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2 Disclaimer This slide deck in its original and unaltered format is for educational purposes and is current as of September The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of Creative Educational Concepts or the supporter. These materials may discuss therapeutic products that have not been approved by the US Food and Drug Administration and off-label uses of approved products. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies described in this educational activity.
3 Usage Rights This slide deck is provided for educational purposes and slides may be used for personal, non-commercial presentations only as long as content and references remain the same. No part of this slide deck may be published or distributed in print or electronic format without prior written permission from Creative Educational Concepts.
4 Accreditation Physicians: 1.0 AMA PRA Category 1 Credit(s) Pharmacists: 1.0 ACPE contact hours (.10 CEUs) Nurses: 1.0 contact hour Faculty Information: You can find your faculty member s full bio and disclosure in your handout or online at Special Thanks! Supported through an independent educational grant from AstraZeneca. Presented by Creative Educational Concepts, Inc. (CEC)
5 Learning Objectives 1. Examine the role of clinical practice guidelines in the management of patients with acute coronary syndromes (ACS) and cardiovascular disease (CVD) and understand how to interpret class of recommendation (COR) and level of evidence (LOE) classifications. 2. Review recent updates to the ACC/AHA practice guidelines focusing on the management of patients with acute coronary syndromes (NSTE-ACS and STEMI) and other secondary prevention measures. 3. Discuss optimal oral antiplatelet therapy for patients following ACS in terms of P2Y 12 inhibitor (clopidogrel, prasugrel, ticagrelor) selection, aspirin dosing, and duration of dual antiplatelet therapy (DAPT). 4. Evaluate strategies members of the healthcare team can employ to actively engage patients in self-management to promote long-term adherence to antiplatelet and other ACS secondary prevention therapies following hospital discharge.
6 Association Between Hospital Guideline Adherence and In-hospital Mortality CRUSADE In-Hospital Mortality, % CRUSADE=Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines NSTE-ACS Hospital Composite Guideline Adherence Quartiles Adapted with permission from Peterson ED, et al. JAMA
7 Class I Applying Classification of Recommendations and Level of Evidence Class IIa Class IIb Class III Benefit >>> Risk Procedure/ Treatment SHOULD be performed/ administered Benefit >> Risk Additional studies with focused objectives needed IT IS REASONABLE to perform procedure/administer treatment Benefit Risk Additional studies with broad objectives needed; Additional registry data would be helpful Procedure/Treatment MAY BE CONSIDERED Risk Benefit No additional studies needed Procedure/Treatment should NOT be performed/administere d SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL Level A Level B Level C Recommendation based on evidence from multiple randomized trials or meta-analyses population risk strata evaluated; General consistency of direction and magnitude of effect Recommendation based on evidence from a single randomized trial or non-randomized studies population risk strata evaluated Recommendation based on expert opinion, case studies, or standardof-care population risk strata evaluated Multiple (3-5) Limited (2-3) Very limited (1-2)
8 Pathophysiologic Differences Between STEMI and NSTE-ACS STEMI Clot Totally Blocking Channel Clot Partially Obstructing Channel NSTE-ACS Ruptured Plaque Cross Section Longitudinal Section Cross Section Longitudinal Section
9 Acute Coronary Syndromes Hospitalizations in the United States 1.19 million hospital admissions UA/NSTEMI 0.81 million admissions per year STEMI 0.38 million admissions per year NSTEMI, non ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; UA, unstable angina. Roger VL, et al. Circulation
10 Key ACS Management Questions 1.Dx/Pathway: STEMI vs. NSTE-ACS 2.Risk? (troponin, ECG; TIMI, GRACE risk scores) 3.General management: bedrest, aspirin, highintensity statin, beta-blocker 4.Initial strategy? Invasive vs. ischemia-guided? 5.Antiplatelet: ASA dose? Choice of P2Y 12 inhibitor 6.Anticoagulant: UFH? LMWH? bival?
11 Reperfusion Therapy for Patients with STEMI *Patients with cardiogenic shock or severe heart failure initially seen at a non PCI-capable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from MI onset (Class I, LOE: B). Angiography and revascularization should not be performed within the first 2 to 3 hours after administration of fibrinolytic therapy.
12 Cumulative Incidence TRANSFER-AMI Primary Efficacy Endpoint Primary endpoint: composite of death, reinfarction, recurrent ischemia, new or worsening CHF, or shock within 30 days Standard Treatment 17.2% P = Days Routine Early PCI RR = 0.64 (95 CI%, ) N=1,059 STEMI patients treated with fibrinolysis and randomized to either early (<6 h) transfer for angiography/pci (median, 2.8 h) or standard care. CHF=Congestive Heart Failure; CI=Confidence Interval; RR=Relative Risk; TRANSFER-AMI=Trial of Routine Angioplasty and Stenting After Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction 11.0% Cantor WJ, et al. N Engl J Med
13 Reperfusion Therapy and Time-to-Treatment Goals I IIa IIb III Reperfusion therapy should be administered to all eligible patients with STEMI with symptom onset within the prior 12 hours. I IIa IIb III Primary PCI is the recommended method of reperfusion when it can be performed in a timely fashion by experienced operators.
14 Antiplatelet Therapy to Support Primary PCI for STEMI I IIa IIb III Aspirin 162 to 325 mg should be given before primary PCI. I IIa IIb III After PCI, aspirin should be continued indefinitely. I IIa IIb III It is reasonable to use 81 mg of aspirin per day in preference to higher maintenance doses after primary PCI.
15 Acute Coronary Syndromes Hospitalizations in the United States 1.19 million hospital admissions UA/NSTEMI 0.81 million admissions per year STEMI 0.38 million admissions per year NSTEMI, non ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; UA, unstable angina. Roger VL, et al. Circulation
16 I I I I I IIa IIb III IIa IIb III IIa IIb III IIa IIb III IIa IIb III AHA/ACC NSTE-ACS Guidelines: Early Risk Stratification Perform rapid determination of likelihood of ACS, including a 12-lead ECG within 10 min of arrival at an ED. Perform serial ECGs at 15- to 30-min intervals during the first hour in symptomatic patients with initial non-diagnostic ECG. Measure cardiac troponin (ctni or ctnt) in all patients with symptoms consistent with ACS. Measure serial cardiac troponin I or T at presentation and 3-6 hours after symptom onset in all patients with symptoms consistent with ACS to identify a rising and/or falling pattern.. Use risk scores to assess prognosis in patients with NSTE-ACS. Amsterdam EA, et al. Circulation
17 TIMI Risk Score* for NSTE-ACS TIMI Risk Score All-Cause Mortality, New or Recurrent MI, or Severe Recurrent Ischemia Requiring Urgent Revascularization Through 14 d After Randomization, % *The TIMI risk score is determined by the sum of the presence of 7 variables at admission; one point is given for each of the following variables: 65 y of age; 3 risk factors for CAD; prior coronary stenosis 50%; ST deviation on ECG; 2 anginal events in prior 24 h; use of aspirin in prior 7 d; and elevated cardiac biomarkers. Antman EM, et al. JAMA
18 Considerations for Choice of Strategy Strategy Candidate Characteristics Immediate Invasive Refractory angina strategy Signs/symptoms of HF, new/worsening mitral regurgitation (within 2 h) Hemodynamic instability Recurrent angina/ischemia at rest or low-level activity Sustained VT or VF Ischemia-guided Low-risk score (e.g., TIMI 0/1, GRACE <109) strategy Low-risk, troponin-negative females Patient/clinician preference and no high-risk features Early invasive strategy None of above, but GRACE risk score >140 (within 24 h) Temporal change in troponin New or presumably new ST depression Delayed invasive None of the above but diabetes mellitus strategy Renal insufficiency (GFR <60 ml/min/1.73 sq-m) (within h) Reduced LV systolic function (EF<0.40) Early post-infarction angina PCI within 6 months Prior CABG GRACE score ; TIMI score >=2. Amsterdam EA, et al. Circulation
