pakistan in 1990. After that, he worked as a Lecturer of Pharmacology at the Chandka Medical College, Larkana, Pakistan. He obtained his M.Phil in Pharmacology from Jinnah Postgraduate Medical Centre, Karachi in 1996 and returned to Chandka Medical College to work as an Assistant Professor. In 1999, he was awarded the prestigious Monbusho scholarship by the Ministry of Education, Japan to pursue PhD.

Abstract:

Adrenoceptors AR are important targets in therapeutics. Competitive antagonists at -AR are among the most widely used drugs in cardiovascular medicine. It has been shown that 1-AR are present and functional in inner ear epithelial cells as well as in neuronal cells that are involved in auditory transmission. Beside the presence of 1-AR in marginal cells, these are also present in outer hair cells, outer sulcus, supporting cells and transitional cells of vestibular labyrinth and in inner hair cells. If -AR are present and functional in areas which are concerned with auditory system, then decreasing the function of those physiologically active receptors may result in defects in the hearing. Thus the current study was conducted to test the hypothesis that patients in cardiology department who are prescribed β-blockers will have a hearing loss compared to patients in the same department who do not receive β-blockers. The specific aim was to determine the association of use of β-blockers and hearing loss. This was a cross-sectional study conducted on the patients visiting the Adult Cardiology Clinic or admitted at Heart Centre of King Faisal Specialist Hospital & Research Centre (KFSHRC), Riyadh, Saudi Arabia. All recruited study participants were divided into two groups based on their usage and non-usage of β-blockers. Group A were patients taking β-blockers and Group B were patients not taking β-blockers. Audiometry was performed on all the patients. A total of 212 patients were screened; however hearing test was performed on 151 patients. Out of those then 25 participants were excluded because of the presence of middle ear pathology. Therefore, the study population consisted of 126 patients. 68 patients were males (54%), and mean age was 40±11.47 years. Sixty patients were on β-blockers (β-blocker group); and 66 patients were not on β-blockers (non- β-blocker group). There was no significant difference in patients’ age, gender, and the presence of diabetes mellitus, hypertension or dyslipidemia between the two groups. However, cardiac failure and dilated cardiomyopathy were more frequent in β-blocker group. Accordingly, concomitant use of frusemide was significantly higher in β-blocker group, which is also an important drug for the management of these diseases. Audiometric analysis revealed that patients on β-blockers had significantly higher prevalence of hearing loss at high frequencies (4000-8000Hz). This finding of more hearing loss with use of -blockers was also noted at different frequencies while analyzing each β-blocker separately (carvedilol, metoprolol, and atenolol). Concluding, this is the first study which shows that use of -blockets on chronic basis is associated with some degree of hearing loss.

Biography:

Dr Sibel Catirli Enar has completed her MD degree from Istanbul University in 1981.She has become Anestesiology specialist in 1985 and Cardiology specialist in 1992 after completing her education in Ä°stanbul University and Institute of Cardiology (Istanbul University). She is Associate Prof.of Cardiology,FESC and FASE.She is working at Turkiye Hospital and Ä°stanbul Memorial Hospital.She is a member of cardiac societies,involved in multicenter trials,and served as speakeror moderator or abstract grader in national and international conferences.She has published more than 25 papers and,contributed to book chapters .She is also serving as associate member at the board of Turkish Society of Cardiology (for 2016-2018).

Abstract:

