Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 5th International Conference on Clinical & Experimental Cardiology Philadelphia, USA.

Day 1 :

  • Track 2: Congenital Heart Diseases
    Track 4: Biophysics and Systems Biology
Speaker

Chair

Arthur T. Martella

Our Lady of Lourdes Medical Center, USA

Speaker

Co-Chair

Michael Chorny

The Children’s Hospital of Philadelphia, USA

Session Introduction

Arthur T. Martella

Our Lady of Lourdes Medical Center, USA

Title: Minimally invasive coronary artery bypass grafting

Time : 15:25-15:45

Speaker
Biography:

Arthur Martella graduated from Jefferson Medical College (Philadelphia, Pa) in 1989. He completed his general surgery training at Albert Einstein Medical Center in The Bronx, NY. He then went on to University of Rochester for his Cardiothoracic Surgical Training. He is currently the Chief of Cardiothoracic Surgery at Our Lady of Lourdes Medical Center and has interest in robotic coronary surgery and minimally invasive valve surgery.

Abstract:

The invasiveness of coronary artery bypass grafting (CABG) surgery has not decreased since the operation was introduced over 40 years ago. Although the benefits of bilateral mammary artery use are well known, only 4 percent of CABG procedures utilize both mammary arteries. We have utilized two strategies to reduce the use of the sternotomy incision for multivessel coronary artery disease. The first is hybrid coronary revascularization (HCR) which combines a minimally invasive, sternal-sparing left internal mammary artery to left anterior descending coronary artery bypass (LIMA-LAD) with percutaneous coronary intervention (PCI) to non-LAD coronary lesions. We have utilized a robotic platform for mammary harvesting which facilitated the transition to a totally endoscopic (TECAB) approach for selected patients. The second is multivessel minimally invasive direct coronary artery bypass with utilization of bilateral mammary arteries and radial artery when appropriate. This approach has also been facilitated by the use of the Davinci Robot for bilateral mammary artery harvesting and the ability to reach the ascending aorta from the left thoracotomy for proximal anastomoses. We review our experience of the last 24 months with 182 patients and discuss how the procedures and the selection process have evolved during this time.

Christine Burgmeier

University Medical Center Ulm, Germany

Title: Reported cardiovascular events during laparoscopy in term and preterm neonates

Time : 16:40-17:00

Speaker
Biography:

Christine Burgmeier is a surgeon in training in the Department of General, Visceral and Pediatric Surgery at the University Medical Center Ulm, Germany. She completed her studies at the Ludwigs-Maximilians-University (LMU) Munich, Germany in 2006. Then she started her surgical training in Cardiothoracic and Vascular surgery, before she specialized in Pediatric Surgery in 2010. Her main research interest is minimal invasive surgery in term and preterm infants with cardiac anomalies.

Abstract:

Laparoscopy is progressively performed in pediatric surgery. Cardiac anomalies are supposed to be a contraindication to minimally invasive surgery, but until today there are no general recommendations. A few retrospective studies have reported promising results, but reports on intraoperative complications are scarce, especially in infants and neonates. The aim of this study was to review the literature for reported cardiovascular events during laparoscopy in neonates. Therefore, a systematic review of the literature using Pubmed, Medline and ScienceDirect was performed. Altogether, four single case reports presenting neonates who developed cardiovascular events during a laparoscopic procedure were identified. Two neonates were supposed to undergo laparoscopic pyloromyotomy and two laparoscopic repair of duodenal atresia. During the laparoscopic procedure three neonates developed a cardiac arrest and required CPR. One neonate presented bradycardia, hypotension and decrease of oxygen saturation a few minutes after creation of a capnoperitoneum. In all cases gas embolism through a patent umbilical vein was assumed to be responsible for the cardiovascular events during laparoscopy. Post- or intraoperative echocardiography revealed persistent fetal circulation in three of four neonates. All neonates were successfully resuscitated and did not present neurological or cardiopulmonary sequelae. In summary, gas (carbon dioxide or air) embolism is a rare but serious complication of laparoscopic surgery in neonates. Presence of an open umbilical vein and persistent fetal circulation are the most important risk factors. In case of surgical injury of the umbilical vein during open or closed placement of the trocar the risk of gas embolism has to be respected.

