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- 2. The global obesity pandemic: shaped by global drivers and local environments Boyd A Swinburn, MD, Gary Sacks, PhD, Kevin D Hall, PhD, Klim McPherson, PhD, Diane T Finegood, PhD, Marjory L Moodie, DrPH and Steven L Gortmaker, PhD The Lancet Volume 378, Issue 9793, Pages 804-814 (August 2011) DOI: 10.1016/S0140-6736(11)60813-1 Copyright © 2011 Elsevier Ltd Terms and Conditions
- 3. Figure 1 Source: The Lancet 2011; 378:804-814 (DOI:10.1016/S0140-6736(11)60813-1) Terms and Conditions
- 4. Figure 2 Source: The Lancet 2011; 378:804-814 (DOI:10.1016/S0140-6736(11)60813-1) Terms and Conditions
- 5. Figure 3 Source: The Lancet 2011; 378:804-814 (DOI:10.1016/S0140-6736(11)60813-1) Terms and Conditions
- 6. Figure 4 Source: The Lancet 2011; 378:804-814 (DOI:10.1016/S0140-6736(11)60813-1) Terms and Conditions
- 7. STANDARDS OF MEDICAL CARE IN DIABETES—2011
- 9. A1C 6.5 – 7.5% ** Monotherapy 2 - 3 Mos. *** 2 - 3 Mos. *** 2 - 3 Mos. *** Dual Therapy A1C > 9.0% No Symptoms Drug Naive Under Treatment Symptoms Triple Therapy AACE/ACE Algorithm for Glycemic Control Committee Cochairpersons: Helena W. Rodbard, MD, FACP, MACE Paul S. Jellinger, MD, MACE Zachary T. Bloomgarden, MD, FACE Jaime A. Davidson, MD, FACP, MACE Daniel Einhorn, MD, FACP, FACE Alan J. Garber, MD, PhD, FACE James R. Gavin III, MD, PhD George Grunberger, MD, FACP, FACE Yehuda Handelsman, MD, FACP, FACE Edward S. Horton, MD, FACE Harold Lebovitz, MD, FACE Philip Levy, MD, MACE Etie S. Moghissi, MD, FACP, FACE Stanley S. Schwartz, MD, FACE * May not be appropriate for all patients ** For patients with diabetes and A1C < 6.5%, pharmacologic Rx may be considered *** If A1C goal not achieved safely † Preferred initial agent 1 DPP4 if PPG and FPG or GLP-1 if PPG 2 TZD if metabolic syndrome and/or nonalcoholic fatty liver disease (NAFLD) 3 AGI if PPG 4 Glinide if PPG or SU if FPG 5 Low-dose secretagogue recommended 6 a) Discontinue insulin secretagogue with multidose insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% when added to GLP-1 or DPP-4 8 If A1C < 8.5%, combination Rx with agents that cause hypoglycemia should be used with caution 9 If A1C > 8.5%, in patients on Dual Therapy, insulin should be considered A1C 7.6 – 9.0% Dual Therapy 8 2 - 3 Mos. *** 2 - 3 Mos. *** Triple Therapy 9 Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE MET + GLP-1 or DPP4 1 TZD 2 Glinide or SU 5 TZD + GLP-1 or DPP4 1 MET + Colesevelam AGI 3 MET + GLP-1 or DPP4 1 + TZD 2 Glinide or SU 4,7 INSULIN ± Other Agent(s) 6 INSULIN ± Other Agent(s) 6 INSULIN ± Other Agent(s) 6 MET + GLP-1 or DPP4 1 ± SU 7 TZD 2 GLP-1 or DPP4 1 ± TZD 2 INSULIN ± Other Agent(s) 6 MET + GLP-1 or DPP4 1 or TZD 2 SU or Glinide 4,5 MET + GLP-1 or DPP4 1 + TZD 2 GLP-1 or DPP4 1 + SU 7 TZD 2 MET † DPP4 1 GLP-1 TZD 2 AGI 3
- 10. A1C 6.5 – 7.5% ** Monotherapy 2 - 3 Mos. *** Dual Therapy Triple Therapy 2 - 3 Mos. *** 2 - 3 Mos. *** *** If A1C goal not achieved safely † Preferred initial agent 1 DPP4 if PPG and FPG or GLP-1 if PPG 2 TZD if metabolic syndrome and/or nonalcoholic fatty liver disease (NAFLD) 3 AGI if PPG 4 Glinide if PPG or SU if FPG 5 Low-dose secretagogue recommended 6 a) Discontinue insulin secretagogue with multidose insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% when added to GLP-1 or DPP-4 Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE LIFESTYLE MODIFICATION AACE/ACE DIABETES ALGORITHM FOR GLYCEMIC CONTROL MET + GLP-1 or DPP4 1 TZD 2 Glinide or SU 5 TZD + GLP-1 or DPP4 1 MET + Colesevelam AGI 3 MET + GLP-1 or DPP4 1 + TZD 2 Glinide or SU 4,7 INSULIN ± Other Agent(s) 6 MET † DPP4 1 GLP-1 TZD 2 AGI 3
- 11. A1C 7.6 – 9.0% LIFESTYLE MODIFICATION AACE/ACE DIABETES ALGORITHM FOR GLYCEMIC CONTROL Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE Dual Therapy 8 2 - 3 Mos. *** Triple Therapy 9 2 - 3 Mos. *** *** If A1C goal not achieved safely † Preferred initial agent 1 DPP4 if PPG and FPG or GLP-1 if PPG 2 TZD if metabolic syndrome and/or nonalcoholic fatty liver disease (NAFLD) 4 Glinide if PPG or SU if FPG 5 Low-dose secretagogue recommended 6 a) Discontinue insulin secretagogue with multidose insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% when added to GLP-1 or DPP-4 8 If A1C < 8.5%, combination Rx with agents that cause hypoglycemia should be used with caution 9 If A1C > 8.5%, in patients on Dual Therapy, insulin should be considered MET + GLP-1 or DPP4 1 + TZD 2 GLP-1 or DPP4 1 + SU 7 TZD 2 MET + GLP-1 or DPP4 1 or TZD 2 SU or Glinide 4,5 INSULIN ± Other Agent(s) 6
- 12. No Symptoms Drug Naive Under Treatment Symptoms A1C > 9.0% LIFESTYLE MODIFICATION AACE/ACE DIABETES ALGORITHM FOR GLYCEMIC CONTROL Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE 1 DPP4 if PPG and FPG or GLP-1 if PPG 2 TZD if metabolic syndrome and/or nonalcoholic fatty liver disease (NAFLD) 6 a) Discontinue insulin secretagogue with multidose insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% when added to GLP-1 or DPP-4 MET + GLP-1 or DPP4 1 ± SU 7 TZD 2 GLP-1 or DPP4 1 ± TZD 2 INSULIN ± Other Agent(s) 6 INSULIN ± Other Agent(s) 6
- 14. Correlation of A1C with Estimated Average Glucose (eAG) ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S18. Table 9. These estimates are based on ADAG data of ~2,700 glucose measurements over 3 months per A1C measurement in 507 adults with type 1, type 2, and no diabetes. The correlation between A1C and average glucose was 0.92. A calculator for converting A1C results into estimated average glucose (eAG), in either mg/dl or mmol/l, is available at http://professional.diabetes.org/GlucoseCalculator.aspx. Mean plasma glucose A1C (%) mg/dl mmol/l 6 126 7.0 7 154 8.6 8 183 10.2 9 212 11.8 10 240 13.4 11 269 14.9 12 298 16.5
- 15. Glycemic Recommendations for Non-Pregnant Adults with Diabetes (1) *Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peak levels in patients with diabetes. ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S21. Table 10. A1C <7.0%* Preprandial capillary plasma glucose 70–130 mg/dl* (3.9–7.2 mol/l) Peak postprandial capillary plasma glucose† <180 mg/dl* (<10.0 mmol/l)
- 25. Type 2 diabetes across generations: from pathophysiology to prevention and management Christopher J Nolan, FRACP, Peter Damm, DMSc and Marc Prentki, PhD The Lancet Volume 378, Issue 9786, Pages 169-181 (July 2011) DOI: 10.1016/S0140-6736(11)60614-4 Copyright © 2011 Elsevier Ltd Terms and Conditions
- 26. Figure 1 Source: The Lancet 2011; 378:169-181 (DOI:10.1016/S0140-6736(11)60614-4) Terms and Conditions
- 27. Figure 2 Source: The Lancet 2011; 378:169-181 (DOI:10.1016/S0140-6736(11)60614-4) Terms and Conditions
- 28. Figure 3 Source: The Lancet 2011; 378:169-181 (DOI:10.1016/S0140-6736(11)60614-4) Terms and Conditions
- 29. Figure 4 Source: The Lancet 2011; 378:169-181 (DOI:10.1016/S0140-6736(11)60614-4) Terms and Conditions
- 30. Figure 5 Source: The Lancet 2011; 378:169-181 (DOI:10.1016/S0140-6736(11)60614-4) Terms and Conditions
- 33. Metformin. In most of the world, metformin is the only biguanide available. Its major effect is to decrease hepatic glucose output and lower fasting glycemia. Typically, metformin monotherapy will lower A1C levels by 1.5 percentage points (27,49). It is generally well tolerated, with the most common adverse effects being gastrointestinal. Metformin monotherapy is not usually accompanied by hypoglycemia and has been used safely, without causing hypoglycemia, in patients with prediabetic hyperglycemia (50). Metformin interferes with vitamin B12 absorption but is very rarely associated with anemia (27). The major nonglycemic effect of metformin is either weight stability or modest weight loss, in contrast with many of the other blood glucose–lowering medications. The UKPDS demonstrated a beneficial effect of metformin therapy on CVD outcomes (7), which needs to be confirmed. Renal dysfunction is considered a contraindication to metformin use because it may increase the risk of lactic acidosis, an extremely rare (less than 1 case per 100,000 treated patients) but potentially fatal complication (51). However, recent studies have suggested that metformin is safe unless the estimated glomerular filtration rate falls to 30 ml/min (52).