Systemic hypertension causes,  hypertensive heart disease.Chronic systemic pressure loading results in left ventricular hypertrophy in order to maintain normal wall stress.In earlier stages of hypertension systolic function is preserved.But in later stages or with concomittant coronary artery disease,systolic function is also impaired. The echocardiographic findings related with hypertension are as follows: Left ventricular hypertrophy (LVH),left atrial (LA) dilatation,diastolic dysfunction,systolic dysfunction,mitral anular calcification,aortic sclerosis,aortic root dilatation. LVH is symmetrical in hypertension. ASE/EAE guidelines and cut off limits for LVH: LV septal wall thickness>0.9 cm for women and >1.0 cm for men.Mild LVH:LV septal thickness 1.-1.2 cm/1.1-1.3cm.Moderate LVH:1.3-1.5/1.4-1.5cm.Severe LVH:>1.6/>1.7 cm. Left ventricular hypertrophy causes different changes in longutidunal,radial and circumferential mechanics in patients with hypertensive patients.Longitudinal strain is significantly decreased,while radial strain is increased. Left atrial dilatation is commonly seen in hypertensive patients. Left atrial dilation is related to diastolic dysfunction. Left atrial size is also a predictor of paroxysismal atrial fibrillation in hypertensive patients. Recent studies have shown that measurement of left atrial strain with speckle tracking may be useful in determining left atrial function in hypertensive patients. According to the studies,it has been shown that LA strain values are lower in hypertensive patients when compared to normals, irrespective to the presence of LA enlargement or LVH.Decrease in SR values are present in all three phases of LA function. Reason for LA dysfunction in hypertensive patients is explained by the chronic pressure exposure of the LA,LA pressure rise and reduction of reservoir and conduit functions. In the earliest stages of the disease,systolic function is preserved unless coronary artery disease accompanies.Small,hypertrophic left ventricule is typical for this form of the disease. However, recent studies using 2D speckle tracking strain demonstrate that impaired myocardial systolic deformation occurs in hypertensive patients.Therefore,systolic left ventricular longitudinal strain decreases in the early stages of left ventricular remodelling. Mitral anular calcification is frequently seen in chronic hypertensive patients.It is the reason for mild or moderate mitral regurgitation in these patients. Measures of right ventricular deformation are reduced in patients with LVH secondary to hypertension.So,LVH may cause early sub clinical RV dysfunction as well. According to the most recent guidelines,it is stated that initiation or monitoring the response to antihypertensive response is based on clinical parameters. However,periodic evaluation of cardiac function and morphology by echocardiography are necessary because of the progressive charasterstics of hypertensive cardiomyopathy

Biography:

Dr. Wellnhofer has completed his MD in 1984 at Technical University in Munich and his PhD 2010 at Charité University Medicine Berlin on the field of “modelling and simulation in cardiac imaging”. He has done studies in informatics and statistics as well as health economy. He is clinical cardiologist, scientist and university teacher. His current fields of work are cardiac imaging in particular of coronary atherosclerosis, biomedical informatics and statistics, regulatory issues regarding software as medical device and health technology assessment. He published  more than  90 papers in reputed journals and holds several patents. His h-index is 23

Abstract:

Dobutamine stress CMR (DCMR) is an accurate and safe non-invasive test for coronary artery disease (CAD) with high negative predictive value. Direct catheterization (CA) is still an alternative approach that is incentivized by the current reimbursement policy in many countries. Since long-term outcome and cost data from randomized controlled prospective trials are rarely available when new health technologies emerge, evidence based reimbursement policy requires retrospective data mining and lags behind medical and technical evolution. This paper presents level five HTA data on DCMR based on a long term follow-up of patients with suspected stable CAD (sCAD) who underwent DCMR and controls with direct CA. We expected that a DCMR guided approach would be at least as effective as direct CA with respect to survival and more patient friendly in terms of fewer hospitalizations during follow-up by avoiding direct CA. Generally, we suggest data mining digital documentation of early adoption phases of new technologies as source of evidence. This study was a single center retrospective cohort trial that compares two different pathways for managing patients with sCAD and intermediate event risk. Groups (CMR: 209 pts. CA: 293 pts) were matched by propensity scores. Clinical data were collected from institutional quality assurance and research databases. Median patient follow-up was 7.9 years. Primary clinical endpoints were death and cardiac re-hospitalizations. The cost data were calculated per patient and hospital stay from original resource utilization data provided to the German federal InEK/G-DRG database. We chose cost contribution accounting as method to compare both approaches. 

Biography:

Dr. Maass joined NYU School of Medicine in 2008 after completing her PhD at the Rheinische Friedrich-Wilhelms-Universität in Bonn, Germany and a postdoctoral fellowship in experimental electrophysiology at Upstate Medical University in Syracuse, NY. She is research assistant professor of medicine at the NYU Leon H. Harney Divison of Cardiologyy, and specializes in mouse molecular genetics, embryonic stem cell biology and experimental models of cardiovascular development and disease, evidenced by numerous publications. Dr. Maass serves as associate F1000 faculty member for cardiovascular pharmacology and as scientific peer-reviewer, including the American Heart Association’s regenerative cell biology Peer Review Committee.

