STEMI Case

MI GOING TO BE OKAY?

June 18, 2015

Cam Roessner, BSc(Pharm), PharmD Student

ST-ELEVATION MYOCARDIAL INFARCTION IN A PREVIOUSLY HEALTHY INDIVIDUAL

2

LEARNING OBJECTIVES

Briefly describe the pathophysiology, clinical presentation and treatment of acute ST-Elevation Myocardial Infarction (STEMI)

Outline post-MI risk assessment, prognostic variables, and goals of treatment

Understand the evidence, rationale, and impact of the common treatment options used for post-MI risk reduction

3

PRESENTATION OUTLINE

Introduction to Patient Case

ST-Elevation Myocardial Infarction Background

Goals of Therapy & Drug Therapy Problems DRP #1 – Antiplatelet

DRP #2 – Beta-Blockers

DRP #3 – ACE Inhibitions

DRP #4 – Statins

Case Resolution and Monitoring

Summary

References

4

PATIENT CASE

History of Presenting Illness 55 year old ♂ RM developed right sided chest pain at

20:45 with accompanying diaphoresis, nausea, and vomiting

EMS called and at arrival patient experienced VF arrest requiring 2 min of CPR and cardioversion × 1

Past Medical History Unremarkable

Social and Family History Smoker

No known family history of coronary artery disease

Medications None

Past Medications None

5

INVESTIGATIONS

System Relevant Labs, Vital Signs, and Physical Examination Findings

CNS A & O × 3, GCS 15/15

CVS BP 140/87mmHgHR 87JVP 2cm ASAnormal S1/S2Ø murmurs

Troponin-T 1. 244ng/L (23:10)2. 3062ng/L

(06:40)

Lipids• Total Cholesterol: 5.21mmol/L• HDL Cholesterol: 1.75mmol/L• LDL Cholesterol: 2.88mmol/L

Respiratory RR 20, 96% on room air CXR – atelectasis, Ø consolidation

GI Nausea and vomiting, soft non-tender abdomen

Renal Scr 81umol/L, CrCl = 137mL/min, eGFR 94mL/min

Endocrine HbA1C 5.7%, BG 9.5mmol/L, FPG 6.9mmol/L

Hematology & Electrolytes

WBC 12.6 10E9/L (4.0 – 11.0 10E9/L)Neutrophils 9.4 10E9/L (2.0 – 8.0 10E9/L)

K+ 3.1mmol/LCa2+ 2.00mmol/L

Phosphate 0.64mmol/L

6

CARDIAC DIAGNOSTICS

ECG ECHO

1. Sinus bradycardia2. Normal valves and left ventricle size3. Distal anterior septal hypokinesis

(possible akinesis)4. Preserved function (EF = 60%)

7

PATIENT DIAGNOSIS & ACUTE TREATMENT

Anterolateral ST-Elevation Myocardial Infarction Urgent revascularization → Sent to the “cath lab”

Acute Treatment: Acetylsalicylic acid 320mg

Ticagrelor 180mg (loading dose)

Unfractionated heparin 4000 units IV bolus followed by 12 units/kg/hr

Primary percutaneous coronary intervention (PCI) - No thrombolysis necessary

Plan for beta blocker, angiotensin-converting enzyme inhibitor, and statin

8

CARDIAC ANGIOGRAM

Before After

9

NEXT STEPS

PCI has been performed and a Drug-Eluding Stent (DES) has been placed

Patient has been transferred to RGH CCU for follow-up care

What now? What is the patient’s prognosis and risk of recurrent MI or complications?

What can we do to reduce the risk?

How much can we reduce the risk?