- 34. Las Guías reconocen a la Metformina como el tratamiento base en la Diabetes Tipo 2 1-4 Pacífico Asiático 4 2009 2 Metformina 1. UK National Clinical Guidelines for T2DM 2002. Rev 2005 2. Nathan DM et al. Diabetes Care 2009;31(1):193-203 3. IDF Clinical Guidelines Task Force. Diabet Med 2006;23:579-93 4. Asian Pacific Type 2 Diabetes Practical Targets & Treatment. 4th Ed IDF 2005 3 NICE 2002 1
- 35. Metformin Institution: COMPLEJO HOSP DR AAM | Sign Out | Sign In as Individual | Contact Subscription Administrator at your institution | FAQ
- 47. IV. PREVENTION/DELAY OF TYPE 2 DIABETES
- 49. Volume 352:1223-1236 March 24, 2005 Number 12
- 52. Drug Insight: insulin-sensitizing drugs in the treatment of polycystic ovary syndrome—a reappraisal Andrea Dunaif
- 55. Clinical Therapeutics Metformin for the Treatment of the Polycystic Ovary Syndrome John E. Nestler, M.D. N Engl J Med Volume 358(1):47-54 January 3, 2008
- 66. Original Article Metformin versus Insulin for the Treatment of Gestational Diabetes Janet A. Rowan, M.B., Ch.B., William M. Hague, M.D., Wanzhen Gao, Ph.D., Malcolm R. Battin, M.B., Ch.B., M. Peter Moore, M.B., Ch.B., for the MiG Trial Investigators N Engl J Med Volume 358(19):2003-2015 May 8, 2008
- 69. UKPDS: Post –Trial Monitoring Survival and Myocardial Infarction Metformin* Sulfonylureas * / Insulin * Survival MI Holman RR. NEJM ,2008; 359: 1577 - 89 -33% -36% -39% -27% -15% -13% * Including glibenclamide, ** vs Lifestyle -8% -14% *
- 71. A1C 6.5 – 7.5% ** Monotherapy 2 - 3 Mos. *** 2 - 3 Mos. *** 2 - 3 Mos. *** Dual Therapy A1C > 9.0% No Symptoms Drug Naive Under Treatment Symptoms Triple Therapy AACE/ACE Algorithm for Glycemic Control Committee Cochairpersons: Helena W. Rodbard, MD, FACP, MACE Paul S. Jellinger, MD, MACE Zachary T. Bloomgarden, MD, FACE Jaime A. Davidson, MD, FACP, MACE Daniel Einhorn, MD, FACP, FACE Alan J. Garber, MD, PhD, FACE James R. Gavin III, MD, PhD George Grunberger, MD, FACP, FACE Yehuda Handelsman, MD, FACP, FACE Edward S. Horton, MD, FACE Harold Lebovitz, MD, FACE Philip Levy, MD, MACE Etie S. Moghissi, MD, FACP, FACE Stanley S. Schwartz, MD, FACE * May not be appropriate for all patients ** For patients with diabetes and A1C < 6.5%, pharmacologic Rx may be considered *** If A1C goal not achieved safely † Preferred initial agent 1 DPP4 if PPG and FPG or GLP-1 if PPG 2 TZD if metabolic syndrome and/or nonalcoholic fatty liver disease (NAFLD) 3 AGI if PPG 4 Glinide if PPG or SU if FPG 5 Low-dose secretagogue recommended 6 a) Discontinue insulin secretagogue with multidose insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% when added to GLP-1 or DPP-4 8 If A1C < 8.5%, combination Rx with agents that cause hypoglycemia should be used with caution 9 If A1C > 8.5%, in patients on Dual Therapy, insulin should be considered A1C 7.6 – 9.0% Dual Therapy 8 2 - 3 Mos. *** 2 - 3 Mos. *** Triple Therapy 9 Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE MET + GLP-1 or DPP4 1 TZD 2 Glinide or SU 5 TZD + GLP-1 or DPP4 1 MET + Colesevelam AGI 3 MET + GLP-1 or DPP4 1 + TZD 2 Glinide or SU 4,7 INSULIN ± Other Agent(s) 6 INSULIN ± Other Agent(s) 6 INSULIN ± Other Agent(s) 6 MET + GLP-1 or DPP4 1 ± SU 7 TZD 2 GLP-1 or DPP4 1 ± TZD 2 INSULIN ± Other Agent(s) 6 MET + GLP-1 or DPP4 1 or TZD 2 SU or Glinide 4,5 MET + GLP-1 or DPP4 1 + TZD 2 GLP-1 or DPP4 1 + SU 7 TZD 2 MET † DPP4 1 GLP-1 TZD 2 AGI 3
- 72. Current Guidelines for Diabetes Management Country or region UK (NICE) Australia Asia-Pacific Fra (AFSSAPS) Germany (DDG) S Afr (SEMDSA) Lat Am (ALAD) USA (ADA) Europe (EASD) IDF (global) Year 2005/8 2004 2005 1999 2003 2002 2007 2006/8/9 2006/8/9 2005 BMI definition of overweight (kg/m2) >25 None >23 > 28 >25-27 >25 > 27 > 25 >25 >25 Overweight Metformin Metformin Metformin Metformin Metformin Consider met Metformin Metformin Metformin Metformin Non-overweight Consider metformin Initiate with metformin Metformin, SU,TZD,AGI Metformin, SU or AGI Insulin secretagogue No recommendation Metformin Metformin Metformin Metformin,SU Recommendations for initiating pharmacologic therapy after failure of diet and exercise Big Question is what to add to Metformin
- 73. Choice of agents for combination therapy Metformin Acarbose Miglitol Voglibose Rosiglitazone Pioglitazone Glipizide Gliclazide Glimepiride Glibenclamide Repaglinide Nateglinide Sitagliptin Vildagliptin Emerging Established
- 75. Fixed dose combinations - proof of better adherence Adherence rate (%) Glucovance ® Met + glib co-administered p<0.001 Melikian C et al. Clin Ther 2002;24:460-7 Post monotherapy patients
- 76. Glucovance ® vs Metformin + Glibenclamide Co-administered: HbA 1C Duckworth et al. JMCP 2003; 9: 256-62 Mean HbA 1C (%) All patients (n=72) Mean HbA 1C (%) Base HbA 1C > 8% (n=37) ® ® -0.6% p<0.01 -1.3% p<0.001
- 77. Glucovance Evidence Base 1999-2006 Patients uncontrolled on diet Patients uncontrolled on monotherapy Patients uncontrolled on combination therapy 22 Publications 9 Controlled Clinical Trials
- 78. HbA 1C Response with Glucovance in Metformin Failures Marre. Diabet Med 2002; 19: 673-80 Low dose HbA 1C (%) *p= 0.0001 vs. monotherapies * 6.5 7.0 7.5 8.0 8.5 Baseline Week 16 Maintain on Metformin 500 mg 1660 mg Switch to Glibenclamide 5 mg 13.4 mg Switch to Glucovance ® 500 mg/2.5 mg 1225 mg / 6.1 mg Mean final doses
- 79. Proportion of Patients Achieving HbA 1C < 7%: Post-Metformin Study Marre M et al. Diabet Med 2002;19:673-80 0 10 20 30 40 50 60 70 80 % Patients 75% more patients Glibenclamide 5mg Metformin 500mg Glucovance 500/2.5 mg
- 80. Choice of agents for combination therapy Metformin Acarbose Miglitol Voglibose Rosiglitazone Pioglitazone Glipizide Gliclazide Glimepiride Glibenclamide Repaglinide Nateglinide Sitagliptin Vildagliptin Emerging Established
- 99. Management of type 2 diabetes: new and future developments in treatment Abd A Tahrani, MD, Clifford J Bailey, PhD, Stefano Del Prato, MD and Anthony H Barnett, MD The Lancet Volume 378, Issue 9786, Pages 182-197 (July 2011) DOI: 10.1016/S0140-6736(11)60207-9 Copyright © 2011 Elsevier Ltd Terms and Conditions
- 100. Figure 1 Source: The Lancet 2011; 378:182-197 (DOI:10.1016/S0140-6736(11)60207-9) Terms and Conditions
- 114. Figure 2 Source: The Lancet 2011; 378:182-197 (DOI:10.1016/S0140-6736(11)60207-9) Terms and Conditions
- 115. Figure 3 Source: The Lancet 2011; 378:182-197 (DOI:10.1016/S0140-6736(11)60207-9) Terms and Conditions
- 116. Figure 4 Source: The Lancet 2011; 378:182-197 (DOI:10.1016/S0140-6736(11)60207-9) Terms and Conditions
- 117. Figure 5 Source: The Lancet 2011; 378:182-197 (DOI:10.1016/S0140-6736(11)60207-9) Terms and Conditions
- 118. Figure 6 Source: The Lancet 2011; 378:182-197 (DOI:10.1016/S0140-6736(11)60207-9) Terms and Conditions
- 119. Figure 6 Source: The Lancet 2011; 378:169-181 (DOI:10.1016/S0140-6736(11)60614-4) Terms and Conditions
- 120. VI. PREVENTION AND MANAGEMENT OF DIABETES COMPLICATIONS
- 137. Kaplan–Meier Curve for the Primary End Point. The AIM-HIGH Investigators. N Engl J Med 2011. DOI: 10.1056/NEJMoa1107579
- 138. Causal Diagram of the Relationships among Niacin, Major Lipid Levels, and Clinical Outcomes. Giugliano RP. N Engl J Med 2011. DOI: 10.1056/NEJMe1112346
- 144. Recommendations: Glycemic, Blood Pressure, Lipid Control in Adults *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. A1C <7.0% * Blood pressure <130/80 mmHg † Lipids LDL cholesterol <100 mg/dl (<2.6 mmol/l) ‡
- 149. Gracias...
- 150. Hypertension Implementing NICE guidance August 2011 NICE clinical guideline 127
- 164. Care pathway CBPM ≥160/100 mmHg & ABPM/HBPM ≥ 150/95 mmHg Stage 2 hypertension Consider specialist referral Offer antihypertensive drug treatment Offer lifestyle interventions If younger than 40 years If target organ damage present or 10-year cardiovascular risk > 20% Offer annual review of care to monitor blood pressure, provide support and discuss lifestyle, symptoms and medication Offer patient education and interventions to support adherence to treatment CBPM ≥140/90 mmHg & ABPM/HBPM ≥ 135/85 mmHg Stage 1 hypertension
- 165. Summary of antihypertensive drug treatment Step 4 Aged over 55 years or black person of African or Caribbean family origin of any age Aged under 55 years C 2 A A + C 2 A + C + D Resistant hypertension A + C + D + consider further diuretic 3, 4 or alpha- or beta-blocker 5 Consider seeking expert advice Step 1 Step 2 Step 3 Key A – ACE inhibitor or low-cost angiotensin II receptor blocker (ARB) 1 C – Calcium-channel blocker (CCB) D – Thiazide-like diuretic See slide notes for details of footnotes 1-5
- 170. Costs and savings for total population of England Costs and savings of using ABPM to confirm diagnosis of hypertension Year Change in diagnosis cost (£m) Change in treatment cost (£m) Net resource impact (£m) Year 1 £5.1 − £2.5 £2.6 Year 2 £5.1 − £5.8 − £0.7 Year 3 £5.1 − £9.1 − £4.0 Year 4 £5.1 − £12.4 − £7.3 Year 5 £5.1 − £15.7 − £10.5
Notas del editor
- Good afternoon. It's my pleasure to share with you the overall messages and key findings of this new WHO global report: Preventing chronic diseases: a vital investment. Several misunderstandings about chronic diseases have contributed to their global neglect. This report dispels these misunderstandings with the strongest evidence and proposes a way forward for stopping the rising global epidemic.