Abstract:

The majority of cardiac fatalities occur due to cardiac arrhythmias. Clinical data implicate distal parts of the specialized cardiac conduction system, the Purkinje fiber network, as main trigger of ventricular tachyarrhythmia. Owing to the rareness of this cell type, deficiencies in understanding processes governing Purkinje cell differentiation and physiology remain. The discovery of induced cell reprogramming has made generation of target cells from somatic human tissue practical. We recently published a reporter gene based embryonic stem cell model of murine Purkinje cells. Using this cell model, we could perform high throughput transcriptional profiling and compare the expression profile to previous published data obtained from adult hearts. We detected high expression of described Purkinje cell transcription factors, including Tbx3, Tbx5, Irx3, Irx5, Etv1, Hopx, and Nkx2.5. Ongoing work characterizes the top-enriched transcription factors towards their transdifferentiation potential, namely generation of Purkinje cells from pluripotent stem cells or fibroblasts. Towards translational applications, we extended our research to human induced pluripotent stem cells (hiPS). We identified cardiomyocyte subpopulations expressing Purkinje cell markers, including Etv1 and Cntn2 (2.9% Cntn2+TroponinT+; 2.7% Cntn2+Etv1+) and detected increased Cntn2 expression over time. Additionally, we have developed a human iPS Purkinje cell reporter line by targeting the Cntn2 locus with a fluorescent reporter gene using CRISPR/Cas9 technology. Using these complementary approaches, we seek to optimize the generation of cardiac conduction system cells for downstream applications, including screening platforms for urgently needed anti-arrhythmic drugs, as clinical tools in personalized medicine approaches or for regenerative cell replacement therapies.

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:

A 5 years old child died suddenly beside his father watching television. The immediate appeal of the EMS and Fire Brigade did not allow resuscitation practiced under ideal conditions. The child had a bipolar, epicardial, dual-chamber PM, for complete AV Block detected in utero. A lead fracture discovered during follow-up led to unipolarize the atrial lead system.. However, another lead fracture was also visible at the bifurcation of the ventricular lead system. Nevertheless pacing of both atrial and ventricular chambers was OK.  LVEF was borderline lower limit can be explained by abnormal area of contraction near the LV apex. The case is still in Court after failure of two conciliation committees. Two university hospitals, eight lawyers with one PM technician, 17 doctors and cardiologists, four experts including two super-experts (including GF) were involved. Up to now this case has been presented to 212 doctors and cardiologists who have not found the solution. Seven half-days to study a 500-pages file were necessary to completely elucidate the mechanism of this irreversible death. The conclusion which needs knowledge in Medicine, Cardiology, PM technology and heart Pathology (despite absence of autopsy) suffers no alternative...

The case will be presented step by step asking participation of the audience. The first more important document is the last standard ECG recorded before the catastrophe showing a consistent but difficult to see abnormal phenomenon, the second are laboratory data concerning an asymptomatic lupus detected in the mother by specific antibodies which may explain AV block in utero. The third is the standard X-Ray showing the two leads fracture which was the point of major discussion. The last is the post-mortem interrogation of PM memories, which was overlooked by the expert technician of the pacemaker company. 

Biography:

Abstract:

It is estimated that 30% to 40% of hypertensive patients have OSA, and 50% to 56% of OSA patients have hypertension. Scientific data about the interaction between OSA and hypertension are continuously increasing. However, it had been difficult to clarify the cause-effect relationship between the two disorders. Data from some studies support a dose-response relationship of OSA at baseline and the cumulative incidence of hypertension.^1,2 In contrast, other studies have reported that the unadjusted risk of hypertension increases in concert with AHI (apnea-hypopnea index), but this association was not significant after adjustment for potential confounding variables.^3,4 Latest data from a retrospective study published in the ‘‘Journal of Clinical Hypertension’’ have revealed that age, BMI, comorbidity (CCI), daytime oxygen saturation, and indices of hypoxia during sleep are the most precise predictors for hypertension. In contrast, AHI and DI (desaturation index) participated weakly in the statistical model. Therefore, although AHI and DI were independent predictive factors for hypertension, both were not included in the most accurate predictors for development of hypertension. It seems that AHI and DI are more complex measures reflecting the degree of intermittent hypoxia, and therefore are susceptible to variability in the clinical setting. It is suggested that daytime and nocturnal hypoxemia as consequences of chronic intermittent hypoxia play a central role in OSA-related hypertension. In particular, the shift from chronic intermittent hypoxia to daytime and nocturnal hypoxia may represent a direct prelude to the development of hypertension.⁵

