Global Cardiology Summit October 22-23, 2018 Osaka, Japan

Barkov Ivan, doctor cardiac surgeon of the Children\'s Department of the FSBE « The federal center of cardiovascular surgery» of the Russian Ministry of Health. Astrakhan.rnEducation:rnGraduated from medical university in 2007,гesidency in cardiovascular surgery 2009-2011.rnSince 2011 the doctor is a cardiosurgeon.rnThe spectrum of interests is pediatric cardiosurgery, minimally invasive methods of correction congenital heart diseases. rnStudy:rnSince 2016 the participant of research perventricular closing defect of interventricular septum, data base more than 100 operations.rnPrepared a report with video: periventricular closure in children before one year.rn

Purpose: To present results of perventricular closing of defects of an interventricular partition with occluder of various types in pediatric group.rnMaterials and methods: In the department of surgery of congenital heart diseases of the federal center of cardiovascular surgery Astrakhan from 2014 to 2017 were operated 50 patients with VSD with use of a method of perventricular closing of defect without use of artificial blood circulation under control of TEE ECHO. Age of patients - from 2,1 to 11.8 months ±8,6. Body weight - from 3,9 to 9,8, kg.±8,4. Defects size from 4,5 to 8,5 mm, localization: the subaortal – 17(34%) cases, in aneurism – 10(20%) cases, subtrikuspidal – 16 (32%) cases, muscular-7(14%) cases. The Qp/Qs index from 1,6 to 2,5. Size of occluder: from 5 to 9 mm. CHF of patients of the I-IIb FC on NYHA.rnResults: Successful closing of VSD is reached in 94%. Duration of procedure was from 29 to 68 min. (on average 40 min.).Were used occluders SQFDQ II(symmetric) - 32 (64%), SQFDQ IV (asymmetric) -11 (22%), SQFDQ I(muscular)-7 (14%). Frequency of conversion - 3 (6%) it is connected with underestimation of the sizes and localizations of defect. Blood loss 0,6-4,3 ml/kg ±1,1. Intraoperative the ECHO the shunt from 1 to 2 mm at 12 patients (24%), freedom from shunts in 3 months of-90%, the tricuspid, aortic and mitral regurgitation didn\'t exceed 0-1 degrees. Mean duration of mechanical ventilation was 238,6±160,5 min. Mean hospital stay was 6,73±2 days. Cardiotonics applied 4 patients whith pulmonary hipertezion . There were no intraoperative rhythm disorders. One patient has late complete atrioventricular block two month after operation with implanted pacemaker. rnConclusions: The technology of perventricular closing of VSD provides good cosmetic effect, fast rehabilitation of patients, takes a certain place in surgical treatment of VSD along with traditional techniques (with use of artificial circulation, transkateter closure).rn Keywords: congenital heart diseases, defect of interventricular septum, perventricular closing.rn

Rose Chinly Mae Ortega is a graduate of Bachelor of Science in Biology (2016) in Mindanao State University-Iligan Institute of Technology in the Philippines. She is now a full-time Masters in Biology (Advanced) student of the same institution under the scholarship of the Department of Science and Technology-ASTHRDP. As a young fellow, she is interested and working on physical examination on early detection of Cardiovascular diseases of any parts of a human body using Geometric Morphometric Analysis. Other field of interest includes Metagenomic Analysis on microbial flora on internal and external organs.

Facial investigations using geometric morphometrics has been used in many studies to affirm that a particular disease can attribute to an individual’s facial morphology. A landmark based geometric morphometric analysis was used in this study to asses if facial shape changes is associated with cardiovascular diseases (CVD) and if facial morphology of the CVD individuals differ from the normal ones. In the Municipality of Cantilan, Surigao del Sur, frontal face images taken from 32 cardiovascular disease patients and 32 normal individuals were examined using forty-one manually positioned landmarks. Result showed that facial morphology of the CVD group differ from non-CVD group. Procrustes ANOVA showed significant values for the individual symmetry and directional asymmetry. The analysis of structure by the Principal Components reveals particular variations and the scatter plot of the residual asymmetry shows distinct differences between CVD and non-CVD. Therefore, cardiovascular diseases contributes to facial shape changes and that development of facial morphology differ between CVD and non-CVD group.

Dr. Shaun Khanna has completed his MBBS in 2016 from Bond University and is currently completing his Master of Medicine (Advanced) with the University of Sydney. He has a current appointment with Blacktown Hospital as a medical officer and as a conjoint lecturer with the University of Western Sydney. He is heavily involved in research with interests in arrhythmias and cardiovascular imaging.

