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Scientific Tracks & Abstracts conferenceseries.com 985th Conference 18th Annual Cardiologists Conference June 19-21, 2017 Paris, France Scientific Tracks & Abstracts Day 1 Cardiologists 2017 Page 31 Oral Sessions Day 1 June 19, 2017 Cardiac Regeneration|Heart Disease| Electrocardiography | Cardiomyopathies | Diabetes & Heart | Cardiac Nursing Session Chair Session Co-chair Guy Hugues Fontaine William E. Feeman Jr. La Salpêtrière Hospital, France Wood County Hospital, USA Session Introduction Enhanced prediction of the population at risk of atherothrombotic disease Title: William E Feeman Jr., Wood County Hospital, USA Genetic ventricular arrhythmia: Clinical presentation and disease modeling using iPSC- Title: derived cardiomyocytes Katriina Aalto-Setala, University of Tampere & Tampere University Hospital, Finland Cardiologists 2017 Page 32 William E Feeman Jr., J Clin Exp Cardiolog 2017, 8:6(Suppl) conferenceseries.com DOI: 10.4172/2155-9880-C1-071 18th Annual Cardiologists Conference June 19-21, 2017 Paris, France Enhanced prediction of the population at risk of atherothrombotic disease William E Feeman Jr. Wood County Hospital, USA Statement of the Problem: To be able to prevent atherothrombotic disease (ATD), one must be able to predict the population at risk of ATD. Many risk predictors have been advocated for such prediction, but none have been universally accepted. Methodology & Theoretical Orientation: The Framingham Heart Study has demonstrated that the population that develops ATD differs from the population that does not by the severity of certain ATD risk factors and the duration during which those risk factors have been operative. The author has examined his entire ATD population to determine the constellation of ATD risk factors that separates population from the population that did not develop some form of clinical ATD. Findings: The population at risk of ATD is characterized by cigarette smoking, dyslipidemia, and (often) hypertension, with some contribution from the very high blood sugar levels of uncontrolled diabetes. These risk factors are not independent, but rather dependent, interacting with one another leading to ATD. Dyslipidemia is defined as a ratio between LDL- and HDL-cholesterol (Cholesterol Retention Fraction, or CRF, defined as [LDL-HDL]/LDL). The predictive tool is a graph with the CRF on the ordinate and systolic blood pressure (SBP) on the abscissa. The graph exhibits a threshold line with CRF-SBP co-ordinates (0.74, 100) and (0.49, 140), above which lie the CRF-SBP of 93% of all the ATD patients in the author’s practice. The outcomes of those patients can be found in the Table. Further fine-tuning can be done by stratifying the CRF by SBP or by LDL-cholesterol. Any therapy that brings the CRF-SBP plot below the threshold line results in plaque stabilization/regression in a minimum average of 75% of cases. Conclusions: The population at risk of ATD is predictable and hence, ATD is preventable. Biography William E Feeman Jr is a Physician at Wood County Hospital, and private practice in Bowling Green, Ohio. He is the Founder of Association for the Prevention of Atherothrombotic Disease in Northwest Ohio to facilitate the spread of knowledge about this disease. [email protected] J Clin Exp Cardiolog, an open access journal Cardiologists 2017 Volume 8, Issue 6 (Suppl) ISSN: 2155-9880 June 19-21, 2017 Page 33 Katriina Aalto-Setälä, J Clin Exp Cardiolog 2017, 8:6(Suppl) conferenceseries.com DOI: 10.4172/2155-9880-C1-071 18th Annual Cardiologists Conference June 19-21, 2017 Paris, France Genetic ventricular arrhythmia: Clinical presentation and disease modeling using iPSC-derived cardiomyocytes Katriina Aalto-Setälä1, 2 1University of Tampere, Finland 2Tampere University Hospital, Finland Background & Aim: Genetic cardiac arrhythmias are often severe, but due to their rare nature, no specific treatment exists. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe arrhythmia caused by mutations in the RyR2 gene. This gene is important in regulating Ca2+ release from sarcoplasmic reticulum. The purpose of this study was to create induced pluripotent stem cells (iPSCs) from individuals having CPVT and to study the functional properties of the cardiomyocytes. Methodology: iPSC lines were derived from six individuals carrying different RyR2 gene mutations. Arrhythmias of cardiomyocytes were analyzed using Ca2+ imaging. Findings: Patients’ heart rates were increased by stress exercise test and this induced in all of them polymorphic ventricular extra beats. When their cardiomyocytes were treated with adrenaline, similar irregular beating was observed. If the patients were treated with dantrolene, in some individuals all arrhythmias were abolished, but in some, it did not have any effect. As