ST-Elevation Myocardial Infarction

Tauhid Ahmed Bhuiyan, PharmD
PGY-1 Resident
King Faisal Specialist and Research Center (KFSH&RC)
ST-ELEVATION MYOCARDIAL
INFARCTION (STEMI): A TOPIC REVIEW
AND CASE PRESENTATION
King Faisal Specialist Hospital and Research Center (KFSHRC) is accredited by the Accreditation Council for Pharmacy Education as a
provider of continuing pharmacy education. (UAN# 0833-0000-14-064-L01-P, 0833-0000-14-064-L01-T)

OBJECTIVES
• Provide an overview of STEMI in terms of epidemiology, etiology,
pathophysiology, and risk factors
• Identify key diagnostic criteria to diagnose STEMI
• Review current guideline directed standard of care in the
management of STEMI
• Analyze a patient case related to the topic
I do not have financial relationship and no actual or potential conflict of interest in relation to this activity

BACKGROUND
• STEMI:
– An acute coronary event that results in complete occlusion of the coronary
artery Myocardial Ischemia
• Myocardial infarction (MI) is the manifestation of prolonged ischemic event
• Ischemia is associated with
– Persistent ST segment elevation on electrocardiography (ECG)
– Release of cardiac biomarkers of myocardial necrosis
• Emergency requiring immediate medical intervention

SPECTRUM OF ACUTE CORONARY
SYNDROME
Fox K. Heart 2004; 90:698-706

EPIDEMIOLOGY
• Estimated annual incidence of myocardial infarction (MI) in the
United States:
– New: 565 K
– Repeat: 300 K
• STEMI accounts for 30%-40%
– ~20%-30% patients die before reaching to the hospital
– In-hospital and 30-day mortality rates have been estimated to be 8.8% and
18.4%, respectively
O’Gara PT et al. Circulation; 2013; 127

KINGDOM OF SAUDI ARABIA
• Osman et al. conducted a prospective observational trial of 205
patients at Prince Sultan Cardiac Center in Riyadh, Saudi Arabia
– STEMI accounted for 19.5% of diagnosis at admission and has the highest
direct medical cost (58K SAR/patient)
• Gulf RACE – 2 study by AlHabib et al:
– 9 month prospective, multicenter study
– Evaluated data on patients with acute coronary syndromes and their long
term outcomes in the Arabian Gulf countries
– STEMI accounted for 45.6% of the cases (N=7930)
Osman AM et al. Saudi Med J; 2011; 32(12):1279-84
Alhabib KF et al. Ann Saudi Med; 2012; 32(2):9-18

ETIOLOGY
• Most common:
 Atherosclerotic disease
• Less common:
 Coronary embolism
 Coronary vasospasm (e.g. prinzmetal’s angina)
 Drug induced (e.g. cocaine, chemotherapeutic agents)
 Spontaneous coronary dissection or aortic dissection

CORONARY
CIRCULATION
• Originates from the aorta
• Right coronary artery bifurcates into:
• Right marginal artery
• Posterior descending artery
• Left coronary artery bifurcates into:
• Left anterior descending artery (LAD)
• Circumflex artery
http://labelled-diagram-of-the-human-heart.blogspot.com/2009/07/coronary-
arteries.html

PATHOPHYSIOLOGY
Rupture of “vulnerable”
atherosclerotic plaque
Activation of coagulation cascade and
fibrin deposition
Partial (NSTMI) or totally occlusive
(STEMI) coronary vessel
Myocardial ischemia and necrosis
http://pmtwww.uptodate.com/contents/image?imageKey=PI/60394&topicKey=PI%2F3428&source=outline_link

COAGULATION
CASCADE
http://openi.nlm.nih.gov/imgs/512/349/2496975/2496975_vhrm0402-305-01.png

RISK FACTORS
Non-modifiable
Age
Gender
Family history of
atherosclerotic coronary
artery disease
Modifiable
Hyperlipidemia
Diabetes Mellitus
Hypertension
Tobacco use
Bolooki MH et al. Acute Myocardial Infarction. Available at: http://www.clevelandclinicmeded.com

EARLY RISK ASSESSMENTS
• Global Registry of Acute Coronary Event (GRACE) risk score:
– Predicts in-hospital and 6-months mortality rate
– http://www.outcomes-
umassmed.org/grace/acs_risk/acs_risk_content.html
• Thrombolysis In Myocardial Infarction (TIMI) risk score:
– Estimates overall mortality of STEMI
– http://www.mdcalc.com/timi-risk-score-for-stemi/