Pratibha Nallari

Osmania University, India

Title: Biomarkers and drug responsive genotype in long QT syndrome

Time : 17:00-17:20

Speaker
Biography:

Pratibha Nallari is a Professor at Dept. of Genetics, Osmania University, and Hyderabad carrying out considerable research in Indian population on Dilated Cardiomyopathy (DCM) and Hypertrophic Cardiomyopathy (HCM), Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) and Primary Pulmonary Hypertension (PPH) / Idiopathic Pulmonary Arterial Hypertension (IPAH). She has received an international grant from GlaxoSmithKline, UK apart from international collaboration with Sick kids hospital for research on ARVC. She has 125 papers to her credit in national and international peer reviewed journals apart from being one of the co-authors in a study published in Nature Genetics (2009). Dr. Nallari is also a member of various National/International bodies of human genetics, and has 70 novel variations patented in NCBI database to her credit.

Abstract:

Long QT Syndrome (LQTS), an ion channelopathy is a fatal cardiovascular disorder with a propensity to ventricular tachyarrhythmias. Although, gene's encoding the cardiac sodium, potassium and calcium-sodium channels are implicated in LQTS, apart from the influence of environmental factors and/or modifying genetic effects. Hence, the modifier genes - Beta-1 adrenergic receptor (ADRB1), Beta-2 adrenergic receptor (ADRB2), Atrial Natriuretic Peptide (NPPA) and Tumor Necrosis factor-alpha (TNF-α) gene/s were considered in the study in view of the variants being susceptible alleles, having pharmacogenomic importance. PCR-RFLP analysis was carried out on 46 LQTS, 69 first degree relatives (FDRs) and 150 controls of South Indian origin followed by statistical and In-silico analyses. ADRB1 polymorphism genotyping revealed that the South Indian cohort was monomorphic for S49 and R389 and ADRB2 exhibited R16 and E27 homozygous genotypes respectively. It was also hypothesized that the presence of R389 allele of ADRB1 may pave way for beta-blockers as a good therapeutic agent in LQTS patients and R16/E27 rare haplotype carriers can be evaluated for resistance to agonist-induced down regulation. TNF-α -308A allele of -308G/A and -1031C allele of -1031C/T were found to be predominant, and -238A allele of -238G/A was found to be significantly associated implying its role in LQTS etiology. Genotyping of NPPA -664C>G and 1766T>C revealed only ‘CC’ genotype and ‘TT’ genotypes respectively. In 1364 C>A polymorphism, predominanace of 1364C allele frequency points to its role in LQTS etiology. Three families each with two clinically affected/symptomatic LQTS probands exhibited CC genotype of 1364 C>A substitution. In-silico analysis of the polymorphisms predicted their effect on mRNA thermodynamic stability; splice site and spliceosome factor binding sites influencing the downstream signalling cascade. It was thus hypothesized that TNF-α promoter and NPPA polymorphisms may impair the ion channels causing prolonged APD and hence can be considered as potential biomarkers/diagnostic markers in case of LQTS. These polymorphisms play a role in cardiac remodelling/cardiogenesis and may be helpful in risk stratification of FDRs. The ADRB1 and ADRB2 genotypes seems to be of pharmacogenomic implication paving way for beta-blockers in the treatment and management of LQTS.

  • Track 1: Heart Diseases
Speaker

Chair

Anastasia Susie Mihailidou

Royal North Shore Hospital & Kolling Institute
Australia

Speaker

Co-Chair

Anthony Martin Gerdes

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

Session Introduction

Anastasia Susie Mihailidou (Conference Moderator)

Royal North Shore Hospital & Kolling Institute, Australia

Title: Standardizing skills for taking the pressure off

Time : 10:35-10:55

Speaker
Biography:

Anastasia Susie Mihailidou is Head of the Cardiovascular & Hormonal Research Laboratory and Director of the Ambulatory Blood Pressure Service, Cardiology Department, Royal North Shore Hospital and also Clinical Senior Lecturer, Sydney Medical School, The University of Sydney. Anastasia is a Fellow of the American Heart Association (AHA) and has both clinical and basic research interests into hypertension, diabetes and regulation of aldosterone/mineralocorticoid receptors in the heart. Her research has made a significant contribution to understanding the role of corticosteroid hormones (and antagonists) in the heart. As a clinical scientist, she was a member of the High Blood Pressure Research Council of Australia (HBPRCA) and National Heart Foundation Ambulatory Blood Pressure (ABP) Working Group which revised the Australian Guidelines for ABP monitoring.

