Evidence-Based Medicine for CAD: Take 5 to Stay Alive

EVIDENCE-BASED MEDICINE FOR POST MI CARE

presented by Paul St. Laurent, MSN, RN, ACNP, CCRNAcute Care Nurse PractitionerBaylor Heart and Vascular Hospital

What Do We Already Know?Aspirin reduces the risk of myocardial infarctionAntiplatelet therapy reduces stent thrombosisBeta blockers reduce post MI mortalityACE inhibitors and angiotensin receptor blockers inhibit LV remodelingStatins reduce major coronary events2TRUE OR FALSE?How do we know these things? Its because of evidence based medicine. What is evidence based medicine?2

Evidence Based Medicine (EBM)The conscientious, explicit and judicious use of current best evidence in making decisions about the care of the individual patient. It means integrating individual clinical expertise with the best available external clinical evidence from systematic research."

3Sackett DL, BMJ, 1996:312 (7023): 71-72

David Lawrence Sackett, Canadian doctor, pioneer of evidence based medicine. Founded Oxford Center for Evidenced-Based Medicine.

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Steps in EBM Process1: THE PATIENTClinical problem arises from care of patient2: THE QUESTIONConstruct question derived from case3: THE RESOURCESelect resource, conduct search4: THE EVALUATIONAppraise evidence for validity and applicability5: THE PATIENTIntegrate evidence with clinical expertise, patient preferences and apply it to practice6: SELF-EVALUATIONEvaluate your performance with this patient

4http://www.hsl.unc.edu/services/tutorials/ebm/index.htmEBM process involves several steps. The patient is the key to this entire process. The patient generates the question, and if we are to be patient centered, we must consider the patient in the clinical decision making process. 4

Case ScenarioSTEP 1: The patientMrs. Jones BP is 160/80STEP 2: The questionWhat BP medication should she take?PMH: DM and chronic kidney diseaseThiazide, BB, ACEI, ARB, CCB, other?STEP 3: The resourcesNational hypertension guidelinesNational Heart, Lung, and Blood Institute (JNC 7), National Kidney Foundation, European Society of Hypertension

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JNC 7Published in 2003Coalition of 39 major professional, public, and voluntary organizations, and seven federal agenciesIncorporates results of many large-scale clinical trials6

Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JNC 1 1976, JNC 8 will be available for review in December 2010 and will be published in 2011.This report gives the most recognized authoritative recommendations for diagnosis and management of hypertension in the United States.6

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In JNC 7, specific medications are recommended based on the presence of medical conditions. Based on Mrs. Jones PMH of DM and CKD, she has compelling indications to be on either an ACEI or ARB.7

Case ScenarioSTEP 4: The evaluationWhich ACEI or ARB is best?Review literature for validity and applicabilitySTEP 5: The patientPrefers once a day dosingPrefers generic$4 listYou prescribe lisinopril 20 mg dailySTEP 6: Self-evaluationMrs. Jones returns for follow up in 4 weeksBP 140/72

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Doing a literature review can be very time-consuming. But whats nice about guidelines is that the research has already been done for you. The bibliography list for JNC 7 has 386 references, which illustrates the extent of scholarly research that went into the development of these guidelines.

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Coronary Artery DiseasePROVEN THERAPIESAnti-platelet therapyAspirinADP receptor blockers (thienopyridines)Beta blockersACE inhibitors/angiotensin receptor blockersLipid-lowering therapy

9Each of the categories of medications is commonly used in CAD. They are used because that been proven to be effective in reducing mortality and morbidity. The categories are antiplatelet drugs, BB, ACEI/ARBS, and lipid-lowering therapy. What Id like to do next is discuss each of these classes of medications, and review the mechanism of action, clinical benefits, and evidence for use in CAD.9

Antiplatelet Medications10

In the first class of medications, antiplatelet medications, we have 2 drugs, aspirin and thienopyridines. Lets begin with aspirin.