CLINICAL PRESENTATION
• Differ by gender and age
• Midline anterior and/or retrosternal chest pain/discomfort lasting >20 minutes in
duration
– May radiate to shoulder, arm, back, jaw
– Unremitting
– May describes as pressure sensation, fullness, or heaviness
– Associated symptoms: nausea and vomiting, palpitations, diaphoresis or sweating, dyspnea or
shortness of breath, cough, syncope, or low grade fever
• Patient may present with acute heart failure, tachycardia, bradycardia, or heart block
• Hypotension or cerebrovascular symptoms in elderly
Koda-Kimble MA et al. Myocardial Infarction. In: Applied Therapeutics: The Clinical Use of Drugs, 2009

• New ST-elevation at the J point (at least 2 contiguous
leads):
– ≥ 2 mm (0.2 mV) in men
– ≥ 1.5 mm(0.15 mV) in women
OR
– ≥ 1 mm (0.1 mV) in other contiguous chest leads or limb leads
• ST-depression:
– ≥ 2 precordial leads (V1 – V4): may indicate transmural posterior
injury
• Established MI
– Presence of Q waves of ≥ 0.03 s in leads V1 – V6 or II, aVL, aVF
12-LEAD ELECTROCARDIOGRAM (ECG)
V2 – V3

LOCATION OF MI
http://imgarcade.com/1/septal-mi/

LABORATORY MARKERS
• Biomarkers
– CK
• Less specific for cardiac muscle necrosis
– CK-MB
• Detectable within 6 hours, falls within
48 hours
– Troponin I or T
• Detectable within 6 hours, remains
elevated for 7-14 days
DiPiro J. Acute Coronary Syndrome. In: Pharmacotherapy: A Pathophysiological Approach, 2011

COMPLICATIONS OF MI
Ventricular remodeling
Cardiogenic shock
Death
Valvular dysfunction
Arrhythmias (VF/VT)
Heart failure
Bradycardia
Heart block
Pericarditis
CVA secondary to LV
thrombus
Free wall rupture (e.g. VSD,
papillary muscle
dysfunction)

GOALS OF THERAPY
• Short term:
– Early restoration of epicardial blood flow and myocardial
perfusion in the infarct zone
– Relief ischemic chest discomfort and restoration of ECG
changes
• Long term:
– Prevent death or MI complications
– Prevent reocclusion or reinfarction

ACC/AHA CLASSIFICATION OF
RECOMMENDATIONS

MANAGEMENT
Reperfusion Therapy
Pharmacological
Non-
Pharmacological

REPERFUSION THERAPY
• Prompt and effective reperfusion therapy is the cornerstone for
treatment of STEMI
• Selection of reperfusion depends on chance of achieving early and
persistent reperfusion with lowest risk of major complications
• Guideline recommendation:
– Should be administered to all eligible patients with STEMI with symptoms onset
within the prior 12 hours(Class 1; LOE: A)
– 12-24 hours for patient with ongoing ischemia (Class IIa; LOE: B)

TYPES OF REPERFUSION
Primary Percutaneous Coronary Intervention (PPCI) Fibrinolytics
Balloon angiography 1. Strptokinase
2. Alteplase
3. Reteplase
4. Tenecteplase
Placement of intracoronary stent:
 Bare-metal stent (BMS)
 Drug-eluting stent (DES)

Rescue PCI
PCI: percutaneous
coronary
intervention
FMC: first medical
contact
CABG: coronary
artery bypass graft
ALGORITHM OF THERAPY

TIMING TO REPERFUSION THERAPY
Treatment
Recommended Time for Initiation
of Treatment
PCI Door-to-balloon time ≤ 90 min
Fibrinolytic
agents
Door-to-needle time ≤ 30 min
Hilleman DE et al. Pharmacotherapy. 2007;27(11):1558-1570

PRIMARY PCI (PPCI)
http://www.youtube.com/watch?v=S9AqBd4RExk

PPCI
• Indications:
ACC/AHA Recommendations COR† LOE†
1. Ischemic symptoms <12 h I A
2. Ischemic symptoms <12 h and contraindications to fibrinolytic
therapy irrespective of time delay from FMC
I B
3. Cardiogenic shock or acute severe HF irrespective of time delay
from MI onset
I B
4. Evidence of ongoing ischemia 12 to 24 h after symptom onset IIA B
5. PCI of a non-infarct artery at the time of primary PCI in patients
without hemodynamic compromise III: Harm B
COR: Classification of recommendation; LOE: level of evidence