10

ST-ELEVATION MYOCARDIAL INFARCTIONA BRIEF OVERVIEW

Scirica, B. M., & Morrow, D. A. (2015) 11

DEFINITION OF ACUTE MYOCARDIAL INFARCTION (AMI)

Detection of a rise and/or fall in cardiac biomarker values with at least one value above the 99th percentile of the upper reference limit and with at least one of the following: • Symptoms of ischemia

• New or presumed new significant ST-segment T wave (ST-T) changes or new LBBB

• Development of pathologic Q waves on the ECG

• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

• Identification of an intracoronary thrombus by angiography or autopsy


PATHOPHYSIOLOGY

Atherosclerosis A slow process, beginning early in life and

progressing silently over decades

Major risk factors accelerating atherosclerosis include high plasma LDL-C, low plasma HDL-C, cigarette smoking, hypertension, chronic kidney disease, and diabetes mellitus

Collections of subintimal fat, smooth muscle cells, fibroblasts, and intercellular matrix reduce luminal diameter

Narrowing of the luminal diameter by >70% affects myocardial perfusion during exertion (angina pectoris) and narrowing ≥80% has the potential to affect myocardial perfusion at rest


PATHOPHYSIOLOGY

Acute Coronary Syndromes Plaque disruption exposes substances that

promote platelet activation and aggregation, thrombin generation, and thrombin formation leading to either partial occlusion (UA/NSTEMI) or total occlusion (STEMI) of the infarct-related artery

A resulting myocardial oxygen supply-demand mismatch precipitates ischemic symptoms, and when severe or prolonged, leads to myocardial necrosis of the supplied area and release of ischemic biomarkers (troponins)

Ventricular damage and loss of viable tissue leads to altered conduction patterns on ECG and associated complications


CLINICAL PRESENTATION

Pain Quality – Constricting, crushing, oppressing, or compressing pain, often described as being

“heavy” or “squeezing”

Location – Retrosternal with possible radiation to the left arm/hand (tingling sensation), shoulders, neck, and/or jaw

Duration – As long as there is ongoing ischemia (infarcted or re-perfused regions unlikely to cause pain)

Other Nausea and vomiting

Weakness, dizziness, palpitations, diaphoresis

Sense of impending doom

Levine sign (clutching chest)


ELECTROCARDIOGRAM

Electrocardiogram (ECG/EKG) Most important diagnostic tool for patients with ST-Elevation MI

Identification of the occluded artery is possible via ECG as well as the success of reperfusion

Extent of ST elevation, the location of infarct, and the QRS duration correlate with a risk for adverse outcomes

Definition of STEMI on ECG New ST elevation at the J point in two contiguous leads with the following cut points:

≥0.1 mV in all leads (except V2-V3)

In leads V2-V3 the following cut points apply:

≥0.2 mV in men ≥40 years

≥0.25 mV in men <40 years

≥0.15 mV in women


BIOMARKERS OF CARDIAC DAMAGE

Cardiac-Specific Troponins Troponins (T, I) are released from damaged

myocardial cells An abnormally increased level is a value

exceeding that of 99% of a reference control group

Plasma levels begin to rise 3 hours after the onset of chest pain and remain elevated for up to 10-14 days Advantageous for late diagnosis but at a

disadvantage for detecting re-infarction Measurements are taken serially (at initial

evaluation and 3-8 hours later) STEMI – Awaiting biomarker results should not

delay reperfusion treatment – ECG results are sufficient


CLASSIFYING ISCHEMIA

Multiple disease processes result in myocardial ischemia and infarction

1. Type 1 – Spontaneous MI (thrombus)

2. Type 11 – Ischemic imbalance MI (no thrombus formation)

Scirica, B. M., & Morrow, D. A. (2015). 18

CLASSIFYING ISCHEMIA

Multiple disease processes result in myocardial ischemia and infarction

1. Type 1 – Spontaneous MI (thrombus)

2. Type 11 – Ischemic imbalance MI (no thrombus formation)


CONSEQUENCES OF ISCHEMIA

Myocardial Infarction (“wave front of necrosis”)

Reperfusion (restoration of “stunned” myocardium)