Abstract:

Blood pressure (BP) is one of the vital indicators of an individual’s health and an independent risk factor for cardiovascular and renal disease. Hypertension is one of the most frequent conditions treated in primary practice, and accounts for 51% of stroke deaths and 45% of ischemic heart disease deaths, while hypotension may be an early symptom alerting a change in the patient’s health. Increasingly busy clinical environments raise the risk that accurate BP measurement may be overlooked; this is a problem identified across health services nationally and internationally and not unique to a single health discipline. Health professionals must therefore be able to implement best practice procedures for accurately measuring and acting appropriately upon these measures to ensure patient safety and management. An initial random audit of 23 clinical wards and outpatient clinics identified more digital than manual BP monitors in use with only 17% sites having annual in-service training for measurement of BP and only 50% of medical students (Stage 1 and 2) retaining BP measurement skills. Busy clinical environments require multimedia technology and hence we developed an e-learning module that would be accessible and available for self-directed learning. For the platform to have active engagement and sustainability requires a multi-disciplinary approach. The strategy involved extensive consultation with stakeholders that included health professionals, patients and students to identify challenges encountered both in the clinic and as part of the learning experience, so that program content was not only consistent and accurate but also relevant. Advantages include distance-learning, flexible scheduling with immediate access to content at any time without limitations of access to facilities, easy access from any multimedia device and easily updated to include the latest best practice information. Our goal is that health professionals will have improved knowledge of the limitations of different devices and use standardized procedures for BP measurement, which will provide excellence in patient care.

Speaker
Biography:

Anthony Martin Gerdes has done PhD in Anatomy (1978), from University of Texas Medical Branch at Galveston. He was the Professor/Chair of Anatomy, University of South Dakota. Also the founding Scientist for Sanford Research-University of South Dakota. His Current position is Professor/Chair Biomedical Sciences, NYIT College of Osteopathic Medicine, Old Westbury, NY, 2011-present. Publications: ~120 peer reviewed journal articles. 2013 Distinguished Alumnus, Graduate School of Biomedical Sciences, UTMB at Galveston Anthony Martin Gerdes developed a precise method to determine cardiac myocyte shape. He then provided a comprehensive understanding of how cardiac myocytes remodel during growth, maturation, aging, cardiac hypertrophy, and heart failure (HF) from many etiologies. After demonstrating that low thyroid hormone function alone can cause heart failure, he showed remarkable beneficial changes in myocyte shape and vascular remodeling, reduced fibrosis, and improved LF function after thyroid hormone treatment of various models of HF (including ischemia, diabetes, hypertension).

Abstract:

Myocardial Infarction (MI) activates cardiac D3 deiodinase, contributing to low tissue T3 and Heart Failure (HF). Potential improvements in LV remodeling and function with a therapeutic T3 dose after MI are not clear. We hypothesize that a safe, low-dose T3 treatment/monitoring regimen will lead to significant cardioprotection in rats following MI-induced HF. MI was produced in adult rats by LAD ligation. T3 (4-5 μg/kg/day) in drinking water was started after MI and continued for 2 months (Mo). Vehicle (V) was used in MI controls (n=16-20/group). Infarct size was similar in both MI groups. D3 mRNA expression increased in MI+V (2.7-fold) and was reversed in MI+T3 (0.49-fold). MI+T3 improved ejection fraction by 51% at 1 Mo and by 47% at 2 Mo post-MI as assessed by magnetic resonance imaging (MRI). Mean MRI wall thickness was increased at both latter time-points. Histologically, non-infarct area and wall thickness increased significantly (30% and 18% respectively). Non-infarct length was also increased. Remarkably, following MI, the incidence of atrial tachyarrhythmias that persisted following discontinuation of experimental atrial tachypacing was significantly diminished by 63% with T3. T3 did not affect heart rate. The selected dose led to feedback inhibition of Thyroid-Stimulating Hormone (TSH) but no significant change in serum T3. Conclusion: Results demonstrate a safe and effective post-MI/HF T3 treatment strategy that dramatically improves LV function, atrial arrhythmogenesis, non-infarct tissue remodeling, and myocyte survival with no adverse effects. This study describes an effective, translatable, treatment/monitoring protocol for T3 treatment of MI.