A 72 year old male presented to our institution with worsening dyspnoea, orthopnea and decreased exercise tolerance. This is on a known background of an idiopathic cardiomyopathy, atrial fibrillation (AF), and cardiovascular risk factors. \r\nOn examination, the patient appeared fluid overloaded. Chest examination revealed coarse crackles to bilateral mid-zones with an audible wheeze. Precordial examination revealed a holosystolic murmur at the apex with radiation to the axillary regions. He had evidence of peripheral to the sacrum. \r\nA diagnosis of decompensated congestive cardiac failure (CCF) was made and he was commenced on appropriate inpatient heart failure treatment. Chest radiograph showed gross cardiomegaly with evidence of mild pulmonary venous congestion. See Figure 1. \r\nA transthoracic echocardiogram revealed severely dilated bi-ventricular sizes with normal left ventricular ejection fraction but severely impaired right ventricular ejection fraction. Strikingly, there was evidence of severely dilated bi-atrial size. Left atrial volume was indexed at 438.3 ml/m2 relative to body surface area. See Figure 2 & 3. There was also presence of severe mitral regurgitation in the setting of non-coaptation of the mitral valve leaflets. See Figure 4. These findings are consistent with a Giant Atrial Myopathy in the setting of an idiopathic dilated cardiomyopathy. \r\nGiant Atrial Myopathies are typically associated with rheumatic valve disease, however there are several case reports demonstrating its presence in primary cardiomyopathies. This atrial disease forms a composite substrate for AF, CCF and thrombus formation. Management strategies in this disease are often supportive, with the condition often portending a poor prognosis.\r\n

Dr. Shaun Khanna has completed his MBBS in 2016 from Bond University and is currently completing his Master of Medicine (Advanced) with the University of Sydney. He has a current appointment with Blacktown Hospital as a medical officer and as a conjoint lecturer with the University of Western Sydney. He is heavily involved in research with interests in arrhythmias and cardiovascular imaging.

Here, we explore a case of a 65-year-old female who presented to our facility with a constellation of symptoms including chest pain, dizziness and headache over the last day. \r\nAn MRI Brain was performed revealing multiple scattered focal sites of abnormal diffusion restriction in the posterior and anterior circulation with additional ischemic foci in the left cerebellar hemisphere. See Figure 1. This was concerning for cardio-embolic source. \r\nSubsequently an echocardiogram revealed a large mass in the left atrium attached to the inter-atrial septum. See Figure 2. Cardiothoracic surgery was consulted for excision of the atrial myxoma. In the Interim, intravenous heparin infusion with a target low APTT (40-60) was commenced in light of risk of further embolism versus risk of haemorrhagic transformation of the ischemic stroke. In the interim, the patient was monitored with BD non-contrast CT Brain scans.\r\nThe patient successfully had excision of the atrial myxoma and patch repair of the intra-atrial septum. Findings were of a gelatinous, friable tumour measuring 35 x 25 x 15mm with histopathology consistent with atrial myxoma.\r\nThe prevalence of cardiac tumours ranges from 0.001% to 0.3% with cardiac myxoma being the most common primary cardiac tumour with a 2:1 female preponderance. Cardiac myxomas, specifically atrial origin myxomas (75%) have several presentations with the most serious being systemic embolization through tumour thrombi and rarely tumour fragments. This phenomenon is currently responsible for approximately 0.5% of strokes. Further studies are required to delineate timing of surgery, in light of potential haemorrhagic transformation.\r\n

Dr. Shaun Khanna has completed his MBBS in 2016 from Bond University and is currently completing his Master of Medicine (Advanced) with the University of Sydney. He has a current appointment with Blacktown Hospital as a medical officer and as a conjoint lecturer with the University of Western Sydney. He is heavily involved in research with interests in arrhythmias and cardiovascular imaging.

Mitochondrial disorders are genetic disorders that result in dysfunction in the energy metabolism pathway. The prevalence of mitochondrial disease is estimated at 9 – 16 per 100,000 with the most common type being MELAS. \r\nA 61-year-old female has presented to our facility on numerous occasions over the last ten year period, with thorough inpatient and outpatient investigations. \r\nShe was diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke (MELAS) syndrome in 2015 after 6-7 years of a constellation of symptoms including muscle weakness, ataxia, fatigue, headaches and sensorineural hearing loss. Her other past medical history includes an initial diagnosis of hypertrophic cardiomyopathy (with an IVDd of 19mm), chronic kidney disease and recurrent bowel obstruction. See Figure 1. \r\nDuring the last few years there were concerns that her heart function was worsening and hence the patient was arranged for a right ventricular cardiac biopsy. The tissue histopathology slides showed hypertrophied myocytes with diffuse vacuolisation but no evidence of myocyte disarray. See Figure 2. This is most consistent with mitochondrial cardiomyopathy. \r\nThis case presents a patient with mitochondrial cardiomyopathy that has possibly presented itself initially as a phenocopy of HCM. Studies have also shown that cardiac involvement possibly stems from mitochondrial dysfunction with hypertrophy present in the early remodelling stage, with progression to dilated cardiomyopathy. This link has already been hypothesised in our patient and she is currently being monitored for further progression of her potential mitrochondrial cardiomyopathy.\r\n\r\n