July 17-18, 2023 | 09:00 AM GST


Osaka, Japan

Speakers Interview

Conference Agenda

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Keynote Session:

Meetings International -  Conference Keynote Speaker Atef Khamis Saleh photo

Atef Khamis Saleh


Title: Impact Of Regional Network On The Management Of STEMI Patients In North Cairo


Atef Saleh has completed his PhD at the age of 25 years from Ain University and postdoctoral studies from the same University School of Medicine. He is now working as cardiology specialist at Nasser institute for treatment and research at north Cairo and active member in the cardiology department.


Coronary artery disease is most frequent cause of death. Over seven million people every year die from ischemic heart disease. The management of patients with ST-Elevation myocardial infarction is influenced by health care service organizations. Regional STEMI networks for acute myocardial infarction facilitate primary percutaneous coronary intervention (PPCI) and its efficacy in reducing mortality and improving outcomes. The aim of the present study was to assess the feasibility of establishment of regional STEMI network in north Cairo governorate, Egypt and to assess the impact of this network on the practice of hospitals in the network and on patients' outcomes.

Results: The number of patients upon implementation of STEMI network increased from 140 to 212 (51.4%) to the same hospitals with the same facilities and in equal periods of time (6 months). It was found that the mean time of chest pain to first medical contact between the two groups before and after establishment of STEMI network did not change, it was 4 hours in both groups (P=0.36) while the mean door to balloon time improved from 54.3 to 44.1 minutes (P=0.01). In our study thrombolytic therapy use declined from 36.4% before STEMI network set up to only 7.5% (P>0.001), Ejection fraction improved from 51.3% to 55.4% (P>0.001), mitral regurge (MR) also improved upon establishment of STEMI network from 53.6% to 78.8 with (P>0.001),  the mean CCU stay in group II was 2 days versus 3 days before implementation of STEMI network (P>0.001), the mean door in door out from the spokes was 40 minutes. In-hospital mortality improved upon establishment of STEMI network from 6.4% to 2.8% (P=0.10).

Conclusions: Establishment of the STEMI network in Egypt is feasible and can lead to improvement of patients' outcomes. Thrombolytic therapy was no longer the main reperfusion therapy and primary PCI was offered to most patients after establishment of STEMI network.

Meetings International -  Conference Keynote Speaker  Ramy Mohamed Atlm photo

Ramy Mohamed Atlm

Lecturer of Cardiology - Faculty of Medicine Tanta University . EGYPT



Master degree (2009)
Fellowship of critical care medicine (2008-2009)
Fellowship of interventional cardiology- Ravenna , Italy  (2009-2011)
MD (2019)


Male patient 54 years old , hypertensive 4 years ago on ACE1 , diabetic on oral hypoglycemic drugs 10 years ago, hypercholesterolemic with positive family history .

 Anterior  STEMI   2019 underwent 1ry PCI  to LAD with one  DES. During this session we discovered that his RCA was CTO receiving retrograde collateral from septal branch of  LAD and epicardial collateral from circumflex. Stress MPI was decided to detect viability and ischemic burden which was positive (ischemic viable ).Ischemic burden was 15%

So , we decided to do CTO  PCI  to his RCA.

Meetings International -  Conference Keynote Speaker VINOD NIKHRA photo


Medical Doctor Hindu Rao Hospital & NDMC Medical College India

Title: Highlighting the Relationship Between NAFLD Metabolic Syndrome and Cardiovascular Disease


Dr.Vinod Nikhra is a Senior Consultant Physician and Faculty at NDMC Medical College and Hindu Rao Multi-specialty Public Hospital, New Delhi, India. He is a healthcare administrator, academician and clinician. He has been a Visitor at Cleveland Clinic Foundation, Cleveland and an Observing Physician at Alabama Medical Center a tertiary care hospital in Opelika, Alabama, USA. He has been elected a Fellow by International Medical Sciences Academy and the Royal Society of Medicine, London. He has been Editor of Madhya, the midage, the official Journal of Association for Health in Middle Age during 2003-2006. He has been on Reviewer panel of, among others, the Family Practice, an Oxford University medical journal and International Journal of Obesity. His published books include,ËœAging slowly, Living longer and The Anti-obesity Guide. Over the years he has contributed about hundred papers in leading national and international medical journals, some of which are available on


