html5-img
1 / 71

Practical Approaches to Managing Hypertension: Reducing Global Cardiovascular Risk

Practical Approaches to Managing Hypertension: Reducing Global Cardiovascular Risk. John S. Banas, MD Professor Emeritus of Clinical Medicine Columbia University College of Physicians and Surgeons New York, New York Dorothy and Lloyd Huck Chairman Emeritus

ronda
Télécharger la présentation

Practical Approaches to Managing Hypertension: Reducing Global Cardiovascular Risk

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Practical Approaches to Managing Hypertension: Reducing Global Cardiovascular Risk John S. Banas, MD Professor Emeritus of Clinical Medicine Columbia University College of Physicians and Surgeons New York, New York Dorothy and Lloyd Huck Chairman Emeritus Department of Cardiovascular Medicine Morristown Memorial Hospital Morristown, New Jersey

  2. ? Key Question Which class of agents do you presently consider first-line treatment for patients with hypertension? • Diuretics • β-Blockers (BBs) • Calcium channel blockers (CCBs) • Angiotensin-converting enzyme inhibitors (ACEIs) • Angiotensin receptor blockers (ARBs) • All of the above Use your keypad to vote now!

  3. Faculty Disclosure • Dr Banas:speakers bureau: Bristol-Myers Squibb Company, Pfizer Inc, sanofi-aventis Group; speakers bureau, consultant: King Pharmaceuticals, Inc.

  4. Learning Objectives • State the prevalence of hypertension and its role in the cardiovascular disease continuum • Formulate hypertension management according to risk stratification • Describe the importance of targeting improvement in vascular function in patients with hypertension

  5. Progression of Cardiovascular Disease: The Cardiovascular Continuum Myocardial infarction Myocardialischemia Ventricular dysfunction SD PAD Endothelialdysfunction and atherothrombosis Ventricular dilation and hypertrophy Stroke Congestive heart failure and death Hyperlipidemia,HTN, diabetes, smoking, obesity, etc Adapted from Dzau V, Braunwald E. Am Heart J. 1991;121:1244-1263.

  6. Diastolic dysfunction LVH Death/ Sudden Death HF Systolic dysfunction ACS Atherothrombosis, left ventricular remodeling Subclinical left ventricular dysfunction Overt heart failure Progression From Hypertension to Heart Failure/Sudden Death Obesity Diabetes Hypertension Smoking Dyslipidemia Risk Factors Time Adapted from Vasan RS, Levy D. Arch Intern Med. 1996;156:1789-1796.

  7. Development and Progression of Vascular Disease RISK FACTORS LDL BP Diabetes Smoking Oxidative Stress Endothelial Dysfunction andSmooth Muscle Activation NO •  Local Mediators •  Tissue ACE, AII EndothelinCatecholamines PAI-1, PlateletAggregation, Tissue Factor VCAM/ICAMCytokines Proteolysis Inflammation Growth Factors Cytokines Matrix Inflammation PlaqueRupture Vasoconstriction Thrombosis Vascular Lesionand Remodeling CLINICAL SEQUELAE Dzau V. Hypertension. 2001;37:1047-1052.

  8. Hypertension and Global CV Risk

  9. What Is Global CV Risk? • Treating hypertension to goal is good • Addressing all CV risk factors is better • Achieve optimal BP level • Avoid CV and renal morbidity and mortality Chobanian AV et al, for the NHBPEPCC. Bethesda, Md: NHLBI; 2004. NIH Publication No. 04-5230. Available at: www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.

  10. JNC 7 Cardiovascular Risk Factors • Microalbuminuria or estimated GFR <60 mL/min • Age (men >55 yr; women >65 yr) • Family history of premature CVD • Hypertension • Cigarette smoking • Obesity (BMI ≥30 kg/m2) • Physical inactivity • Dyslipidemia • Diabetes mellitus Chobanian AV et al, for the NHBPEPCC. Bethesda, Md: NHLBI; 2004. NIH Publication No. 04-5230. Available at: www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.