- Estimates of percentage of childhood population overweight, including obese (with use of International Obesity Taskforce cutoffs) in a selection of countries Based on data from Wang and Lobstein,11 International Association for the Study of Obesity,12 and Matsushita and colleagues.13
- Prevalence of obesity (body-mass index [BMI] >30 kg/m2) in adult women in a selection of countries in the 2000s Data from International Association for the Study of Obesity.17
- Food availability for the USA, 1910–200658 There are two distinct phases: a decrease in food energy supply (postulated to be pulled down by reduced energy expenditure requirements for daily living), followed by an increase in food energy supply (postulated to be pushed up by increasing food access). An energy balance flipping point is proposed, marking the change in how the US population generally achieved energy balance.
- A framework to categorise obesity determinants and solutions The more distal drivers are to the left and the environmental moderators that have an attenuating or accentuating effect are shown, along with some examples. The usual interventions for environmental change are policy based, whereas health promotion programmes can affect environments and behaviours. Drugs and surgery operate at the physiological level. The framework shows that the more upstream interventions that target the systemic drivers might have larger effects, but their political implementation is more difficult than health promotion programmes and medical services.
- “ 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 Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S11-12. Available online at http://care.diabetesjournals.org/content/34/Supplement_1
- Glycemic control is fundamental to the management of diabetes; recommendations for glycemic goals in nonpregnant adults are reviewed on this slide Lowering A1C to below or around 7% has been shown to reduce microvascular and neuropathic complications of type 1 and type 2 diabetes; therefore, for microvascular disease prevention, the A1C goal is <7% (A) In type 1 and type 2 diabetes, randomized controlled trials of intensive versus standard glycemic control have not shown a significant reduction in cardiovascular disease (CVD) outcomes during the randomized portion. Long-term follow-up of the Diabetes Control and Complications Trial (DCCT) and UK Prospective Diabetes Study (UKPDS) cohorts suggests treatment to A1C targets ≤7% in years soon after a diagnosis of diabetes is associated with long-term reduction in risk of macrovascular disease; until more evidence is available, a goal of <7% appears reasonable for many adults for macrovascular risk reduction (B) Subgroup analyses of clinical trials (e.g., DCCT, UKPDS, ADVANCE) suggest a small but incremental benefit in microvascular outcomes with A1C values closer to normal; therefore, providers might reasonably suggest even lower A1C goals than <7%, if achievable without significant hypoglycemia, for example. Such patients might include those with short duration of diabetes, long life expectancy, and no significant CVD (B) Conversely, less-stringent A1C goals than the general goal of <7% may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, and extensive comorbid conditions and those with longstanding diabetes in whom the general goal is difficult to attain despite diabetes self-management education, appropriate glucose monitoring, and effective doses of multiple glucose-lowering agents including insulin (C) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S19.
- Table 9, as shown on this slide, contains the correlation between A1C levels and mean plasma glucose (PG) levels based on data from the international A1C-Derived Average Glucose (ADAG) trial using frequent SMBG and continuous glucose monitoring (CGM) in 507 adults (83% Caucasian) with type 1, type 2, and no diabetes 1 The ADA and the American Association of Clinical Chemistry have determined that the correlation ( r = 0.92) is strong enough to justify reporting both an A1C result and an estimated average glucose (eAG) when a clinician orders the A1C test 2 A calculator for converting A1C results into eAG, in either mg/dl or mmol/l, is available at http://professional.diabetes.org/eAG. Reference Nathan DM, Kuenen J, Borg R, et al., for the A1c-Derived Average Glucose Study Group. Translating the A1C assay into estimated average glucose values. Diabetes Care . 2008;31:1473-1478. American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S18, Table 9.
- Recommended glycemic goals for nonpregnant adults (Table 10) are shown on three slides Slide 1 of 3 These recommendations are based on those for A1C values, with listed blood glucose levels that appear to correlate with achievement of an A1C of <7% The issue of preprandial versus postprandial self-monitoring of blood glucose (SMBG) is complex; in some epidemiological studies, elevated postchallenge two-hour oral glucose tolerance test (2-h OGTT) glucose values have been associated with increased cardiovascular risk independent of fasting plasma glucose (FPG) In diabetic subjects, some surrogate measures of vascular pathology, such as endothelial dysfunction, are negatively affected by postprandial hyperglycemia Postprandial hyperglycemia, like preprandial hyperglycemia, contributes to elevated A1C levels, with its relative contribution being higher at A1C levels that are closer to 7% However, outcome studies have clearly shown A1C to be the primary predictor of complications, and landmark trials such as the Diabetes Control and Complications Trial (DCCT) and the UK Prospective Diabetes Study (UKPDS) relied overwhelmingly on preprandial SMBG For individuals who have premeal glucose values within target but A1C values above target, a reasonable recommendation for postprandial testing and targets is monitoring postprandial plasma glucose 1-2 hours after the start of the meal and treatment aimed at reducing PPG values to <180 mg/dl to help lower A1C Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S20-21. Table 10.
- Prevalence of diabetes-specific retinopathy (moderate to severe) by distribution of FPG, 2 h plasma glucose, and HbA1c concentrations Each vigintile includes individuals with a glycaemia range from the number stated to just below that of the next. FPG=fasting plasma glucose. PG=plasma glucose. HbA1c=glycated haemoglobin A1c. Reproduced from Colagiuri S et al, with permission of Elsevier.24
- Overview of normal glucose homoeostasis In the fasting state blood glucose concentration is determined by the balance between EGP production, mainly through hepatic glycogenolysis and gluconeogenesis, and use by insulin-independent tissues, such as the brain. EGP prevents hypoglycaemia and is supported by a low insulin-to-glucagon ratio in plasma. The brain is dependent on glucose and, therefore, other tissues, such as heart and skeletal muscle, are mainly provided with non-glucose nutrients (eg, non-esterified fatty acids from adipose tissue lipolysis). In the fed state (meal with carbohydrate) glucose concentrations in the blood rise because of absorption in the gut, which stimulates insulin secretion by islet β cells and suppresses glucagon secretion from α cells. EGP is suppressed (which helps to curtail total glucose input into blood) and uptake into insulin-sensitive peripheral tissues, such as the heart, skeletal muscle, and adipose tissue is activated (which increases the rate of glucose disposal). Neurohormonal processes include the release of the incretin hormones, such as GLP-1, which increases glucose-stimulated insulin secretion and glucose-suppression of glucagon secretion. Adipose tissue lipolysis is suppressed and anabolic metabolism is promoted. Glucose concentrations become close to the fasting level within 2 h. GLP-1=glucagon-like peptide 1. EGP=endogenous glucose production.
- Pathway to type 2 diabetes and related complications Complex interactions between the environment early and later in life and the neurohormonal weight control network, especially in the brain, lead to chronic fuel surfeit, which drives the development of type 2 diabetes. Overnourished diabetes-resistant individuals are able to safely contain a chronic fuel overload due to robust islet β cells that are able to sustain adequate compensatory insulin secretion as required, and by healthy expansion of SAT. In this way, blood nutrient levels are maintained within the normal range and other tissues, such as the liver, skeletal muscle, heart, and ovaries, are not damaged. In diabetes-susceptible individuals the chronic fuel surfeit is not contained due to islets that are susceptible to failure if overworked and adipose tissue that develops an abnormal phenotype when stressed. The combination results in so-called nutrient spillover into non-adipose tissues and raised concentrations of inflammatory cytokines in plasma, which lead to stress and injury in multiple tissues, including the liver, skeletal muscle, heart, and ovaries. Type 2 diabetes eventually develops, which aggravates nutrient-induced tissue injury, including that to the pancreatic islets. The relative contributions of islet β cells and adipose tissue to the disease phenotype depends on the underlying mix of genetic and acquired tissue susceptibilities (including epigenetic) of the individual. SAT=subcutaneous adipose tissue. VAT=visceral adipose tissue. NAFLD=non-alcoholic fatty liver disease. NASH=non-alcoholic steatohepatitis.
- Role of islet β-cell metabolic activation by fuels and neurohormonal agonists in insulin secretion Glucose is metabolised via glycolysis to pyruvate and in the mitochondria to acetyl-CoA, which is then oxidised in the TCA cycle. These actions lead to an increased cytosolic ratio of ATP to ADP, which closes the K+ATP channels, depolarises the plasma membrane potential, and opens voltage-gated Ca2+ channels, causing influx of Ca2+ and the triggering of insulin-granule exocytosis. Pyruvate from glucose can also be metabolised via PC into the anaplerosis-cataplerosis pathway. Anaplerosis refers to the processes by which Kreb's cycle intermediates in the mitochondrion are replenished or increased, whereas cataplerosis refers to their egress from the mitochondrion. Changes in concentrations of cataplerosis-derived signalling molecules, including NADPH from pyruvate shuttles, and citrate-derived Mal-CoA, can lead to augmentation of insulin secretion. Glucose interacts with NEFA by promoting activity in a GL/FA cycle when raised concentrations of Mal-CoA, via the anaplerosis pathway, inhibits partitioning of LC-CoA into FA oxidation, which increases the availability of the LC-CoA for esterification. Glucose also provides glycerol-3-phosphate, which is necessary for FA esterification. Glycerolipids are rapidly hydrolysed by lipases back to NEFA and glycerol to create the GL/FA cycle process. This cycle produces lipid signalling molecules, such as diacylglycerols, that enhance glucose-stimulated insulin secretion. Aminoacids, such as glutamine and leucine, also interact with the glucose metabolism pathways to increase the coupling signals produced by glucose alone. The β cell responds to other neurohormonal and metabolic extracellular signals via various plasma membrane receptors. PC=pyruvate carboxylase. PDH=pyruvate dehydrogenase. Ach-R=acetylcholine receptor. GIP-R=gastric inhibitory polypeptide receptor. GLP-1-R=glucagon-like peptide-1 receptor. FFAR1=free-fatty-acid receptor-1. α-ADR-R=α2-adrenergic receptor. SSN-R=somatostatin receptor. OAA, oxaloacetate; CoA=coenzyme A. MAG, monoacylglycerides; DAG=diacylglycerides. TG=triacylglycerides. Δψm=change in plasma membrane potential. Mal-CoA=malonyl-CoA. LC-CoA=long-chain acyl-CoA. GL=glycerolipid. FA=fatty acid. NEFA=non-esterified fatty acids.
