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Macro complications 2018
The document discusses atherosclerosis and macrovascular complications of diabetes. It describes the pathogenesis of atherosclerosis, including endothelial dysfunction, LDL oxidation, foam cell formation, and plaque development. It notes that macrovascular complications of diabetes include increased risks of coronary heart disease, cerebrovascular disease, and peripheral vascular disease. The document also discusses some potential mechanisms contributing to accelerated atherosclerosis in diabetes, including abnormalities in lipoproteins, advanced glycation end products, procoagulant states, and insulin resistance.
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Macro complications 2018
- 1. PBRC 2005 Macrovascular complicationsMacrovascularcomplications Pr. Dr. M. A. BADR
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- 4. Atherosclerosis Focal plaqueswithin the intima containing cholesterol and cholesterol esters (CE) Affects large and medium sized arteries Causes coronary heart diseases (CHD) Peripheral vascular disease Cerebral vascular disease Diabetic , accelerated , arteriolar, distal, multiple vessels,associated with microvascular affection and autonomic neuropathy =silent ischemia
- 5. April 28, 20185 Chronic Coronary Artery Disease in the Elderly
- 6. PBRC 2005 1. Atheroscleroticlesions Fatty streaks. Gelatinous plaques. Fibrous plaques. Complicated plaques. 2. Theories of atherogenesis Lipid hypothesis. Thrombogenetic hypothesis. Mesenchymal hypothesis. Monoclonal hypothesis. Response to injury hypothesis.
- 7. April 28, 20187 VSMC migration Foam-cell formation Adherence and aggregation of platelets Adherence and entry of leukocytes T-cell activation Atherosclerosis: An Inflammatory Disorder VSMC, vascular smooth muscle cell migration.
- 8. Pathogenesis Chronic inflammatoryresponse of the vascular wall to endothelial injury or dysfunction Elevated plasma LDL levels causing the deposit of LDL in the subendothelium of blood vessels Oxidation of transmigrated LDL Activation of endothelial cells Recruitment of monocytes/macrophages which ingest oxLDL through scavenger receptors Formation of foam cells – fatty streaks Proliferation of smooth muscle cells Deposition of extracellular matrix proteins
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- 10. Lipid Core lumen neointima Formation ofAtherosclerotic Plaques
- 11. Plaque Rupture andThrombosis Lipid Core Tissue Factor Platelet Aggregation
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- 16. April 28, 201816 Potential Mechanisms of Atherogenesis in Diabetes Abnormalities in apoprotein and lipoprotein particle distribution Glycosylation and advanced glycation of proteins in plasma and arterial wall “Glycoxidation” and oxidation Procoagulant state Insulin resistance and hyperinsulinemia Hormone, growth-factor, and cytokine-enhanced SMC proliferation and foam cell formation
- 17. Coronary HeartDisease Increased 2 fold in men; 4 fold in women Responsible for 50-60% of adult deaths Cerebrovascular Disease Risk for stroke increased 4 fold Peripheral Vascular Disease Present in 8% at diagnosis, 45% at 20 years Foot or ankle ulcers occur in 15% Accounts for 40-50% of nontraumatic amputations 50% 3-year survival after amputation
- 18. PBRC 2005 What isthe metabolic syndrome? Clustering of Metabolic Risk Factors (3+) Atherogenic dyslipidemia Elevated blood pressure Elevated plasma glucose Prothrombotic state Proinflammatory state
- 19. PBRC 2005 Global cardiometabolicrisk* Gelfand EV et al, 2006; Vasudevan AR et al, 2005 * working definition
- 20. PBRC 2005 Insulin-resistance andInsulin-resistanceand ββ-cell function-cell function Amiloyd storeAmiloyd store GlucotoxicityGlucotoxicity (hyperglycemia(hyperglycemia)) Hyper-Hyper- insulinaemiainsulinaemia ProteinProtein GlycosilationGlycosilation LipotoxicityLipotoxicity ((↑↑ FFA e TG)FFA e TG) Insulin-Insulin- resistanceresistance ⇩⇩ ββ-cell-cell functionfunction
- 21. PBRC 2005 Public HealthPublicHealth ApproachApproach
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- 24. PBRC 2005 PublicEducation Screening for at risk individuals: Blood Sugar/ HbA1c Lipids Blood pressure Tobacco use Body habitus Family history Screening/Public Health ApproachScreening/Public Health Approach
- 25. PBRC 2005 Intensive therapyIntensivetherapy AggressiveAggressive TTOTTO Maximum TherapMaximum Therap dosedose
- 26. PBRC 2005 Recommendations: Glycemic,Blood Pressure,Recommendations: Glycemic, Blood Pressure, Lipid Control in AdultsLipid Control in Adults A1C <6.5 %* Blood pressure <130/80 mmHg† Lipids LDL cholesterol <100 mg/dl (<2.6 mmol/l)‡ *More or less stringent glycemic goals may be appropriate for individual patients. Goals should be individualized based on: duration of diabetes, age/life expectancy, comorbid conditions, known CVD or advanced microvascular complications, hypoglycemia unawareness, and individual patient considerations. †Based on patient characteristics and response to therapy, higher or lower systolic blood pressure targets may be appropriate. ‡In individuals with overt CVD, a lower LDL cholesterol goal of <70 mg/dl (1.8 mmol/l), using a high dose of statin, is an option. ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S31. Table 12.