  11. Age (y) 20–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–74 75–79 Points –9 –4 0 3 6 8 10 11 12 13 PointsTotal-C Age (y)(mg/dL) 20–39 40–49 50–59 60–69 70–79 <160 0 0 0 0 0 160–199 4 3 2 1 0 200–239 7 5 3 1 0 240–279 9 6 4 2 1 ≥280 11 8 5 3 1 HDL-C (mg/dL) Points ≥60 –150–59 040–49 1<40 2 Systolic BP Points(mm Hg) Untreated Treated <120 0 0120–129 0 1130–139 1 2140–159 1 2≥160 2 3 Age (y) 20–39 40–49 50–59 60–69 70–79 Nonsmoker 0 0 0 0 0 Smoker 8 5 3 1 1 Point total: <0 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 >1710-yr risk (%) <1 1 1 1 1 1 2 2 3 4 5 6 8 10 12 16 20 25 ≥30 NCEP/Framingham Risk Scores: Estimate of 10-yr CHD Risk in Men Without CHD Reilly MP, Rader DJ. Circulation. 2003;108:1546-51.

  12. ? Key Question What percentage of patients with hypertension have 2 or more additional CV risk factors? • 20% • 30% • 40% • 50% • >50% Use your keypad to vote now!

  13. CV Risk Factor Clustering With Hypertension: Framingham Offspring, Aged 18 to 74 Years >50% of Hypertension Occurs in Presenceof 2 or More Risk Factors Men Women 1 RF 2 RFs 1 RF 2 RFs 25% 24% 26% 27% 20% 22% 19% 17% 8% 12% No Additional RFs No Additional RFs 3 RFs 3 RFs 4 or More RFs 4 or More RFs RF = risk factor. Adapted from Kannel WB. Am J Hypertens. 2000;13:3S-10S.

  14. Risk of CHD in Mild Hypertension by Intensity of Associated Risk Factors 40 42 36 30 21 10-Year Probability of Event (%) 24 18 14 10 12 6 4 6 0 Risk Factors SBP 150-160 mm Hg + + + + + + TC 240-262 mg/dL − + + + + + HDL-C 33-35 mg/dL − − + + + + Diabetes − − − + + + Cigarette smoking − − − − + + ECG-LVH − − − − − + Adapted from Kannel WB. Am J Hypertens. 2000;13:3S-10S.

  15. STAGE 2 SBP 160 mm Hg or DBP 100 mm Hg Treatment recommended STAGE 1 SBP 140-159 mm Hg or DBP 90-99 mm Hg Consider treatment in those with diabetes or renal disease who fail lifestyle modification PREHYPERTENSION SBP 120-139 mm Hg or DBP 80-89 mm Hg NORMAL SBP <120 mm Hg and DBP <80 mm Hg JNC 7 Classification of Blood Pressure Chobanian AV et al, for the NHBPEPCC. Bethesda, Md: NHLBI; 2004. NIH Publication No. 04-5230. Available at: www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.

  16. JNC 7: Algorithm for Hypertension LIFESTYLE MODIFICATIONS Not at Goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease) INITIAL DRUG CHOICES With Compelling Indications Without Compelling Indications Stage 2 Hypertension 2-drug combos for most (usually thiazide-type diuretics and ACEI, or ARB, or BB, or CCB) Compelling Indications Other drugs (diuretic, ACEI, ARB, BB, CCB) as needed Stage 1 Hypertension Thiazide-type diuretics for most; may consider ACEI, ARB, BB, CCB, or combo If not at goal BP, optimize dosages or add drugs until goal BP achieved; consider consultation with hypertension specialist Chobanian AV et al, for the NHBPEPCC. Bethesda, Md: NHLBI; 2004. NIH Publication No. 04-5230. Available at: www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.

  17. Nonpharmacologic Interventionsand BP Reduction Low-SaltDiet Weight Loss(19.4 lb) Alcohol Reduction Exercise 0 1 2 3 BP Decrease(mm Hg) 4 5 6 SBP DBP 7 Adapted from: Stevens VJ et al. Ann Intern Med. 2001;134:1-11; Messerli FH et al. In: Griffin BP et al, eds. 2004. Manual of Cardiovascular Medicine. 2nd ed; Whelton SP et al. Ann Intern Med. 2002;136:493-503; Cutler JA et al. Am J Clin Nutr. 1997;65(suppl):643S-651S; Xin X et al. Hypertension. 2001;38:1112-1117; Whelton PK et al. JAMA. 1997;277:1624-1632.

  18. Antihypertensive Medications: Mechanism of Action American Heart Association. December 11, 2006. Available at:http://www.americanheart.org/presenter.jhtml?identifier=3038158.