Biography:

Oguzhan YILDIZ, MD, has completed his PhD at the age of 29 years from Hacettepe University and postdoctoral studies from University of California, Irvine. He is professor of Medical Pharmacology at Gulhane Faculty of Medicine. He has published more than 60 papers in reputed journals and has been serving as an editorial board member of repute. 

Abstract:

Interest has increased in the use of arterial conduits for CABG significantly in most major cardiac surgery centers around the world, because the number of patients receiving arterial grafts and our knowledge about the biologic characteristics of arterial grafts have increased. In addition, more advanced clinical protocols for the use of grafts have been developed and midterm results with alternative arterial grafts are encouraging. The internal mammary artery (IMA) has been shown to have greater long-term patency for coronary artery bypass grafting when compared with the saphenous vein graft. Because of the superior long-term results of the IMA, other arterial grafts which have recently been advocated include the radial artery (RA), the gastroepiploic artery (GEA), the inferior epigastric artery (IEA), the splenic artery, the subscapular artery, the inferior mesenteric artery, the descending branch of lateral femoral circumflex artery, the intercostal artery and the ulnar artery. One ofthe  various  manifestations  clinically  observed  among  these  arterial  grafts  is  a  different tendency to develop spasm during surgical dissection and during the perioperative period which could be the cause of perioperative morbidity and mortalitiy. For example, there are reports of vasoactive drugs altering IMA graft flow. Moreover, there is accumulating evidence that blood flow in arterial grafts is insufficient in some circumstances. Many vasoconstrictors  (spasmogens)  may  cause  arterial  grafts  spasm.  Accordingly,  antispastic therapy  is  important  in  the  development  of  arterial  grafts  and  the  nature  of  constrictor substances that cause arterial graft spasm needs to be determined. In recent years, the problem of  graft  spasm  has  become  more  frequent  with  the  increasing  use  of  new  arterial  grafts. Therefore, it is essential for surgeons to understand the causes of vascular graft spasm, to improve  patency  rates  and  to  use  the  optimal  vasodilator  in  the  most  appropriate  way  to counteract vasospasm. Surgeons have studied graft pharmacology by measuring the effects of vasodilators on blood flow through arterial grafts before they were attached to the heart. Pharmacologists have also joined the study of graft pharmacology by evaluating endothelial and smooth muscle function  of  bypass  grafts  using  their  standard  in  vitro  method,  the  isolated  vessel  ring preparation in the organ bath. However, results from these in vitro studies need to be carefully extrapolated to the clinical situations, where the conditions of the arterial grafts are complicated. Even so, the organ bath method can provide very useful information about the effects of vasoactive substances in the arterial grafts. Several vasodilators have been tested and various antispastic methods have been suggested to prevent graft spasm; including papaverine, phenoxybenzamine, calcium antagonists and nitrates etc. Choice of a pharmacological agent to overcome the vasospasm encountered in the arterial grafts must be on the basis of pharmacological studies. Accordingly, current state of knowledge based on experiments to study the pharmacological effect of a number of vasoconstrictor and vasodilator substances and the practical application of this knowledge will be summarized.

