Day 2 :
Thomas Jefferson University Hospital, USA
Michael P. Savage is the Ralph J. Roberts Professor of Cardiology at Thomas Jefferson University and Director of the Cardiac Catheterization Laboratory at the Thomas Jefferson University Hospital in Philadelphia. He was instrumental in the formation of the recently opened Jefferson Angioplasty Center as a second-opinion center for high-risk patients with complex cardiovascular disease. The Jefferson team under Dr. Savage has pioneered many advances in interventional cardiology and was at the forefront of clinical research in the development of coronary stents that have revolutionized the treatment of heart disease. Dr. Savage's research continues to advance the care of cardiac patients by perfecting techniques for less invasive alternatives to heart surgery. His work includes over 230 publications of original research, book chapters, and abstracts. He has lectured nationally and internationally on a variety of cardiac disease topics and is an editorial consultant for numerous journals. He has received multiple honors for patient care, research, and teaching. Dr. Savage is a Fellow of the American College of Cardiology, the Society of Cardiac Angiography and Interventions, and the American College of Physicians..
Background: Saphenous vein grafts (SVG) are the most common conduit used in coronary artery bypass surgery. However, within a decade from surgery approximately 50% of SVG will develop significant disease. Percutaneous coronary intervention (PCI) of diseased SVG is associated with a high risk of distal embolization, no-reflow, periprocedural myocardial infarction (MI), and late restenosis [1,2]. This review examines the evolutionary advances and current status of PCI for this challenging problem. Role of Stents: The preeminent role of coronary stenting for SVG disease was established by the SAVED trial . Compared to balloon angioplasty, bare metal stents resulted in improved procedural and angiographic outcomes. At 240 days, event-free survival was significantly higher in the stent group (73 vs. 58%, p=0.04). The role of drug-eluting stents (DES) remained uncertain initially due to the mixed results of smaller randomized trials. The superiority of DES was solidified by the 610 patient ISAR-CABG trial which demonstrated fewer cardiac events at 1 year with DES (15.4 vs. 22.1%, p=0.03) . Optimal duration of dual antiplatelet therapy after SVG stenting has not been established. However, late and very late stent thrombosis occur more frequently in SVG. Distal Embolization: SVG intervention is fraught with a high risk of ischemic complications due to distal embolization. In the landmark SAFER trial, use of a distal protection device (DPD) resulted in a 42% relative reduction in early cardiac events . Despite the evidence of clinical benefit and guideline class I recommendation, DPD are used in <25% of SVG PCI. Delivery of filter devices can be technically challenging in complex SVG and this likely contributes to the reticence of some operators to use them. We have recently reported the value of simple adjunct techniques to facilitate the successful deployment of DPD in SVG . No-Reflow: The development of no-reflow during PCI is a significant risk factor for MI and death. DPD have reduced but not eliminated no-reflow, which is a complex phenomenon involving both debris embolization and microvascular spasm. A variety of vasodilating drugs have been used to treat no-reflow including calcium channel blockers, adenosine, and nitroprusside. In the largest series of patients treated with drug therapy for no-reflow, intracoronary nicardipine was found to be over 98% successful in reversing no-reflow during PCI . It has been suggested that pretreatment with intracoronary nicardipine or other vasodilating agents may reduce the incidence of SVG no-reflow . In current practice, we utilize the apparent synergistic effect of prophylactic intracoronary nicardipine and distal protection filters in vein graft PCI. Compared to use of DPD alone, the combination of drug + device is associated with significantly fewer periprocedural death/MI (10 vs. 1%, p<0.01) . Conclusion: Significant technical and procedural advances have improved the outcome of high risk SVG intervention
New York Medical College, USA
Keynote: List of 13 possible causes of Atrial Fibrillation (AF) by leading institute do not include Lyme Disease. However, in majority of ECGs of AF, we often find various degree of Borrelia Burgdorferi (BB) infection of the heart with increase in ANP & Cardiac Troponin I from analysis of ECGs. It is possible to detect & treat these abnormalities before AF develops
