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Prevention and Management of Cardiovascular Disease

Prevention and Management of Cardiovascular Disease. Dr. Juliette Gordon Montego Bay, Jamaica National Diamondback Alumni Convention June 17, 2009. Presentation Outline. Introduction Definition of CVD Prevalence of CVD Economic burden of CVD Risk factors of CVD

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Prevention and Management of Cardiovascular Disease

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  1. Prevention and Management of Cardiovascular Disease Dr. Juliette Gordon Montego Bay, Jamaica National Diamondback Alumni Convention June 17, 2009

  2. Presentation Outline • Introduction • Definition of CVD • Prevalence of CVD • Economic burden of CVD • Risk factors of CVD • Identify and assess cardiovascular disease risk in women • Endothelial function and its impact on CVD

  3. Presentation Outline • Hypertension prevention and management • Heart failure management • Summary

  4. Learning Objectives • Define CVD • List the significant Disorders associated with CVD • Prevalence of CVD • Identify the types of patients to refer for cardiac or vascular follow-up • Summarize differences in the manifestation of CVD between women and men; • Identify and assess cardiovascular disease risk in women

  5. Learning Objectives Hypertension • Define hypertension, its role in cardiovascular disease (CVD) morbidity and mortality, and its US economic burden • Describe the role of endothelial function in hypertension and its impact on CVD • Review etiology of hypertension • Review management of hypertension • Explain the benefits and limitations of current and emerging beta blockers in hypertension and CVD management

  6. Learning Objectives Heart Failure in women • Discuss the management of heart failure in women • Classify secondary prevention, assess risk and implement the latest treatment plans

  7. Definition Cardiovascular diseases (CVD) Generic term that covers a wide range of vascular and heart-related diseases and disorders. CVD in many cases, is caused by atherosclerosis: an excess build-up of plaque on the inner wall of a large blood vessel, which restricts the flow of blood.

  8. Cardiovascular Diseases • Hypertension • Heart Failure • CAD – angina and MI • Arrhythmia • Peripheral Vascular disease • Heart Valve disease • Shock • Endocarditis • Diseases of the aorta and its branches • Congenital Heart Disease

  9. Prevalence of CVD(NHANES 2005-6) • In 2006, an estimated 80,000,000 American adults (one in three) have one or more types of cardiovascular disease (CVD) • 38,100,000 - 60 years or older.

  10. Prevalence of CVD(NHANES 2005-6)

  11. Prevalence of Cardiovascular Disease by Age and Sex

  12. Ethnic Groups And Cardiovascular Diseases Total Cardiovascular Disease Whites Blacks Mexican Both Sexes M F M F M F Prevalence 2006: 80.0 M (36.3%) 37.8% 33.3% 45.9% 45.9%26.1% 32.5% Mortality 2005: 864.5 K 329.6 K 372.2 K 47.4 K 52.4 K NA NA Heart Disease and Stroke Statistics — 2009 Update, American Heart Association

  13. Estimated Direct & Indirect Costs (Billions$$) of CVD And Stroke: USA 2009 Heart Dz* CAD Stroke HTN HF Tot CV Direct Cost Hospital $106.3 $54.6 $20.2 $8.2 $20.1 $150.1 Nursing home $23.4 $12.3 $16.2 $4.8 $4.5 $48.2 Physicians/others HC $23.8 $13.4 $3.7 $13.4 $2.4 $46.4 Drugs/other Medical Durables $22.1 $10.3 $1.4 $25.4 $3.3 $52.3 Home Health Care $7.4 $2.2 $4.4 $2.4 $3.4 $16.8 Total Expenditures $183.0 $92.8 $45.9 $54.2 $33.7 $313.8 Indirect Cost Lost prod./morbidity $24.0 $10.6 $7.0 $8.4 .... $39.1 Lost prod/mortality $97.6 $62.0 $16.0 $10.8 $3.5* $122.4 Grand totals $304.6 $165.4 $68.9 $73.4 $37.2 $475.3 Prepared by Thomas Thom, NHLBI.;Heart Disease&d Stroke Statistics ;2009 Update, AHA

  14. Non Modifiable Risk Factors • Family History • Gender • Advancing age • Racial or Ethnic Background • Elevated levels of homocysteine

  15. Modifiable Risk Factors • Smoking • Obesity • Lack of exercise • Diabetes • Elevated Blood Pressure • Dyslipidemia

  16. Identify the types of patients to refer for cardiac or vascular follow-up • All adults over age 20 should be screened for heart disease risk factors every two to five years • Over weight • Elevated blood pressure • Diabetics • Cholesterol • Smoking and exercise habits • Family history.

  17. Differences in the Manifestation of CVD between men and women • Underrepresented in randomized clinical trials • CVD not diagnosed in women • Symptoms can differ by sex and race • Outcomes can differ by sex and age • Black women less likely to receive life threatening therapies

  18. Differences in the Manifestation of CVD between men and women • Difference in response to drug therapies • PK and PD differences • Lower body wt, smaller organ size, >fat tissues, hormone levels and differences in metabolism may affect absorption and elimination of drugs • Gender differences in enzyme activity • Adverse effects

  19. Identify and assess cardiovascular disease risk in women Non-controllable risk factors: • Family history of coronary artery disease or stroke • Age 55 or older • Being post-menopausal, or having your ovaries removed

  20. Identify and assess cardiovascular disease risk in women Controllable risk factors: • Obesity & Sedentary lifestyle • Smoking • Hypertension • Dyslipidemia • Diabetes

  21. Identify and assess cardiovascular disease risk in women Controllable risk factors: • Metabolic syndrome • Complicated pregnancy • Increased C-reactive protein (CRP)

  22. Single cell layer lining inside of arteries Plays a critical role in development of CVD Dysfunction precedes atherosclerosis Endothelium

  23. Endothelium Function Has 4 major physiologic responsibilities: • Barrier between the blood and underlying structures, regulating the flow of substances from blood to tissue • Regulates vasomotor tone • Regulates hemostasis and fibrinolysis • Regulates inflammatory responses

  24. Endothelium Function Endothelial cells produce both relaxing and contracting factors: NITRIC OXIDE ENDOTHELIN 1 – (ET – 1)

  25. Endothelium Function In the physiologic state, EC’s promote vasodilation, platelet dissolution, anticoagulation, and anti-inflammation However, in the face of injury EC’s can promote vasoconstriction, platelet aggregation, coagulation, and inflammation

  26. What is Endothelial Dysfunction? • Decreased production of NO - Increased endothelial permeability - Impaired anti-coagulation and fibrinolysis - Decreased ability to deal with inflammation

  27. Endothelial Dysfunction in Atherosclerosis NEJM Jan 1999:115-125

  28. Fatty-Streak Formation in Atherosclerosis NEJM Jan 1999:115-125.

  29. Advanced, Complicated Lesion of Atherosclerosis NEJM Jan 1999:115-125

  30. Unstable Fibrous Plaques in Atherosclerosis NEJM Jan 1999:115-125.

  31. Endothelial Dysfunction

  32. Aging Smoking Obesity Mental Stress Menopause Homocysteine Hypertension Diabetes Hyperlipidemia Hypertriglyceridemia Oxidized LDL C Reactive Protein Insulin resistance Sources of Endothelial Dysfunction

  33. Hypertension Introduction • Most common adult medical problem in the world. • Affect 65 million Americans. • Significant risk factor for the development of atherosclerotic coronary artery disease; major cause of heart failure, renal failure, and stroke.

  34. Etiology of Hypertension • Primary (essential) hypertension: 90-95% • Secondary hypertension: 5-10% • Generally asymptomatic • No cure • Treatment generally is life-long.

  35. DEFINITION AND CLASSIFICATION OF HYPERTENSION BY JNC 7

  36. TRENDS IN AWARENESS, TREATMENT AND CONTROL OF HYPERTENSION IN US (%)

  37. How can pharmacists make a difference in hypertension? • Prevention • Identification • Treatment gap • Treatment intensity gap

  38. Proposed Pathophysiologic Mechanisms of Primary (Essential) Hypertension

  39. Why Treat Hypertension? Target Organ damage for HTN Cardiac Cerebrovascular Peripheral vascular Renal Retinopathy

  40. Treatment of Hypertension First Line Agents Diuretics BBs ACEI/ARB CCBs

  41. Treatment of Hypertension Second Line agents Alpha blocker Aldosterone Receptor Blockers Centrally acting Agents Direct Vasodilators Renin Inhibitors

  42. Beta Blockers in hypertension Various Clinical conditions Hypertension CAD HF Arrhythmia

  43. Classes • 1st Generation – Non-selective e.g. Propranolol • 2nd Generation – selective e.g. Metaprolol, Atenolol, Bisoprolol • 3rd Generation – alpha receptor blockade and release of Nitric Oxide

  44. Proposed Mechanisms of action • Reduction in Cardiac output by blocking adrenoreceptors • Reduction in sympathetic activity • Inhibit release of renin

  45. BB in Uncomplicated HTN • Identifies as 1st line by many national and international guidelines e.g.. JNC7 • No evidence of reduction in morbidity and mortality • Many clinical trials show that BB may be associated with worst clinical outcomes

  46. Older Trials(re BB) • STOP • STOP 2 • SHEP • CONVINCE • NORDIL • CAPP

  47. Recent Trials (re BB) • British MCR • ASCOT • LIFE • Other Meta- analyses

  48. Reasons for BB Ineffectiveness • Anti-hypertensive Efficacy • Metabolic side effects • Decreased Compliance • Cost effectiveness

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