Qiangarong Liang

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

Title: Dysregulation of mitochondrial quality control and diabetic cardiomyopathy

Time : 11:15-11:35

Speaker
Biography:

Qiangrong Liang was MD, in 1986, Xian Medical University, Xian, China. He has completed his PhD, 1999, from University of North Dakota, Grand Forks, ND. also did the Postdoctoral Training, in 1999-2003, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio He was the Assistant and Associate Professor, 2003-2012, Sanford Research-University of South Dakota, Sioux Falls, SD. Currently he is the Associate Professor, 2013, Department of Biomedical Sciences, NYIT College of Osteopathic Medicine, Old Westbury, NY. Peer-reviewed publications: 35. Dr. Liang’s research interest is in the cellular and molecular mechanisms that underlie acquired heart disease, cardiac hypertrophy and heart failure. His laboratory is conducting research in three areas: 1) Investigate why diabetes exacerbates progression to heart failure and explore mechanism-based approaches to reduce this susceptibility. 2) Explore mechanisms of myocardial protection by caloric restriction (CR) and develop drugs that mimic the beneficial effects of CR. 3) Investigate why the anti-cancer drug doxorubicin (DOX) can cause heart failure and how myocardial homeostasis can be restored by coordinately promoting survival mechanisms and blocking cell death pathways.

Abstract:

Mitochondrial dysfunction and reactive oxygen species (ROS) are critical to diabetic heart damage. However, antioxidant therapies have failed to reduce heart failure in clinical trials, underscoring the need to develop new therapeutic strategies. A healthy pool of mitochondria is maintained through a number of quality control mechanisms including mitochondrial autophagy known as mitophagy which degrades dysfunctional mitochondrial fragments that are segregated by the fission process. This study investigates the functional status and roles of mitophagy and mitochondrial fission in type 1 diabetic heart. A novel dual fluorescent mitophagy reporter was used to label and quantify mitochondrial fragments that are being degraded within the lysosome in isolated cardiomyocytes and in type 1 diabetic hearts. The functional roles of mitophagy and mitochondrial fission were determined in cardiomyocytes by using genetic gain- and loss-of-function approaches. Using this mitophagy reporter, we found that mitophagic flux is inhibited in cardiomyocytes cultured in media that mimic hyperglycemic conditions. Parkin overexpression diminishes, while parkin knockdown exaggerates high glucose toxicity, as measured by the levels of ROS generation, oxidative injury and cardiomyocyte death. Further, high glucose increases mitochondrial fragmentation and Drp1 knockdown inhibits this effect, predisposing cells to high glucose toxicity. Similarly, mitophagy is inhibited in type 1 diabetic heart as assessed by mitophagy reporter mice, which is associated with increased small-sized mitochondria. These findings not only demonstrate a mismatch between mitochondrial fission and mitophagy in high glucose-treated cardiomyocytes and in the diabetic heart but also suggest that improving mitochondrial quality control processes may protect the heart against hyperglycemic toxicity in type 1 diabetes.