- Timelines for prevention of gestational and permanent diabetes Owing to guidelines, women are frequently not diagnosed and do not receive interventions for gestational diabetes until around 28 weeks' gestation. Thus, the fetus might have been exposed to an adverse intrauterine environment during the previous two trimesters. Before pregnancy mothers could optimise their health, which might be helped by health checks, advice, and public health programmes. Mothers with gestational diabetes are at high risk of permanent diabetes after pregnancy. This period yields an opportunity for diabetes prevention, including gestational diabetes in later pregnancies. Most health advice given after gestational diabetes is directed at the mother, but advice for the whole family could achieve reductions in the risk of diabetes for multiple generations simulatenously. GDM=gestational diabetes mellitus.
- Section IV, “Prevention/Delay of Type 2 Diabetes,” includes one slide: Recommendations: Prevention/Delay of Type 2 Diabetes
- Recommendations for the prevention/delay of type 2 diabetes are summarized on this slide Individuals at high risk for developing diabetes (i.e., those with impaired fasting glucose [IFG], impaired glucose tolerance [IGT] or both) can be given interventions that significantly decrease rate of onset of diabetes 1 Based on results of clinical trials and known risks of progression of prediabetes to diabetes, person with an A1C of 5.7%-6.4%, IGT or IFG should be counseled on lifestyle changes: 7% weight loss and moderate physical activity of at least 150 minutes/week Regarding the more controversial issue of drug therapy for diabetes prevention, a consensus panel believed that metformin should be the only drug considered[39] Metformin may be recommended for very high-risk individuals (those with risk factors for diabetes and/or those with more severe or progressive hyperglycemia) Of note, in the Diabetes Prevention Program (DPP), metformin was most effective compared to lifestyle in individuals with BMI ≥35 kg/m 2 and was not significantly better than placebo in those over age 60 years For other drugs, issues of cost, side effects, and lack of persistence of effect in some studies led the panel to not recommend use for diabetes prevention References American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S16. Nathan DM, Davidson MB, DeFronzo RA, et al., for the American Diabetes Association. Impaired fasting glucose and impaired glucose tolerance: implications for care. Diabetes Care 2007;30:753-759.
- Choice of agents in current use Sulfonylureas, -glucosidase inhibitors, thiazolidinediones and meglitinides, and of course metformin, are all available for use in type 2 diabetes. Metformin is located in the pivotal position given its role in reducing hyperglycaemia and excess risk of morbidity from life-threatening complications. The choice of single-agent therapy has never been so broad with at least a dozen candidate agents to select from. As a result there are a large number of potential combinations of oral antidiabetic agents to choose from.
- Evidence base for metformin combinations Metformin is a much-used antidiabetic agent that has been well studied alone and in combination. Examination of the literature, however, reveals that the vast majority of evidence underpinning its use in combination relates to the evaluation of metformin-glibenclamide combinations. Combinations of metformin with other sulphonylureas or with other classes of oral antidiabetic agents are described in only a handful of publications in each case.
- Improved compliance with Glucovance ® vs. metformin and glibenclamide co-administered Glucovance ® replaces two separate medications with a single treatment, and therefore has the potential to simplify regimens and to improve patient compliance. This has been evaluated in a retrospective survey which measured adherence to an antidiabetic regimen in 1920 patients receiving either Glucovance ® or metformin and glibenclamide co-administered. Adherence was measured as the sum of days’ supply of medication obtained by patients during the analysis period divided by the duration of the analysis period (180 days). The average rate of adherence to therapy was significantly greater in the Glucovance ® group, compared with patients receiving metformin and glibenclamide co-administered. Melikian C, White TJ, Vanderplas A et al. Adherence to oral antidiabetic therapy in a managed care organization: a comparison of monotherapy, combination therapy and fixed-dose combination therapy. Clin Ther 2002;24:460-7.
- Switching from metformin + glibenclamide co-administered to Glucovance ®: HbA 1C This was a retrospective chart review of data from 4 US hospitals. Patients had received metformin plus a sulphonylurea co-administered for at least 6 months prior to the period of analysis, and then received Glucovance ® for a mean of 283 days. Records from 72 patients were evaluated. The switch to Glucovance ® was associated with a mean change from baseline in HbA 1C of -0.6% (p<0.01) in the overall patient group. Larger changes were observed in patients with HbA 1C > 8% at baseline (-1.3%). HbA 1C did not change to a significant extent in patients with HbA 1C <8% at baseline. Changes in the dosages of drugs, additional medications, or adherence to regimens were not sufficient to explain the magnitude of the improvement in HbA 1C following the switch. As in the analysis described in the previous slide, earlier absorption of glibenclamide with Glucovance ® , compared with metformin and glibenclamide co-administered, has been associated with enhanced insulin release and this may have contributed to the improved efficacy following the switch. Duckworth W, Marcelli M, Padden M et al. Improvements in glycaemic control in type 2 diabetes patients switched from sulfonylurea co-administered with metformin to glyburide-metformin tablets. J Managed Care Pharmacy 2003;9:256-62.
- Evidence base for metformin combinations Metformin is a much-used antidiabetic agent that has been well studied alone and in combination. Examination of the literature, however, reveals that the vast majority of evidence underpinning its use in combination relates to the evaluation of metformin-glibenclamide combinations. Combinations of metformin with other sulphonylureas or with other classes of oral antidiabetic agents are described in only a handful of publications in each case.
- HbA 1C response in metformin failures In patients previously inadequately controlled by metformin, both dosage strengths of Glucovance ® were significantly more effective than either monotherapy in reducing HbA 1C . Furthermore, the superior antihyperglycaemic effects of Glucovance ® were achieved at lower mean final doses of metformin and glibenclamide compared with each agent given as monotherapy . The effects on HbA 1C in the study are summarised below: HbA 1C Glucovance ® 500 mg/2.5 mg -1.2% 500 mg/5 mg -0.9% Metformin 500 mg -0.2% Glibenclamide 5 mg -0.3% Allavoine TH, Marre M. Efficacy of a fixed combination metformin/ glibenclamide in metformin failure type 2 diabetes patients. Diabetes Res Clin Pract 2000;50 Suppl 1:P1368.
- Proportion of patients achieving HbA 1C <7%: post-metformin study Less than half of the patients in the post-metformin study achieved HbA 1C <7% with either monotherapy. In contrast, 75% of the Glucovance ® 500 mg/2.5 mg group and 62% of the Glucovance ® 500 mg/5 mg group achieved this treatment goal. Overall, 75% more patients achieved HbA 1C <7% with Glucovance ® than with either metformin or glibenclamide monotherapy. As described above, these benefits were achieved at lower mean daily dosages of metformin and glibenclamide compared with those used as monotherapy. Marre M, Howlett H, Lehert P et al. Improved glycaemic control with metformin-glibenclamide combined tablet therapy (Glucovance ® ) in Type 2 diabetic patients inadequately controlled on metformin. Diabet Med 2002;19:673-80.
- Choice of agents in current use Sulfonylureas, -glucosidase inhibitors, thiazolidinediones and meglitinides, and of course metformin, are all available for use in type 2 diabetes. Metformin is located in the pivotal position given its role in reducing hyperglycaemia and excess risk of morbidity from life-threatening complications. The choice of single-agent therapy has never been so broad with at least a dozen candidate agents to select from. As a result there are a large number of potential combinations of oral antidiabetic agents to choose from.
- Typical pathogenic features of hyperglycaemia in type 2 diabetes Adapted from DeFronzo8 with permission.
- Role of glucokinase in glucose metabolism and metabolic stimulus–secretion coupling in the β cell Adapted from Pal68 with permission. Solid lines represent single-step pathways. Dashed lines represent multiple-step pathways. Glucose is phosphorylated by glucokinase, which determines the rate of metabolism and ATP production. ATP-sensitive potassium-ion (K+) channels in the plasma membrane close in response to ATP production, evoking membrane depolarisation and opening voltage-gated calcium-ion (Ca2+) channels. As a result intracellular Ca2+ concentrations increase, activating Ca2+-dependent enzymes that control exocytosis of insulin. Glucokinase activation in the liver also results in reduction of glucose concentrations by increasing glycogen synthesis. GLUT2=glucose transporter 2. ΔV=change in voltage.
- Potential sites for intervention in intracellular pathways of insulin signalling Adapted with permission from Bailey.86 Dashed line with a bar at the end means inhibition. Solid line with an arrowhead means a stimulatory effect. SOCS-3=suppressor of cytokine signalling 3. PIP2=phosphatidylinositol-3,4-bisphosphate. PP2C=pyruvate dehydrogenase phosphatase (protein phosphatase 2C). TNFα=tumour necrosis factor α. JNK=c-Jun N-terminal kinase. IRS=insulin receptor substrate. PI3K=phosphatidylinositol 3-kinase. PIP3=phosphatidylinositol-3,4,5-trisphosphate. PTEN=protein phosphatase. SHIP-2=src homology-2-inositol phosphatase. PTP-1B=protein tyrosine phosphatase 1B. IKKB=inhibitor κ-B kinase-β. PDK=phosphoinositide-dependent protein kinase. Grb=growth-factor-receptor-binding protein. SOS=sons of sevenless. Ras=guanosine trisphosphatase. Raf=serine-threonine protein kinase. MEK=mitogen-activated protein kinase kinase. MAPK=mitogen-activated protein kinase. PKC=protein kinase C. mTOR=mammalian target of rapamycin. Akt=protein kinase B. FAs=fatty acids. DAG=diacylglycerol. ROS=reactive oxygen species. FOXO1=forkhead box protein O1A. eNOS=endothelial nitric oxide synthase. GLUT=glucose transporter isoform. GSK3=glycogen synthase kinase 3. PPAR=peroxisome-proliferator-activated receptor. RXR=retinoid-X receptor. PGC-1α=PPAR coactivator 1α. AMPK=adenosine monophosphate-activated protein kinase.