  19. JNC 7: Compelling Indications for Antihypertensive Drug Classes Recommended Drugs AldoCompelling Indication Diuretic ACEI BB ARB CCB ANT Heart failure • • • •   • Post MI   • •     • High coronary disease risk • • •   •   Diabetes • • • • •   Chronic kidney disease   •  •     Recurrent stroke prevention •• Aldo ANT = aldosterone antagonist.Chobanian AV et al, for the NHBPEPCC. Bethesda, Md: NHLBI; 2004. NIH Publication No. 04-5230. Available at: www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.

  20. ? Key Question On average, how many drugs will a patient need to control hypertension? • 1 • 2 • 3 • 4 Use your keypad to vote now!

  21. Multiple Antihypertensive Agents Frequently Required to Achieve BP Goal UKPDS (<150/85 mm Hg) MDRD (<92 mm Hg, MAP) HOT (<80 mm Hg, diastolic) AASK (<92 mm Hg, MAP) RENAAL (<140/90 mm Hg) IDNT (135/85 mm Hg) 1 2 3 4 Average No. of BP Medications Patients had either diabetes or renal impairment. Bakris GL et al. Am J Kidney Dis. 2000;36:646-661; Brenner BM et al. N Engl J Med. 2001;345:861-869; Lewis EJ et al. N Engl J Med. 2001;345:851-860.

  22. Hypertension and Diabetes: Global CV Risk Reduction With Evidence-Based Intervention

  23. DM ApproximatelyDoubles CVD Risk in Patients With Hypertension Adapted from Curb JD et al. JAMA. 1996;276:1886-1892; Hansson L et al. Lancet. 1998;351:1755-1762; Tuomilehto J et al. N Engl J Med. 1999:340:677-684.

  24. Syst-Eur: CV Protection Resulting From BP Lowering Was Greatest in Patients With Diabetes Diabetic Nondiabetic Fatal and Nonfatal Stroke Fatal and Nonfatal Cardiac Events All CV Events Overall Mortality CVD Mortality 0 –10 8% P = .55 16% P = .37 –20 22% P = .10 25% P = .02 Reduction in Event Rate for Active Treatment Group (%) –30 36% P = .02 –40 41% P = .09 –50 57% P = .06 –60 62% P = .002 –70 69% P = .02 70% P = .01 Patients with hypertension received nitrendipine  enalapril or HCTZ. N = 4695. DM = 492. Syst-Eur = Systolic Hypertension in Europe; CV = cardiovascular. Adapted from Tuomilehto J et al. N Engl J Med. 1999;340:677-684.

  25. HOT Study: Fewer Major CV Events in Patients With Diabetes Randomized to Lower BP Goal P = .005 25 20 15 Stroke, MI, or CV Death (per 1000 patient-years) 10 5 0 80 90 85 Target DBP (mm Hg) Patients with hypertension and diabetes were given baseline felodipine, plus other agents in a 5-step regimen. Study N = 18790; diabetes n = 1501. HOT = Hypertension Optimal Treatment; MI = myocardial infarction. Adapted from Hansson L et al, for the HOT Study Group. Lancet. 1998;351:1755-1762.

  26. UKPDS: Tight Glucose Versus Tight BP Control and CV Outcomes Tight glucose control (goal <6.0 mmol/L or 108 mg/dL) Tight BP control (average 144/82 mm Hg) Stroke Any Diabetic Endpoint DM Deaths Microvascular Complications 0 5% -10 10% 12% -20 Relative Risk Reduction (%) 24% * -30 32% 32% * 37% -40 * *P <.05 compared to tight glucose control 44% * -50 Patients had hypertension and Type 2 diabetes. N = 1148. UKPDS = United Kingdom Prospective Diabetes Study. Bakris GL et al. Am J Kidney Dis. 2000;36:646-661.

  27. Antihypertensive Medications: Mechanism of Action American Heart Association. December 11, 2006. Available at: http://www.americanheart.org/presenter.jhtml?identifier=3038158.

  28. The Renin-Angiotensin-Aldosterone System (RAAS) Angiotensinogen Kininogen Kallikrein Renin Bradykinin Angiotensin I ACE Angiotensin II Inactive Peptides • Blood Pressure • Vascular Proliferation • Oxidative Stress • Vascular Inflammation • Thrombogenesis • Aldosterone AT1 Adapted with permission from Brown NJ et al. Circulation. 1998;97:1411-1420; Endemann DH. J Am Soc Nephrol. 2004;15:1983-1992.

  29. The Renin-Angiotensin-Aldosterone System (RAAS) Angiotensinogen Kininogen Renin Inhibitors  Kallikrein Renin Bradykinin Angiotensin I ACE Angiotensin II Inactive Peptides ARBs ¯Blood Pressure ¯Vascular Proliferation ¯Oxidative Stress ¯Vascular Inflammation • Thrombogenesis • Aldosterone AT1 Adapted with permission from Brown NJ et al. Circulation. 1998;97:1411-1420; Endemann DH. J Am Soc Nephrol. 2004;15:1983-1992.

  30. The Renin-Angiotensin-Aldosterone System (RAAS) Angiotensinogen Kininogen Kallikrein Renin Bradykinin Angiotensin I ACE Angiotensin II Inactive Peptides ARBs  ARBs AT2 AT2 ¯Blood Pressure ¯Vascular Proliferation ¯Oxidative Stress ¯Vascular Inflammation • Thrombogenesis • Aldosterone AT1 Adapted with permission from Brown NJ et al. Circulation. 1998;97:1411-1420; Endemann DH. J Am Soc Nephrol. 2004;15:1983-1992.

  31. Hazard Ratio Valsartan/Amlodipine Primary cardiac composite endpoint Cardiac mortality Cardiac morbidity All myocardial infarction All congestive heart failure All stroke All-cause death New-onset diabetes 0.5 1 2.0 Favors Valsartan Favors Amlodipine VALUE: Hazard Ratios for Prespecified Analyses in Patients With Hypertension at High CV Risk • Patients had hypertension and were at high CV risk. • VALUE = Valsartan Antihypertensive Long-term Use Evaluation. • Julius S et al, for the VALUE trial group. Lancet. 2004;363:2022-2031.

  32. Kininogen Kallikrein Nitric Oxide Bradykinin  Inactive Peptides The Renin-Angiotensin-Aldosterone System (RAAS) Angiotensinogen Renin ACEIs Angiotensin I  ACE Angiotensin II ¯Blood Pressure ¯Vascular Proliferation ¯Oxidative Stress ¯Vascular Inflammation • Thrombogenesis • Aldosterone AT1 Adapted with permission from Brown NJ et al. Circulation. 1998;97:1411-1420; Endemann DH. J Am Soc Nephrol. 2004;15:1983-1992.

  33. ACEI Trials in CAD Without HF: Primary Outcomes EUROPA: CV Death/MI/Cardiac Arrest HOPE: CV Death/MI/Stroke 14 20 Placebo Placebo 12 20% Risk Reduction HR = 0.80 (0.71–0.91) P = .0003 22% Risk Reduction HR = 0.78 (0.70–0.86) P <.001 15 10 Percent 8 Ramipril 10 mg 10 6 Perindopril 8 mg Percent 4 5 2 Time (years) Time (years) 0 0 0 1 2 3 4 5 0 1 2 3 4 QUIET: All CV Events PEACE: CV Death/MI/CABG/PCI 50 30 Quinapril 20 mg Placebo 4% Risk Increase HR = 1.04 (0.89–1.22) P = .6 40 25 4% Risk Reduction HR = 0.96 (0.88–1.06) P = .43 20 30 Percent Percent Trandolapril 4 mg 15 Placebo 20 10 10 Time (years) Time (years) 5 0 0 1 2 3 4 5 6 0 1 2 3 EUROPA Investigators. Lancet. 2003;362:782-788; HOPE Study Investigators. N Engl J Med. 2000;342:145-153; PEACE Trial Investigators. N Engl J Med. 2004;351:2058-2068; Pitt B, et al. Am J Cardiol. 2001;87:1058-1063.

  34. MICRO-HOPE, PERSUADE: CV Events in Patients With Diabetes MICRO-HOPE(n = 3577)CV death/MI/stroke PERSUADE(n = 1502)CV death/MI/cardiac arrest 25 25 Placebo Placebo 20 20 25% RRRP = .0004 19% RRRP = .13 15 15 Primary Outcome (%) Perindopril8 mg 10 10 Ramipril10 mg 5 5 0 0 5 0 1 2 3 4 5 0 1 2 3 4 Follow-Up (years) Follow-Up (years) MICRO-HOPE = Microalbuminuria, Cardiovascular, and Renal Outcomes (Heart Outcomes Prevention Evaluation); PERSUADE = Perindopril Substudy in Coronary Artery Disease and Diabetes. HOPE Study Investigators. Lancet. 2000;355:253-259; Daly CA et al. Eur Heart J. 2005;26:1369-1378.

  35. MICRO-HOPE: Albuminuria in Patients With Diabetes 3.0 Placebo 2.5 Ramipril 2.0 P = .02 Mean Albumin/Creatinine Ratio (urine) 1.5 P = .001 1.0 0.5 0.0 1 0 4-5 2 3 Time (y) HOPE Study Investigators. Lancet. 2000;355:253-259.

  36. Multiple Mechanisms of ACEIin Cardiovascular Disease Blood pressure lowering Cardioprotective effects •  Preload and afterload •  LV mass •  Sympathetic stimulation •  Reperfusion injury • Improved myocardial remodeling Metabolic syndrome • Lipid neutral • Improved glucose metabolism • Increases adiponectin • Decreased insulin resistance Vasculoprotective effects • Direct antiatherogenic • Enhance endogenous fibrinolysis • Inhibit platelet aggregation • Antimigratory for mononuclear cells •  Matrix formation • Improve endothelial function • Antioxidant • Anti-inflammatory • Protection from plaque rupture • Improved arterial compliance and tone Modified from: Lonn E et al. Eur Heart J Suppl. 2003;5:A43-A48.

  37. Definition of the Metabolic Syndrome Abdominal Obesity Waist Circumference Men: >40 in (>102 cm); (>94 cm [37 in]) Women: >35 in (>88 cm); (>80 cm [32 in]) Plus Two Risk Factors • Triglycerides ≥150 mg/dL (1.7 mmol/L) • HDL cholesterol Men: <40 mg/dL (<1.0 mmol/L) Women: <50 mg/dL (<1.3 mmol/L) • BP ≥30/85 mm/Hg • Glucose ≥110 mg/dL (>6.1 mmol/L); (≥100 mg/dl) (≥5.6 mmol/L) Grundy SM et al. Circulation. 2004;109:433-438. IDF Consensus. Berlin 2005.

  38. Large (Visceral/Peritoneal) Insulin-ResistantAdipocytes Metabolic Syndrome (cont’d)

  39. Relationship Between Visceral Adipose Tissue and Insulin Action Decreased Adiponectin* Resistin FFA* TNF-alpha* Leptin* IL-6 (CRP)* Tissue Factor* PAI-1* Retinol-binding protein Adipsin Angiotensinogen* Acylation-stimulating protein *Probable CAD Risk Factor Banerji M et al. Am J Physiol. 1997;273:E425-E432.

  40. Abdominal obesity Glucose intolerance/ Insulin resistance Hypertension Atherogenic dyslipidemia Proinflammatory/ Prothrombotic state Diabetes CVD Characteristics of the Metabolic Syndrome: NCEP-ATP III National Cholesterol Educational Program (NCEP); Adult Treatment Panel (ATP) III; 2001.

  41. AHA/ACC Guidelines Update in Patients With Atherosclerotic CV Disease Medication Recommendations as Supplements* toLifestyle Modification (TLC) (DASH, weight loss, exercise, smoking cessation): • Lipid-lowering therapy to achieve LDL-C of <100 mg/dL (optional: <70 mg/dL); non-HDL <130 mg/dL (optional: <100 mg/dL) • Antiplatelet therapy, aspirin and/or clopidogrel • Antihypertensive therapy to achieve BP of <140/90 mm Hg • <130/80 mm Hg in the patient with diabetes • Ideal BP 120/80 (JNC 7) • Hypoglycemic therapy to achieve near normal fasting glucose (HbA1C <7%) (ADA: <6.5) • ACE inhibitor • Beta-blocker • Influenza vaccine *In the absence of specific contraindications Updated from: AHA/ACC. Circulation. 2001;104:1577-1579; Braunwald E et al. J Am Coll Cardiol. 2002;40:1366-1374; Grundy SM et al. Circulation. 2004;110:227-239; Krumholz HM et al. Circulation. 2006;113:732-761; Smith S et al. J Am Coll Cardiol. 2006;47:2130-2139.

  42. Adherence

  43. 48.2 44.3 37.0 35.8 33.9 29.0 7.3 5.2 CV Risk Factor Control Among Adults With Diagnosed Diabetes Fewer than half of adults with diabetes achieve treatment goals for CV risk factors NHANES III, 1988-1994 (n = 1204) 60 NHANES 1999-2000 (n = 370) 50 40 Adults (%) 30 20 10 0 Blood Pressure <130/80 mm Hg Total Cholesterol* <200 mg/dL Achieved All 3 Treatment Goals A1CLevel<7% *LDL-C and TG not evaluated. Saydah SH, et al. JAMA. 2004;291:335-342.

  44. Factors Which Contribute to Poor Adherence • Lack of understanding • Dementia/senility • Side effects • Lack of discharge planning • Cost • Lack of symptoms • Complexity of Rx regimen • Poor mobility • Little or no support system • Modified from: Vermeire E, et al. J Clin Pharm and Ther. 2001;26:331-342; Cheng JWM, et al. Pharmacotherapy. 2001;21:828-841.

  45. Practical Tips to Improve Adherence • Talk to your patient • Explain the condition and why specific therapy is important • Ask about adherence • Involve the patient as a partner in treatment • Provide clear written and oral instructions • Tailor the regimen to the patient’s lifestyle and needs • Use motivational interviewing techniques • Look for • Different ways to approach patients based on individual patient attitudes • Allies in patient care—family, friends • Ways to simplify the regimen • Refill dates (if the patient has not refilled the prescription, the medication is not being taken) Ockene IS et al. J Am Coll Cardiol. 2002;40:630-640.

  46. Practical Tips to Improve Adherence • Use systematic approaches • Disease management programs • Periodic review of electronic medical records or manual chart audits • Group/shared medical appointments blend care, education, social support • Other techniques • Follow-up (telephone/mail/e-mail) and reminder cards • Signed agreements/contracts • Self-monitoring tools (eg, tape measure, pedometer, home testing devices) • Patient assistance programs • Support patients where medication costs are a barrier to adherence Fonarow GC et al. Am J Cardiol. 2001;87:819-822; Ockene IS et al. J Am Coll Cardiol. 2002;40: 630-640; NCEP ATP III. September 2002. NIH publication no. 02-5215; Pfizer Helpful Answers Web site. Available at: http://www.pfizerhelpfulanswers.com.

  47. Summary: The Case for Global CV Risk Management • CV disease remains the leading cause of death in both men and women in the United States • Data from the Framingham Heart Study have demonstrated “clustering” of risk factors—and that risk of death from CHD and stroke increases further with each added risk factor • Hypertension, a pivotal risk factor for CV disease, should prompt the search for the presence of additional risk factors • Recent clinical trials have provided the “evidence” supporting a “standard of care” for the management of global CV risk

  48. Case Study

  49. Case Study: 55-Year-Old Man From India With Hypertension and Type 2 Diabetes The patient is in for a checkup • History • Hypertension • Type 2 diabetes • Nonsmoker • No symptoms • Physical examination • BP: 148/96 mm Hg • Height: 64" • Weight: 178 lb • BMI: 30 kg/m2 • Waist circumference: 38" • Cardiac dysfunction status: normal ventricular function (LVEF 68%) • Laboratory values • Glucose: 148 mg/dL (fasting) • A1C: 8.8% • Creatinine: 1.5 mg/dL • Urinalysis: 1+ proteinuria • Lipid profile (mg/dL): • TC: 268; LDL-C: 168; HDL-C: 42; TG: 296 • Medications • HCTZ 25 mg/d • Glyburide 5 mg/d

  50. Age (y) 20–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–74 75–79 Points –9 –4 0 3 6 8 10 11 12 13 PointsTotal-C Age (y)(mg/dL) 20–39 40–49 50–59 60–69 70–79 <160 0 0 0 0 0 160–199 4 3 2 1 0 200–239 7 5 3 1 0 240–279 9 6 4 2 1 ≥280 11 8 5 3 1 HDL-C (mg/dL) Points ≥60 –150–59 040–49 1<40 2 Systolic BP Points(mm Hg) Untreated Treated <120 0 0120–129 0 1130–139 1 2140–159 1 2≥160 2 3 Age (y) 20–39 40–49 50–59 60–69 70–79 Nonsmoker 0 0 0 0 0 Smoker 8 5 3 1 1 Point total: <0 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 >1710-yr risk (%) <1 1 1 1 1 1 2 2 3 4 5 6 8 10 12 16 20 25 ≥30 NCEP/Framingham Risk Scores: Estimate of 10-yr CHD Risk in Men Without CHD VBWG Reilly MP, Rader DJ. Circulation. 2003;108:1546-51.

More Related