19 TIMACS: Timing of PCI in NSTE-ACS Rates of death, MI, or stroke within 6 mo by GRACE score: HR (95% CI), early vs. delayed invasive strategy EARLY (%) DELAYED (%) Hazard Ratio (95% CI) P Value Low/Intermediate (N=2070) ( ).48 High (N=961) ( ).006 *Low/intermediate risk=grace score <140 High risk=grace score 140 Early: Within 24 h (mean, 15 h); Delayed: After 36 h (mean, 50 h) Mehta SR, et al. N Engl J Med
20 I I I I I IIa IIb III IIa IIb III IIa IIb III IIa IIb III IIa IIb III AHA/ACC NSTE-ACS Guidelines: General Early Hospital Care Administer supplemental oxygen only with oxygen saturation <90%, respiratory distress, or other high-risk features for hypoxemia. Administer sublingual NTG every 5 min x 3 for continuing ischemic pain, then assess need for IV NTG. Administer oral beta blockers within the first 24 h in the absence of HF, low-output state, risk for cardiogenic shock, or other contraindications to beta blockade. Calcium channel blockers are recommended for ischemic symptoms when beta blockers are not successful, are contraindicated, or cause unacceptable side effects. Initiate or continue high-intensity statin therapy in patients with no contraindications. Amsterdam EA, et al. Circulation
21 Dual Antiplatelet Therapy DAPT What is the optimal dose of ASA? Which P2Y 12 should I select for my patient? How long should DAPT be continued?
22 Aspirin Meta-analysis Aspirin Dose # Trials OR* (%) Odds Ratio 500-1,500 mg mg mg <75 mg 3 13 Any aspirin Antiplatelet Better Antiplatelet Worse *Odds reduction Treatment effect P<.0001 Antithrombotic Trialists Collaboration. BMJ
23 Antiplatelet Therapy for NSTE-ACS I I IIa IIb III IIa IIb III Non-enteric-coated aspirin ( mg/d) should be given to all NSTE-ACS patients promptly after presentation, and a maintenance dose ( mg/d) should be continued indefinitely. A loading dose of a P2Y 12 receptor inhibitor (clopidogrel, prasugrel, or ticagrelor) should be given before the procedure in patients undergoing PCI with stenting. I IIa IIb III A P2Y 12 inhibitor (either clopidogrel or ticagrelor) in addition to aspirin should be given for patients treated with an initial ischemia-guided strategy. Amsterdam EA, et al. Circulation
24 Cumulative Hazard Rate CURE Trial Primary Endpoint: MI/Stroke/CV Death Placebo + ASA Clopidogrel + ASA Months of Follow-Up 20% RRR P<.001 N=12,562 Yusuf S, et al. N Engl J Med
25 Clinical Issues With Clopidogrel Genetic polymorphisms in metabolism Prodrug that must undergo two CYP450 enzymes conversion steps CYP 2C19 loss-of-function alleles Heterozygous vs. homozygous Connection of clinical outcomes debated Drug Interactions Proton pump inhibitors (omeprazole vs. others) Other drugs that inhibit (CYP2C19) Variability of platelet inhibition Up to 40% of patients are nonresponsive Role of platelet function testing? What to do with the results? FDA Prescribing Information; Gurbel PA, et al. J Am Coll Cardiol
26 TRITON-TIMI 38 ACS (STEMI or UA/NSTEMI) & planned PCI CLOPIDOGREL 300 mg LD/75 mg MD N=13,608 PRASUGREL 60 mg LD/10 mg MD Median duration of therapy - 12 months 1 o endpoint: CV death, MI, stroke 2 o endpoints: CV death, MI, stroke, rehosp-recurr. ischemia CV death, MI, UTVR Stent thrombosis (ARC definite/probable) Safety endpoints: TIMI major bleeds, life-threatening bleeds Wiviott SD, et al. N Engl J Med
27 Endpoint (%) TRITON-TIMI 38 Trial Results CV Death / MI / Stroke Clopidogrel Prasugrel events HR=0.81 ( ) P=.0004 NNT= TIMI Major Non-CABG Bleeds Days Prasugrel Clopidogrel events HR=1.32 ( ) P=.03 NNH=167 Wiviott SD, et al. N Engl J Med
28 TRITON-TIMI 38 Trial: Prasugrel vs. Clopidogrel by Subgroup Net Clinical Benefit by Subgroup Prior Stroke or TIA 75 Years of Age Weight 60 kg HR=1.54 ( ); P=.04 HR=0.99 ( ); P=.92 HR=1.03 ( ); P= % 16% Remaining 80% of patients in TRITON-TIMI 38 demonstrated a significant reduction in CV death, MI, or stroke without an increase in bleeding CV Death/MI/Stroke: 11.0% clopidogrel vs. 8.3% prasugrel; P<.0001 Major Bleeding: 1.5% clopidogrel vs. 1.9% prasugrel; P=.17 Wiviott SD, et al. N Engl J Med. 2007; Wiviott SD, et al. Am J Cardiol
29 Prasugrel Warnings and Contraindications History of stroke or TIA Prasugrel is contraindicated Patients with weight 60 kg Caution due to increased risk of bleeding Patients age 75 years Prasugrel generally not recommended EXCEPT: STEMI or Diabetes mellitus
30 PLATO Study Design NSTE-ACS (moderate-to-high risk) STEMI (if primary PCI) Clopidogrel-treated or -naive; randomised within 24 hours of index event N=18,624 Clopidogrel If pre-treated, no additional loading dose; if naive, standard 300 mg loading dose, then 75 mg daily maintenance Ticagrelor 180 mg loading dose, then 90 mg bid maintenance; (additional 90 mg pre-pci) Primary endpoint: CV death + MI + Stroke Primary safety endpoint: Total major bleeding Wallentin L, et al. N Engl J Med
31 Cumulative Incidence (%) PLATO Trial: Results CV Death/MI/Stroke Clopidogrel P<.001 HR 0.84 ( ) NNT=53 Ticagrelor 11.7% 9.8% Days after Randomization Wallentin L, et al. N Engl J Med
32 % of Patients PLATO Results Major Bleeding Non-CABG and CABG Related 9% 6% 3% P= % 3.8% Ticagrelor Clopidogrel P = % 2.2% P=NS 7.4% 7.9% P=NS 5.3% 5.8% 0% Non-CABG PLATO Non-CABG TIMI CABG PLATO CABG TIMI Total PLATO major bleeding: 11.6% Ticagrelor vs. 11.2% Clopidogrel; P=.43 Total TIMI major bleeding: 7.9% Ticagrelor vs. 7.7% Clopidogrel; P=.57 Wallentin L, et al. N Engl J Med
33 PLATO Trial Other Adverse Effects All Patients Ticagrelor (N=9,325) Clopidogrel (N=9,186) P-value Dyspnea, % Any With D/C of study treatment <.001 <.001 Ventricular pauses, % First Week 3 seconds 5 seconds At 30 days 3 seconds 5 seconds Wallentin L, et al. N Engl J Med
34 Summary of P2Y 12 Inhibitors Clopidogrel Prasugrel Ticagrelor Class Thienopyridine Thienopyridine Triazolopyrimidine Reversibility Irreversible Irreversible Reversible Activation Prodrug, limited by metabolism Prodrug, not limited by metabolism Active drug Onset of effect 2-4 hr 30 min 30 min Duration of effect 3-10 days 5-10 days 3-4 days Withdrawal before major elective surgery Contraindications/ Caveats 5 days 7 days 5 days 600 mg loading dose (not FDA approved) provides faster, greater, and more reliable platelet inhibition CYP2C19 *2 or *3 alleles are poor metabolizers and have reduced antiplatelet effects Contraindicated in patients with hx CVA/TIA Generally not recommended in patients age >75 years (bleeding risk) Increased bleeding risk if body weight <60 kg *clarithromycin, ketoconazole, indinavir, itraconazole, etc. **rifampin, carbamazepine, dexamethasone, phenytoin, phenobarbital Concomitant ASA dose should be <100 mg Contraindicated if severe hepatic impairment Avoid use with strong CYP3A inhibitors* or CYP3A inducers** Based in part from Hamm CW, et al. Eur Heart J. 2011, as well as drug PIs and study protocols.
35 What is the optimal duration of DAPT? Should DAPT duration be extended?
36 MACE, % Randomized Trials: Primary Endpoint HR=0.98 (95% CI ) P= HR= 1.14 (95% CI ) P= EXCELLENT DES-LATE PRODIGY 12 vs. 6 mo N=1,443 HR= 0.67 (95% CI) P= vs. 12 mo N=2, vs. 6 mo N=1,970 Long Short Park SJ, et al. N Engl J Med. 2010; Gown HC, et al. Circulation. 2012; Valgimigli M, et al. Circulation. 2012; Kim B-K, et al. J Am Coll Cardiol
37 Major Bleeding, % Randomized Trials: Bleeding HR=0.46 (95% CI ) P= HR=0.50 (95% CI ) P= EXCELLENT DES-LATE PRODIGY 12 vs. 6 mo N=1,443 HR=0.67 (95% CI) P= vs. 12 mo N=2, vs. 6 mo N=1,970 Long Short Park SJ, et al. N Engl J Med. 2010; Gown HC, et al. Circulation. 2012; Valgimigli M, et al. Circulation. 2012; Kim B-K, et al. J Am Coll Cardiol
38 Pooled RESOLUTE Timing of Permanent Discontinuation and ST through 1 Year Subsequent Stent Thrombosis (ARC Def/Prob) (%) Patients who permanently discontinued DAPT after 1-month show a low number of stent thrombosis events out to 1 year in this larger patient population. 10.0% 8.0% 6.0% Timing of Permanently Discontinued DAPT and ST Through 1 Year 5.05% 4.0% 2.0% 0.0% 0.72% Not Permanently Discontinued Permanently Discontinued 0-1 Months 0.00% Permanently Discontinued 1-12 Months # of pts at risk at baseline # of events Bhatt DL, et al. Presented at TCT
39 DAPT Study 30 vs. 12 months of DAPT (clopidogrel or prasugrel + ASA) in patients post DES placement 9961 patients enrolled Co-primary efficacy endpoint 1% ARR in stent thrombosis (P<.001) 2% ARR in MACE (P<.001) Safety 0.9% increase in severe/moderate bleeding (P=.05) All-cause mortality higher in DAPT group (2% vs. 1.5%) Mauri L, et al. N Engl J Med
40 Cumulative Incidence (%) DAPT Study Co-Primary Effectiveness End Points and Components: Months 5.9% 6% <0.001 < % 4.3% 4.1% 4% 3% <0.001 < % 1.4% 1.2% % 2.1% 1.5% % 0% 0.4% 0.3% 0.1% 0.1% 0.5% 0.7% 0.3% 0.2% Thienopyridine (N=5020) Placebo (N=4941) Mauri L, et al. N Engl J Med
41 Cumulative Incidence (%) DAPT Study Primary Safety End Point (Moderate or Severe Bleeding): Months 3.5% < % % < % 2.5% 2.6% 2.0% 1.5% 1.0% 0.5% 1.6% % 1.0% % 0.6% 1.5% 1.5% % Moderate or Severe 0.1% 0.1% Moderate Severe BARC Type 2 BARC Type 3 BARC Type 5 Thienopyridine (N=4710) Placebo (N=4649) Mauri L, et al. N Engl J Med
42 CV Death, MI, or Stroke (%) PEGASUS-TIMI 54: Primary Endpoint (composite of CV death, MI, or stroke) N = 21,162 Median follow-up 33 months Placebo (9.0%) Ticagrelor 90 (7.8%) Ticagrelor 60 (7.8%) Months from Randomization Ticagrelor 90 mg HR 0.85 (95% CI ) P=.008 Ticagrelor 60 mg HR 0.84 (95% CI ) P= Bonaca MP, et al. N Engl J Med
43 3-Year KM Event Rate (%) PEGASUS-TIMI 54: Bleeding 5 Ticag 90: HR 2.69 ( ) Ticag 60: HR 2.32 ( ) P< P< Ticagrelor 90 mg Ticagrelor 60 mg Placebo P=NS P=NS P=NS TIMI Major TIMI Minor Fatal bleeding or ICH ICH Fatal Bleeding Based on PEGASUS data ticagrelor 60 mg twice daily was approved for use after one year following ACS 60 mg twice daily was as effective as 90 mg twice daily and associated with less bleeding Bonaca MP, et al. N Engl J Med
44 Summary of DAPT Duration Guidelines generally recommend 1 year post ACS Subgroup trial data suggest longer duration in ACS patients, especially if at higher ongoing risk More recent second generation DES trials suggest shorter is OK, but low risk populations were studied
45 General Plan of Outpatient Care for Patients with NSTE-ACS I IIa IIb III Post-hospital systems of care designed to prevent hospital readmissions should be used to facilitate the transition to effective, coordinated outpatient care for all patients with NSTE-ACS. I I IIa IIb III IIa IIb III An evidence-based plan of care that promotes medication adherence, timely follow-up, appropriate dietary and physical activities, and compliance with secondary prevention should be provided to patients with NSTE-ACS. Annual influenza vaccination for all patients. Amsterdam EA, et al. Circulation
46 Triple Therapy Patients on chronic oral anticoagulation therapy (OAC) with CAD are 7x more likely to receive concomitant antiplatelet therapy Addition of single antiplatelet therapy to OAC increases risk of major bleeding by ~40-60% or more Addition of dual antiplatelet therapy to OAC increases risk of major bleeding by ~ % Meta-analysis of triple therapy found risk of major bleeding at 2.2% at 1 month and 4-12% at one year Majority of studies evaluated primarily warfarin Johnson SG. Chest. 2007; Dentali F. Arch Intern Med. 2007; Hansen ML. Arch Intern Med. 2010; Dans A. Circulation. 2012; Faxon DP. Circ Cardiovasc Interv. 2011; Paikin JS. Circulation
47 WOEST (What is the Optimal Antiplatelet and Anticoagulant Therapy in Patients with Oral Anticoagulation and Coronary Stenting) Dual Therapy (warfarin + clopidogrel) Triple Therapy (warfarin + clopidogrel + aspirin) P Value All TIMI Bleeding 19.5% 44.9% <.001 TIMI Major Bleeding 3.3% 5.8% Composite Efficacy* 11.3% 17.7%.025 Death 2.6% 6.4%.027 Stent thrombosis 1.5% 3.2%.165 *Composite Efficacy=death, MI, TVR, CVA, stent thrombosis Dewilde W, Berg JT. Am Heart J
48 Triple Therapy: Summary Triple therapy greatly increases risk, use for shortest duration Consider lower range in INR WOEST had weaknesses Small trial so findings need confirmed Exceptionally high bleeding rates in triple therapy and dual Preferential use of low-dose ASA, in all patients and definitely in those with ticagrelor Use of BMS over DES in high-risk patients Use of clopidogrel, as well as the addition of PPI therapy in highest risk of bleeding
49 Secondary Prevention * Recommendations COR LOE Lipid management with lifestyle modification and lipid-lowering therapy Lifestyle modification I B Statin therapy mod/high intensity I A Beta-blocker therapy For 3 y in pts with normal LVF All pts with EF <40, HF, prior MI I B A RAAS blocker therapy ACEI if HTN, DM, EF <40, CKD Use ARBs if intolerant of ACEIs I A Blood pressure control (with a blood pressure goal of <140/90 mm Hg) Lifestyle modification I B Pharmacotherapy I A Diabetes management (eg, lifestyle modification and pharmacotherapy) coordinated with the patient s primary care physician and/or endocrinologist. I C Complete smoking cessation I A In addition, referral to a cardiac rehabilitation program (IB). *Comprehensive secondary prevention recommendations in the ACC/AHA Secondary Prevention and Risk Reduction 2011 and 2013 Updates, and 2012 SIHD Guidelines. LVF=Left Ventricular Function; EF=Ejection Fraction; CKD=Chronic Kidney Disease; ARB=Angiotensin Receptor Blocker; ACEI=Angiotensin-Converting Enzyme Inhibitor; HTN=Hypertension; RAAS=Renin- Angiotensin-Aldosterone System Smith SC, et al. Circulation. 2011; Stone NJ, et al. J Am Coll Cardiol. 2014; Fihn SD, et al. J Am Coll Cardiol
50 Why is Adherence Important?
51 Resistance to Antiplatelet Therapy Mechanism of Non-adherence Genetic Adverse effects Complex Regimens Environment Nonadherence Expense Uneducated Priorities Unspecified (~30%) Self-reported moderate to low adherence =? % ALMOST 30% Kolandaivelu K, Bhatt DL. Nat Rev Cardiol. 2010; Mathews R, et al. Circ Cardiovasc Qual Outcomes
52 Adherence as a Problem Approximately 70% of all Americans are taking one medication Prescriptions never filled 20-30% Of those filled, 50% are not taken correctly Cost >$100 Billion in avoidable healthcare costs This is not just a problem in cardiology Zhong W, et al. Mayo Clinic Proceedings
53 Mortality (%) at 12 months Importance of Dual Antiplatelet Therapy Adherence % Continued 7.5% Discontinued Hazard Ratio: % CI: ; P=.02 Spertus JA, et al. Circulation
54 Early Medication Nonadherence After Acute Myocardial Infarction Nonadherence associated with: Lack of clearly communicated instructions Depression Lower education level Financial hardship Immigrant status Patients more likely to be adherent if: Follow-up appointments scheduled prior to discharge Provider explain potential side effects of their medications. Mathews R, et al. Circ Cardiovasc Qual Outcomes. 2015; Czarny MJ, et al. Clin Cardiol
55 Patient Barriers to Adherence Patient perception of illness Health literacy levels-reading the direction on the bottles Insurance coverage or cost of medication Social support Polypharmacy Medication availability Kuntz JL, et al. Patient Education and Counseling
56 Prescriber Barriers Patient/Clinician Relationship Trust Ability to discuss missed mediations Clinician not educating patient about disease process Regimens not perceived by the patient as being safe, effective and necessary, due to lack of communication Imprecise instructions Changes in ordering policy 90-day supply Mail order Mantri P. Practice Nurse
57 Clinician-Patient Discord: Differences in Perspectives in Post-MI Patients after Drug-Eluting Stent Placed Patients who discontinued antiplatelet drug: Unaware they should be taking the drug and didn t know for how long I was just taking it because they were telling me to Patient who continued drug: Could explain the purpose and benefit could relate to it keeps the pipes open so things won t stick Clinicians mentioned cost as the greatest perceived barrier even in patients with insurance Garavalia L, et al. Eur J Cardiovasc Nurs
58 Shared Decision Making Engaging the patient in prescribing decisions by communicating why a medication is indicated, its risks and benefits, and the likely impact on the patient s health Patient Values guide care Preferences Needs Values
59 Patient Centered Medication Management Framework Shared decision-making Methods to enhance effective prescribing System for eliciting and acting on patient feedback and treatment goal Support for medication-taking behavior Kuntz JL, et al. Patient Education and Counseling
60 Medication-Taking Behavior Use accessible, understandable and useful tools Enhance accurate medication-taking Provide systems and resources in obtaining medications in a timely manner Offer options to help taking medications at home
61 Strategies to Improve Adherence Patient education supplemental coaching, motivational approaches or social support Ability to obtain medication Verify that obtained medication with follow up phone call Verify at follow up Kuntz JL, et al. Patient Education and Counseling
62 ADHERENCE MATTERS: Impact of Adherence to Evidence-based Therapies on 6-mo Survival in the GRACE Registry Cohort* NUMBER OF THERAPIES (vs. 0 or 1 therapy) OR (95% CI) 2 therapies 3 therapies 4 therapies 5 therapies 6 therapies 7 therapies 8 therapies 0.80 ( ) 0.74 ( ) 0.59 ( ) 0.51 ( ) 0.40 ( ) 0.27 ( ) 0.31 ( ) OR = odds ratio *Registry of patients with ACS OR Chew DP, et al. Heart
63 Summary: Early Diagnosis, Risk Stratification, Strategy Selection, and Appropriate Antithrombotic and Other Guideline- Directed Medical Therapy followed by Outpatient Prevention Measures Make a Difference in ACS (and Stable IHD) Outcomes!
Optimizing Oral Antiplatelet Therapy: Using the Guidelines to Direct Agent Selection Thomas M. Maddox, MD, MSc, FACC, FAHA
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