- 27. PBRC 2005 Lifestyle modification Diet Exercise Weight loss Smoking cessation If a 1% reduction in HbA1c is achieved, you could expect a reduction in risk of: • 21% for any diabetes-related endpoint • 37% for microvascular complications • 14% for myocardial infarction However, compliance is poor and most patients will require oral pharmacotherapy within a few years of diagnosis Stratton IM et al. BMJ 2000; 321: 405–412.
- 28. PBRC 2005 Weight lossmay be obtainedWeight loss may be obtained through:through: • Therapeutic lifestyle changeTherapeutic lifestyle change • Drug therapyDrug therapy (if Therapeutic lifestyle change is not sufficient)(if Therapeutic lifestyle change is not sufficient) • Bariatric surgeryBariatric surgery (in selected cases; to estimate the risk/benefit ratio)(in selected cases; to estimate the risk/benefit ratio)
- 29. PBRC 2005 REVERSIBILITY OFATHEROMATOUS PLAQUES Apo A Milano HDL
- 30. PBRC 2005 REVERSIBILITY OFATHEROMATOUS PLAQUES Apo A Milano HDL
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- 35. Lomitapide, mipomersen: Twonovel agents for homozygous familial hypercholesterolemia
- 38. PBRC 2005 QUALITY IMPROVEMENT& ASSURANCE CONSENSUS GUIDELINES EVIDENCE BASED MEDICINE PERSONALIZED MEDICINE
- 39. PBRC 2005 ADA EvidenceGrading System for ClinicalADA Evidence Grading System for Clinical RecommendationsRecommendations Level ofLevel of EvidenceEvidence DescriptionDescription A Clear or supportive evidence from adequately powered well-conducted, generalizable, randomized controlled trials Compelling nonexperimental evidence B Supportive evidence from well-conducted cohort studies or case-control study C Supportive evidence from poorly controlled or uncontrolled studies Conflicting evidence with the weight of evidence supporting the recommendation E Expert consensus or clinical experience ADA. Diabetes Care 2011;34(suppl 1):S12. Table 1.
- 40. April 28, 201853 Atherosclerosis Timeline Foam cells Fatty streak Inter- mediate lesion Athe- roma Fibrous plaque Complicated lesion / rupture
- 41. PBRC 2005 STANDARDS OFMEDICAL CARESTANDARDS OF MEDICAL CARE IN DIABETES—2016IN DIABETES—2016
- 42. PBRC 2005 Tools Neededfor Prediction and Personalized CareDiseaseBurden Time Cost 1/reversibility Typical Current Intervention Earliest Clinical Detection Earliest Molecular Detection Initiating Events Baseline Risk Decision Support Tools: Baseline Risk Preclinical Progression Disease Initiation and Progression Assess Risk Refine Assessment Predict/Diagnose Monitor Progression Predict Events Inform Therapeutics Sources of New Biomarkers: Stable Genomics: Single Nucleotide Polymorphisms (SNPs) Haplotype Mapping Gene Sequencing Dynamic Genomics: Gene Expression Proteomics Therapeutic Decision Support
- 43. Genomic and proteomic approaches Genomic and proteomic approaches to cardiovascular medicine promise to revolutionize our understanding of disease initiation and progression PBRC 2005
- 44. Genomic and proteomic approaches . This improved appreciation of pathophysiology may be translated into avenues of clinical utility. Gene-based presymptomatic prediction of illness, finer diagnostic subclassifications and improved risk assessment tools will permit earlier and more targeted intervention. PBRC 2005
- 45. Genomic and proteomic approaches Pharmacogenetics will guide our therapeutic decisions and monitor response to therapy. Personalized medicine will require the integration of clinical information, stable and dynamic genomics, and molecular phenotyping PBRC 2005
- 46. Genomic and proteomic approaches . Bioinformatics will be crucial in translating these data into useful applications, leading to improved diagnosis, prediction, prognostication and treatment. The present paper reviews the potential contributions of genomic and proteomic approaches in developing a more personalized approach to cardiovascular medicine. PBRC 2005
- 48. Commonly prescribed medications CVS Diabetes HTN Dyslipidemia Sedatives OA/GIT preparation Over the counter med
- 49. Possibilities Drug Druginteraction Drug disease interaction Adverse drug effects ADE Inappropriate drug Expenses Quality of life
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Editor's Notes
- #2 “Standards of Medical Care in Diabetes—2011” contains all of the current and key clinical recommendations of the American Diabetes Association (ADA) These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, general treatment goals, and tools to evaluate the quality of care While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided These standards are not intended to preclude clinical judgment or more extensive evaluation and management of the patient by other specialists as needed The recommendations included are screening, diagnostic, and therapeutic actions that are known or believed to affect health outcomes of patients with diabetes favorably The slides are organized to correspond with sections within the “Standards of Medical Care in Diabetes—2011” While not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement These standards of care are revised annually by the ADA’s multidisciplinary Professional Practice Committee, incorporating new evidence; subsequently, they are reviewed and approved by the Executive Committee of ADA’s Board of Directors
