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Diabetes Mellitus 101 for Cardiologists (and Alike): 2015

Diabetes Mellitus 101 for Cardiologists (and Alike): 2015. An Aggressive Pathophysiologic Approach to Therapy of Type 2 Diabetes in Cardiometabolic Patients: Looking at Diabetes Medications with a Cardiologists Eye. Part 2. Stan Schwartz MD,FACP Affiliate, Main Line Health System

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Diabetes Mellitus 101 for Cardiologists (and Alike): 2015

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  1. Diabetes Mellitus 101 for Cardiologists (and Alike): 2015 An Aggressive Pathophysiologic Approach to Therapy of Type 2 Diabetes in Cardiometabolic Patients: Looking at Diabetes Medications with a Cardiologists Eye Part 2 Stan Schwartz MD,FACP Affiliate, Main Line Health System Emeritus, Clinical Associate Professor of Medicine, U of Pa. 6105472000

  2. 21% 50% Retinopathy1 ASVD 18% Nephropathy2 20% Erectile dysfunction1 12% Neuropathy1 Type 2 diabetes – the microvascular and macrovascular burden is already present at diagnosis 1. UKPDS Group. Diabetes Res 1990; 13: 1–11.2. The Hypertension in Diabetes Study Group. J Hypertens 1993; 11: 309–317.

  3. Metabolic Sydrome, IGT, Diabetes, CV Disease 1. Beginning at 83 mg/dL, rising 2-hr pp glucose levels correlated linearly with CHD mortality 2. Even mild glucose elevations (fbs >110) increase mortality in patients undergoing PCI 3. Almost 70% of patients with first MI have IGT or undiagnosed diabetes 4. In multiple studies stress hyperglycemia in AMI is associated with 3-10 x mortality risk in patients without known diabetes 5. In a group of >31,000 patients without known diabetes but with CV disease (CVD), patients, an 18 mg/dL-higher FPG was associated with a 23% increase in the risk of hospitalization for HF 6. Inc mortality in hosp if admitted wth CVA

  4. Cardiovascular disease and diabetes No A1C threshold is apparent Finnish study by Kuusisto et al; UKPDS epidemiologic analysis; EPIC-Norfolk Study ~65% of deaths are due to CV disease Cardiovascular complications of T2DM Coronary heart disease deaths2- to 4-fold Stroke risk 2- to 4-fold Impaired glucose tolerance (IGT) and postprandial hyperglycemia are CV risk factors Funagata Diabetes Study; Honolulu Heart Program; DECODE Study; Rancho Bernardo Study Heart failure 2- to 5-fold Bell DSH. Diabetes Care. 2003;26:2433-41. Centers for Disease Control (CDC). www.cdc.gov. T2DM = type 2 diabetes mellitus

  5. A1C Predicts Coronary Heart Disease in Type 2 Diabetes 30 28.4 Men Women 25 21.9 20 CHD events (events/100 persons) 16.7 16.2 15.7 15 10.2 9.6 10 8.7 7.3 6.4 5 3.8 3 2.1 1.7 0 <5.0% 5.0%- 5.5%- 6.0%- 6.5%- ³7.0% Known 5.4% 5.9% 6.4% 6.9% diabetes A1C concentration* *P<0.001 for linear trend across A1Ccategories. Khaw KT et al. Ann Intern Med. 2004;141:413-420.

  6. THE PREVALENCE OF CHRONIC ANGINA POSES A SIGNIFICANT BURDEN TO THE US HEALTH CARE SYSTEM New Cases of Stable Angina Per Year (Among Americans ≥45 Years of Age) • ~16 million Americans have CHD • ~9.1 million Americans have angina pectoris 500,000 new cases are reported annually • Mean angina frequency is ~2 episodes per week > 18 million episodes each week or ~30 episodes each second Incidence (# of New Cases) 500,000 320,000 180,000 Men Women Total American Heart Association. Heart Disease and Stroke Statistics, 2008 Update. Pepine CJ, et al. Am J Cardiol. 1994;74:226-231.

  7. Pathophysiology of Diabetic Complications: Implications for Goals of Therapy Epidemiology • Hyperglycemia is a continuous Risk Factor • No A1C threshold is apparent • Worse >A1C, longer duration DM II Individual Susceptibility Genetic/ethnic ?Acquired IV Early Metabolic a\memory I Metabolic Disorder Glucose, insulin hormones, enzymes, metabolites, etc. (i.e., control) Point of metabolic“no return” Delayed Complications Retinal, renal neural, CV, cutaneous, etc. Eg: Macro- albuminuria; Proliferative retinopathy III Modulating Factors Hypertension, diet, smoking, etc. Mechanisms • Unified Theory of Brownlee • Oxidative stress • AGE, PKC, Hexosamine,Aldose Reductase V Late

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