- Schematic representation of the renal handling of glucose and sodium by SGLTs in the kidneys Adapted with permission from Bailey and Day.94 All solid lines represent single-step pathways. Dashed line represents reduced amount of glucose reabsorbed in segment 3 of the proximal tubule. SGLT=sodium–glucose cotransporter. Na+=sodium ion. K+=potassium ion.
- Targets for antihyperglycaemic drugs in liver Adapted from Agius70 with permission. Solid lines represent biochemical pathways. Dashed lines represent regulatory control pathways. (1) Binding of glucagon to its receptor and coupling with G proteins activates adenyl cyclase. The cAMP activates protein kinase A, which converts phosphorylase kinase from an inactive to an active form. The active form of the enzyme activates glycogen phosphorylase by converting the inactive form to the active form by phosphorylation. The reverse reaction (conversion of active form to inactive form) is catalysed by phosphorylase phosphatase. (2) The active form of glycogen phosphorylase catalyses the degradation of glycogen to glucose-1-phosphate and is also a potent inhibitor of glycogen synthase phosphatase, which converts glycogen synthase from a less active to a more active form. Glucose-1-phosphate formed during glycogenolysis is converted to glucose-6-phosphate and then to glucose by glucose-6-phosphatase. (3) Gluconeogenesis from lactate and other three-carbon precursors is an alternative source of glucose-6-phosphate. (4) Fructose-1,6-bisphosphatase catalyses the penultimate reaction in gluconeogenesis to glucose-6-phosphate. (5) Increased glucose entry activates glucokinase by dissociation from its inhibitory protein. Glucokinase catalyses the phosphorylation of glucose to glucose-6-phosphate—a precursor for glycogen synthesis, and activates glycogen synthase and inactivates glycogen phosphorylase. GRA=glucagon receptor antagonist. GR=glucagon receptor. GS=G-protein. AC=adenyl cyclase. GKRP=glucokinase inhibitory protein. G6Pase=glucose-6-phosphatase. cAMP=cyclic AMP. PEP=phosphoenol pyruvate. PKi=inactive phosphorylase kinase. PKA=protein kinase A. PKa=active phosphorylase kinase. G6P=glucose-6-phosphate. G1P=glucose-1-phosphate. F6P=fructose-6-phosphate. F1,6P2=fructose-1,6-bisphosphatase. GPb=inactive glycogen phosphorylase. GPa=active glycogen phosphorylase. GSa=active glycogen synthase. GSi=inactive glycogen synthase. Pi=phosphate. PP=phosphate phosphatase. SP=glycogen synthase phosphatase.
- Summary of metabolic effects of PPAR agonists Adapted from Bailey86 with permission. The actions of PPAR agonists are mediated through stimulation of the nuclear PPARs (γ, α, or δ). PPARs form heterodimeric complexes with the retinoid-X receptor. The activated complexes bind to the PPRE, which is a nucleotide sequence in the promoter regions of the genes that are regulated by PPARs. PPAR=peroxisome-proliferator-activated-receptor. PGC-1α=PPAR coactivator-1α. FA=fatty acid. PPRE=PPAR response element.
- Natural history of type 2 diabetes and possible inadequacies of the standard therapeutic approach Type 2 diabetes mellitus is a progressive disease in which islet β-cell function and mass decrease and metabolic stress and tissue injuries worsen over time. The current approaches to diabetes management are largely based on the expectation of this pattern. Thus, treatments are increased or added only if glycaemic therapy is inadequate (ie, glycated haemoglobin A1c remains above target). A change in the main goals of therapy towards healing of the pathogenic defects, with the aim of preventing and altering the natural history of the disease, might improve outcomes and be more cost effective. NGT=normal glucose tolerance.
- Section VI, “Prevention and Management of Diabetes Complications,” includes 48 slides (1 slide unless otherwise noted): Cardiovascular Disease (CVD) in Individuals with Diabetes Recommendations: Hypertension/Blood Pressure Control (8 slides) Recommendations: Dyslipidemia/Lipid Management (7 slides) Secondary Prevention: Reduction in 10-Year Risk of Major CVD Endpoints Primary Prevention: Reduction in 10-Year Risk of Major CVD Endpoints Recommendations: Glycemic, Blood Pressure, Lipid Control in Adults Recommendations: Antiplatelet Agents (3 slides) Recommendations: Smoking Cessation Recommendations: Coronary Heart Disease Screening Recommendations: Coronary Heart Disease Treatment (2 slides) Recommendations: Nephropathy Recommendations: Nephropathy Screening Recommendations: Nephropathy Treatment (5 slides) Definitions of Abnormalities in Albumin Excretion Stages of Chronic Kidney Disease Management of CKD in Diabetes Recommendations: Retinopathy Recommendations: Retinopathy Screening (4 slides) Recommendations: Retinopathy Treatment (2 slides) Recommendations: Neuropathy Screening/Treatment (2 slides) Recommendations: Neuropathy Foot Care (4 slides)
- For those with diabetes, cardiovascular disease (CVD) is the major cause of morbidity and mortality and the largest contributor to the direct and indirect costs of diabetes 1,2 Common conditions that coexist with type 2 diabetes, such as hypertension and dyslipidemia, are clear risk factors for CVD, and diabetes itself confers independent risk 1,2 Numerous studies have shown the efficacy of controlling individual cardiovascular risk factors in preventing of slowing CVD in people with diabetes 1,2 Large benefits are seen when multiple risk factors are addressed globally 1,2 Risk for coronary heart disease and CVD in general can be estimated using multivariable risk factors approaches, and such a strategy may be desirable to undertake in adult patients prior to instituting preventive therapy 3 References Gaede P, Lund-Andersen H, Parving HH, Pedersen O. Effect of a multifactorial intervention on mortality in type 2 diabetes. N Engl J Med 2008;358:580- 591. Buse JB, Ginsberg HN, Bakris GL, et al., for the American Heart Association, American Diabetes Association. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Diabetes Care 2007;30:162–172. American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- Hypertension is a common comorbidity of diabetes that affects the majority of patients, with prevalence depending on type of diabetes, age, obesity, and ethnicity Hypertension is a major risk factor for both CVD and microvascular complications In type 1 diabetes, hypertension is often the result of underlying nephropathy, while in type 2 diabetes it usually coexists with other cardiometabolic risk factors The following eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 1 of 8 – Screening and Diagnosis Blood pressure should be measured at every routine diabetes visit Patients found to have systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥80 mmHg should have blood pressure confirmed on a separate day Repeat systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥80 mmHg confirms a diagnosis of hypertension (C) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 2 of 8 – Goals A goal systolic blood pressure <130 mmHg is appropriate for most patients with diabetes (C) Based on patient characteristics and response to therapy, higher or lower systolic blood pressure targets may be appropriate (B) Patients with diabetes should be treated to a diastolic blood pressure <80 mmHg (B) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 3 of 8 – Treatment (Slide 1 of 6) Patients with a systolic blood pressure 130-139 mmHg or a diastolic blood pressure 80-89 mmHg may be given lifestyle therapy alone for a maximum of 3 months, and then if targets are not achieved, patients should be treated with the addition of pharmacological agents (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 4 of 8 – Treatment (Slide 2 of 6) Patients with more severe hypertension (systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg) at diagnosis or follow-up should receive pharmacologic therapy in addition to lifestyle therapy (A) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 5 of 8 – Treatment (Slide 3 of 6) Lifestyle therapy for hypertension consists of weight loss if overweight, DASH-style dietary pattern including reducing sodium and increasing potassium intake, moderation of alcohol intake, and increased physical activity (B) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 6 of 8 – Treatment (Slide 4 of 6) Pharmacologic therapy for patients with diabetes and hypertension should be paired with a regimen that included either an ACE inhibitor or an angiotensin II receptor blocker (ARB); if one class is not tolerated, the other should be substituted If needed to achieve blood pressure targets, a thiazide diuretic should be added to those with an estimated glomerular filtration rate (GFR) ≥30 ml x min/1.73 m 2 and a loop diuretic for those with an estimated GFR <30 ml x min/1.73 m 2 (C) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 7 of 8 Treatment (Slide 5 of 6) Multiple drug therapy (two or more agents at maximal doses) is generally required to achieve blood pressure targets (B) If ACE inhibitors, angiotensin II receptor blockers (ARBs), or diuretics are used, kidney function and serum potassium levels should be closely monitored (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- This set of eight slides summarize recommendations for screening and diagnosis, goals, and treatment for hypertension/blood pressure control in patients with diabetes Slide 8 of 8 – Treatment (Slide 6 of 6) In pregnant women with diabetes and chronic hypertension, blood pressure target goals of 110-129/65-79 mmHg are suggested in the interest of long-term maternal health and minimizing impaired fetal growth ACE inhibitors and angiotensin II receptor blockers (ARBs) are contraindicated during pregnancy (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S27.
- Patients with type 2 diabetes have an increased prevalence of lipid abnormalities, contributing to their high risk of CVD This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 1 of 7 – Screening In most adult patients, measure fasting lipid profile at least annually In adults with low-risk lipid values (LDL cholesterol <100 mg/dl, HDL cholesterol >50 mg/dl, and triglycerides <150 mg/dl), lipid assessments may be repeated every 2 years (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 2 of 7 – Treatment Recommendations and Goals (Slide 1 of 6) Lifestyle modification focusing on the reduction of saturated fat, trans fat, and cholesterol intake; increase of n-3 fatty acids, viscous fiber, and plant stanols/sterols; weight loss (if indicated) and increased physical activity should be recommended to improve the lipid profile in patients with diabetes (A) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 3 of 7 – Treatment Recommendations and Goals (Slide 2 of 6) Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels, for diabetic patients With overt CVD (A) Without CVD who are over the age of 40 years and have one or more other CVD risk factors (A) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 4 of 7 – Treatment Recommendations and Goals (Slide 3 of 6) For patients at lower risk than described on Slide 2 of 6 (e.g., without overt CVD and under the age of 40 years), statin therapy should be considered in addition to lifestyle therapy if LDL cholesterol remains >100 mg/dl or in those with multiple CVD risk factors (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 5 of 7 – Treatment Recommendations and Goals (Slide 4 of 6) In individuals without overt CVD, the primary goal is an LDL cholesterol <100 mg/dl (2.6 mmol/l) (A) In individuals with overt CVD, a lower LDL cholesterol goal of <70 mg/dl (1.8 mmol/l), using a high dose of a statin, is an option (B) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 6 of 7 – Treatment Recommendations and Goals (Slide 5 of 6) If drug-treated patients do not reach the targets outlined on the previous slide (Slide 4 0f 6) on maximal tolerated statin therapy, a reduction in LDL cholesterol of ~30-40% from baseline is an alternative therapeutic goal (A) Triglyceride levels <150 mg/dl (1.7 mmol/l) and HDL cholesterol >40 mg/dl (1.0 mm/l) in men and >50 mg/dl (1.3 mmol/l) in women, are desirable; however, LDL cholesterol-targeting statin therapy remains the preferred strategy (C) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 7 of 7 – Treatment Recommendations and Goals (Slide 6 of 6) If targets are not reached on maximally tolerated doses of statins, combination therapy using statins and other lipid-lowering agents may be considered to achieve lipid targets but has not been evaluated in outcome studies for either CVD outcomes or safety (E) Statin therapy is contraindicated in pregnancy (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
- Figure 1. Kaplan–Meier Curve for the Primary End Point.