- #3 “Standards of Medical Care in Diabetes—2011” contains all of the current and key clinical recommendations of the American Diabetes Association (ADA) These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, general treatment goals, and tools to evaluate the quality of care While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided These standards are not intended to preclude clinical judgment or more extensive evaluation and management of the patient by other specialists as needed The recommendations included are screening, diagnostic, and therapeutic actions that are known or believed to affect health outcomes of patients with diabetes favorably The slides are organized to correspond with sections within the “Standards of Medical Care in Diabetes—2011” While not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement These standards of care are revised annually by the ADA’s multidisciplinary Professional Practice Committee, incorporating new evidence; subsequently, they are reviewed and approved by the Executive Committee of ADA’s Board of Directors
- #4 “Standards of Medical Care in Diabetes—2011” contains all of the current and key clinical recommendations of the American Diabetes Association (ADA) These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, general treatment goals, and tools to evaluate the quality of care While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided These standards are not intended to preclude clinical judgment or more extensive evaluation and management of the patient by other specialists as needed The recommendations included are screening, diagnostic, and therapeutic actions that are known or believed to affect health outcomes of patients with diabetes favorably The slides are organized to correspond with sections within the “Standards of Medical Care in Diabetes—2011” While not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement These standards of care are revised annually by the ADA’s multidisciplinary Professional Practice Committee, incorporating new evidence; subsequently, they are reviewed and approved by the Executive Committee of ADA’s Board of Directors
- #6 Several age-associated cardiovascular changes directly impact the development and progression of atherosclerosis and CAD.1 Over a century ago, it was recognized that arterial walls stiffen with age in both animals and man. Major aging changes in the arterial wall include increased calcium and collagen content and loss of elastin fibers. An increase in collagen cross-linking also occurs. Greater wall thickness is observed in both central and peripheral arteries and can be detected by ultrasound as increased intima-medial thickness. The loss in arterial resiliency results in increases in the systolic blood pressure and pulse pressure, both of which are potent cardiovascular and coronary risk factors in older patients. Pulse wave velocity, a more direct measure of arterial stiffness, also increases with age. The central arterial pressure wave contour is also altered with age, typically demonstrating late systolic augmentation, thought to represent the effects of early wave reflection returning from the periphery. Stiffer arteries with higher systolic and pulse pressures coupled with late systolic pressure augmentation combine to increase the left ventricular (LV) pulsatile load with age. Thus, the older adult heart requires greater LV stroke work, wall tension and myocardial oxygen consumption during systole than does the younger heart, thereby increasing the risk of ischemia, even in the absence of CAD. In addition, vascular wall stress is increased, predisposing to vascular injury, an important stimulus to the development and progression of atherosclerosis. [1] Lakatta EG, et al. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises – part I: aging arteries: a “set up” for vascular disease. Circulation. 2003; 107:139–146 [2] Lakatta EG, et al. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises – part II: the aging heart in health: links to heart disease. Circulation. 2003; 107:346–354
- #20 We have understood for decades the roles of ‘classical’ risk factors – elevated LDL-cholesterol, hypertension, elevated blood glucose and smoking – in the pathogenesis of cardiovascular disease. More recent research is continuing to define the contribution of emerging risk factors to the risk of developing type 2 diabetes and cardiovascular disease, particularly in the setting of insulin resistance. Abdominal obesity is associated with multiple cardiometabolic risk factors such as atherogenic elevated blood glucose (hypertriglyceridaemia and low HDL-cholesterol), elevated blood glucose and inflammation, which are major drivers of cardiovascular disease and type 2 diabetes. In addition, atherosclerosis is increasingly regarded as an inflammatory condition.