Yoshiaki Omura received Oncological Residency training at Cancer Institute of Columbia University & Doctor of Science Degree through research on Pharmaco-Electro-Physiology of Single Cardiac Cells in-vivo and in-vitro from Columbia University. He researched EMF Resonance phenomenon between 2 identical molecules for non-invasive detection of molecules, at Graduate Experimental Physics Dept., Columbia University, for which he received U.S. patent. He is also the creator of Bi-Digital O-Ring Test. He published over 270 original research articles, many chapters, & 9 books. He is currently Adjunct Prof. of Family & Community Medicine, New York Medical College; President & Prof. of Int’l College of Acupuncture & Electro-Therapeutics, NY; Editor in Chief, Acupuncture & Electro-Therapeutics Research, Int’l Journal of Integrative Medicine, (indexed by 17 major int’l Indexing Periodicals); Formerly, he was also Adjunct Prof. or Visiting Prof. in Universities in USA, France, Italy, Ukraine, Japan, Korea, & China
According to the currently available lists of possible causes of Atrial Fibrillation (A.F.), none of them mention Lyme Disease, Borrelia Burgdorferi (B.B.) infection. Using very high sensitivity of Electromagnetic Field (EMF) Resonance Phenomenon between 2 identical molecules with identical weight, we can detect almost any molecules or infection including B.B. Spirochete infection non-invasively from chest wall or recoded electrocardiograms (ECGs). The B.B. infections are often found in ECGs corresponding to SA-node area, right atrium, left atrium, etc. This non-invasive, sensitive method of detecting different molecules or specific cancer tissues was given US Patent in 1993. When we examine ECG of A.F., we found in majority of recoded ECGs, various degrees of B.B. infection exist at SA-node area, right atrium and left atrium. However, small degree of B.B. infection such as less than 1000ng we do not find A.F. When degree of infection increased over 2000 or 3000ng and only when ANP (Atrial Natriuretic Peptide) significantly increased over 150~200ng at where B.B. infection is significantly increased, they often develop A.F. When there was A.F, due to B.B. there was always very significant increase in ANP & Cardiac Troponin I (while in normal heart ANP is less than 10ng) and increased Cardiac Troponin I with decrease in Vitamin D3 & Taurine. It is well known that ANP is released from atrial muscle and it has function of reducing blood pressure as well as increasing excretion of sodium from kidney. Our study indicates significantly high percentage of various degrees of B.B. infection were detected in ECG showing presence of A.F. Therefore, even when the patient does not have A.F. by non-invasively examining the degree of infection of Borrelia Burgdorferi Spirochete & abnormal increased ANP at atriums, we may be able to prevent development of atrial fibrillation since it indicates high probability of development of atrial fibrillation. For eliminating B.B. infection of heart, commonly used Doxycycline often have some problem for various reasons, more effective result can be obtained by combined use of optimal doses of Vitamin D3 or Taurine & Amoxicillin average 3 times a day, since Vitamin D3 was found to have excellent urinary excreting effect of virus, bacteria, & fungi as one of 7 unique beneficial effects.
- Interventional Cardiology | Cardiovascular Diseases & Vascular Heart Diseases | Cardiac & Cardiovascular Research | Cardiac and Heart Regeneration
Cesca Therapeutics Inc., USA
To be Updated Soon...
Cardiovascular Diseases are a major burden on healthcare in modern society. Diseases, such as Critical Limb Ischemia (CLI), are debilitating. Many of the cardiovascular ischemic disease patients have limited surgical or medical options. Regeneration of vascular system is an attractive treatment strategy and is actively pursued in various preclinical and clinical settings. One of the options in regenerative medicine is the use of autologous bone-marrow concentrate (aBMC) containing stem & progenitor cells. Autologous bone-marrow concentrate (aBMC) is derived from the bone marrow aspirate (BMA) by density centrifugation and can be delivered either intra-muscularly (IM) or intra-coronary in the affected region. The aBMC consists of a) an acellular fraction comprised of autologous plasma and the cytokines & b) Cellular Fraction which is a source of (i) proangiogenic cells such as hematopoietic stem cells, mesenchymal progenitor cells, and endothelial progenitor cells; (ii) other cells of immune system at different levels of maturity and multi-potency. The acellular and cellular components participate in tissue repair and regeneration and have made aBMC an attractive source of cells and cytokines for therapeutic angiogenesis in the treatment of ischemic diseases.