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 has been conducting women and heart disease-specific campaigns for the past two years with the goal of formulating key policy and research recommendations to advance the prevention, diagnosis, and treatment of heart disease in women. Drawing from our database of 20,000 members, we developed and conducted national patient education surveys approved by the Institutional Review Board and led telephone focus groups and patient round-tables. We obtained valuable input from women heart patients on specific topics related to heart disease. We then held key opinion leader workshops, in which researchers and policy experts discussed the results gathered from these surveys, focus groups, and round-tables and formulated key recommendations. WomenHeart released the results of these studies and key opinion leader workshops at briefings on Capitol Hill, thereby raising awareness among congressional staff. Additionally, these findings were published in peer reviewed journals such as Elsevier’s Women’s Health Issues, consequentially underscoring the importance of these heart health issues throughout the medical community. In this workshop, we will highlight how our topic-specific campaigns on heart disease in women have the potential to draw the attention of policy-makers, healthcare professionals, and the public. We will focus on the following three recent topic-specific campaigns:

·         Cholesterol and Familial Hypercholesterolemia

·         Heart Failure and Women

·         Atrial Fibrillation and Stroke Risk in Women

Biography:

I am a PhD.candidate, 29 years old, male and study in Nanjing medical university, Nanjing, China. My Ph.D. supervisor is Dr. Zhijian Yang. He has published more than 20 papers in reputed journals and has been serving as an editorial board member of repute. As his Ph.D. student, I am now engaged in the study regarding the regeneration of the infarcted heart. Our study results are encouraging and the abstract is shown above.

Abstract:

Ischemic heart disease is the leading cause of morbidity and mortality worldwide due to the inability of the heart to replace lost myocytes. While the discovery of c-kit⁺ cardiac stem cells (CSCs) provides us a new opportunity to repair the damaged heart, the proliferation, differentiation and regulation of the CSCs remains elusive. Therefore, here we investigated whether adenovirus vector containing hepatocyte growth factor gene (Ad-HGF) can promote the proliferation and differentiation of c-kit⁺ CSCs into cardiomyocytes, smooth muscle cells or endothelial cells. We firstly discovered a positive correlation between the expression levels of HGF and c-kit⁺ CSCs among neonatal, adult and senior SD rats in vivo. Notably, epicardial injection of Ad-HGF following MI activates c-kit⁺ CSCs and promotes proliferation and differentiation into cardiomyocyte, endothelial cell and smooth muscle cell in vivo. Ad-HGF treatment promotes angiogenesis, inhibits fibrosis and improves the cardiac function of the rat following MI. The protective role of HGF may be due to the activation of c-Met receptor, and subsequent activation of the p-Akt-p21/p27-cell cycle pathway. Meanwhile, the levels of Bcl-2/Bcl-xL were elevated, while the levels of cleaved caspase 3 and Bax were reduced. Taken together, Ad-HGF promotes heart repair by regulating c-kit⁺ cardiac stem cell proliferation and differentiation and prevents heart failure following MI. This approach may provide new strategy for the treatment of ischemic heart disease.

Biography:

Yunle Wang is a Ph. D. student in Nanjing Medical University. She is major in cardiology and works for the team of Prof. Zhijian Yang. Her studies focus on the protection effect of hepatocyte growth factor on myocardial infarction, and the function of autophagy in myocardial ischemia disease.

Abstract:

Hepatocyte growth factor (HGF) is widely known as a protective factor in ischemic myocardium, however the mechanism remains unclear. Autophagy at early stage of hypoxia has been demonstrated to play an important role in protecting myocardium both in vivo and in vitro. We performed this study to investigate the association between the protective effect of HGF and autophagy. We found that autophagy in neonatal rat ventricular myocytes (NRVMs) increased at early stage after hypoxia and HGF release was consistent with the change of autophagy. Then we added exogenous HGF to the cells and enhanced autophagy was detected, while neutralizing HGF got opposite effects. However, after inhibition of autophagy using 3-methyladenine, apoptosis of myocytes increased, indicated that the protective effect of HGF was autophagy-dependent. This may be associated with clearance of injured mitochondria as the marker of mitochondrial autophagy, Parkin, was induced when HGF was added to cell medium. Our results provided insight into a potential mechanism in which exogenous HGF prevented NRVMs from apoptosis after hyoxia. Upregulation of Parkin through administration of exogenous HGF may be a potential therapeutic strategy for myocytes ischemia.

Biography:

Waleed Al-Darzi has completed his medical school from Ain Shams University, Faculy of Medicine, Egypt. He is ECFMG certified. He is currently a second year Internal Medicine resident at Henry Ford Hospital, Detroit, Michigan, USA.         
 