- #21 1. Paolisso G, Howard BV. Role of non-esterified fatty acids in the pathogenesis of type 2 diabetes mellitus. Diabet Med 1998; 15(5):359 2. Weyer C, Bogardus C, Mott DM, Pratley RE. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest 1999; 104(6):787-94 3. Maedler K, Spinas GA, Lehmann R, et al. Glucose induces beta-cells apoptosis via upregulation of the Fas receptor in human islets. Diabetes 2001; 50(8):1683-90 4. DeFronzo RA, Bonadonna R, Ferrannini E. Pathogenesis of NIDDM. A balanced overview. Diabetes Care 1992; 15(3):318-68 1. Weyer C, Bogardus C, Mott DM et al. J Clin Invest 1999; 104: 787–94. 2. UK Prospective Diabetes Study Group. Diabetes 1995; 44: 1249–58. 3. Maedler K, Spinas GA, Dyntar D et al. Diabetes 2001; 50: 69–76. 4. Paolisso G, Howard BV. Diabet Med 1998; 15: 360–66. 5. Jones NP, Charbonnel B, Lönnqvist F et al. Diabetologia 1999; 42(suppl 1): A229, Abs 859 and poster.
- #23 “Standards of Medical Care in Diabetes—2011” contains all of the current and key clinical recommendations of the American Diabetes Association (ADA) These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, general treatment goals, and tools to evaluate the quality of care While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided These standards are not intended to preclude clinical judgment or more extensive evaluation and management of the patient by other specialists as needed The recommendations included are screening, diagnostic, and therapeutic actions that are known or believed to affect health outcomes of patients with diabetes favorably The slides are organized to correspond with sections within the “Standards of Medical Care in Diabetes—2011” While not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement These standards of care are revised annually by the ADA’s multidisciplinary Professional Practice Committee, incorporating new evidence; subsequently, they are reviewed and approved by the Executive Committee of ADA’s Board of Directors
- #26 These data are from the Nurses’ Health Study (Carey VJ et al, 1997), an observational study that followed a cohort of 43,581 women between 1986 and 1994 in the USA. The analysis presented here was designed to define the association between waist circumference and the risk of developing type 2 diabetes. The risk of developing type 2 diabetes increased linearly with an increasing waist circumference. The relative risk for women at the 90th percentile of waist circumference (equivalent to a waist measurement of 92 cm [36 in]) was 5.1 (95% CI 2.98.9) compared with women at the 10th percentile (waist measurement of 67 cm [26.2 in]). High waist circumference is a powerful predictor of an increased risk of developing type 2 diabetes (Wang Y et al, 2005).
- #27 The prospective Nurses Health Study set out to assess the impact of factors such as waist circumference in determining risk of CHD in a cohort of 44,702 US female registered nurses, aged 40 to 65 years, recruited between 1986 and 1994. Study subjects were free of prior CHD at baseline. During 8 years of follow-up, there was a direct, independent and continuous relationship between waist circumference and age-adjusted risk of CHD.
- #28 This analysis from the Heart Outcomes Protection Evaluation (HOPE) study evaluated the effects of abdominal obesity (tertiles of waist circumference) on the risk of all-cause or cardiovascular death, or MI in 6,620 men and 2,182 women followed for an average of 4.5 years. Results were adjusted for BMI, age, smoking, sex, previous MI, stroke, peripheral arterial disease, microalbuminuria, use of antiplatelet agents, diuretics, lipid-lowering agents, and anti-hypertensives, history of hypertension, diabetes, or total cholesterol &gt;5.2 mmol/L, or HDL-cholesterol &lt;0.9 mmol/L. The risk of cardiovascular death, MI, or death from any cause increased in line with increasing tertiles of waist circumference. These data from this major intervention study add to the growing database of evidence linking high waist circumference with a clinically significant increase in the risk of an adverse cardiovascular outcome.
- #30 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #31 Malik and colleagues demonstrated that the cardiometabolic risk factors associated with metabolic syndrome increase the CVD mortality rate. Relative to an individual with no metabolic syndrome risk factors, having 1 to 2 risk factors increased a patient’s hazard ratio by more than 70%. Persons with metabolic syndrome (having ≥3 of the 5 risk factors) were found to have a hazard ratio of 2.71. The ratio increased with the onset of type 2 diabetes, CVD, and was greatest in persons with existing CVD and T2DM. Malik S, Wong ND, Franklin SS, et al. Impact of the metabolic syndrome on mortality from coronary heart disease, cardiovascular disease, and all causes in United States adults. Circulation. 2004;110:1245-1250.
- #33 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #34 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #35 This slide represents a summary of recommendations for glycemic, blood pressure, and lipid control for most adults with diabetes
- #36 Type 2 diabetes is a progressive disease and lifestyle adjustments alone are rarely sufficient in the long term – almost all patients will eventually require drug treatment to control their glucose levels.1 References 1.Turner RC et al. JAMA 1999; 281: 2005–2012.
- #44 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #45 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #46 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #47 Public education is key! Recognizing risk factors and dealing with them is important, Recognizing clusters of risk factors is important, i.e, when some of the factors are recognized others should be investigated. Using the correct drugs to treat the various risk factors is important. ACEI or ARB TZD’s or Glitazars Metformin Statins with or without fibric acid derivatives Treating to goal. Smoking cessation.
- #53 The American Diabetes Association has developed a grading system for clinical recommendations (Table 1) This grading system was used to clarify and codify evidence that forms the basis for each of the recommendations in the “Standards of Medical Care in Diabetes—2011” The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E This slide summarizes the description for each of these levels of evidence
- #54 Atherosclerosis timeline Content Points: The pathological effects of atherosclerosis occur over decades. A subtle injury to the endothelium initiates the atherosclerotic process.3 Endothelial dysfunction underlies many stages in the progression of atherosclerosis from earliest onset to the lesions that result in coronary heart disease (CHD).4 Foam cells may infiltrate the vessel, progressing to a fatty streak. As the lesion progresses, small pools of extracellular lipid form within the smooth muscle layers, disrupting the intimal lining of the vessel. Progression to an advanced lesion, or atheroma, occurs when accumulated lipid, cells, and other plaque components disrupt the arterial wall. Progression of atheroma involves accumulation of smooth muscle cells that elaborate extracellular matrix macromolecules. Once the plaque becomes fibrous, the danger of rupture increases. This type of advanced lesion can be found beginning in the fourth decade of life. The clinically important complication of atheroma usually involve thrombosis. Arterial stenoses by themselves seldom cause acute unstable angina or acute myocardial infarction. Indeed, sizable atheroma may remain silent for decades or produce only stable symptoms, such as angina, precipitated by increased demand. Thrombus formation usually occurs because of physical disruption of atherosclerotic plaque. The majority of coronary thromboses result from a rupture of the plaque’s protective fibrous cap, which permits contact between blood and the highly thrombogenic material located in the lesion’s lipid core. The endothelium participates in the atherosclerotic process and remodeling through secretion of specific compounds.1 These will be discussed in later slides. (Adapted from Pepine CJ. Am J Cardiol. 1998.)
- #55 “Standards of Medical Care in Diabetes—2011” contains all of the current and key clinical recommendations of the American Diabetes Association (ADA) These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, general treatment goals, and tools to evaluate the quality of care While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided These standards are not intended to preclude clinical judgment or more extensive evaluation and management of the patient by other specialists as needed The recommendations included are screening, diagnostic, and therapeutic actions that are known or believed to affect health outcomes of patients with diabetes favorably The slides are organized to correspond with sections within the “Standards of Medical Care in Diabetes—2011” While not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement These standards of care are revised annually by the ADA’s multidisciplinary Professional Practice Committee, incorporating new evidence; subsequently, they are reviewed and approved by the Executive Committee of ADA’s Board of Directors