Lecture 47 Acute Coronary Syndrome Chua CLINICAL PRESENTATION:

Chest pain, chest pressure, chest tightness (radiating to jaw and back)

Diaphoresis

Shortness of breath

Lightheadedness, nausea, vomiting

ASSESSMENT AND DIAGNOSIS:

Do STAT ECG

Draw laboratory blood work (cardiac biomarkers)

Give initial routine measures: MONA Drug Dose Efficacy Toxicity

Morphine Class IIb

2-8 mg IV q5-15 mins PRN Reduction in chest pain (also in anxiety and pulmonary edema)

Hypotension

Known hypersensitivity

Rash, pruritis

Decreased respiration

Decreased LOC

Oxygen Class IB

If experiencing clinical significant hypoxia (O2stat <90%), HF, or dyspnea

2-4 L/min by nasal cannula

Can increase rate or change to face mask if needed

Reduction in hypoxia

Caution with COPD and CO2 retention

Possible concerns with excessive oxygen

Nitroglycerin Class IC

0.4 mg SL q 5 min up to 3 doses as BP allows

If after 3 SL doses, use IV beginning at 10 mcg/min titrate to desired effect

Reduction in chest pain (anti-anginal / anti-ischemic)

Avoid in suspected RV infarction

Hypotension

Headache

Avoid with SBP < 90 mmHg

Avoid if recent (24-48 h) use of PDE inhibitors

ASA Class IA

162-325 mg on day 1 of ACS and continued indefinitely on a daily base thereafter at a lower dose of 75-162 mg

Mortality reduction Known hypersensitivity

Bleeding

RISK STRATIFICATION:

ECG and cardiac biomarkers help with risk stratification of ACS which ultimately determines rapidity of treatment, and also choices in drug therapy

o ECG abnormalities indicates presence of MI o Cardiac biomarkers of cardiac myocyte death (indicating MI): CK, CKMB, Troponin (T, I, N)

Troponin: most sensitive & specific biomarker for acute MI up to one week (isoforms T and I are specific to myocardium)

Unstable angina Myocardial infarction

NSTEMI STEMI

Chest pain Chest pain Chest pain

Normal ECG

ST depression, T-wave inversion, non-specific ECG changes

ST elevation

Negative cardiac enzymes Elevated cardiac enzymes (troponin) Elevated cardiac enzymes (troponin)

Low risk Intermediate risk High risk

Needs revascularization Requires IMMEDIATE REVASCULARIZATION

Lecture 47 Acute Coronary Syndrome Chua

REVASCULARIZATION OPTIONS OVERVIEW: Description Drug Related Implications Implications for pharmacists

PCI BMS: bare metal (stainless steel) stents

Drug eluting stent (DES) o Stent coated with anti-proliferative drugs

(zotarolimus, everolimus, sirolimus) to prevent restenosis of lesion

DAPT critical after PCI

Bleeding

Adherence to DAPT is paramount

CABG High risk surgery Pain

Infection

Delirium

Post op AF

HF

Bleeding

Pain control

Treat infections

Antipsychotics

Anticoagulation

Treatment of HF

Medical Therapy

No PCI

No CABG

Optimal medical therapy critical after ACS

Bleeding

Ensure optimal medical therapy for medical management of ACS

Modality of revascularization (PCI, CABG, medical therapy) the same between a STEMI and UA/NSTEMI ***

Difference is how fast you revascularize the patient

STEMI is immediate revascularization

STEMI – IMMEDIATE PERFUSION TREATMENT: timings are IDEAL times 1. Primary PCI (Door to Balloon (DB) time < 90 minutes or transfer for PCI < 120 mins)

Immediate transfer from ER to cardiac catheterization lab and activation of cath lab team 2. Fibrinolysis (Door to Needle (DN) time < 30 mins)

Indication: chest pain duration < 12 hours AND ST elevation of > 1 mm on 2 contiguous leads on ECG