ABSTRACT :- CARDIOVASCULAR DISEASE, METS AND NAFLD: There exists a near-ubiquitous relationship between Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (METS or MetS). Both, MetS and NAFLD have been, in turn, related to increased incidence and prevalence of cardiovascular disease (CVD). Further, as a fallout of the modern-day sedentary lifestyle and altered dietary practices with enhanced intake of sweetened non-alcoholic and alcoholic drinks, there is increased prevalence of adiposity, MetS and type 2 diabetes mellitus (T2DM). NAFLD - PREVALENCE AND ASSOCIATIONS: NAFLD is a highly prevalent metabolic disorder having as key feature, the insulin resistance (IR), accompanied with impaired insulin sensitivity (IS) in liver and other organs including muscles and adipose tissues. Further, the incidence of NAFLD is high in conditions associated with IR such as obesity, type 2 diabetes mellitus (T2DM), dyslipidemia and metabolic syndrome (MetS). Intrahepatic triglyceride accumulation, or steatosis, is the hallmark of NAFLD that develops when the rate of fatty acids (FAs) influx (FAs uptake from plasma and de novo lipogenesis) exceeds the rate of FAs efflux (FA oxidation and secretion of triglycerides as VLDL). A subset of NAFLD patients go on to develop non-alcoholic steatohepatitis (NASH), which can progress to fibrosis and cirrhosis. ETIOLOGY AND PATHOLOGICAL MECHANISMS: The pathogenesis of NAFLD has been described by the ‘two hits’ hypothesis. The first ‘hit’ is deposition of FAs and triglyceride in hepatocytes (steatosis), and the second ‘hit’ is the progression of steatosis to NASH. The etiology of NAFLD is complex with factors like overnutrition, dysbiosis, increased fat mass, endocrine disruptors and oxidant injury, pro-inflammatory cytokines and altered adipokines involved to variable extent. The pro-inflammatory cytokines appear to interfere with insulin signaling by activating various inflammatory pathways. The pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α), activate intracellular kinases such as JNK and IKKβ and the activation of downstream transcription factors like AP-1 and NF-κB results in the impairment of insulin receptor signaling. METABOLIC CROSS-TALKS - LIVER AND OTHER ORGANS: The target organs can have differential responses to insulin and the skeletal muscle is more sensitive to insulin than the liver and adipose tissue. Thus, IR in skeletal muscle is observed early during development of NAFLD, T2DM and MetS, occurring long before IR in the liver and adipose tissue. There results a metabolic cross-talk involving liver, muscles and adipose tissue, which brings about a cascade of metabolic alterations: (a) The skeletal muscle IR impairs insulin-stimulated muscle glucose uptake → ↑ glucose delivery to the liver; (b) The hepatic selective IR leads to decreased hepatic glycogen synthesis, increased hepatic gluconeogenesis and ↑ liver triglyceride levels and hepatic de novo lipogenesis (DNL); (c) The adipose IR impairs insulin-mediated suppression of lipolysis → ↑ release of glycerol and fatty acid (FAs) → redirected to the liver, driving hepatic lipid synthesis further; (d) ↑ glycerol delivery to the liver → hepatic gluconeogenesis via substrate push; (e) Diacylglycerol (DAG)-mediated activation of protein kinase C epsilon  impairs hepatic insulin signaling →↓ insulin-stimulated hepatic glycogen synthesis; (f) The ↑ glucose uptake in the liver activating the carbohydrate response element-binding protein (ChREBP), stimulates intracellular glycolysis, providing metabolic precursor materials for DNL; and (g) The increased FAs may activate the intrinsic apoptosis pathway in hepatocytes via c-Jun N-terminal kinase (JNK), which promotes progression from simple steatosis to NASH and advanced hepatic fibrosis. The adipocyte secretome, including FFAs and adipokines, is closely linked to the evolution and progression of NAFLD. THERAPEUTIC OPTIONS AND IMPLICATIONS: Hepatic steatosis is defined by the presence of ≥5% lipid laden hepatocytes on a liver biopsy or ≥10% fatty infiltration of the liver on magnetic resonance imaging (MRI). The presence of hepatic steatosis alone is associated with a low risk for progression to cirrhosis. But, those with NASH or NAFLD and fibrosis are at risk of progressive liver disease and require therapeutic intervention. The lifestyle modifications include dietary modifications and increasing physical activity. Pioglitazone increases adiponectin levels and decreases in hepatic fat. Omega-3 fatty acids and pentoxifylline are useful. Vitamin E supplementation may Improve steatosis and inflammation, whereas metformin, ursodiol and orlistat have no therapeutic benefit. Bariatric surgery may help and its impact on NAFLD may extend beyond through weight loss alone. CONCLUSION – THE PROGNOSTIC IMPLICATIONS: The accumulation of fat affects physiology of hepatocytes and is accompanied by various homeostatic and metabolic alterations. The presence of hepatic steatosis alone is associated with a low risk for progression to cirrhosis, but those with NASH or NAFLD and fibrosis are at risk of progressive liver disease and carry adverse prognostic implications. In addition, there are various associated metabolic disorders like T2DM and CVD resulting from enhanced atherosclerosis afflict health status and complicate the QOL issues. The NAFLD associated liver diseases present a modern-day clinical challenge due to their meagre response to lifestyle measures and available treatment options. There is observed a poor adherence to the treatment and follow up due to overnutrition, overweight and obesity often being considered normal health variables.