- Figure 1. Causal Diagram of the Relationships among Niacin, Major Lipid Levels, and Clinical Outcomes. In the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes trial (AIM-HIGH), niacin was compared with placebo, with a primary outcome of a composite of cardiovascular events. Niacin also has many favorable effects on the lipid profile, including a reduction in low-density lipoprotein (LDL) cholesterol and triglyceride levels and an increase in high-density lipoprotein (HDL) cholesterol levels. It has been clearly established that lowering LDL cholesterol levels reduces cardiovascular outcomes, whereas the clinical benefits of lowering triglyceride levels and raising HDL cholesterol levels with pharmacologic therapy are less well established. Given the design of the AIM-HIGH trial, any benefit (or harm) observed with niacin could not be attributed solely to its effect on HDL cholesterol levels.
- This slide represents a summary of recommendations for glycemic, blood pressure, and lipid control for most adults with diabetes Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S31. Table 12.
- The ADA and the American Heart Association have, in the past, jointly recommended low-dose aspirin therapy be used as a primary prevention strategy in those with diabetes at increased cardiovascular risk, including those who are >40 years of age or with additional risk factors, such as family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria 1 ; these recommendation were derived from several older trials that included small numbers of patients with diabetes Aspirin has been shown to be effective in reducing cardiovascular morbidity and mortality in high-risk patients with previous MI or stroke (secondary prevention); its net benefit in primary prevention among patients with no previous cardiovascular events is more controversial, both for patients with and without a history of diabetes 2 Recommendations for the use of antiplatelet agents 3 are summarized in three slides Slide 1 of 3 Consider aspirin therapy (75-162 mg/day) as a primary prevention strategy in those with type 1 or type 2 diabetes at increased cardiovascular risk (10-year risk >10%) This includes most men >50 years of age or women >60 years of age who have at least one additional major risk factor (family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria) (C) References Buse JB, Ginsberg HN, Bakris GL, et al., for the American Heart Association, American Diabetes Association. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Diabetes Care 2007;30:162-172. Baigent C, Blackwell L, Collins R, et al., for the Antithrombotic Trialists’ (ATT) Collaboration. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials . Lancet 2009;373:1849-1860. American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S31.
- Recommendations for the use of antiplatelet agents are summarized in three slides Slide 2 of 3 Aspirin should not be recommended for CVD prevention for adults with diabetes at low CVD risk (10-year CVD risk <5%, such as in men <50 and women <60 years of age with no major additional CVD risk factors), since the potential adverse effects from bleeding likely offset the potential benefits (C) In patients in these age groups with multiple other risk factors (e.g., 10-year risk 5%-10%) clinical judgment is required (E) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S31.
- Recommendations for the use of antiplatelet agents are summarized in three slides Slide 3 of 3 Use aspirin therapy (75-162 mg/day) as a secondary prevention strategy in those with diabetes with a history of CVD (A) For patients with CVD and documented aspirin allergy, clopidogrel (75 mg/day) should be used (B) Combination therapy with ASA (75-162 mg/day) and clopidogrel (75 mg/day) is reasonable for up to a year after an acute coronary syndrome (B) Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S31.
- ABOUT THIS PRESENTATION: This presentation has been written to help you raise awareness of the NICE clinical guideline on hypertension. This guideline has been written for healthcare professionals caring for adults with hypertension in secondary care (excluding emergency care) and community settings in which NHS care is received. The guideline is available in a number of formats, including a quick reference guide. You may want to hand out copies of the quick reference guide at your presentation so that your audience can refer to it. See the end of the presentation for ordering details. You can add your own organisation’s logo alongside the NICE logo. We have included notes for presenters, broken down into ‘key points to raise’, which you can highlight in your presentation, and ‘additional information’ that you may want to draw on, such as a rationale or an explanation of the evidence for a recommendation. Where necessary, the recommendation will be given in full. DISCLAIMER This slide set is an implementation tool and should be used alongside the published guidance. This information does not supersede or replace the guidance itself. PROMOTING EQUALITY Implementation of this guidance is the responsibility of local commissioners and/or providers. Commissioners and providers are reminded that it is their responsibility to implement the guidance, in their local context, in light of their duties to avoid unlawful discrimination and to have regard to promoting equality of opportunity. Nothing in this guidance should be interpreted in a way which would be inconsistent with compliance with those duties.
- NOTES FOR PRESENTERS: This guidance updates and replaces NICE clinical guideline 34 (published in 2006). NICE clinical guideline 34 updated and replaced NICE clinical guideline 18 (published in 2004). The original 2004 guideline was developed by the Newcastle Guideline Development and Research Unit. The guideline was updated by the National Collaborating Centre for Chronic Conditions [NCC-CC] (now the National Clinical Guideline Centre [NCGC]) in collaboration with the British Hypertension Society (BHS) in 2006 and by the NCGC in 2011.
- NOTES FOR PRESENTERS: Key points to raise The recommendations from this guideline have been incorporated into a NICE pathway, which is available from http://pathways.nice.org.uk/pathways/hypertension If you are showing this presentation when connected to the internet, click on the orange button to go straight to the NICE Pathways website. The front page includes a two minute video giving an overview of the features and content within the site, as well as the list of topics covered. NICE Pathways: guidance at your fingertips Our new online tool provides quick and easy access, topic by topic, to the range of guidance from NICE, including quality standards, technology appraisals, clinical and public health guidance and NICE implementation tools. Simple to navigate, NICE Pathways allows you to explore in increasing detail NICE recommendations and advice, giving you confidence that you are up to date with everything we have recommended.
- NOTES FOR PRESENTERS: In this presentation we will start by providing some background to the guideline and why it is important. We will then present the key priorities for implementation. The NICE guideline contains 12 key priorities for implementation, which you can find on pages 7,8, and 9 of the NICE guideline. We will then look at areas which that have not been identified as key priorities but where new recommendation have been added. We will then briefly summarise areas where the recommendations have not been updated. Next, we will summarise the costs and savings that are likely to be incurred in implementing the guidance. Then we will open the meeting up with a list of questions to help prompt a discussion on local issues for incorporating the guidance into practice. Finally, we will end the presentation with further information about the support provided by NICE.
- NOTES FOR PRESENTERS: Key points to raise: Hypertension is a major risk factor for ischaemic and haemorrhagic stroke, myocardial infarction, heart failure, chronic kidney disease, cognitive decline and premature death. Untreated hypertension is usually associated with a progressive rise in blood pressure. The vascular and renal damage that this may cause can culminate in a treatment-resistant state. Blood pressure is normally distributed in the population and there is no natural cut-off point above which 'hypertension' definitively exists and below which it does not. The risk associated with increasing blood pressure is continuous, with each 2 mmHg rise in systolic blood pressure associated with a 7% increased risk of mortality from ischaemic heart disease and a 10% increased risk of mortality from stroke. Routine periodic screening for high blood pressure is now commonplace in the UK as part of National Service Frameworks for cardiovascular disease prevention. Consequently, the diagnosis, treatment and follow-up of people with hypertension is one of the most common interventions in primary care, accounting for approximately 12% of Primary Care consultation episodes and approximately £1billion in drug costs in 2006.
- NOTES FOR PRESENTERS: Key points to raise: Primary hypertension is remarkably common in the UK population and the prevalence is strongly influenced by age and lifestyle factors. Systolic and/or diastolic blood pressures may be elevated. Systolic pressure elevation is the more dominant feature of hypertension in older patients and diastolic pressure is more commonly elevated in younger patients (those younger than 50 years). At least one quarter of adults (and more than half of those older than 60) have hypertension (blood pressure ≥140/90mmHg). As the demographics of the UK population shift towards an older, more sedentary and obese population, the prevalence of hypertension and its requirement for treatment will continue to rise.
- NOTES FOR PRESENTERS: Definitions In this guideline the following definitions are used: Stage 1 hypertension Clinic blood pressure is 140/90 mmHg or higher and subsequent ambulatory blood pressure monitoring (ABPM) daytime average or home blood pressure monitoring (HBPM) average blood pressure is 135/85 mmHg or higher. Stage 2 hypertension Clinic blood pressure is 160/100 mmHg or higher and subsequent ABPM daytime average or HBPM average blood pressure is 150/95 mmHg or higher. Severe hypertension Clinic systolic blood pressure is 180 mmHg or higher or clinic diastolic blood pressure is 110 mmHg or higher. Additional information: ABPM – ambulatory blood pressure monitoring HBPM – home blood pressure monitoring
- NOTES FOR PRESENTERS. Key points to raise: This guidance and NICE clinical guideline 34 were developed in collaboration with the British Hypertension Society. This guideline is for the clinical management of primary hypertension in adults (aged 18 years and older) who may, or may not, have pre-existing cardiovascular disease. Groups that have been covered - Adults with hypertension (18 years and older). - Particular consideration has been given to the needs of black people of African and Caribbean descent and minority ethnic groups where these differ from the needs of the general population. - People aged 80 years or older. Groups that have not been covered - People with diabetes. - Children and young people (younger than 18 years). - Pregnant women. - Secondary causes of hypertension (for example, Conn's adenoma, phaeochromocytoma and renovascular hypertension). - People with accelerated hypertension (that is, severe acute hypertension associated grade III retinopathy and encephalopathy). People with acute hypertension or high blood pressure in emergency care settings. Additional information: Primary hypertension: Primary hypertension was previously termed ‘essential hypertension’ because of a long-standing view that high blood pressure was sometimes ‘essential’ to perfuse diseased and sclerotic arteries. It is now recognised that the diseased and sclerotic arteries were most often the consequence of the hypertension and thus the term ‘essential hypertension’ is redundant and ‘primary hypertension’ is preferred. The majority of people (approximately 90%) with sustained high blood pressure encountered in clinical practice, for which there is no obvious, identifiable cause are said to have primary hypertension. The remaining 10% of cases are termed ‘secondary hypertension’, for which specific causes for the blood pressure elevation can be determined (for example, Conn's adenoma, renovascular disease, or phaeochromocytoma). Drug recommendations in the guideline: The guideline will assume that prescribers will use a drug’s summary of product characteristics to inform decisions made with individual patients. This guideline recommends drugs for indications for which they do not have a UK marketing authorisation at the date of publication, if there is good evidence to support that use. Where recommendations have been made for the use of drugs outside their licensed indications (‘off-label use’), these drugs are marked with an † in the presenters’ notes. If the drug does not have UK marketing authorisation for a particular use, informed consent should be obtained and documented.