their cardiomyocytes were treated with the same drug, adrenaline-induced arrhythmias were abolished, but only from those cardiomyocytes derived from individuals who also clinically responded to the treatment. However, arrhythmias were not abolished from cardiomyocytes derived from the patients having no response to the medication. Conclusion & Significance: With this drug, we could demonstrate that all individuals did not respond to this medication the same way even though their clinical phenotype was the same and they had mutations in the same gene. Importantly, iPSC-derived cardiomyocytes demonstrated the very same phenomenon: If the patient responded, also his cardiomyocytes responded, but if the drug did not remove arrhythmias from the patient, they were not abolished from his cardiomyocytes either. This study demonstrate that iPSC-derived cells reproduce the effect observed in the patients and they could be used to tailor medication especially in patients having severe, potentially lethal arrhythmias. Biography Katriina Aalto-Setala is the Professor of Physiology at School of Medicine, University of Tampere and a Cardiologist at Heart Hospital, Tampere University Hospital, Finland. She works as an invasive Cardiologist and is In-charge of the genetic cardiac outpatient clinic at Heart Hospital. Her research at University of Tampere focuses on Human Genetic Cardiac Diseases such as genetic arrhythmias and atherosclerosis with the help of induced pluripotent stem cell (iPSC) technology. The main aim of the research group is to learn more about the basic pathology of the genetic diseases as well as to test current and new pharmaceutical agents to correct the abnormalities. Her research group in collaboration with researches at Tampere Technical University has also invented new methods to monitor and analyze the maturity and functionality cardiomyocytes. [email protected] Notes: J Clin Exp Cardiolog, an open access journal Cardiologists 2017 Volume 8, Issue 6 (Suppl) ISSN: 2155-9880 June 19-21, 2017 Page 34 conferenceseries.com 985th Conference 18th Annual Cardiologists Conference June 19-21, 2017 Paris, France Special Session Day 1 Cardiologists 2017 Page 36 Fabiola B Sozzi, J Clin Exp Cardiolog 2017, 8:6(Suppl) conferenceseries.com DOI: 10.4172/2155-9880-C1-071 18th Annual Cardiologists Conference June 19-21, 2017 Paris, France Fabiola B Sozzi University Hospital Policlinico of Milan, Italy Diastolic stress echocardiography: How and when to perform it here is growing evidence that the diastolic stress test can provide important diagnostic findings helpful in the management of patients presenting with dyspnea of an unclear etiology. Many patients present with exertional dyspnea and exercise Tintolerance, but have normal left ventricular filling pressures at rest. In these patients, it is important to evaluate filling pressure with exercise. Exercise can be performed using a supine bicycle or treadmill protocol. Alternatively dobutamine can be used, though its vasodilator as well as inotrope effect determine a very different hemodynamic response compared to that of exercise. We need to record mitral inflow by pulsed Doppler echocardiography at the level of the mitral tips, mitral annular velocities by spectral Doppler echocardiography, and tricuspid regurgitation jet by continuous-wave Doppler at baseline and after the termination of exercise. Diastolic function parameters can be obtained soon after the assessment of regional wall motion abnormalities, especially when an exercise echocardiogram is performed for the evaluation of dyspnea. In patients with diastolic heart failure, left atrial pressure is increased, leading to an increase in mitral E velocity, whereas annular e’ velocity remains reduced given the limited preload effect on e’. Moreover, an increase in the pulmonary artery systolic pressure can be detected by the increase in peak velocity of the tricuspid regurgitation jet. On the other hand, in the absence of cardiac disease, e’ increases to a similar extent to the increase in mitral E velocity, and the normal E/e’ ratio essentially is unchanged with exercise. The concept of the diastolic stress test was introduced more than 10 years ago. Subsequently, exercise E/e’ ratio was validated against invasive measurements. Importantly, exercise septal E/e’ ratio was an important determinant of exercise capacity, and its decline with age was noted in a large series of patients referred for exercise echocardiography. Furthermore, a recent study showed the incremental prognostic value of exercise E/e’ ratio over clinical variables and exercise wall motion score index. In conclusion, diastolic stress test has an interesting role in patients with heart failure and preserved ejection fraction that present
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