Meetings International -  Conference Keynote Speaker JIE TIAN photo


Ministry of Education Key Laboratory of Child Development and Disorders Chongqing Medical University China

Title: Pediatric Diastolic Heart Failure: Clinical Features Description of 421 Cases


Jie Tian completed his PhD from Chongqing Medical University and then devoted himself to the clinic, teaching and research of childrens cardiovascular diseases for 32 years.


Background and Aim: Heart failure in children differs substantially from the adult population. Clinical characteristics of pediatric diastolic heart failure has rarely been reported. In this study, we aimed to summary the causes, clinical features, lab tests, and treatment effect of pediatric diastolic heart failure.

Methods: This study was a single center, retrospective study conducted in Children’s Hospital of Chongqing Medical University. Children who were diagnosed with diastolic heart failure (DHF) without systolic heart failure (SHF) between 2006 and 2014 were included. Meanwhile, SHF (without DHF) cases were also collected from 2013 to 2014. Results A total of 421 DHF and 42 SHF cases were included. The average age of pediatric DHF was 1.89 ± 3.29 years old, significant younger than that of SHF (4.65 ± 4.90). The top three cardiovascular causes of DHF were complex congenital heart malformations (53.4%), simple congenital heart defect (15.7%), and cardiomyopathy (7.4%). Alternatively, number of cardiomyopathy cases (57.1%) ranked first in SHF group. Simple congenital heart diseases (CHDs) rarely caused SHF. The most common symptom and sign were tachypnea and hepatomegaly in pediatric HF. Symptoms like cyanosis, feeding difficulty, be fidgety, pale, fatigue, and edema were valuable in differential diagnosis of DHF and SHF in children. B-type natriuretic peptide (BNP) increase was found in 36.9% of DHF children, and 60% in SHF patients. Sensitivity of BNP greater than 100 pg/ml in diagnosis of DHF was 0.37, and specificity of it was 0.86. Diastolic function indicators, such as E/A (early wave/late wave) ratio, IVRT (isovolumic relaxation time) were significant recovered after treatment in DHF patients. Less therapeutic benefits were achieved in children with cardiomyopathy induced DHF, in compared with non-cardiomyopathy patients.

Conclusion: Pediatric DHF and SHF were largely different in primary causes, clinical symptoms and signs and short-term prognosis. There was a limit diagnostic value of BNP with 100 pg/ml as cut-off value in pediatric DHF. Larger, multicenter studies of pediatric DHF are required in the future.

Keynote Session: