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John B. Crider, M.D. Family Medical Clinic

Improving Cardiovascular Risk: Effective Therapy. Managing High-Risk CV Patients: Understanding the Neuronal Hormonal Mechanisms and End-Organ Protection. John B. Crider, M.D. Family Medical Clinic. A ’- Rab, AL. Arab, AL. No Pharmaceutical Industry Affiliations. Salvador Dali.

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John B. Crider, M.D. Family Medical Clinic

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  1. Improving Cardiovascular Risk: Effective Therapy Managing High-Risk CV Patients: Understanding the Neuronal Hormonal Mechanisms and End-Organ Protection John B. Crider, M.D. Family Medical Clinic A’- Rab, AL Arab, AL No Pharmaceutical Industry Affiliations

  2. Salvador Dali “The only difference between myself and a mad man is that I am not mad.”

  3. “Would you like a Bypass with that ?” Reprinted with permission

  4. “It’s the hottest new diet ! Just attach this modem to your stomach and upload your fat to a skinny person on the Internet.” Reprinted with permission

  5. “What fits your busy schedule better, exercising one hour a day or being dead 24 hours a day ?” Reprinted with permission

  6. “Give it to me straight Doc… How much longer do I have to ignore your advice ?” Reprinted with permission

  7. Learning Objectives • State of the Union: A Discussion of Patient Outcomes • What do the Guidelines Say About Cardiovascular Risk — JNC 7? • Defining Cardiovascular Risks in Patients with Co-morbid Conditions — Case Studies • Understanding Modes of Action of Antihypertensive Drugs

  8. The World’s Greatest Public Health Problem WHO, 2002 http://www.who.int/mdg/publications/04MDGChapter4.pdf

  9. Adults with High Blood Pressure Source: CDC, Behavioral Risk Factor Surveillance System, 2007.

  10. CHD Mortality: Missouri http://hp2010.nhlbihin.net/hrmaps/_cvdmaps.html

  11. HTN: Cardiovascular Disease Risk Kannel WB. JAMA. 1996; 275:1571-1576

  12. Audience Response Question

  13. HTN: Awareness, Treatment & Control NHANES: 2003-2006. Source: NCHS and NHLBI.

  14. 14.0 12.0 10.0 8.0 Population (millions) 6.0 NOT MEETING GOAL 4.0 2.0 0.0 91–100 81–90 131–140 231–240 141–150 151–160 161–170 171–180 181–190 241–250 111–120 121–130 221–230 191–200 201–210 101–110 211–220 SBP Range (mm Hg) Majority Are Not at SBP Goal Whyte JL et al. J ClinHypertens. 2001;3:211-216. Lapuerta P, L’Italien GJ. Am J Hypertens. 1999;12:92A. Adapted from Whyte JL et al. J ClinHypertens. 2001;3:211-216.

  15. Learning Objectives • State of the Union: A Discussion of Patient Outcomes • What do the Guidelines Say About Cardiovascular Risk — JNC 7? • Defining Cardiovascular Risks in Patients with Co-morbid Conditions — Case Studies • Understanding Modes of Action of Antihypertensive Drugs

  16. Audience Response Question

  17. JNC 7 Blood Pressure Definitions JAMA. 2003;289:(doi:10.1001/jama.289.19.2560) (JNC-7).

  18. “High Normal” BP and CVD Risk 130-139/85-89 120-129/80-84 <120/80 130-139/85-89 120-129/80-84 <120/80 VasanVasanRS et al. RS et al. N N EnglEngl J Med. J Med. 2001;345:1291 2001;345:1291- -1297. (Framingham)

  19. 8 7 6 4 3 2 1 0 115/75 135/85 155/95 175/105 SBP/DBP (mm Hg) CV Mortality Doubles with Each 20/10 BP Increase 8x CVMortalityRisk 4x 2x Chobanian AV et al. JAMA. 2003;289:2560-2572. LewingtonS et al. Lancet. 2002;360:1903-1913.

  20. Case Study: “Pre-hypertension” • 40-year-old male presents for routine examination. • No complaints or problems. • ROS: CV & Neuro unremarkable. • PMSH: Unremarkable. • BP 136/86, P 72 PE: Normal • U/A: Protein (-), Renal Panel: WNL, Lipid: WNL • EKG: NSR What are the patient’s risks based on the blood pressure?

  21. Case Study: “Pre-hypertension” • Does not increase Stroke risk • Triples the risk of MI “Pre-hypertension”: (120-139) / (80-90) 1. Mohammad Y, Qureshi AI, Suri MFK, et al. Is pre-hypertension a risk factor for stroke and myocardial infarction? Program and abstracts from the 29th International Stroke Conference; February 5-7, 2004; San Diego, California. Abstract P326. 2. M. Fareed K. Suri, M.D.; Jawad F. Kirmani, M.D.; Afshin A. Divani, Ph.D.; and Yousef Mohammad, M.D. American Heart Association (2005, August 6).

  22. “Lower is Better” Diastolic BP Systolic BP CV event % RR CV event % RR Adapted from Hansson L et al. Lancet. 1998;351:1755-1762 (HOT TRIAL).

  23. Importance of Systolic Blood Pressure >130/85 >120/80 SBP >160 • MRFITT Arch Int Med, 1992

  24. SBP, DBP, Age and CHD Risk Franklin SS et al. Circulation. 2001;103:1245-1249

  25. MIDAS/NICS/VHAS UKPDS C vs A NORDIL INSIGHT HOT L vs H STOP ACEIs HOT M vs H MRC1 MRC2 STOP CCBs HEP SHEP STONE HOPE EWPHE CAPPP Syst-Eur UKPDS L vs H Syst-China RCT70-80 PART 2/SCAT ATMH STOP-1 SBP Reduction and CV Mortality P = 0.003 1.50 1.25 1.00 Odds Ratio 0.75 0.50 0.25 - 5 0 5 10 15 20 25 Difference in SBP (mm Hg) Staessen JA, et al. Lancet. 2001;358:1305-15.

  26. Audience Response Question

  27. Targets in HTN Treatment • Treating BP ≤ (140-160)/(90-100) does not reduce mortality or morbidity • Systematic reviews regarding recommendations for lower targets in DM and CKD are in progress1 • ADA recommends Tx if BP >130/802 1. Arguedas JA, Perez MI, Wright JM. Treatment blood pressure targets for hypertension. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.: CD004349. DOI: 10.1002/14651858.CD004349.pub2. 2. Diabetes Care January 2010 vol. 33 no. Supplement 1 S11-S6

  28. Achieving Target BP Bakris GL et al. Am J Kidney Dis. 2000;36:646-661. Cushman WC et. al J ClinHypertens 2002; 4:393-404

  29. Case Study: Hypertension • 50-year-old male presents for routine examination. • No complaints or problems. • ROS: CV, Neuro unremarkable • PMSH: Unremarkable. • BP 150/94, P 80 PE: Normal • U/A: Protein (-), Renal Panel: WNL, Lipid: WNL • EKG: NSR What are the patient’s risks based on the blood pressure?

  30. HTN and Stroke Odds ratios and95% confidence intervals 0.63(0.55 to 0.72) 0 2 0.5 1.5 1 Active treatment worse than placebo Active treatment better than placebo Reprinted from He J, et al. Am Heart J. 1999; 138:211-219.

  31. HTN & CV Risk • HTN confers >50% lifetime risk of Stroke vs. “Optimal BP” (120/80) • 2 separate BP factors impact the 10-year CVD Risk Calculator (SBP & Treatment of HTN) • Seshadri S, Beiser A, Wolf PA. Lifetime risk of stroke: results from the Framingham Study. Program and abstracts from the 29th • International Stroke Conference; February 5-7, 2004; San Diego, California. Abstract 43. 2. NCEP ATP III JAMA. 2001;285:2486-2497 (Framingham Point Scores).

  32. Audience Response Question

  33. 20 10 0 -10 -20 -30 -40 -50 HTN & DM Any DM Endpoint Death fromDM Microvascular Complications Stroke 11 Risk Reduction (%) 10 12 24* 25 32* 37* 44* Tight glucose control (HgbA1c7.0%) Tight BP control (<150/85 mm Hg) *P<0.05 vs tight glucose control. BakrisGL et al. Am J Kidney Dis. 2000;36:646-661. (UKPDS)

  34. HTN & DM • 75% of CVD in DM may be attributable to HTN • Therefore, Treat BP <130/85 in DM Hypertension. 2001;37:1053.

  35. HTN & End-Stage Renal Disease JAMA. 2003;289:(doi:10.1001/jama.289.19.2560) (JNC-7).

  36. HTN & Mortality Overall life expectancy at age 50 with High Blood Pressure: Reduced by ~5 years Hypertension. 2001;37:1053.

  37. Learning Objectives • State of the Union: A Discussion of Patient Outcomes • What do the Guidelines Say About Cardiovascular Risk — JNC 7? • Defining Cardiovascular Risks in Patients with Co-morbid Conditions — Case Studies • Understanding Modes of Action of Antihypertensive Drugs

  38. Without Compelling Indications With Compelling Indications Drug(s) for the compelling indications Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. Stage 1 Hypertension(SBP 140–159 or DBP 90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination. Stage 2 Hypertension(SBP >160 or DBP >100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB) Not at Goal Blood Pressure Optimize dosages or add additional drugs until goal blood pressure is achieved.Consider consultation with hypertension specialist. JNC7 Treatment Algorithm Lifestyle Modifications Not at Goal Blood Pressure (<140/90 mmHg) (<130/80 mmHg for those with diabetes or chronic kidney disease) Initial Drug Choices JAMA. 2003;289:(doi:10.1001/jama.289.19.2560) (JNC-7).

  39. Reprinted with permission

  40. Ways to Lower Pressure Vasodilators • Reduce Cardiac Output • ß-Bs, CCBs • Reduce Plasma Volume • Diuretics • Reduce Peripheral Vascular Resistance • Vasodilators (RASI, ß-Bs, CCBs, α-Bs, Diuretics) ß-Bs CCBs Vasodilators Diuretics MAP = CO X TPR

  41. Antihypertensive Modes of Action ß-Bs CCBs

  42. Modes of Action: Diuretics • Inhibit Na+/CL- reabsorption • in the nephron Reabsorption Na+ H2O DistalTubule Blood Urine Distal Tubular Cell Clˉ ATP Na+ Na+ K+ Na+/ClˉCotransporter Na+/K+ Pump • Hyperosmolar renal tubules pull water • into the urine for excretion Brater DC. In: Principles of Pharmacology: Basic Concepts and Clinical Applications. 1995;657-672.

  43. β-Blockers in HTN • Block β receptors  Sympathetic tone  CO: (-) ionotropic & (-) chronotropic effect  Renin release  Vasoconstriction (mild in older β-B’s) 1)http://www.mc.uky.edu/Pharmacology/instruction/decor/ar/bhkbbl.jpg. 2)Cleveland Clinic Journal of Medicine. February 2010, 77 (2)

  44. Audience Response Question

  45. RAAS in HTN Bradykinin-----//----- AT II http://upload.wikimedia.org/wikipedia/commons/a/a2/Renin-angiotensin-aldosterone_system.png

  46. RAAS in HTN Angiotensin II Stimulates ADH  H20 retention Super-stimulates sympathetic response  Myocardial norepinephine  Arterial & venous vasoconstriction  Renin Stimulates Thirst  Blood volume • Potent venous vasocontriction  SBP • Potent arterial vasoconstriction  DBP • Stimulates Aldosterone  Na+ & H20 retention • Stimulates Myocardial Growth Factor  Cardiac Remodeling Am Fam Physician 1999;60:1185-90

  47. RAAS in HTN ARB ACEI Bradykinin-----//----- Bradykinin AT II DRI http://upload.wikimedia.org/wikipedia/commons/a/a2/Renin-angiotensin-aldosterone_system.png

  48. RAASIs in HTN Medication Effects ARBs:  Prevent AT II from acting on target tissue β-Bs:  Block Renin formation in the kidney • DRIs:  Prevent formation of AT I (“upstream”)  No Bradykinin effect • ACEIs:  Prevent formation of AT II  Augment Bradykinin  Vasodilation (arteriolar & veinules)

  49. Audience Response Question

  50. HTN & Renin • 15% High Renin • 60% Normal Renin • 25% Low Renin • Elderly • African American • More salt-sensitive • More responsive to Diuretics & CCBs 1.) Am J Med 1984 Aug 20;77(2A):36-4. 2.) J Hum Hypertens. 2001 Jan;15(1):17-25. 3.) Kidney IntSuppl 1988 Sep;25:S162- 74. 4.) JAMA 1992 Mar 4;267(9):1221-5. 5.) Kidney IntSuppl 1988 Sep;25:S162-74.

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