- NOTES FOR PRESENTERS: The NICE guideline contains 65 recommendations about how care can be improved, but the experts who wrote the guideline have chosen key recommendations that they think will have the greatest impact on care and are the most important priorities for implementation. They are divided into two main areas of key priority and within these there are 12 recommendations that we will consider in turn. Key points to raise: Recommendations are marked as [2004], [2004, amended 2011], [2006], [2008], [2009], [2010] or [new 2011]. [2004] indicates that the evidence has not been updated and reviewed since 2004 [2004, amended 2011] indicates that the evidence has not been updated and reviewed since 2004 but a small amendment has been made to the recommendation. These amendments are likely to represent a change to clinical practice. [2006] indicates that the evidence has not been updated and reviewed since 2006 [2008] applies to recommendations from ‘Lipid modification’ (NICE clinical guideline 67), published in 2008 [2009] applies to recommendations from ‘Medicines adherence’ (NICE clinical guideline 76), published in 2009 [2010] applies to recommendations from ‘Hypertension in pregnancy’ (NICE clinical guideline 107), published in 2010 [new 2011] indicates that the evidence has been reviewed and the recommendation has been updated or added. Additional information: All of the key priorities for implementation are labelled as [new 2011] This slide set will focus upon presenting the recommendations which are new or amended and will signpost to the other relevant recommendations which have not been updated since 2004 and 2006.
- NOTES FOR PRESENTERS: Recommendation 1.2.3 [new 2011] in full: shown on the slide. Related new recommendations When considering a diagnosis of hypertension, measure blood pressure in both arms. If the difference in readings between arms is more than 20 mmHg, repeat the measurements. If the difference in readings between arms remains more than 20 mmHg on the second measurement, measure subsequent blood pressures in the arm with the higher reading. [new 2011] [1.2.1] If blood pressure measured in the clinic is 140/90 mmHg or higher take a second measurement during the consultation. If the second measurement is substantially different from the first, take a third measurement. Record the lower of the last two measurements as the clinic blood pressure. [new 2011] [1.2.2] If a person is unable to tolerate ABPM, home blood pressure monitoring (HBPM) is a suitable alternative to confirm the diagnosis of hypertension. [new 2011] [1.2.4] If the person has severe hypertension, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM. [new 2011] [1.2.5] While waiting for confirmation of a diagnosis of hypertension, carry out investigations for target organ damage (such as left ventricular hypertrophy, chronic kidney disease and hypertensive retinopathy) (see recommendation 1.3.3, slide 19) and a formal assessment of cardiovascular risk using a cardiovascular risk assessment tool (see recommendation 1.3.2, slide 19). [new 2011] [1.2.6] Additional information See slide 18 for recommendations about measuring blood pressure.
- NOTES FOR PRESENTERS: Recommendations in full: When using ABPM to confirm a diagnosis of hypertension, ensure that at least two measurements per hour are taken during the person’s usual waking hours (for example, between 08:00 and 22:00). Use the average value of at least 14 measurements taken during the person’s usual waking hours to confirm a diagnosis of hypertension. [new 2011] [1.2.9] When using HBPM to confirm a diagnosis of hypertension, ensure that: for each blood pressure recording, two consecutive measurements are taken, at least 1 minute apart and with the person seated and blood pressure is recorded twice daily, ideally in the morning and evening and blood pressure recording continues for at least 4 days, ideally for 7 days. Discard the measurements taken on the first day and use the average value of all the remaining measurements to confirm a diagnosis of hypertension. [new 2011] [1.2.10] Related new recommendations If hypertension is not diagnosed but there is evidence of target organ damage such as left ventricular hypertrophy, albuminuria or proteinuria, consider carrying out investigations for alternative causes of the target organ damage. [new 2011] [1.2.7] If hypertension is not diagnosed, measure the person’s clinic blood pressure at least every 5 years subsequently, and consider measuring it more frequently if the person’s clinic blood pressure is close to 140/90 mmHg. [new 2011] [1.2.8] Additional information: An extensive review of the evidence by the guideline development group has identified that ABPM multiple blood pressure measurements away from the clinic setting are the best predictor of blood pressure-related clinical outcomes. They concluded that ABPM appeared to provide the best method of confirming a diagnosis of hypertension. They stated that ABPM would not only be a more effective means of diagnosis but also, a more cost-effective means of establishing the diagnosis of hypertension. Recommendations 1.2.11 and 1.2.12 covering specialist assessment and investigation have been amended since the previous guideline in 2004. It is possible that this amendment may reflect a change in practice.
- NOTES FOR PRESENTERS: Recommendations in full: Offer antihypertensive drug treatment to people aged under 80 years with stage 1 hypertension who have one or more of the following: target organ damage established cardiovascular disease renal disease diabetes a 10-year cardiovascular risk equivalent to 20% or greater. [new 2011] [1.5.1] Offer antihypertensive drug treatment to people of any age with stage 2 hypertension. [1.5.2] [new 2011] . For people aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes, consider seeking specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage. This is because 10-year cardiovascular risk assessments can underestimate the lifetime risk of cardiovascular events in these people. [new 2011] [1.5.3] Additional information See slide 20 for recommendations about lifestyle interventions and patient education and adherence to treatment.
- NOTES FOR PRESENTERS: These recommendations are not key priorities but have been included as they direct the management of hypertension. Recommendations in full: Use clinic blood pressure measurements to monitor the response to antihypertensive treatment with lifestyle modifications or drugs. [new 2011] [1.5.4] Aim for a target clinic blood pressure below 140/90 mmHg in people aged under 80 years with treated hypertension. [new 2011] [1.5.5] Aim for a target clinic blood pressure below 150/90 mmHg in people aged 80 years and over, with treated hypertension. [new 2011] [1.5.6]
- NOTES FOR PRESENTERS: Recommendation 1.5.7 in full: For people identified as having a ‘white-coat effect’ (a discrepancy of more than 20/10 mmHg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis) consider ABPM or HBPM as an adjunct to clinic blood pressure measurements to monitor the response to antihypertensive treatment with lifestyle modification or drugs. [new 2011] Related recommendation: When using ABPM or HBPM to monitor the response to treatment (for example, in people identified as having a ‘white-coat effect’ and people who choose to monitor their blood pressure at home), aim for a target average blood pressure during the person’s usual waking hours of: below 135/85 mmHg for people aged under 80 years below 145/85 mmHg for people aged 80 years and over. [new 2011] [1.5.8]
- NOTES FOR PRESENTERS. Key priority recommendations are identified with [KPI] in these notes Step 1 treatment: Offer people aged under 55 years step 1 antihypertensive treatment with an angiotensin-converting enzyme (ACE) inhibitor or a low-cost angiotensin-II receptor blocker (ARB). If an ACE inhibitor is prescribed and is not tolerated (for example, because of cough), offer a low-cost ARB. [new 2011] [1.6.6] Do not combine an ACE inhibitor with an ARB to treat hypertension. [new 2011] [1.6.7] Offer step 1 antihypertensive treatment with a calcium-channel blocker (CCB) to people aged over 55 years and to black people of African or Caribbean family origin of any age. If a CCB is not suitable, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. [new 2011] [1.6.8] [KPI] If diuretic treatment is to be initiated or changed, offer a thiazide-like diuretic, such as chlortalidone (12.5–25.0 mg once daily) or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide or hydrochlorothiazide. [new 2011] [1.6.9] [KPI] For people who are already having treatment with bendroflumethiazide or hydrochlorothiazide and whose blood pressure is stable and well controlled, continue treatment with the bendroflumethiazide or hydrochlorothiazide. [new 2011] [1.6.10] [KPI] Related recommendations: Recommendations 1.6.11 and 1.6.12 have not been updated and reviewed since ‘Hypertension’ (NICE clinical guideline 34, 2006). Step 2 treatment If blood pressure is not controlled by step 1 treatment, offer step 2 treatment with a CCB in combination with either an ACE inhibitor or an *ARB. [new 2011] [1.6.13] If a CCB is not suitable for step 2 treatment, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. [new 2011] [1.6.14] For black people of African or Caribbean family origin, consider an ARB* in preference to an ACE inhibitor, in combination with a CCB. [new 2011] [1.6.15] *Choose a low-cost ARB Additional information : the pathway above focuses on stage 1 and 2 hypertension. For the full care pathway see page 35 of the NICE guideline.
- NOTES FOR PRESENTERS. Key priority recommendations are identified with [KPI] in these notes. Step 3 treatment Before considering step 3 treatment, review medication to ensure step 2 treatment is at optimal or best tolerated doses. [new 2011] [1.6.16] If treatment with three drugs is required, the combination of ACE inhibitor (or angiotensin-II receptor blocker), calcium-channel blocker and thiazide-like diuretic should be used. [2006] [1.6.17] Step 4 treatment Regard clinic blood pressure that remains higher than 140/90 mmHg after treatment with the optimal or best tolerated doses of an ACE inhibitor or an ARB plus a CCB plus a diuretic as resistant hypertension, and consider adding a fourth antihypertensive drug and/or seeking expert advice. [new 2011] [1.6.18] For treatment of resistant hypertension at step 4 : Consider further diuretic therapy with low-dose spironolactone 4 (25 mg once daily) if the blood potassium level is 4.5 mmol/l or lower. Use particular caution in people with a reduced estimated glomerular filtration rate because they have an increased risk of hyperkalaemia. Consider higher-dose thiazide-like diuretic treatment if the blood potassium level is higher than 4.5 mmol/l. [new 2011] [1.6.19] [KPI] When using further diuretic therapy for resistant hypertension at step 4, monitor blood sodium and potassium and renal function within 1 month and repeat as required thereafter. [new 2011] [1.6.20] If further diuretic therapy for resistant hypertension at step 4 is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker. [new 2011] [1.6.21] If blood pressure remains uncontrolled with the optimal or maximum tolerated doses of four drugs, seek expert advice if it has not yet been obtained. [new 2011] [1.6.22] Footnotes (1) Choose a low-cost ARB. (2) A CCB is preferred but consider a thiazide-like diuretic if a CCB is not tolerated or the person has oedema, evidence of heart failure or a high risk of heart failure. (3) Consider a low dose of spironolactone 4 or higher doses of a thiazide-like diuretic. (4) At the time of publication (August 2011), spironolactone did not have a UK marketing authorisation for this indication. Informed consent should be obtained and documented. (5) Consider an alpha- or beta-blocker if further diuretic therapy is not tolerated, or is contraindicated or ineffective.
