Nawel Jaafar has received the BSc. degree in Medical Biotechnology and MASc. degree in Genetics and Biodiversity in the High Institute of Biotechnology, Monastir – Tunisia. Currently, she is a PhD student (3rd year) in Biological sciences and Biotechnology. She achieved several projects in molecular biology and genetics fields.

Hypertrophic Cardiomyopathy (HCM) is a common genetic cardiac disorder, caused by mutations in genes encoding for sarcomere proteins and transmitted in an autosomal dominant form. Data about the mutational spectrum in HCM patients from North Africa is limited. We performed semiconductor ship (Ion Torrent PGM) next generation sequencing of the main sarcomeric genes (MYH7, MYBPC3, TNNT2, TNNI3, ACTC1, TNNC1, MYL2, MYL3, TPM1) in 45 Tunisian HCM patients. Overall, we found a total of 14 carriers (31%) with MYH7and MYBPC3 presenting 75% of the mutations. A patient was homozygous for a new MYL3 mutation and two patients were double mutation carriers (MYBPC3+MYH7). In conclusion, we did report the mutationnal spectrum of the main genes in Tunisian HCM patients and like studied other ethnic groups, mutations in MYBPC3 and MYH7 are the most frequent.

Artur Gabriyelyan dedicated his professional life to treatment of people heart diseases. He now has more than 25-year experience in cardiovascular surgery. His latest researches in CBSC transplantation were based on both hospital and educational institutions, which should lead to further investigations in the area with a wide potential for opinion pluralism.

Statement of the Problem: Prevalence of heart failure (HF) is expected at 2-3% of the population. One-year survival with medical therapy is about 57-64%. Due to the shortage of donor organs transplantation waiting time can stretch up to two years. For some patients with severe chronic HF medication is not effective. Cord blood stem cells (CBSC) is perspective, but is not enough researched in the treatment of HF. Methodology & Theoretical Orientation: 14 patients at the age of 49±6 years, with ejection fraction (EF) 22+5%, NYHA Class ІІІ-ІV, with intravenous infusion of CBSC treatment effectiveness were analyzed. The results of clinical and special methods of patients with CBSC transplantation during 1-year research were investigated. Findings: In comparison with the initial state all of the patients failed to compensate manifestations of HF, achieved target of therapeutic doses of β-blockers, diuretics doses were significantly reduced. EF of left ventricle was improved from 22% to 28,5%, level NT-proBNP was decreased by 21,3±7%. Analysis on quality of life questionnaire MLHFQ showed improvement in subjective patient\'s status. Questionnaire SF-36 showed improvement in clinical and psychological health component. Risk of one- and three-year death on a scale MAGGIS was decreased from 16-20% to 11-17% respectively. Analysis of arrhythmias according to Holter monitoring prior to and during follow-up showed no progression in arrhytmological events after CBSC transplantation. Immunological analysis revealed no reactivation of viral infection, no rejection. Conclusion & Significance: The best results were obtained at 3-6 months after CBSC transplantation. Despite of the negative trend in the period from 9 to 12 months, the condition of patients was significantly better. These results demonstrated the efficiency of CBSC transplantation in complex conservative treatment of refractory HF, improvement of life quality and allow to extend waiting time of a donor organ.

Ramesh is a core medical trainee at the cardiology department at Queen Elizabeth Hospital Woolwich, London. This provides management for a broad range of cardiology diagnoses with a particular focus on interventional treatment for angina and acute coronary syndromes. The department is currently focusing on improving services by reducing the number of unnecessary normal coronary angiograms through intelligent application of the latest guidelines. My personal interest is how the use of invasive coronary angiography in the assessment of coronary artery disease might be curtailed by advances in CT coronary angiography.

Introduction: The authors present a rare case of a spontaneous intradural extramedullary spinal haematoma complicating percutaneous coronary intervention (PCI) for acute myocardial infarction (MI). We review potential aetiologies, pathological mechanisms and treatment options in this challenging subset of patients.\r\nCase Report: A 65-year-old man was admitted with a non-ST-elevated Myocardial infarction (NSTEMI). Angiogram showed significant left anterior descending (LAD) and left circumflex (LCX) disease. After discussion the patient opted for staged PCI over CABG. After the second PCI to LAD he developed severe neuropathic pain down the lateral aspect of his right arm. Magnetic Resonance Imaging (MRI) of the cervical-spine showed an intraspinal canal haematoma at the levels C5/6 and C6/7 with some compression on the cord. He did not develop weakness so neurosurgeons opted for conservative management. Antiplatelets were continued as he had drug-eluting stents (DES) but heparin was held. A repeat scan suggested the lesion was reducing in size and the patient was discharged with analgesia and follow up.\r\nDiscussion: This is only the second case in the literature of a spontaneous intraspinal haematoma complicating PCI.(1) Anticoagulant therapy represents the second most common aetiology of intraspinal haematoma.(2) Possible pathological mechanisms include that sudden sharp increases in thoracic pressure elevate intravascular pressure in the spinal subdural space to the extent that it could overcome extravascular pressure and result in the tearing of spinal vessels.(3) If symptoms are stable case reports have shown that haematomas can resolve by stopping anticoagulant treatment.(4) However if neurological status is deteriorating, early neurosurgical intervention gives the best outcomes.(5) \r\nConclusion: Interventional cardiologists should bear this condition in mind if faced with neurological symptoms after antiplatelets, anticoagulants or PCI. This case also highlights the difficulty in striking the right balance between bleeding risk during treatment of NSTEMI and prevention of in-stent thrombosis. \r\n