Absolute contraindications: o Any prior ICH o Known structural cerebral vascular lesion (ex// arteriovenous malformation) o Known malignant intracranial neoplasm (primary or metastatic) o Ischemic stroke within 3 month (EXCEPT acute ischemic stroke within 4.5 h) o Suspected aortic dissection o Active bleeding or bleeding diathesis (excluding menses) o Significant closed-head or facial trauma within 3 mo o Intracranial or intraspinal surgery within 2 mo o Severe uncontrolled hypertension (unresponsive to emergency therapy) o For streptokinase, prior treatment within the previous 6 mo

Adverse effects: hemorrhage, intracranial hemorrhage

Drugs: Streptokinase, t-PA, r-PA, TNK 2. Urgent CABG: not routinely performed, unless pt is very unstable and other revascuarization options not viable

TREATMENT OF ACS:

Lecture 47 Acute Coronary Syndrome Chua

TREATMENT EFFICACY DURATION MONITORING

DAPT = dual antiplatelet therapy

ASA + clopidogrel

ASA + prasugrel

ASA + ticagrelor

CRITICAL and MANDATORY after coronary stent insertion

Reduces reinfarction, death and stent thrombosis

MORTALITY REDUCTION

PCI o BMS: min 1 month DAPT o DES: min 12 months DAPT

Medical therapy / CABG o Ideally 1 year

After 1-12 month course of DAPT is done, stop clopidogrel/ prasugrel / ticagrelor BUT CONTINUE ASA 81 MG DAILY LIFELONG

Adherence: #1 cause of stent thrombosis is non-compliance o Not taking DAPT after a

BMS/DES has 30x increase in risk of stent thrombosis

Bleeding

Thrombocytopenia

Rash

Anticoagulation:

IV heparin (UFH)

LMWH (enoxaparin)

Factor Xa inhibitors (fondaparinux)

Reduction in chest-pain

Reduces re-infarction

1. Continue anticoagulation until pt receives revascularization

2. 2-8 days if pt receives only medical therapy

DO NOT continue anticoagulation on discharge for ACS (unless there is another indication – LV thrombus, AF, etc)

Bleeding: CBC (platelets, Hg) o UFH: monitor aPPT (target

is 1.5 – 2.5x control aPPT) o Enoxaparin or

fondaparinux: can monitor anti-Xa

Heparin induced thrombocytopenia

Osteoporosis (UFH)

Cardiac catheter thrombosis (fondaparinux)

Beta-blocker:

Metoprolol (IV & PO)

Atenolol (IV and PO)

Acebutolol

Timolol

Propranolol

Decreases and limits size of infarct by decreasing myocardial demand during an acute ACS

Prevent lethal arrhythmias (VF/VT)

Initiated in the first 24 hours in patients with ACS who do not have: o Signs of HF o Evidence of a low output state o Increased risk for cardiogenic

shock o Bradycardia o Other contraindications to oral

beta blockers

Initiate at small doses and up-titrate as tolerated

IV only if there is strong indication (ex// uncontrolled AF)

ACEI/ARB Use of ACEI/ARB during acute phase of ACS decreases afterload, prevents negative cardiac remodelling and HF

Reduces mortality, re-infarction and HF

ACEI administered within first 24 hours to all patients with ACS with: o Anterior location o HF o Ejection fraction ≤ 0.40

ARB given to patients with ACS who have indications for but are intolerant of ACEI

DO NOT USE IV ACEI in ACS – increases mortality

Statin/lipid lowering therapy:

Atorva 80 mg daily

Rosuva 10-40 mg daily

High-intensity statin therapy should be initiated or continued in all patients with ACS and no contraindications to its use

± ezetimibe

MRA (aldosterone antagonist)

Eplerenone

Spironolactone

All patients with ACS and no contraindications who are already receiving an ACEI and beta blocker AND who have an EF ≤ 0.40 and either symptomatic HF or DM

Blood pressure

SCr

Potassium

Gynecomastia (especially with spironolactone)

WHAT DO I NEED TO DO AS A PHARMACIST POST ACS?

STOP SMOKING

Lifestyle changes (diet, exercise)

TAKE YOUR MEDICATION

Manage your cardiac risk factors (ex// HTN, DM, obesity)

Educate patient about benefits of drug therapy and how to prevent recurrent ACS

Drug-drug interactions?

Is patient on optimal drug therapies for ACS?

Is patient tolerating/experiencing side effects of drug therapies?