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Aspirin: Mechanism of ActionMost widely studied antiplatelet drugSome of strongest evidence available about long term effects pertain to patients with coronary diseaseIrreversibly inhibits COX-1 within platelets, prevents formation of thromboxane A2, diminishes platelet aggregationPlatelet inhibition mechanism for clinical benefit1111

Antiplatelet Effect of Aspirin12

Aspirin inhibits COX 1, which in turn blocks arachidonic acid metabolism and prevents the production of prostaglandins. This prevents the formation of thromboxane A2 which diminishes platelet aggregation.12

Aspirin: The EvidenceAntithrombotic Trialists Collaboration (2002)Collaborative meta-analysis of randomized trials287 studies, 135,000 patients 25% REDUCTION in combined outcome of any serious vascular eventNon-fatal MI, non-fatal stroke, death from any vascular cause13Antithrombotic Trialists Collaboration. Collaborative meta-analysis of randomized trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2001;324:71-86.What does the evidence tell us about aspirin?13

Aspirin DosingNo trial has compared different doses of ASA in patients who present with UA/NSTEMIIndirect comparisons of doses ranging from less than 75 mg to up to 1500 mg Similar reductions in the odds of vascular eventsLess than 75 mg dailyBenefit reduced by at least half compared with higher doses

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Aspirin DosingAnalysis from CURE trial suggested no difference in rate of thrombotic events according to ASA dose, but there was a dose-dependent increase in bleeding Major bleeding rate2.0% in patients taking < 100 mg daily2.3% with 100 mg - 200 mg daily4.0% with > 200 mg dailyTherefore, maintenance doses of 75 -162 mg PREFERRED

15Yusuf, S., et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndrome without ST-segment elevation. N Engl J Med 2001;345:494-502.

So What is The Recommended Dose of Aspirin in CAD?

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This is where we rely on guidelines to direct us. The use of aspirin in CAD is clearly delineated in 2 publications. 1 is the ACC/AHA guidelines and the other is the American College of Chest Physicians Guidelines. Today we are going to focus of the ACC/AHA guidelines, which not only cover CAD, but a host of other cardiovascular diseases.17

ACC/AHA GuidelinesACC and AHA jointly engaged in producing guidelines since1980ACC/AHA Task Force on Practice Guidelines charged to develop, update, or revise guidelines for important cardiovascular diseases and proceduresCurrent guidelines include:STEMI (2009), USA/NSTEMI (2007), Chronic stable angina (2007), PCI (2009), chronic heart failure (2009), valvular disease (2008), PAD (2005)

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http://www.americanheart.org/presenter.jhtml?identifier=300454219

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Within the guidelines, each recommendation is graded based on the benefit vs. risk, and strength of supporting evidence. Class I recommendations should always be done (GREEN LIGHT), class IIa are reasonable to perform (YELLOW LIGHT), class IIb may be considered (ORANGE LIGHT), and class III should not be done (RED LIGHT), and may be harmful. The level of evidence to support each recommendation is either A, which means its supported by multiple, randomized clinical trials, B, supported by a single randomized trial or nonrandomized studies, or C, only expert opinion, cases studies, or standard-of-care. Lets look at the ACC/AHA guidelines for aspirin use in CAD.21

Aspirin RecommendationsUA/NSTEMI/STEMI without stentingAspirin 75 162 mg indefinitely (LOE: A)UA/NSTEMI/STEMI with BMSAspirin 162 325 mg at least one month, then 75 162 mg indefinitely (LOE: A)UA/NSTEMI/STEMI with DESAspirin 162 mg 325 mg at least 3 months for sirolimus-eluting, at least 6 months for paclitaxel-eluting, then 75 162 mg indefinitely (LOE: A)

22CLASS IDose range given, must use judgment and decide what is appropriate for that patient.22

Thienopyridines: Mechanism of ActionAdenosine diphosphate (ADP) receptor antagonistsPrevent adenosine diphosphate from binding to its receptor on plateletsStops activation of glycoprotein IIb/IIIa complex thereby inhibiting platelet activationProdrugs: require metabolism by cytochrome P450 enzyme to become activeClopidogrel and prasugrel

23Cytochrome P450 enzyme actives both clopidogrel and prasugrel in the liver, and the active metabolites act on the ADP receptors. 23

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Thienopyridines: Clinical BenefitsMonotherapy and in combination with aspirinClopidogrel: CAPRIE, CURE, CHARISMAPrasugrel: TRITON-TIMI 38CAPRIE (1996)Monotherapy with clopidogrel vs. aspirinPrimary end-point composite of vascular death, MI, strokeFavored clopidogrel (5.3% vs. 5.8%)

25CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996;348:1329-1339.