Mauri, L., & Bhatt, D. L. (2015), Mega, J. L., & Morrow, D. A. (2015) 20

ACUTE TREATMENT – REPERFUSION

Reperfusion Every 30-minutes that elapse from symptom onset until PCI increases the relative risk for 1-year

mortality by 8%

Early reperfusion shortens the duration of coronary occlusion, minimizes the risk of left ventricular dysfunction, and reduces the probability of pump failure or fatal arrhythmias

PCI vs. Fibrinolysis PCI – Generally the preferred reperfusion strategy and ideally is performed within 90 minutes of

first medical contact but is still beneficial within 12 hours or 12-24 hours in those with ongoing ischemia or shock

Fibrinolysis – If the delay from first medical contact to PCI is anticipated to be >120 minutes, a fibrinolytic (i.e. tenectoplase) is indicated for the treatment of STEMI within 12 hours of symptom onset (no benefit >12 hours)

Mega, J. L., & Morrow, D. A. (2015) 21

ACUTE TREATMENT – REPERFUSION

Mega, J. L., & Morrow, D. A. (2015) 22

ACUTE TREATMENT – PHARMACOLOGICAL

Antiplatelet Aspirin reduces mortality by 20-25% if given within 24 hours (additive to benefits of fibrinolysis)

Regardless of reperfusion strategy, the addition of a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) further improves CV mortality outcomes

Antithrombotic Unfractionated heparin (or bivalrudin) preferred in patients undergoing PCI

If fibrinolysis is given, or in patients treated without reperfusion, enoxaparin or fondaparinux are generally superior to UFH

Mega, J. L., & Morrow, D. A. (2015) 23


The composition of the thrombus provides rationale for the acute pharmacological treatment of ACS

“White clot” consists of platelets

“Red clot” consists of red blood cells and interlinked fibrin

Mega, J. L., & Morrow, D. A. (2015) 24


Beta Blockers Beta blockers reduce myocardial oxygen consumption and improve chest pain – general the β1 –

selective or “cardio-selective” (metoprolol, bisoprolol, carvedilol, atenolol) agents are chosen

Beta blockers have beneficial acute and long-term effects in ACS (more on that later)

Nitrates Relief of acute pain and recurrent angina but no effect on mortality in the reperfusion era

Morphine Typically the analgesic of choice for acute ischemic pain

Circulation, 102(17), 2031-2037 25

RISK STRATIFICATION – TIMI STEMI

Killip Class

I. Absent lung crackles and absent S3

II. Crackles in lower half of lung fields and possible S3

III. Crackles more than halfway up the lung fields and frequent pulmonary edema

IV. Cardiogenic shock

GRACE score can also be used to predict 6-month mortality

Mauri, L., & Bhatt, D. L. (2015), Mega, J. L., & Morrow, D. A. (2015) 26

PROGNOSIS

Left ventricular failure Most important predictor of mortality after STEMI

Our patient:

TIMI risk = 1 (anterior MI) which carries 0.3% risk of death at 30 days

GRACE risk is 3% for death OR MI at 6 months

Prompt PCI helped reduce the extent of damage, however hypokinesis and akinesis was still apparent on echocardiography

Stent thrombosis – Rate of 1% within the first year and increases 0.2-0.5% per year after DES implantation

Clinical restenosis – Occurs in 10-15% of BMS and 3-5% of DES within 1 year

Atherosclerosis – Plaques that exist separately from the culprit lesion also at risk of rupture and occlusion

What options are there for secondary prevention?

27

DRUG THERAPY PROBLEMSSECONDARY PREVENTION

28

DRUG THERAPY PROBLEMS

•DTP #1 – Patient RM requires antiplatelet agents for the prevention of stent thrombosis

•DTP #2 – Patient RM will benefit from post-ACS use of a beta blocker

•DTP #3 – Patient RM requires an ACE inhibitor for the reduction of ventricular remodeling and improved hemodynamics

•DTP #4 – Patient RM requires a statin for atherosclerotic secondary prevention after ACS

Journal of the American College of Cardiology, 61(4), e78-140 29

DRUG THERAPY PROBLEM #1

• Patient RM requires antiplatelet agents for the prevention of stent thrombosis• Patient received an everolimus drug-eluting stent (DES)

• Regardless of stent type, aspirin 81mg daily should be continued indefinitely

• Dual antiplatelet therapy with the addition of an Adenosine Diphosphate (ADP) Receptor Antagonist is suggested for at least one year after DES

• Which one do we use? How long?

The New England Journal of Medicine, 361(11), 1045-1057 30

TICAGRELOR VERSUS CLOPIDOGREL IN PATIENTS WITH ACUTE CORONARY SYNDROMESPLATELET INHIBITION AND PATIENT OUTCOMES (PLATO) – WALLENTIN ET AL.

Population – 18,624 patients with UA/NSTEMI or STEMI (38% of patients) The definition for STEMI included the intention to perform primary PCI

TIMI risk – 45% of patients were ≥3 and 20% were ≥5 (higher than ours)

DES – 19% received ≥1 drug-eluting stent

Exclusion – Fibrinolysis within 24 hours, indication for anticoagulants, concomitant CYP 3A4 inhibitors

Intervention – ticareglor 180mg ×1 then 90mg daily (n=9333) or clopidogrel 300mg ×1 then 75mg daily (n=9291) All received ASA 75-100mg daily

Median duration of dual antiplatelet therapy (DAPT) was 277 days and overall adherence was 83%

Follow-up – Completed up to 12 months with only 5 patients lost to follow-up


TICAGRELOR VERSUS CLOPIDOGREL IN PATIENTS WITH ACUTE CORONARY SYNDROMESPLATELET INHIBITION AND PATIENT OUTCOMES (PLATO) – WALLENTIN ET AL.

Outcomes Composite of death from vascular causes, MI, or stroke

Ticagrelor vs. clopidogrel – 9.8% vs 11.7%, HR 0.84 (0.77–0.92)

NNT = 59 (for 1 year)

Stent thrombosis (definite)

Ticagrelor vs. clopidogrel – 1.3% vs 1.9%, HR 0.67 (0.50–0.91)

NNT = 159

No differences in major bleeding but increased dyspnea leading to discontinuation of ticagrelor

Bottom-Line Ticagrelor superior to clopidogrel as part of ACS antiplatelet

therapy

Guidelines – Minimum 1 year treatment DAPT with DES

About 1700 patients received a DES in PLATO with an overall median treatment of 277 days – maybe longer in those with DES implantation?

Is longer better?


LONG-TERM USE OF TICAGRELOR IN PATIENTS WITH PRIOR MYOCARDIAL INFARCTION(PEGASUS-TIMI 54) – BONACA ET AL.

Population – 21,162 patients with UA/NSTEMI or STEMI 1-3 years previously A median of 1.7 years elapsed from MI to randomization

54% of patients suffered an ST-Elevation MI and

17% current smokers

83% had a history of PCI and 96.5% involved stenting - % of patients with a DES is unknown (approx. 10-30% of stents are bare metal)

Exclusion – Planned use of P2Y12 inhibitor or anticoagulant, history of stroke/ICH, GI bleed < 6 months

Intervention – ticagrelor 90mg bid (n=7050), ticagrelor 60mg bid (n=7045) or placebo (n=7067) All (99.9%) were on ASA 75-100mg at enrollment and continued on it

Most patients (≥80%) in each group were on an ACE inhibitor, Beta-blocker, and statin

Follow-up – Median duration was 33 months About 30% of patients discontinued ticagrelor (mostly due to ADRs) while 20% discontinued placebo


LONG-TERM USE OF TICAGRELOR IN PATIENTS WITH PRIOR MYOCARDIAL INFARCTION(PEGASUS-TIMI 54) – BONACA ET AL.

Outcomes Composite of cardiovascular death, MI, or stroke

ticagrelor 90mg vs ticagrelor 60mg vs placebo – 7.9% vs 7.8% vs 9%

HR of 0.85 (0.75-0.96) and 0.84 (0.74-0.95) for 90mg and 60mg, respectively

ticagrelor 90mg NNT = 84 (for 36 months)

ticagrelor 60mg NNT = 79

Increased major bleeding, minor bleeding, bleeding requiring transfusion and bleeding leading to discontinuation with both doses but no differences in fatal bleeding, nonfatal ICH, or hemorrhagic stroke

Bottom-Line Ticagrelor reduces cardiovascular death and MI when continued as

part of DAPT past 1 year, however at the expense of excess bleeding

Guidelines – DAPT can be continued >1 year depending on bleed risk

Consider the costs and long-term adherence rates – a lot of people discontinued treatment (30%) BUT there was still a benefit when these patients were included in analysis (Intention-To-Treat)

34

PREVENTION OF STENT THROMBOSIS

• Data

• Patient at risk of stent thrombosis and recurrent MI

• Assessment

• Dual antiplatelet therapy with ASA and ticagrelor reduces overall mortality when compared to clopidogrel and reduces risk of cardiovascular death, MI, and stroke when used for greater than 1 year (and up to 36 months)

• Patient is without any precautions or contraindications to treatment (i.e. history of bleed, 3A4 interactions)

• Plan

• ASA 81mg po daily (indefinitely)

• Continue ticagrelor po bid post BMI for a minimum of 1 year

• Reassess benefit vs bleed risk at 1 year



Patient RM will benefit from the continued use of a beta-blocker Antiarrhythmic effects and reduced risk of re-infarction are likely the

reason beta-blockers exhibit a long-term mortality benefit

Long-term (≥ 3 years) or indefinite therapy following acute administration of beta-blockers following an ST-Elevation MI is endorsed by practice guidelines

Not many randomized controlled trials in the “reperfusion era”

How can we interpret the results in the context of contemporary treatment modalities such as PCI?

JACC.Cardiovascular Interventions, 7(6), 592-601 36

ASSOCIATION OF BETA-BLOCKER THERAPY AT DISCHARGE WITH CLINICAL OUTCOMES IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION – YANG ET AL

A retrospective review of a South Korean database of 20,344 patients with ACS from 2005-2010

Population – >18 years of age with STEMI (>1mm in 2 contiguous leads with elevated troponins) who underwent PCI (DES used without restriction)

Exclusion – In-hospital death or missing beta-blocker information (8510 patients were included in final analysis)

Cohorts – Beta-blocker at discharge vs no beta-blocker at discharge Follow-up – Information was available at 1, 6, and 12 months

JACC.Cardiovascular Interventions, 7(6), 592-601 37

ASSOCIATION OF BETA-BLOCKER THERAPY AT DISCHARGE WITH CLINICAL OUTCOMES IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION – YANG ET AL

Outcomes Baseline characteristics differed dramatically with the no beta-blocker

cohort having more serious MI presentation, MI history, and reduced medication use (e.g. previous MI, signs of HF, less RAAS agents)

Information on specific agents, doses, adherence and comorbidities was not available

After propensity matching to account for baseline differences beta-blockers exhibited benefits on: All-cause death – 2.8% vs 4.1%, HR 0.46 (0.27-0.78), NNT = 78 (for 1 year)

Cardiac death – 1.5% vs 2.8%, HR 0.39 (0.19-0.79), NNT = 78


BETA-BLOCKADE

• Data

• Patient is at risk of post-MI complications including arrhythmias and re-infarction

• Assessment

• Practice guidelines support the use of beta-blockers in the acute phase as well as for secondary prevention

• A large observational study suggest mortality benefit – with limitations – in patients with STEMI undergoing PCI (in agreement with their RCT proven efficacy in the reperfusion era)

• Potential benefits outweigh risks

• Plan

• Metoprolol 25mg po bid

• Titrated as tolerated on a weekly basis



• Patient RM requires an ACE inhibitor for the reduction of ventricular remodeling and improved hemodynamics• Guidelines prefer the use in ACE inhibitors in all patients with STEMI with

anterior location, heart failure, or ejection fraction ≤ 40% (left ventricular dysfunction)

• In patients without these features, a Level of Evidence of A (highest quality recommendation) is still given for the use of ACE inhibitors following STEMI

• Does this mean they’re beneficial even without evidence of left ventricular dysfunction?

Circulation, 97(22), 2202-2212 40

INDICATIONS FOR ACE INHIBITORS IN THE EARLY TREATMENT OF ACUTE MYOCARDIAL INFARCTION – ACE INHIBITOR MYOCARDIAL INFARCTION COLLABORATIVE GROUP

A meta-analysis of 4 randomized trials (n=98946) in which ACE-inhibitor treatment was begun in the acute phase of MI (0-36 hrs from symptom onset)

Population

Interventions – ACE inhibitor (n=49214) vs. open treatment (GISSI-3) or placebo (n=49269) Agents were captopril, enalapril, and lisinopril at standard doses (i.e. lisinopril

10mg daily) Follow-up – Information was available up to 30 days in all studies

Average age of 63 years Killip class 1 - 83% 83% with no history of MI

62% received a fibrinolytic STEMI (≥52000) 37% anterior MI

Circulation, 97(22), 2202-2212 41

INDICATIONS FOR ACE INHIBITORS IN THE EARLY TREATMENT OF ACUTE MYOCARDIAL INFARCTION – ACE INHIBITOR MYOCARDIAL INFARCTION COLLABORATIVE GROUP

Outcomes 30-day mortality

ACE inhibitor vs placebo – 7.11% vs 7.6%, RR 0.93 (0.89 – 0.98)

NNT = 210 (for 30 days)

Patients with anterior MI had greater benefit

Heart failure rates were also reduced in the 30 day period

Renal Dysfunction (increased serum creatinine ≥ 177umol/L)

ACE inhibitor vs placebo – 1.3% vs 0.6%, RR 1.98 (1.73 – 2.26)

NNH = 160

Bottom-Line ACE inhibitor provided a mortality benefit in patients post-MI

regardless of their baseline risk and left ventricular function

Patients with cardiogenic shock and hypotension were excluded and most patients were of lower baseline risk (higher risk may have more to gain?)

The use of other beneficial therapies is unknown (i.e. stent) or not yet introduced into practice (i.e. clopidogrel) but aspirin and beta-blockers were used


RAAS INHIBITION

• Data

• Patient has anterolateral location of infarct and may benefit from RAAS inhibition with an ACE inhibitor

• Assessment

• Practice guidelines support the use of ACE inhibitors regardless of baseline risk

• Although long term benefits are well documented in patients with heart failure and LV dysfunction, there is good evidence to suggest a mortality benefit in all patients with STEMI

• ACE inhibitors have demonstrated a “class effect” in this regard

• Plan

• perindopril 2mg po daily

• Titrated to 4mg daily prior to discharge and as needed based on tolerance

Jama, 292(11), 1365-1367, Journal of the American College of Cardiology, 61(4), e78-140 43


• Patient RM requires a statin for atherosclerotic secondary prevention after ACS

There have been no trials of non-statin lipid lowering in patients following acute coronary syndromes

Statin therapy is beneficial after ACS even in patient with normal baseline LDL-cholesterol levels – perhaps they’re beneficial due to plaque stabilization or anti-inflammatory effects, commonly referred to as “pleiotropic effects”?

How much does high-intensity statin therapy benefit these patients?


INTENSIVE VERSUS MODERATE LIPID LOWERING WITH STATINS AFTER ACUTE CORONARY SYNDROMES (PROVE-IT-TIMI 22) – CANNON ET AL.