1. Ponemone et al (2017) Safety and Effectiveness of Bone Marrow Cell Concentrate in the Treatment of Chronic Critical Limb Ischemia Utilizing a Rapid Point-of-Care System. Stem Cell International 18: 1-16.
2. Sanghi et al (2016) The Autologous bone marrow concentrate enriched in progenitor cells — an adjuvant in the treatment of acute myocardial infarction. International Journal of Cardiovascular Academy 2: 77-83.
3. Ponemone et al (2016) Enhancement of Atrophic Non-Union Fracture Healing Using Autologous Progenitor Cell-Rich Bone Marrow. HSOA Journal of Stem Cells Research, Development & Therapy. 3: 007.
4. Sanders et al (2013) Effects of Hypoxanthine Substitution in Peptide Nucleic Acids Targeting KRAS2 Oncogenic mRNA Molecules: Theory and Experiment. J. Phys. Chem. B 117(39): 11584-11595.
Sethi et al (2012) Receptor-specific peptides for targeting of liposomal, polymeric, and dendrimeric nanoparticles in cancer diagnosis and therapy. Current Molecular Imaging, 1(1): 3-11
Cardiovascular Device & Imaging Marketing Consultant & Medical Journalist, USA
Clifford Thornton, Cardiovascular Device & Imaging Consultant & Medical Journalist: Graduated from Sanford-Brown Institute, Iselin, NJ with a certification in Cardiovascular Technology, 2004 (emphasis on echocardiography & cardiac pathologies), B.S. Business Admin./Marketing, New York University, Stern School of Business, 1997. Professional experience as a Program Manager with Lucent Technologies/Avaya, Inc. (Enterprise Networking) and led a custom market research practice as a Sr. Analyst for a Telecommunications Industry Research Firm & Consultancy.
Statement of the Problem: The incidence of Cardiovascular Diseases (CVDs) is rising globally, and rapidly. As a result, this is not just a health issue, but an economic one as related costs are ballooning to economically unsustainable levels. For example, in the U.S., total healthcare expenditures, which are significantly driven by heart disease, are nearing 20% of the total gross domestic national product (GDP). As developing economies experience similar increases in CVDs, it will become more challenging to meet their populations’ health needs while sustaining their economies. Some of the key related statistics:
- On a worldwide basis, 17.7 Million people died from CVDs in 2015; this accounts for 31% of all global deaths
- The total global cost of treating CVDs was $863 Billion in 2010; this is projected to reach approximately $1,100 Billion by 2030
- 84 Million people in the U.S. suffer from some form of CVD
- 15.8 Million Americans have Coronary Artery Disease (CAD)
- Heart Failure affects 5 Million U.S. adults
- Heart disease & stroke account for approximately $320 Billion of direct healthcare costs per year in the U.S.
My presentation will address the following key questions and issues:
What is the current “Gold Standard” of care today for each of these heart conditions and what are the 3 leading evolving technologies & related treatments to address these heart diseases through 2030:
- Coronary Artery Disease (CAD)
- Heart Failure
- Heart Valve Disease
- Cardiac Arrhythmias
- Congenital Heart Defects
- What are the leading medical device companies in each of these areas, what are their product roadmaps, and what evolving and advanced technologies are driving these product strategies? When will we see some of these medical breakthroughs integrated into routine practice?
- Preventive Cardiology: What are some practical, proven, and duplicable?