Youhua Zhang

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

Title: Thyroid dysfunction and atrial fibrillation: The role of myocardial hypothyroidism

Time : 11:35-11:55

Speaker
Biography:

Youhua Zhang was MD (1990), in Xinjiang Medical College, Urumqi, China. He completed his PhD (1993), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China. He is the Resident to Attending Physician in Cardiology, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing, China (1990-1999). Also Postdoctoral Fellow to Project Staff/ Research Assistant Professor, Cleveland Clinic, Cleveland, OH (1999-2011). His current position: Assistant Professor, NYIT College of Osteopathic Medicine, Old Westbury, NY, 2011-present.Publications: ~70 peer reviewed journal articles. Zhang has broad interest in cardiac electrophysiology, arrhythmias and heart failure research. He has pioneered the use of selective atrioventricular node vagal stimulation to control ventricular rate during atrial fibrillation and the use of vagus nerve stimulation to treat heart failure. Dr. Zhang is also an expert in studying atrioventricular (AV) node electrophysiology. He discovered a novel index for dual pathway AV node electrophysiology, termed His electrogram alternans- also called Zhang’s phenomenon. This new index permits monitoring dual pathway conduction on a beat by beat basis.

Abstract:

Both hyperthyroidism and hypothyroidism can lead to heart failure (HF) development. HF is associated with an increased risk of atrial fibrillation (AF). While it is well established that hyperthyroidism increases AF incidence, the effect of hypothyroidism on AF is not so well recognized. To investigate the effect of altered thyroid status on AF inducibility, we treated thyroidectomized rats with placebo, 3.3mg L-thyroxine (T4), or 20 mg T4 pellets (60 day release form) for 2 months. At the end of treatment, hypothyroid, euthyroid, and hyperthyroid status was confirmed in the respective groups. Although hypothyroidism and hyperthyroidism had different effects on heart rate and cardiac function, both increased significantly AF susceptibility. AF inducibility was 78% in hypothyroid, 67% in hyperthyroid, compared with 11% in the euthyroid group (both p<0.05). In light of the evidence suggesting the presence of myocardial tissue hypothyroidism in HF, we hypothesized that not only may myocardial tissue hypothyroidism contribute to HF development, but may also increase AF incidence. Hence, we have studied the effect of thyroid hormone (TH) replacement therapy on AF arrhythmogenesis in a rat myocardial infarction (MI) induced HF model. Rats with large MIs (>40%) were randomized into T4 (n=14) and placebo (n=15) groups 2 weeks after MI and treated for 2 months. Compared with the placebo, T4 treatment attenuated atrial effective refractory period prolongation and reduced AF inducibility (AF/atrial flutter /tachycardia were inducible in 11/15 rats, or 73% in placebo vs 4/14 rats, or 29% in the T4 treated group, P<0.05). It is concluded that hypothyroidism, similar to hyperthyroidism, can lead to increased AF vulnerability in rats. Moreover, correcting myocardial tissue hypothyroidism with TH replacement therapy in HF may attenuate atrial remodeling and reduce AF inducibility post MI-HF. Clinical studies are still needed to confirm such benefits in patients.

Ashutosh Wechalekar

University College London Medical School, UK

Title: Progress in cardiac amyloidosis

Time : 11:55-12:15

Speaker
Biography:

Ashutosh Wechalekar is a Reader in Medicine at University College London Medical School and the Royal Free London NHS Foundation Trust. He trained in medicine at Medical College Nagpur, India and when on to do further training in haematology in UK and Canada. He joined the UK National Amyloidosis Centre funded in 2004 and is now a senior faculty at the centre. His scientific interests are focused on biomarkers in cardiac amyloidosis, novel imaging methods for the heart in all types of amyloidosis (especially DPD scintigraphy – he now has the largest cohort in the world of over 700 patients with amyloidosis imaged by this modality), characterization and treatment of systemic AL amyloidosis with a focus on the study new and novel agents in these disorders. He has published extensively in these areas.