Population – Patients with ACS (n=4162) within 10 days STEMI patients made up 34% and 70% of all patients received PCI Average LDL-C was 2.74mmol/L in each group

Exclusion – Expected survival <2 years, other lipid lowering therapies that could not be discontinued, strong CYP 3A4 inhibitor treatment, recent prior PCI or CABG, unexplained CK >3 × ULN

Intervention – Atorvastatin 80mg (n=2099) vs. pravastatin 40mg (n=2063) ASA (93%), ADP antagonist (72%), βB (85%), ACEi (69%), ARB (14%)

Follow-up – 18 to 36 months (average of 24 months)


INTENSIVE VERSUS MODERATE LIPID LOWERING WITH STATINS AFTER ACUTE CORONARY SYNDROMES (PROVE-IT-TIMI 22) – CANNON ET AL.

Outcomes Composite endpoint (death, MI, UA, revascularization, and

stroke)

Atorvastatin 80mg vs pravastatin 40mg – 22.4% vs 26.3%, RR 0.84 (0.74 –0.95)

NNT = 19 (2 years treatment)

No significant differences in rates of myalgias leading to discontinuation, however ALT elevations occurred more often in the atorvastatin arm

Bottom-Line High-intensity statin therapy with atorvastatin 80mg daily

resulted in reduced cardiovascular events after 2 years of treatment

Benefit of high dose atorvastatin emerged at 30 days and was significant at 180 days

Lower baseline LDL-C level and previous statin therapy resulted in a less prominent benefit – still supports the LDL hypothesis that lower is better

46

HIGH-INTENSITY STATIN

• Data

• Patient has is now considered high-risk for ischemic CVD due to MI and PCI

• Measured LDL-C is 2.88mmol/L

• Assessment

• Practice guidelines support targeting lower LDL-C levels of <2.00mmol/L in high-risk patients and high-intensity statin therapy in all patients with STEMI

• PROVE-IT demonstrated a CV risk reduction benefit with high-dose atorvastatin after ACS

• Patients with higher baseline LDL-C levels and greater reductions tended to do better which supports the LDL hypothesis

• Plan

• Atorvastatin 80mg po daily

• Continued on an indefinite basis with goal of LDL-C <2.00mmol/LJOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 61(4), E78-140, THE CANADIAN JOURNAL OF CARDIOLOGY, 29(2), 151-167

47

CASE RESOLUTION

Patient was sent home after a 5 day, uncomplicated stay

Patient ceased smoking during admission and was determined to quit NRT, counselling, and information provided

Discharge Medications: Aspirin 81mg po daily

Ticagrelor 90mg po bid (reevaluated at 1 year)

Metoprolol 25mg po bid (titrated as tolerated)

Perindopril 4mg po daily (titrated as tolerated)

Atorvastatin 80mg po qhs

48

MONITORING

Scheduled for follow-up with cardiologist 3 weeks post-discharge

Blood work ideally every 1, 3, 6 months

Parameter

ASA / Ticagrelor Metoprolol Perindopril Atorvastatin

Efficacy Absence of recurrent CV event

Absence of complications/CV event

HR, BP


BP


LDL-C, TC, HDL-C

Safety Acute bleed (CBC, Hbg, GI bleed, blood in urine, etc.)

Minor bleeding or bruising

Surgical procedures Dyspnea (ticagrelor) CYP 3A4 Intx (ticagrelor)

Fatigue, exercise intolerance

Abnormal dreams Sexual

dysfunction Bradycardia AV block

Renal function (Scr, CrCl)

Potassium Orthostatic

hypotension Falls

Myalgia Diarrhea ALT/AST CK (baseline) CYP 3A4 Intx

49

SUMMARY

Prompt identification of and treatment of STEMI is important for initial reperfusion and implementation of therapies targeted towards the mechanisms of ischemia during the acute phase

A similar combination of agents are used as part of a long-term treatment strategy in the secondary prevention of recurrent MI, arrhythmias, cardiovascular events, and death

An understanding of these medications’ benefits, combined with the ability to identify and communicate with patients who will profit from their use will lead to improved patient outcomes

50

QUESTIONS?

51

REFERENCES

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