“Cardiac Stem Cell Therapies: The Next Revolution in Heart Failure Treatment”, BioInformant, March 14, 2017
“NYU Stern Innovators – Alumni Paving the Way to the Future in Energy Monitoring & Management and Digital Media Software”, Global Innovation Magazine, February 2017 – Issue 10, pg. 20
What's the BIG DEAL about Diastolic Dysfunction? Here's What....”, LinkedIn – Pulse, October 14, 2016
"A Fantastic Vessel-Clearing Innovation", Inventor's Digest, February 2016 Issue, pg. 19
"A Totally New Healthcare System", Modern Health Talk, February 17, 2012
Shengjing Hospital of China Medical Universtiy, China
Wu Na works in Shengjing hospital of China Medical Universtiy. And now she is studying in Cardiovascular Research Center of Lewis Katz School of Medicine in Temple Univeistiy as a vistiting scholar for one .year. Wu Na has her expertise in pathological and metabolic changes in cardiovascular diseases.Her researches focus on investigating the effect and underlying mechanism of metabolic disorder on 1) Atherosclerosis and vascular inflammation, 2) Endothelial function. She goes into rather rigorous surgery techniques in order to established a rat model of acute blood glucose fluctuations and aimed at further investigating the mechanisms underlying increased apoptosis of vascular endothelial cells in the condition.
Statement of the Problem: Compared to persistent hyperglycemia, fluctuant hyperglycemia has more potential to increase microvascular lesions and the risk of death. In the condition of stress, the glucose levels of those with normal metabolic function may be very high. In this case given hypoglycemic therapy, there may be glucose decreases sharply in the hypoglycemic process, leading to acute glucose fluctuations. Chronic hyperglycemia in vivo and in vitro studies showed that fluctuant hyperglycemia could increase the apoptosis of endothelial cells. But to date, few studies have been conducted to investigate the influence of acute fluctuant hyperglycemia on endothelial cells in vivo. Methodology & Theoretical Orientation: In the present study, an in vivo model of acute fluctuant hyperglycemia was successfully established. We examin the influence of acute fluctuant hyperglycemia and persistent hyperglycemia on vascular endothelial cell apoptosis, oxidative stress and inflammation in vivo. Rats were assigned to three different groups (n=8/group) that received 48-h infusions of saline (SAL group), continuous 50% glucose (constant high glucose group [CHG]), or intermittent 50% glucose (acute blood glucose fluctuation group [AFG]). Expression of related protein and mRNAs were measured in endothelial homogenates prepared from endothelial cells harvested from the aorta Findings: Endothelial cells apoptosis were observed significantly in the aortas of the AFG group. The AFG had reduced Bcl-2 levels and enhanced Bax mitochondrial translocation levels in comparison with the CHG group (P <0.05). Compared with SAL and CHG, AFG increased MDA and 8-isoprostaglandin levels in plasma, oxidative stress in vascular endothelial cells, and inflammatory cytokines in plasma and vascular endothelial cells (P <0.05). Conclusion & Significance:Acute glucose fluctuation could cause significant oxidative stress and inflammation in endothelial cells, and elevate endothelial cell apoptosis, resulting in severe cardiovascular injury. Therefore, not only lowering blood glucose, but also reducing glucose fluctuation is very important in clinic.
1. Wu N, Shen H, Liu H, et al.(2016) Acute blood glucose fluctuation enhances rat aorta endothelial cell apoptosis, oxidative stress and pro-inflammatory cytokine expression in vivo. Cardiovascular Diabetology, 15:109.
2. Wu N, Lu Y, He B, et al. (2010) Taurine prevents free fatty acid-induced hepatic insulin resistance in association with inhibiting JNK1 activation and improving insulin signaling in vivo. Diabetes Research & Clinical Practice, 90:288-96.
3. Shen H, Wu N, Liu Z, et al. (2017) Epigallocatechin-3-gallate alleviates paraquat-induced acute lung injury and inhibits upregulation of toll-like receptors[J]. Life Sciences, 170:25-32.