Thienopyridines: The EvidenceCURE (2001)Dual therapy: aspirin + clopidogrel or aspirin + placebo in ACS patientsClopidogrel: 20% REDUCTION in end point of CV death, MI or stroke at 12 monthsCHARISMA (2006)Dual therapy with clopidogrel + aspirin vs. aspirin alone in patients at high risk for atherothrombotic eventsNo statistical difference overallSignificant benefit in subset of patients with prior MI

26Bhatt, DL., et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med 2006;354:1706-1717.Yusuf, S., et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345:494-502.

PrasugrelFDA approved July 10, 2009TRITON-TIMI 38Randomized, double-blind studyCompared prasugrel (60 mg LD, 10 mg MD) to clopidogrel (300 mg LD, 75 mg MD) in patients undergoing PCI19% relative risk reduction in primary composite endpoint of death, nonfatal MI, or nonfatal stroke at expense of significant increase in the risk of major bleeding

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Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357:2001-2015.

Thienopyridine RecommendationsUA/NSTEMI/STEMI without stentingLD: Clopidogrel 300-600 mg/prasugrel (STEMI only) 60 mg (LOE: B)MD: Clopidogrel 75 mg/prasugrel 10 mg for 1 month, ideally for 1 year (LOE: B)UA/NSTEMI/STEMI with BMSClopidogrel 75 mg/prasugrel 10 mg (STEMI only) for at least 1 month (LOE: B)UA/NSTEMI/STEMI with DESClopidogrel 75 mg/prasugrel 10 mg (STEMI only) for at least 1 year (LOE: B)

28CLASS IAs you have noticed, there is a range for the loading doses for clopidogrel. What does this tell us? It tells us that the evidence is not clear.28

Loading DosesClopidogrel 300 mg loading doseWell established for use in patients with acute coronary syndromeInhibition of platelet aggregation 30% - 40%Time to peak effect 4 to 6 hoursClopidogrel 600 mg loading doseInhibits platelet aggregation > 40%Time to peak effect 2 to 3 hoursReduces clopidogrel hyporesponsiveness

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Loading Doses: The EvidenceMeta-analysis of 10 studies1,567 patients undergoing PCI, variety of loading doses (300 mg 900 mg)Result: high loading doses significantly reduce early ischemic events in patients scheduled for PCIHORIZONS-AMI3,311 patients with STEMI receiving either 300 mg or 600 mg loading dose600 mg: 30-day mortality, subacute stent thrombosis, major adverse cardiac events, with no increase in bleeding

30Lotrionte, M., et al. Meta-analysis appraising high clopidogrel loading in patients undergoing percutaneous coronary intervention. Am J Cardiol 2007;100:1199-1206.Dangas, G., et al. Role of clopidogrel loading dose in patients with ST-segment elevation myocardial infarction undergoing primary angioplasty. J Am Coll Cardiol 2009;54:1438-1446.So we have several studies that have tried to determine the optimal loading dose of clopidogrel. Another question that has been often debated is when is the optimal time to give the loading dose?30

Loading Doses: The EvidenceARMYDA-5 PRELOAD Trial409 patients randomized to 600 mg clopidogrel 4-8 hours before PCI or in the cath lab after angiography but prior to PCINo difference in primary end-point of 30-day incidence of cardiac death, myocardial infarction, or unplanned target vessel revascularization31Sciascio, G., et al. Effectiveness of in-laboratory high-dose clopidogrel loading versus routine pre-load in patients undergoing percutaneous coronary intervention. J Am Cardio 2010;56:550-557.We need more randomized controlled studies before we have a definitive answer about what loading dose is most effective, and when should the loading dose be given. This is especially important when patients are found to have MVD and need CABG. Following a loading of clopidogrel or prasugrel, the guidelines recommend waiting 5 7 days before surgery to allow for platelet recovery. This becomes a problem for hospitals because patients end up occupying beds while they wait for their clopidogrel or prasugrel to wear off before they can go to surgery. Some hospitals, however, have opted to do platelet mapping testing, which measures the level of platelet inhibition of these medications, and uses this as a way to determine when its safe to take patient to the OR. This, however, is not yet considered standard of care.31

Beta-Blockers: Mechanism of ActionBlock the action of adrenergic catecholamines (norepinephrine and epinephrine) on -adrenergic receptors1 receptor mainly in heart2 receptor mainly in lungs, vascular smooth muscle, skeletal muscleCardioselective selectively block 1Nonselective block 1 and 2

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Beta Blockers: Clinical BenefitsDecreased oxygen demand due to reduction in BP, HR, contractility, and relief of chest painDecreased risk of VF and sudden cardiac deathDecreased HR prolongs diastole, and enhances coronary artery perfusionReduces remodeling, and enhances hemodynamic function33

Beta Blockers: The EvidenceUS Carvedilol Study (1996)Carvedilol vs placebo in HF patients65% REDUCTION IN MORTALITYCIBIS-II and MERIT-HF (1999)Bisoprolol and metoprolol vs placebo in HF patients34% REDUCTION IN MORTALITYCAPRICORN (2001)Carvedilol vs placebo in AMI patients with EF 40%23% REDUCTION IN MORTALITY

34The pivotal studies were done which overwhelming showed the benefits of BB in patients with LV dysfunction. In each of these studies, there was a very significant decreased in mortality in the BB arm. Most impressive was the US carvedilol study, which showed at 65% reduction in mortality.34

Beta Blockers: The EvidenceEPIC (1994), EPILOG (1997), EPISTENT (1998), CAPTURE (1997), RAPPORT (1998)Pooled results of 2894 patients with UA and AMI undergoing PCI1939 patients received BB, 934 did not50% REDUCTION IN MORTALITY at 30 days and 6 months35Ellis, K. et al. Mortality benefit of beta blockade in patients with acute coronary syndromes undergoing coronary intervention. J Interven Cardiol 2003;16;2999-305A meta-analysis was done of 5 studies looking at patients undergoing PCI. Why this matters goes back to the discussion of EBM that we had earlier on today. Although the US Cardvedilol study showed a 65% reduction in mortality, we have remember that the patients in the study were patients with LV dysfunction. If the results of a study are to applied to another patient population, that patient population should be the same type of patients. So this study looked at patients with UA and AMI undergoing PCI, and there was a 50% reduction in mortality. So now we can say that BB clearly reduce mortality in patients with AMI undergoing PCI.35

Beta Blocker RecommendationsUA/NSTEMI/STEMIIt is beneficial to start and continue beta-blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or LV dysfunction with or without HF symptoms, unless contraindicated (LOE: A)36CLASS I

Beta Blocker: SelectionCardio-selective vs nonselectiveContraindicationsMarked 1st degree, 2nd/3rd degree AVB, significant sinus bradycardia, hypotension, history of asthma, low output state, severe LV dysfunctionSignificant COPD: short-acting B1 agent at low doseReassess when acute problems have resolved37

Cardioselective: Atenolol, Metoprolol (tartrate and succinate), Bisoprolol, Nevibolol. Nonselective: carvedilol, labetalol. AMI may be unstable. Reassess, start when stable in the hospital, otherwise it may never get started.37

Beta-Blocker SelectionDosing considerationsDaily: metoprolol succinate, carvedilol phosphate, atenolol, nevibololBID: metoprolol tartrate, carvedilol, labetalolEvidence-based beta blockersHF: metoprolol succinate, carvedilol, bisoprolol

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ACE Inhibitors: Mechanism of ActionAngiotensin converting enzyme inhibitorsBlock the enzyme that converts antiogensin I to angiotensin II Block bradykinin, which increases nitric oxide release, promotes vasodilationBlock aldosterone

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ACE Inhibitors: Clinical BenefitInhibits LV remodeling, preserves LV functionAfterload reduction (vasodilation)Reduces blood pressureReduce infarct sizeImproves endothelial function Reduces overall cardiovascular mortality

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Inhibition of AT-II related vasoconstriction and to diminishes breakdown of bradykinin, which enhances endothelial release of nitric oxide.NOT JUST A BLOOD PRESSURE DRUG.40

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Remodeling: Myocyte necrosis leads to hypertrophy, and the formation of a collagen scar.41

ACE Inhibitors: The EvidenceSAVE(1992), AIRE (1993),TRACE (1999)5966 patients after with LV dysfunction post MI26% REDUCTION in death, MI, hospital admission for HFHOPE (2003), QUIET (2001), PART-2 (2000), SCAT (2000), EUROPA (2003), PEACE (2004), CAMELOT (2004)14% REDUCTION in death, MI

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ACE Inhibitor RecommendationsUA/NSTEMI/STEMIShould be given and continued indefinitely for patients with HF, LV dysfunction (LVEF < 40%), hypertension, diabetes, and chronic kidney disease, unless contraindicated (LOE: A)43CLASS I43

ACE Inhibitor SelectionContraindicationsHypotension, angioedema, hyperkalemia, bilateral renal artery stenosis, acute renal insufficiencyDosing considerationsDaily: lisinopril, ramipril, enalapril, benazepril, fosinopril, quinaprilBID/TID: captopril

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Angiotensin Receptor Blockers (ARBs): Mechanism of ActionAngiotensin II causes potent vasoconstriction, aldosterone secretion and sympathetic activationARBs bind to specific membrane-bound receptors that displace angiotensin II from its type 1 receptor subtype (AT1)45

ARBs: The EvidenceVALIANT (2003)Valsartan vs captoprilValsartan equally effective at reducing mortality, CV morbidityCan be used as alternative if ACEI not toleratedACEI cough secondary to inhibition of bradykinin pathway46Pfeffer, M., et al. Valsartan, captopril, or both in myocardial infraction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med 2003:349:1893-1906.

ARB RecommendationsUA/NSTEMI/STEMIAngiotensin receptor blocker should be prescribed at discharge to those UA/NSTEMI patients who are intolerant of an ACE inhibitor and who have either clinical or radiological signs of HF and LVEF < 40% (LOE: A)It is beneficial to use angiotensin receptor blocker therapy in other patients who are ACEI intolerant and have hypertension (LOE: B)47CLASS I

ARB SelectionContraindicationsSame as for ACEIDosing considerationsCandesartan, irbesartan, losartan, olmesartan, telmisartan, valsartan All can be given dailyNone available in generic form

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Statins: Mechanism of ActionHMG CoA reductase inhibitors competitively inhibit the activity of HMG CoA reductase, which reduces cellular cholesterol concentrationReduced cholesterol causes up regulation of LDL receptors, and increased uptake of plasma LDLEnd result: decreased plasma LDL49

Statins: Clinical BenefitsPlaque stabilizationUnstable stable plaqueReduces inflammationContributor of atherosclerosis and plaque ruptureReduces CRP levelsReverses endothelial dysfunction endothelial nitric oxideDecreased thrombogenicityDecreased prothrombin activation and thrombin generation 50NOT JUST A CHOLESTEROL LOWERING DRUG50

Statins: The EvidenceLIPID trial9014 patients with CADPravastatin vs placebo22% MORTALITY24% cardiac death, nonfatal myocardial infarction51

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Statins: The Evidence4S Trial4444 patients with CADSimvastatin vs placebo30% MORTALITY 52

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Statin RecommendationsCLASS IStatins, in the absence of contraindications, regardless of baseline LDL-C and diet modification, should be given to post-UA/NSTEMI/STEMI patients, including post revascularization patients (LOE: A)For hospitalized patients, lipid-lowering medications should be initiated before discharge (LOE: A)53

Statin RecommendationsCLASS IFor UA/NSTEMI/STEMI patients with elevated LDL-C (100 mg per dL), cholesterol-lowering therapy should be initiated or intensified to achieve an LDL-C < than 100 mg per dL (LOE: A)CLASS IIaFurther titration to < than 70 mg per dL is reasonable (LOE: A)

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STATINLDL LOWERINGAtorvastatin 35-60%Fluvastatin 20-35%Lovastatin 25-40%Pitavastatin 39-45%Pravastatin 20-35%Rosuvastatin 40-65%Simvastatin 35-50%While few drugs, including LIVALO (pitavastatin) are free from drugdrug interactions, LIVALO may be an attractive option for physicians treating patients on multiple medications metabolized through the cytochrome P450 system. This is because LIVALO is only minimally metabolized by the cytochrome P450 system which may help reduce its potential for drugdrug interactions mediated by this system. 55

56DRUG CLASSLIPID EFFECTSBile Acid SequestrantsLDL 15-30%HDL 3-5%TG No change or increaseNicotinic acidLDL 5-25%HDL 15-35%TG 20-50% Fibric acidsLDL 5-20%HDL 10-20%TG 20-50%

Statin SelectionContraindicationsAbsolute: active or chronic liver diseaseAdverse effectsMyopathy, increased liver transaminasesDosing considerationsGeneric: lovastatin, pravastatin, simvastatinTake any time: atorvastatin, pitavastatin, pravastatin, rosuvastatinTake in the evening: all others57CPK, LFTs57

Putting it Together58

Impact of Combination TherapyAntiplatelet drugs, -blockers, ACE inhibitors/ARBs, and lipid-lowering agents reduce mortalityAspirin: 25%Thienopyridines: 20 %BB: 35%ACEI: 20 %Statins: 25%59

Impact of Combination Therapy1264 patients with acute coronary syndromeCompared number of discharge drugs and 6-month mortalityWhat was the overall reduction in mortality between patients on all evidence-based medications?60Mukherjee, D et al, Impact of Evidence-Based Combination Therapy on Mortality in patients With Acute Coronary Syndromes. Circulation, 2004;109;745-74960

What Was the Reduction in Mortality?A: 30%B: 40%C: 50%D: > 60%6172% - 87% REDUCTION IN MORTALITY!!

So, How are We Doing?186,000 eligible patients with AMI between July 1, 2000 and June 30, 2002National Registry of Myocardial Infarction 4 (NRMI-4) database1247 hospitalsEarly and discharge medications62Roe, M. et al. Quality of care by classification of myocardial infarction. Arch Intern Med. 2005;165:1630-1636200562

Results63

5533 misses21,394 misses276,277 MISSED OPPORTUNITIESEARLYAspirin = 5533 misses15,861 TOTAL=21,394BB = 9024 misses25,944 TOTAL=34,968ACE = 30257 misses73,655TOTAL=103,912DISCHARGEAspirin = 440514,879TOTAL=19,284BB = 446013,961TOTAL=18,421ACE = 13,82240,616TOTAL=54,438Lipid = 710 23,150TOTAL=23,860TOTAL=276,277

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What About After Discharge?National Disease and Therapeutic Index and National Ambulatory Medical Care Survey (physician prescribing practices)1990 to 200235,295 patients with CADAspirin use increased from 18% in 1990, to 19% in 1995, to 38% in 200164Stafford, R., et al. The underutilization of cardiac medications of proven benefit, 1990 to 2002. J Am Coll Cardiol 2003:41:56-61Surveyed physicians about their prescribing practices.64

What About After Discharge?Duke Databank for Cardiovascular Disease 1995 to 2002Self-reported22,539 patientsConsistently used71% aspirin, 46% , 44% lipid-lowering65Newby, K., et al. Long-Term Adherence to Evidence-Based Secondary Prevention Therapies in Coronary Artery Disease. Circulation. 2006;113:203-212.Surveyed patients. Do you noticed that the patients self-reported numbers are MUCH higher than the physicians numbers? It makes you wonder.65

Key StrategiesEnsure patients receive all 5 evidenced-based medicationsMissing medications should be identified, and action takenEducation to providers in all clinical settingsInpatient, outpatient, cardiologists, primary care providers, physicians, nurses, etc.

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TAKE 5.AND STAY ALIVE67

Why Does it Matter?5 medications can prevent a heart attack5 medications can prevent stent thrombosis5 medications can prevent heart failure5 medications can save a life

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At What Cost?69

$4 DrugsBBsACEIsSTATINSCarvedilolLisinoprilLovastatinMetoprolol tartrateBenazeprilPravastatinAtenololEnalaprilPropranololCaptoprilBisoprolol (with HCTZ only)70

Take 5, Costs $6Aspirin = $0.02/dayBB = $0.13/dayACEI = $0.13/dayStatin = $0.13/dayPlavix = $5.50/day (www.drugstore.com)TOTAL = $5.91/day71

Take Home MessageOVERWHELMING body of evidence supports use of AspirinThienopyridinesBeta blockersACE inhibitors/ARBsLipid-lowering therapy

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.IN PATIENTS WITH CORONARY ARTERY DISEASE

5 medications can significantly impact patient outcomesShare this message with your patients and colleagues

73TAKE 5AND STAY ALIVE

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THANK YOU