- NOTES FOR PRESENTERS: Key points to raise: Recommendation [1.6.4] [new 2011] in full on the slide Related recommendations Where possible, recommend treatment with drugs taken only once a day. [2004] [1.6.1] Prescribe non-proprietary drugs where these are appropriate and minimise cost. [2004] [1.6.2] Offer people with isolated systolic hypertension (systolic blood pressure 160 mmHg or more) the same treatment as people with both raised systolic and diastolic blood pressure. [2004] [1.6.3] Offer antihypertensive drug treatment to women of child-bearing potential in line with the recommendations on Management of pregnancy with chronic hypertension and Breastfeeding in ‘Hypertension in pregnancy’ (NICE clinical guideline 107). [1.6.5] [2010] Related recommendations from ‘Hypertension in pregnancy’ (NICE clinical guideline 107, 2010). The recommendations from CG107 on Management of pregnancy with chronic hypertension are available here: http://egap.evidence.nhs.uk/CG107/section_1_2 The recommendations from CG107 on Breastfeeding are available here: http://egap.evidence.nhs.uk/CG107/section_1_9
- NOTES FOR PRESENTERS: These are not key priorities for implementation in this area however this has been included as it is considered an important part of the treatment pathway. Please note these recommendations would be applied during the person’s initial blood pressure measurement and diagnosis stages of the patient pathway. Recommendations in full: Because automated devices may not measure blood pressure accurately if there is pulse irregularity (for example, due to atrial fibrillation), palpate the radial or brachial pulse before measuring blood pressure. If pulse irregularity is present, measure blood pressure manually using direct auscultation over the brachial artery. [new 2011] [1.1.2] When measuring blood pressure in the clinic or in the home, standardise the environment and provide a relaxed, temperate setting, with the person quiet and seated, and their arm outstretched and supported . [new 2011] [1.1.4] If using an automated blood pressure monitoring device, ensure that the device is validated* and an appropriate cuff size for the person’s arm is used. [new 2011] [1.1.5] Related recommendations These have been amended since 2004 and may represent a change in practice. In people with symptoms of postural hypotension (falls or postural dizziness): measure blood pressure with the person either supine or seated measure blood pressure again with the person standing for at least 1 minute prior to measurement. [2004, amended 2011] [1.1.6] If the systolic blood pressure falls by 20 mmHg or more when the person is standing : review medication measure subsequent blood pressures with the person standing consider referral to specialist care if symptoms of postural hypotension persist. [2004, amended 2011] [1.1.7] Additional information: *A list of validated blood pressure monitoring devices is available on the British Hypertension Society’s website (see www.bhsoc.org or www.bhsoc.org/blood_pressure_list.stm ). The British Hypertension Society is an independent reviewer of published work. This does not imply any endorsement by NICE. Recommendations 1.1.1 and 1.1.3 have not been updated and reviewed since ‘Hypertension’ (NICE clinical guideline 18)
- NOTES FOR PRESENTERS: These are not key priorities for implementation in this area, however this has been included as it is considered an important part of the treatment pathway. Please note these recommendations would be applied during the person’s initial blood pressure measurement and at the diagnosis stages of the patient pathway. Key points to raise: Use a formal estimation of cardiovascular risk to discuss prognosis and healthcare options with people with hypertension, both for raised blood pressure and other modifiable risk factors. [2004] [1.3.1] Estimate cardiovascular risk in line with the recommendations on Identification and assessment of CVD risk in ‘Lipid modification’ (NICE clinical guideline 67)*. [2008] [1.3.2] *Clinic blood pressure measurements must be used in the calculation of cardiovascular risk. For all people with hypertension offer to: test for the presence of protein in the urine by sending a urine sample for estimation of the albumin:creatinine ratio and test for haematuria using a reagent strip take a blood sample to measure plasma glucose, electrolytes, creatinine, estimated glomerular filtration rate, serum total cholesterol and HDL cholesterol examine the fundi for the presence of hypertensive retinopathy arrange for a 12-lead electrocardiograph to be performed. [2004, amended 2011] [1.3.3] Additional information: The recommendations in identification and assessment of CVD risk in ‘lipid modification’ are available here: http://egap.evidence.nhs.uk/CG67/section_1_1 For NICE guidance on the early identification and management of chronic kidney disease see ‘Chronic kidney disease’ (NICE clinical guideline 73, 2008).
- NOTES FOR PRESENTERS: These are not key priorities for implementation in this area however this has been included as it is considered an important part of the treatment pathway. Note these recommendations did not require updating in 2011. Please note these recommendations should be applied throughout the patient pathway. Key points to raise: Lifestyle interventions Recommendation s 1.4.1–1.4.8 in the NICE guideline have not been updated and reviewed since ‘Hypertension’ (NICE clinical guideline 18, 2004). Patient education and adherence Recommendations 1.7.1–1.7.3 in the NICE guideline cover recommendations concerning patient education and adherence to treatment. These have not been updated and reviewed since ‘Hypertension’ (NICE clinical guideline 18, 2004). Because evidence supporting interventions to increase adherence is inconclusive, only use interventions to overcome practical problems associated with non-adherence if a specific need is identified. Target the intervention to the need. Interventions might include: suggesting that patients record their medicine-taking encouraging patients to monitor their condition simplifying the dosing regimen using alternative packaging for the medicine using a multi-compartment medicines system. This recommendation is taken from ‘Medicines adherence’ (NICE clinical guideline 76). [2009] [1.7.4] Additional information For NICE guidance on the prevention of obesity and cardiovascular disease see ‘Obesity’ (NICE clinical guideline 43, 2006) and ‘Prevention of cardiovascular disease at population level’ (NICE public health guidance 25, 2010).
- ADAPTING THIS SLIDE FOR LOCAL USE: We are aware that local factors such as incidence and baseline can vary considerably when compared with the national average. NICE has provided a costing template for you to calculate the financial impact recommendation 1.2.3 will have locally. We encourage you to calculate the local impact of this recommendation by amending the local variations in the template such as incidence, baseline and uptake. You can then remove the national figures from the table and replace them with your local figures to present to your colleagues. NOTES FOR PRESENTERS: NICE has worked closely with people within and outside the NHS to look at the major costs and savings related to implementing recommendation 1.2.3: If the clinic blood pressure is 140/90 mmHg or higher, offer ambulatory blood pressure monitoring (ABPM) to confirm the diagnosis of hypertension. [new 2011] [1.2.3] Implementing recommendation 1.2.3 could lead to a significant recurrent saving for the NHS. However, in the first year following implementation it is expected to need additional funding. In year 1 it is estimated the recommendation will cost the NHS around £2.6 million In future years, as more people benefit from more accurate diagnoses using ABPM, a cumulative effect of people not receiving antihypertensive drugs inappropriately starts to be seen. Savings from reduced treatment costs will start to outweigh the additional costs of diagnoses. Expected savings are £4.0 million in year 3 and £10.5 million in year 5. Saving may increase further from a continuation of this cumulative effect. Difficulties with modeling : Unable to model future trends and practice for example people previously diagnoses as not hypertensive (using ABPM) may start to re-attend for testing. This makes estimating patient numbers and impact complex. Calculation does not include potential savings from a reduction in adverse events, such as strokes and myocardial infarction, resulting from more accurate diagnosis and appropriate treatment. Owing to their long term nature these are difficult to calculate. Estimated savings assume population and demographic remain unchanged over time. In practice the incidence of suspected hypertension is increasing. Total spending in real terms may therefore not decrease over time as described. However, the use of ABPM will provide savings compared with continued use of clinic blood pressure monitoring to confirm hypertension diagnoses. For further information please refer to the costing template and costing report for this guideline on the NICE website. The costing report provides detailed estimates on the national costs and savings associated with implementing recommendation 1.2.3
- NOTES FOR PRESENTERS: These questions are suggestions that have been developed to help provide a prompt for a discussion at the end of your presentation – please edit and adapt these to suit your local situation. Additional questions What information can we develop for people who require ABPM and HBPM? Further information: A list of validated blood pressure monitoring devices is available on the British Hypertension Society’s website (see www.bhsoc.org ). Please note the British Hypertension Society is an independent reviewer of published work. This does not imply any endorsement by NICE.
- NOTES FOR PRESENTERS: If you are showing this presentation when connected to the internet, click on the blue button to go straight to the NHS Evidence website topic page for Hypertension. For the home page go to www.evidence.nhs.uk
- NOTES FOR PRESENTERS: You can download the guidance documents from the NICE website. The NICE guideline – all the recommendations. A quick reference guide – a summary of the recommendations for healthcare professionals. ‘ Understanding NICE guidance’ – information for patients and carers. The full guideline – all the recommendations, details of how they were developed, and reviews of the evidence they were based on. For online copies of the quick reference guide or ‘Understanding NICE guidance’, visit the NICE website http://guidance.nice.org.uk/CG127/QuickRefGuide/pdf/English (quick reference guide) and/or http://guidance.nice.org.uk/CG127/PublicInfo/pdf/English (‘Understanding NICE guidance’). NICE has developed tools to help organisations implement this guideline, which can be found on the NICE website. Costing tools – a costing report gives the background to the national savings and costs associated with implementation, and a costing template allows you to estimate the local costs and savings involved. Audit support – for monitoring local practice. Baseline assessment tool – to help you identify which areas of practice may need more support, decide on clinical audit topics and prioritise implementation activities. Clinical case scenarios – illustrate how the recommendations from the guideline can be applied to the care of patients presenting to primary care. Implementation advice – on how to increase capacity for ABPM in order to facilitate implementation of the ABPM recommendations in practice. Podcast – with Professor Bryan Williams discussing implementing the ABPM recommendations in practice For access to the British Hypertension Society website please visit www.bhsoc.org
- NOTES FOR PRESENTERS: Additional information: This final slide is not intended to be part of the presentation. It asks for feedback on whether this implementation tool meets your requirements and whether it will help you to put this NICE guidance into practice: your opinion would be appreciated. To open the links in this slide set, right click over the link and choose ‘open link’.