4. Shen H, Wu N, Wang Y, et al. (2017) Chloroquine attenuates paraquat-induced lung injury in mice by altering inflammation, oxidative stress and fibrosis.[J]. International Immunopharmacology, 46:16.
5. Shen H, Wu N, Wang Y, et al. (2017) MyD88 gene knockout attenuates paraquat-induced acute lung injury.[J]. Toxicology Letters, 269:41
Institute of Radioprotection and Dosimetry, Brazil
Larissa Oliveira is an excellent research scientist who is doing important work in the Medical Physics field - Diagnostic Radiology, Radiation Protection, Dosimetry, Quality Control and Optimization in Brazil. Her researches provided us information regarding about the importance of justification and optimization and the necessity of developing Optimization Programs, as well as the potential of dose reduction for patients without compromise the diagnostic information and the importance of regular education and training. Recently, she studies the impact of the ionization radiation heart injuries during the CT Cardiac angiography. The heart is considered a late response organ. In high doses of radiation, the cardiac effects are already known, though there is no evidence that the cardiovascular system may also be injured by ionizing radiation at low doses. This approach demonstrated the importance to keep the radiation exposure as low as reasonably achievable strategy to reduce the potential risk.
Statement of the Problem: CT Cardiac angiography is increasingly utilized for the noninvasive assessment of coronary artery disease (CAD) due its ability to exclude or diagnose CAD with high accuracy and fast acquisition time. CT delivers high radiation doses to organs that are in the direct path of radiation beam. Thus, there is a potential risk of inducing cellular damage or radiation-induced cancer due to exponentially increased use of this technique in medicine. Exposure of the heart to high doses of ionizing radiation is associated with cardiac lesions, but there are no conclusive studies regarding ionization radiation at low doses and the risks involved for CT Cardiac angiography. The purpose of this study is to review the literature describing the effect of radiation dose on the circulatory system, with emphasis on the heart during the CCTA procedures. Methodology: The research was carried out in a Private Hospital, which has one GE Discovery dual-energy CT scanner. A sample of patients (n= 100) were selected randomly and in each patient, technical parameters and radiation dose were recorded by database. This study was divided in two phases: (1) To evaluate the CT doses using values reported on the equipment console (2) To determine the organ dose using 3D heart with Anthropomorphic Torso Phantom and dosimeter thermoluminescence. Findings: The results demonstrated the median effective dose was similar with the recent studies, approximately 4.6mSv. The second stage (absorbed dose in the heart) is still in progress due to the discrepancy of the values found in this study with the values of the literature.
Conclusion & Significance: The preliminary results demonstrated the importance to record the radiation exposure during the CCTA. Training and improvement of the team involved in the exam to be familiar with the radiation dose received by the patients during clinical practice.
- Einstein AJ, Elliston CD, Groves DW, Cheng B, Wolff SD, Pearson GDN, Peters MP et al (2012) Effects of Radiation Exposure from Cardiac Imaging: How Good Are the Data? Am Coll Cardiol 59(6): 553-565.
Figure 1. Experimental scheme of the 3D heart positioning in the phantom.
- Hashim S, Karim MKA, Bakar KA, Sabarudin A, Chin AW, Saripan MI, Bradley DA (2016) Evaluation of organ doses and specific k effective dose of 64-slice CT thorax examination using an adult anthropomorphic phantom. Rad. Physics and Chemistry 126:14-20.
- Smith-Bindman R, Lipson J, Marcus R, Kim KP, Mahesh M, Gould R, Berrington de González A, Miglioretti DL (2009) Radiation dose associated with common computed tomography examinations and the associated lifetime attributable risk of cancer. Arch Intern Med. 69(22):2078-86.
- Tahvonen P, Oikarinen H, Pääkkö E, Karttunen A, Blanco Sequeiros R and Tervonen O (2013) Justification of CT examinations in young adults and children can be improved by education, guideline implementation and increased MRI capacity. Br J Radiol. 86:1-9.