Abstract:

Intracardiac thrombosis (ICT) during orthotropic liver transplantation (OLT) is not a common event; however, it is associated with high mortality. Although many risk factors are suggested, these events were considered multifactorial. We are reporting a case of right cardiac chamber thrombus during OLT presented as a sudden cardiac arrest during reperfusion stage. A 54-year-old male with history of decompensated liver disease secondary to primary biliary cirrhosis with secondary portal hypertension, ascites, and hydrothorax who presented for liver transplantation with MELD score of 31. Patient was listed for liver transplantation from a deceased donor. Pertinent pre-operative laboratory studies showed PT of 38 seconds, INR of 1.27, PTT of 15.9 seconds, and platelets of 331 X 10⁹/L. Intraoperatively, reperfusion was not well tolerated. Severe hypotension developed followed by cardiac arrest with chest compressions for 1 minute. Ventricular fibrillation and ventricular tachycardia were recorded. Trans-esophageal Echocardiogram (TEE) showed Right sided intra cardiac thrombus. Heparin 5000 Units was administered with clot resolution. Patient developed profound coagulopathy post reperfusion. Despite one hour of packing and resuscitation, reversal was not sufficient for definitive closure. Temporary abdominal closure was performed. Unfortunately, patient’s course postoperatively was further complicated; including liver ischemia, renal failure and wound infection. Eventually, the received liver didn’t recover; patient was relisted and re-transplanted with a favorable outcome. Cardiac thrombosis should always be considered in patients having hemodynamic compromise during liver transplant surgery. TEE is a useful diagnostic tool in identifying these thrombi intraoperatively. Treatment and prevention of ICT is challenging. 

Biography:

Ahmed Abuzaanona has completed his MD from Al-Quds University, Faculty of medicine, Palestine. He is currently a second year internal medicine resident at Henry Ford hospital in Detroit, Michigan, USA.

Abstract:

Introduction:

Infective endocarditis (IE) is most commonly caused by staph, streptococcus or enterococcus species. Vagococcus is a distinct genus that has been identified in 1989.  One case of human infection was reported causing periodontal abscess. We report the first case of IE caused by Vagococcus fluvialis involving both aortic and mitral valves, presenting as an embolic stroke and requiring surgical intervention.

Case presentation:

A 34 year old female with a history of intravenous drug abuse and endocarditis presented with headache, fever and new onset blind spots after two weeks of toothache and purulent discharge in her oral cavity. On exam she was septic, with new left sided facial weakness, inferior quadranopsia and an apical pansystolic murmur. MRI of the brain showed subacute right occipitoparietal infarct. TEE then revealed mobile vegetations involving aortic and mitral valves, causing severe aortic and mitral insufficiency with ulceration of two of the aortic cusps, and felt to be the source of her embolic stroke. She was started on vancomycin and gentamycin, then switched to intravenous ampicillin and ceftriaxone after blood culture growth of Vagococcus fluvialis. She underwent bioprosthetic valve replacement of both valves with repair of aortic defect with pericardial patch four weeks into her treatment, and received 6 total weeks of antibiotics with resolution of her symptoms on follow up.

Discussion:

Embolic stroke due to IE should always be considered in patients presenting with neurological deficit in the setting of poor dentition and intravenous drug abuse. Vagococcus fluvialis appears to have a fulminant course when causing IE.

Biography:

http://cardiac.conferenceseries.com/Dr. jeffrey Maldonado has completed his Medical School from Universidad Nacional Pedro Henriquez Urena (UNPHU) in the Dominican republic in 2008. He is 3rd year resident of Internal Medicine at San Juan City Hospital in San Juan Puerto Rico. He has presented a poster presentation in the ACP in Boston 2015 named “An atypical case of autoimmune hepatitis in a 88 year old men”, Jeffrey also won first place at the research presentation in the ACP in Puerto in October 2015, named “Can Monocytosis be used as Independent Variable for diagnose of Deep vein thrombosis”. Besides that, Jeffrey went to the Jeopardy of the ACP to represent Puerto Rico during years  2014 and 2015.

Abstract:

In this case report a patient presents with high-output cardiac failure in the clinical setting of acute leukemia and leukostasis. Case particulars are presented, literature is reviewed and a potential mechanistic explanation is proposed to describe presentation and clinical findings.