Abstract:

Systemic amyloidoses are a group of rare diseases caused by deposition of protein fibrils. This talk will focus on major advances in the approaches to diagnosis, changing epidemiology and recent advances in treatment. Light chain (AL) amyloidosis remains the most frequently identified type but cardiac transthyretin amyloidosis is being increasingly recognised. Senile cardiac amyloidosis appears to be an epidemic awaiting diagnosis. Mass spectrometry using laser capture microdissection of a tiny amount of amyloid deposits from histological sections has enabled improved amyloid fibril typing. Understanding of proteotoxicity of amyloidogenic precursors has paved the way for new therapeutic approaches. Developments in cardiac magnetic resonance imaging such a Eq-CMR and T-1 mapping has lead to accurate quantitation of the myocardial interstitial deposits for diagnosis and response assessment. 99mTc-DPD/PyP scintigraphy is transforming evaluation of cardiac amyloidosis. The availability of novel chemotherapy agents and better selection of patients for autologous stem cell transplantation have enabled delivery of therapy in AL with less toxicity and improved outcomes. An array of novel agents, including RNA inhibitors, stabilisers of amyloid precursor proteins, inhibitors of fibril formation and immunotherapeutic targeting of amyloid deposits are all now in clinical development offering great hope for specific and effective new therapies.

Salah A. Mohamed

Medical Center Schleswig-Holstein, Germany

Title: MALDI imaging for determining the protein network associated with atrial fibrillation

Time : 12:15-12:35

Speaker
Biography:

Salah A. Mohamed, Laboratory and Group Leader in Department of Cardiac and Thoracic Vascular Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck in Germany, the group dedicated research interests to aortic and aortic valve diseases, Atrial fibrillation, aging, and biomarker. He has published more than 25 papers in reputed journals and has been serving as an editorial board member of repute.

Abstract:

Atrial fibrillation (AF) is associated with increased risks of stroke, cardiac failure, and mortality. We used a comprehensive proteomics approach matrix-assisted laser desorption/ionization and mass spectrometry imaging (MALDI-MSI) to understand the complex cellular processes and networks in the pathology of AF. Left atrial appendage tissue resected routinely during MAZE procedure in surgery were collected of patients with paroxysmal (n = 9, mean age 69.0±3.1 years), persistent (n = 18, mean age 67.0±2.7 years), and long-standing persistent (n = 19, mean age 71.0±2.0 years) arrhythmia. 9 sections of each phenotype were prepared from paraffin blocks and transferred onto Indium-Tin-Oxide slides suitable for MALDI-MSI. Sections were dewaxed and trypsin solutions were applied directly onto the section using an automated spraying device. Spectra were acquired at a mass range of m/z 800-3500Da and lateral resolution of 80 µm. Two hundred laser shots were acquired per pixel and random walk of 50/position. Data analyses were performed using SCiLS Lab software. Component analysis of MALDI Imaging data by probabilistic latent semantic analysis results in a clear discrimination in the first 3 components of atrial fibrillation as shown in figure 1. Intensity distribution of given m/z values, which are discriminative for the considered cluster, was determined to distinguish between paroxysmal vs persistent AF (mean, 4.08±1.21 vs 1.59±0.12, p = 0.09), and persistent vs long-persistent AF (1.59±0.12 vs 6.85±3.02, p = 0.02). Follow-up with case-controlled assessment of neurological events was shown, that persistent AF showed its vulnerability for neurological attacks, compared paroxysmal and long-persistent AF (56% vs 13% and 42%, p = 0.001). Tissue-based proteomic approach provides clinically relevant information that may be beneficial in improving risk stratification in AF patients.

Break: Group Photo

Lunch Break 12:40-13:[email protected] Benjamin’s
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:

In recent years, clinical and genetic markers of coronary heart disease (CHD) and major cardiac events (МАСЕ) were described, which led to the development of various models for diagnostics and prediction of these conditions. However, a search for models with a highest informative value is continued. Researchers propose additional characteristics within the scope of their interests and focus attention on genetic and biochemical markers (lipids, C-reactive protein etc.), data of instrumental examination (heart rate variability, coronary angiography, MRI etc.) and other. Our studies suggest that the accuracy of a model depends on many factors, such as object of prediction (i.e. atherosclerotic plaque or ischemia), signs included, method of machine learning, variable characteristics of selected patients etc. In particular, sensitivity and specificity of prediction of coronary atherosclerosis with the same set of included signs may vary from 0.8364 and 0.3684 (random forest method), 0.8000 and 0.5614 (ANN), 0.6545 and 0.4912 (logistic regression), and 0.6182 and 0.5439 (SVM), respectively. In this respect, it seems important to discuss the trends of the development of prognostic models for CHD from the point of modern understanding of its pathogenesis and goals for decision-making. We propose several multifactorial prognostic and diagnostic models for coronary atherosclerosis, myocardial ischemia, and MACE, and analyze their similarities, differences, informative value in different groups of patients.

Speaker
Biography:

Vera Maravic-Stojkovic has completed her Ph.D. at the age of 41 years from Belgrade University and postdoctoral studies from Medizinicshe Hochcshule Hannover, Germany. She is the Head of Laboratory Services in Dedinje Cardiovascular Institute, Belgrade Serbia. She has published more than 25 papers in reputed journals and has been serving as a member of the Heart and Liver Transplant Team in Serbia.

Abstract:

Infective endocarditis after combined valve repair and coronary artery bypass surgery, multiorgan failure and sepsis, were treated with redo mitral valve replacement, antibiotics and adjunctive therapy. Sepsis caused by Gram-negative bacteria, was identified based on the grave clinical status, hemodynamic findings and high levels of proinflammatory cytokines. On the day of the redo surgery APACHE II score was 26 and SOFA score was 14. IgM-enriched immunoglobulin, Pentaglobin was administered. The cardiac index improved from 1.9 l/m2 to 3.7 l/m2 on the 1st postoperative day (POD), accompanied with increasing values of mixed venous oxygen saturation from 59.3 % to 77%, while systemic vascular resistance 887 dyn•s/cm5 was maintained by vasopressor agent. On the 4thPOD the inotrops and pressors ceased. APACHE II score declined to 10 and SOFA to 2. Significant improvement in clinical curse, stabilized hemodynamic parameters, balanced perfusion and oxygen pattern, accompanied by remarkable reduction of proinflammatory cytokine expression, strongly support presented therapeutic approach.

Ljudmila Stojanovich

University Medical Center, Serbia

Title: Cardiac involvement in the antiphospholipid syndrome

Time : 14:25-14:45

Speaker
Biography:

Ljudmila Stojanovich is Research Professor, and the scientific director in the Bezhanijska Kosa, University Medical Center of Belgrade University. Her research focuses on Systemic Lupus Erythematosus, Antiphospholipid Syndrome, and Vaccination in patients with Autoimmune Rheumatic diseases. She is an author of three monographs and of about 250 articles on various aspects of Rheumatic disorders, published in international journals and in conference proceedings. She is in Editorial Boards /Reviewer in the “Current Contents” or “Science citation index”, like LUPUS, Cellular and Molecular Neurobiology, The Journal of Vaccine, The Journal of Rheumatology, Allergologia et Immunopathologia and others. She is a member of number International Project, like of “the European Forum on Antiphospholipid Antibodies”, “Multicenter Studies Antiphospholipid Antibodies, Infections and Autoimmune Diseases”. She is the member of steering group committee (composed of experts representing 11 European countries) of European League Against Rheumatism (EULAR) for the recommendations for vaccination in patients with autoimmune inflammatory rheumatic diseases.

Abstract:

Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated with a hypercoagulable state and fetal loss and with other clinical manifestations including cardiac involvement. The antiphospholipid syndrome has been associated with multiple cardiac abnormalities. Cardiac manifestations of APS are valve abnormalities (valve thickening and vegetations), occlusive arterial disease (atherosclerosis and myocardial infarction), intracardiac emboli, ventricular dysfunction, and pulmonary hypertension. Antiphospholipid antibodies (aPL) may have a role in the accelerated atherosclerotic arterial disease observed in APS, related to their ability to induce endothelial activation. aPL have been incriminated in the pathogenesis of heart valve lesions in APS patients. Markers of endothelial cell activation are up-regulated with prominent deposition of aPL in heart valves, suggesting aPL deposition initiates an inflammatory process that recruits complement leading to the valve lesion. Autoantibody-mediated endothelial cell activation probably plays a role in sustaining a proadhesive, proinflammatory, and procoagulant phenotype. The heterogeneity of APS clinical manifestations is likely linked to the varied effects that aPL can induce on endothelial cells and to the different functions that endothelial cells display depending on the anatomic localization. The aim of this study was to investigate association between cardiac manifestations in patients with antiphospholipid syndrome (APS) with type of antiphospholipid antibodies (aPL). Among the 446 patients from the Serbian National APS Registry, 330 met the criteria for primary APS (PAPS), 126 were diagnosed with secondary APS (SAPS) in scope of SLE, and 10 presented APS in scope of some other autoimmune rheumatic disorder. Of these patients, 333 (218 with PAPS and 115 with SAPS) were included into this prospective study. Antiphospholipid antibody (aPL) analysis included detection of aCL (IgG/IgM), ß2GPI (IgG/IgM) and LA and served to evaluate associations with distinct cardiac manifestations. Presence of aCL IgG was more common (p=0.001) in SAPS and LA in PAPS patients (p=0.002). In all patients echocardiography study was performed in order to reveal presence of vegetations, pseudoinfective endocarditis, intracardiac thrombus and valve thickening or dysfunction. Data considering acute myocardial infarction, unstable angina, coronary artery bypass grafting (CABG) or percutaneus coronary artery angioplasty (PTCA) as well as manifestations of chronic or acute heart failure were also collected. There was no statisticaly significant difference between overall cardiac manifestations and the type of aPL. There were 27.7% SAPS patients and 9.3% PAPS patients with valve vegetations (p=0.000). Pseudoinfective endocardits was observed in 12.8% SAPS patients and 3.1% in PAPS patients (p=0.004). 30% of the patients with high levels of aCL IgG antibodies (>100PLU/ml) had valve thickening and dysfunction, as compared to 4.1% without valve abnormalities (p=0.002). Highly statistically significant difference was revealed considering presence of aCL-IgG and aCL-IgM antibodies and pseudoinfective endocarditis (p=0.004, p=0.003 respectively) and presence of aCL-IgG and valvular dysfunction (p=0.023). Valvular manifestations in our cohort were significantly related to titers of aCL antibodies. The level of aCL IgG (p=0.005, Pearson +0.138) were in positive correlation with presence of pseudoinfective endocarditis Our study showed that patients with SAPS had higher prevalence of valvular lesions, and that higher levels of aCL IgG were associated with their appearance. Opposite, patients with PAPS were more often presented with coronary artery disease, although without statistical significance Certain aPL type and levels are associated with distinct cardiac manifestation, suggesting their predictive role. There is strong link between some cardiac manifestations in APS patients, suggesting complexity and evolutionary nature of APS.

Speaker
Biography:

Chayakrit Krittanawong has completed his M.D. at the age of 25 years from Phramongkutklao College of Medicine, Mahidol University, Bangkok, Thailand. He is one of the Cardiovascular Disease Research Fellow from Mayo Clinic, Rochester, MN. His researches focus on cardiac rehabilitation and Spontaneous Coronary Artery Dissection (SCAD), transcatheter aortic valve implantation, and healthcare innovation and technology. He is also the founder of Wikiheart. He will be on the board of directors of Dr. Son Aesthetics Inc., and the Dr. Son Group in 2016.

Abstract:

The emergence of web-based educational application has become popular worldwide. It can help patients to understand the healthcare system, disease complications, and secondary prevention. Because we are in the digital world, the healthcare system needs to be transformed. Virtual community is the second-life world in which people can communicate easily and interactively. We tried to develop the ideal collaboration ware between patients, physicians, and researchers. This program can be easily accessed and edited by anyone with high security protection and has a cloud database system. The aim of this pilot project is to globalize online communication among people in the healthcare system to improve clinical outcomes and prevent further complications. Patient confidentiality is still the most important issue and we require de-identification of all images. We not only created a community that lets people talk about their health problems with others anonymously, to share how their habits develop the disease, but this program educates people about medical knowledge with animations or something that’s easy for non-experts to understand. We have a few medical experts that help answer questions or just talk about the users’ problems, after which users/patients can schedule an appointment with the experts they talk to for a real check-up. This pilot program might help patients to understand the disease pattern, improve adherence to their program, and become closer to individualized medicine.