- Boerma M, Sridharan V, Mao XW, Nelson GA, Cheema AK, Koturbash, Singh SP, Tackett AJ, Hauer-Jensen M (2016) Effects of ionizing radiation on the heart. Mutat Res. 770:319-327
- Kataria B, Sandborg M, Althén JN (2016) Implications of patients centring on organ in Computed Tomography. Radiat Prot Dosimetry 169(1-4):130-5.
Pennsylvania State University College of Medicine, USA
Bi-Hua Tan was initially trained as a cardiologist in China after graduated from medical school. Then she joined the arrhythmia and clinical electrophysiological study group at Cardiovascular Division, Hyogo College of Medicine in Japan and obtained her PhD degree there. After that she completed her postdoctoral training at the Cellular and Molecular Arrhythmia Research Program, Department of Medicine, University of Wisconsin-Madison. She was the first to characterize the molecular phenotype of eight common polymorphisms and some genetic basis of disease causing mutations in cardiac Na channel. She also first characterized a marked gain of functional KATPKir6.1 channel mutation in KCNJ8 as a novel pathogenic mechanism for the phenotypic expression of both Brugada syndrome and early repolarization syndrome. She was awarded American Heart Association (AHA) Postdoctoral Fellowship and the American Heart Association National Center Scientist Development Grant.
The gene SCN5A on chromosome 3 encodes the α-subunit of the voltage-gated cardiac sodium channel (hNav1.5) that is responsible for large peak inward sodium current (INa) and late INa. Peak INa underlies excitability and conduction in working myocardium (atrial and ventricular cells) and special conduction tissues (Purkinje cells etc.). Late INa influences repolarization and refractoriness. The importance of INa for normal cardiac electrical activity is emphasized by the occurrence of potentially lethal arrhythmias in the setting of inherited and acquired Na channel diseases. SCN5A in humans has two splice variants, one lacking a glutamine at position 1077 (Q1077del) and one containing Q1077. Common sequence variants ("polymorphisms") have also been implicated as risk factors in multiple diseases. Mutations in the cardiac Na channel gene SCN5A cause loss-of-function or gain-of-function and underlie arrhythmia syndromes, such as Brugada syndrome, cardiac conduction disorder, congenital sick sinus syndrome, idiopathic ventricular fibrillation, sudden infant death syndrome, the type 3 long QT syndrome etc. Here, 3 unrelated inherited arrhythmia cases will be presented to show that the loss-of-function or gain-of-function biophysical phenotypes for sodium channel mutations depend on the splice variant background in which it is expressed and the intracellular acidosis, and is also modulated by common polymorphism.
- Hu RM*, Tan BH*, Tester DJ, Song C, He Y, Dovat S, Peterson BZ, Acherman MJ, Makielski JC (2015) Arrhythmogenic biophysical phenotype for SCN5A mutation S1787N depends upon splice variant background and intracellular acidosis. PLoS ONE. Apr 29: 10(4):e0124921. doi: 10.1371/journal.pone.0124921. eCollection
- Hu RM, Tan BH, Orland KM, Valdivia CR, Peterson A, Pu J, Makielski JC (2013) Digenic inheritance novel mutations in SCN5a and SNTA1 increase late INa contributing to LQT syndrome. Am J Physiol Heart Circ Physiol. Apr: 304(7):H994-H1001.
- Tester DJ*, Tan BH*, Medeiros-Domingo A, Song C, Makielski JC, Ackerman MJ (2011) Loss-of-Function Mutations in the KCNJ8-Encoded Kir6.1 KATP Channel and Sudden Infant Death Syndrome. Circ Cardiovasc Genet. 4:510-515.
- Medeiros-Domingo A*, Tan BH*, Crotti L*, Tester DJ, Eckhardt LL, Cuoretti A, Kroboth SL, Song C, Zhou Q, Kopp D, Schwartz PJ, Makielski JC, Ackerman MJ (2010) Gain-of-Function Mutation, S422L, in the KCNJ8-Encoded Cardiac KATP Channel Kir6.1 as a Pathogenic Substrate for J Wave Syndromes. Heart Rhythm. 7:1466-1471.
- Tan BH, Pundi KN, Van Norstrand DW, Valdivia CR, Tester DJ, Medeiros-Domingo A, Makielski JC. Ackerman MJ (2010)
Sudden Infant Death Syndrome-Associated Mutations in the Sodium Channel Beta Subunits. Heart Rhythm. 7(6):771-778.
- Medeiros-Domingo A*, Tan BH*, Iturralde-Torres P, Tester DJ, Tusié-Luna T, Makielski JC. Ackerman MJ (2009) Unique mixed phenotype and unexpected functional Effect revealed by novel compound heterozygosity mutations involving SCN5A. Heart Rhythm. 6(8):1170-1175.
- Tan BH, Iturralde-Torres P, Medeiros-Domingo A, Nava S, Tester DJ, Valdivia CR, Tusié-Luna T, Ackerman MJ, Makielski JC (2007) A novel C-terminal truncation SCN5A mutation from a patient with sick sinus syndrome, conduction disorder and ventricular tachycardia. Cardiovascular Research. 76:409-417.
- Tan BH, Valdivia CR, Song C, Makielski JC (2006). Partial expression defect for the SCN5A missense mutation G1406R depends upon splice variant background Q1077 and rescue by mexiletine. Am J Physiol Heart Circ Physiol. 291: H1822- H1828.
- Tan BH,, Valdivia CR, Rok BA, Ye B, Ruwaldt KM, Tester DJ, Ackerman MJ, Makielski JC (2005) Common human SCN5A polymorphisms have altered electrophysiology when expressed in the Q1077 splice variants. Heart Rhythm. 2(7): 741-747.
Poona Hospital and Research Centre, India
Ajeya N Ukadgaonkar is pursuing a superspeciality course (DNB) in Cardiology in Poona Hospital and Research Centre, India. He has completed his MD in Internal Medicine and has worked as an assistant professor in Internal Medicine. He has 2 publications in international and 1 publication in a national journal to his name. He bears a special interest in the field of research.
Background : Cyclophilin A (CyPA) is a protein released from vascular smooth muscle cells in response to reactive oxygen species and serves as a marker of oxidative stress and inflammation, which play an important role in atherosclerosis. We tested the correlation of plasma CyPA levels with coronary artery disease (CAD) and its risk factors.
Methods and Results : Plasma CyPA levels were tested in 205 consecutive patients undergoing coronary angiography (CAG) by immunoassay based sandwich technique and were correlated with CAG results and traditional risk factors for CAD. The data was analyzed using Kruskal Wallis and Mann-Whitney U tests. We observed that the median CyPA levels were significantly higher in patients with obstructive CAD (11.8 ng/ml with inter quartile range (IQR) of 9.9 - 16 ng/ml), as compared to non obstructive CAD (8.6 ng/ml with IQR of 7.55 - 9.65 ng/ml) and normal coronaries (5.6 ng/ml with IQR of 4.5 - 6.9 ng/ml ) with p value <0.001. The median CyPA levels were significantly higher in patients with diabetes mellitus (11.5 ng/ml in diabetic versus 9 ng/ml in non diabetic patients, p<0.001), males (10 ng/ml in males versus 7.9 ng/ml in females, p<0.001), smokers (10.6 ng/ml in smokers versus 9.2 ng/ml in non smokers, p=0.008) and post menopausal state (8.8 ng/ml in post menopausal women versus 5.2 ng/ml in pre menopausal women, p=0.005). Statistically significant difference was not found in median CyPA levels with other risk factors such as age, hypertension, dyslipidemia and family history.
Conclusion : CyPA is a strong predictor and emerging biomarker of CAD and an easy, reproducible tool to screen the patients with CAD or suspected CAD.
Keywords : Coronary artery disease, Coronary Angiography, Cyclophilin A, Risk factors.
- Kimio Satoh (2015) Cyclophilin A in Cardiovascular Homeostasis and Diseases. Tohoku journal of experimental medicine 235(1):1-15.
- Ramachandran et al (2014) Plasma level of cyclophilin A is increased in patients with type 2 diabetes mellitus and suggests presence of vascular disease. Cardiovascular diabetology 13:38.
- Satoh K, Fukumoto Y, Sugimura K, Miura Y, Aoki T, Nochioka K et al (2013) Plasma cyclophilin A is a novel biomarker for coronary artery disease. Circulation journal 77(2) : 447 –55.
- Nigro P., Satoh K., O’Dell M.R., Soe N.N., Cui Z., Mohan A (2011) Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E-deficient mice. Journal of experimental medicine 208(1) : 53-66.
- Satoh K, Shimokawa H, Berk BC (2010) Cyclophilin A: Promising new target in cardiovascular therapy. Circulation journal 74(11) : 2249 –56.
- Satoh K, Matoba T, Suzuki J, O’Dell MR, Nigro P, Cui Z et al (2008) Cyclophilin A mediates vascular remodeling by promoting inﬂammation and vascular smooth muscle cell proliferation. Circulation 117(24) : 3088 –98.
Shiraz University of Medical Sciences, Shiraz, Iran
Maryam Hadibarhaghtalab has her expertise in evaluation of cardiovascular risk factors and making new cut off and new model for anthropometric indices. She is also trying to make new method and formula to predict cardiovascular events such as metabolic sx,stent restenosis,and even cardiac surgeries and et al .moreover she is the medical author of almost 10 books including biomimicry, innovations in medical sciences and et al. besides she has had MPH degree along with being the top student in general practitioner duration and she is
In this study we evaluated and redefined the optimum body mass index (BMI) cut-off point for the Iranian population based on metabolic syndrome (MeS) risk factors. We further evaluated BMI cut-off points with and without waist circumference (WC) as a cofactor of risk and compared the differences. This study is part of the largest surveillance programs conducted in Shiraz, Iran, termed the Shiraz Heart study. Our study sample included subjects between the ages of 20 to 65 years old. After excluding pregnant women, those with missing data and those with comorbid disease, a total of 12283 made up the study population. The participants underwent a series of tests and evaluations by trained professionals in accordance with WHO recommendations. Hypertension, abnormal fasting blood sugar (FBS), triglyceride (TG) and high density lipoprotein cholesterol (HDL) (in the context of the definition of metabolic syndrome) were prevalent among 32.4%, 27.6%, 42.1 and 44.2% of our participants, respectively. Women displayed higher rates of overall obesity compared to men (based on the definition by the WHO as higher than 30 kg/m2). Regarding MeS, 38.9% of our population had the all symptoms of MeS which was more prevalent among women (41.5% vs. 36%). When excluding WC in the definition of MeS, results showed that males tend to show a higher rate of metabolic risk factors (19.2% vs. 15.6%). Results of multivariate analysis showed that parallel to an increase in BMI, the odds ratio (OR) for acquiring each component of the metabolic syndrome increased (OR = 1.178; CI: 1.166–1.190). By excluding WC, the previous OR decreased (OR = 1.105; CI: 1.093–1.118). Receiver Operating Characteristic (ROC) curve analysis showed that the optimum BMI cut-off point for predicting metabolic syndrome was 26.1 kg/m2 and 26.2 kg/m2 [Accuracy (Acc) = 69% and 61%, respectively)] for males and females, respectively. The overall BMI cut-off for both sexes was 26.2 kg/m2 (Acc = 65%) with sensitivity and specificity of 69% and 62%, respectively. This cut-off had a positive predictive value of 54% and a negative predictive value of 76%. When we excluded waist circumference, the optimum BMI cut-off for acquiring metabolic risk factors in males decreased to 25.7 kg/m2(Acc = 67%) and increased for women to 27.05 kg/m2 (Acc = 66%). Iranians are at higher risks of morbidity related to metabolic factors at a lower BMI cut-off and prompt action and preventive health policy are required to prevent and educate Iranians regarding diseases associated with obesity.
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