PPCI >>> FIBRINOLYTICS
• Greatest survival benefit in high risk patient
• Higher rates of infarct artery patency with TIMI 3 flow
(90%-PCI vs. <60%-fibrinolysis)
• Reduction in recurrent ischemia/reinfarction
• 30-day mortality reduction (6.5% to 4.4%)
• Reduction in stroke (2.0% to 0.7%)
• Reduced risk of bleeding
Van De Wefr F. et al. Circulation. 2002;105: 2813-16
TIMI Flow
Grade
Characteristics
0 No perfusion
1
Penetration
without
perfusion
2
Partial
reperfusion
3
Complete
perfusion
TIMI: Thrombolysis in Myocardial Infarction

FIBRINOLYTIC THERAPY
• Acts on converting plasminogen to plasmin  cleaves fibrin 
causing clot dissolution and restoration of blood flow
• Indications:
Recommendations COR† LOE†
1. Ischemic symptoms <12 h I A
2. Evidence of ongoing ischemia 12 to 24 h after symptom onset and
a large area of myocardium at risk or hemodynamic instability
IIa C
3. ST depression, except if true posterior MI is suspected or when
associated with ST elevation in lead aVR III: Harm B

CHOICE OF FIBRINOLYTIC AGENTS
• Adjunctive antiplatelet and/or anticoagulant therapies are
indicated, regardless of the choice of fibrinolytic agent
Agents Fibrin Specificity Half-life (h) Patency Rate
Alteplase (tPA)
(Activase®)
++ 5 73%-84%
Reteplase (rPA)
(Retavase®)
++ 13-16 84%
Tenecteplase
(TNKase®)
++++ 20-24 85%
Streptokinase
(Streptase®)
No 18-23 60%-68%

EFFICACY AND SAFETY DATA

DOSE AND ADMINISTRATION
Agents Dose and Administration
Alteplase (tPA)*
90 min infusion:
• 15 mg bolus, then
• Infusion 0.75 mg/kg for 30 min (max 50 mg), then 0.5 mg (max 35 mg) over
the next 60 min; total dose not to exceed 100 mg; 60 mg administered within
first hour, then 20 mg during second and third hour
Reteplase (rPA) Two 10 unit boluses, each administered over 2 min, 30 min apart
Tenecteplase
(TNK)
Single bolus administration over 5 sec; dose based on patient weight (max dose
50 mg):
<60 kg: 30 mg; 60-69 kg: 35 mg; 70-79 kg: 40 mg; 80-89 kg: 45 mg; and ≥ 90 kg:
50 mg
Streptokinase 1,500,000 units IV infusion over 30-60 min
*KFSH&RC formulary

CONTRAINDICATIONS TO FIBRINOLYTIC
THERAPY

DUAL ANTIPLATELET
THERAPY/DAPT

PLATELET ACTIVATION AND MECHANISMS
OF ADVERSE CLINICAL OUTCOME
Alexopoulos D. Int J Card; 2013; 163:249-55

ASPIRIN
• Irreversibly inhibits cyclooxygenase-1 and 2 enzymes  decreased
formation of prostaglandin and thromboxane A2  inhibit platelet
aggregation
ACC/AHA Recommendations
PPCI
162-325 mg loading dose (IB) followed by ASA 81 mg daily (indefinitely) (IA)
Fibrinolysis
162-325 mg loading dose (IA) followed by ASA 81 mg daily (indefinitely) (IA)

THIENOPYRIDINES
• Prevents P2Y12 component of ADP receptors on the platelet surface
blocking activation of GPIIb/IIIa receptor complex, thereby reduce platelet
aggregation
PPCI:
1. Clopidogrel: 600 mg PO as early as possible or at the time of PCI (IB) followed by 75 mg daily (IB)
2. Prasugrel: 60 mg as early as possible or at the time of PCI (IB) followed by 10 mg daily (IB)
3. Ticagrelor: 180 mg as early as possible or at the time of PCI (IB) followed by 90 mg twice a day
[Note: maintenance therapy continue for 1 year for both BMS/DES ; dose of ASA should not exceed 100 mg with
ticagrelor as DAPT]
Fibrinolytics:
1. Clopidogrel:
a. Age ≤ 75 years: 300 mg loading dose (IA) followed by 75 mg daily for at least 14 days (IA) to 1 year in
absence of bleeding (IC)
b. Age >75 year: 75 mg once (IA) then daily for at least 14 days (IA) up to 1 year (IC) in absence of
bleeding

COMPARATIVE
ADVANTAGE/DISADVANTAGE
Agents Characteristics Contraindications
Onset
of
Action
Potency
Variable
Response
Clopidogrel
(Plavix®)
Produrg, binds
irreversibly
Hypersensitivity, active
pathological bleeding ++ + ++++
Prasugrel
(Effient®)
Produrg, binds
irreversibly
pathological bleeding, prior
TIA or stroke, age ≥ 75 years
or body weight <60 kg
++++ +++ ̶
Ticagrelor
(Brilinta®)
Nonthienopyridine,
reversible binding
pathological bleeding ,
severe hepatic impairment
++++ +++ ̶

MAJOR TRIALS—OUTCOME
COMPARISON

Caterina RD et al. Thromb Haemost; 2013; 109:769-86

PPCI
Unfactionated Heparin (UFH)
• With GP IIb/IIIa receptor antagonist planned: 50-70 U/kg IV bolus to
achieve ACT (IC)
• With no GP IIb/IIIa receptor antagonist planned: 70-100 U/kg IV
bolus to achieve ACT (IC)
Bivalirudin (preferred over UFH in high bleeding risk patients)
• 0.75 mg/kg IV bolus then 1.75 mg/kg/h infusion with or without
prior treatment with UFH (dose adjustment to 1mg/kg/h with CrCl
<30 mL/min) (IB)
Fondaparinux: not recommended as sole agent for PPCI (IIIB: Harm)
ACT: activated clotting time
Anticoagulation

FIBRINOLYTIC THERAPY

GP IIB/IIIA RECEPTOR ANTAGONIST

CLINICAL USE
• Block the final common pathway of platelet aggregation (inhibiting cross-
linking of platelets through fibrinogen bridges)
• Rationale to use in combination with UFH:
– Reduce likelihood of reinfarction
– Prevent distal embolization of thrombi during PPCI
• Should not be administered for medical management of the patients with
STEMI not undergoing PCI
• Administration of GP IIb/IIIa inhibitors should be avoided, if possible, with
bivalirudin due to increased bleeding risk Beygui F et al. Eur Heart J Supp; 2005; 7: 110-114

CHOICE OF AGENTS
Agent Molecule Dose Contraindications
Abciximab
(ReoPro®)
Monoclonal
antibody
Bolus: 0.25 mg/kg
Infusion: 0.125 mg/kg/hr x 12
hrs
Active bleeding,
thrombocytopenia,
prior stroke, renal
dialysis (eptifibatide)
Eptifibatide
Integrilin®)
Peptide Bolus: 180 mcg/kg x 2
Infusion: 2 mcg/kg/min x 18-24
hrs
(1 mcg/kg/min if CrCL <50)
Tirofiban
(Aggrastat®)
Non-
peptide
Bolus: 25 mcg/kg
Infusion: 0.15 mcg/kg/min x 18
hrs
Beygui F et al. Eur Heart J Supp; 2005; 7: 110-114

ROUTINE MEDICAL THERAPIES
Therapy Indications Contraindications (CI) ACC/AHA
Recommendations
B-blockers
Initiated in the first 24
hours in all patient s
without CI
CHF, shock, reactive airway disease,
PR interval >0.24 secs, 2nd or 3rd
degree AV block, HR <60 bpm, SBP
<90 mmHg
IB
ACEI
Initiated in the first 24
hours for patients with
anterior infarction, LV
dysfunction (EF ≤
0.40) or HF
SBP <100 mmHg, intolerant to
ACEI, bilateral renal stenosis,
serum potassium >5.5 mmol/L,
ARF, Pregnancy
IA
ARB
For patient intolerant
to ACE
Same as ACEI
IB

ROUTINE MEDICAL THERAPIES
Therapy Indications
Contraindications
(CI)
ACC/AHA
Recommendations
Aldosterone
Antagonists
LVEF ≤ 0.40 and either
DM or HF who are
already on ACEI and b-
blockers
Hypotension,
hyperkalemia (serum
potassium >5.0 mmol/L),
SCr >2.5 mmol/L or CrCl
<30 mL/min
IB
Statin
High intensity statin to
all patients without CI
Serum transaminase 3X
ULN, Pregnancy, active
liver disease
IB
Nitroglycerin
Patient with ongoing
ischemic discomfort,
hypertension and HF
Hypotension , use of
sildenafil/vardenafil
within 24 h or tadalafil
within 48 h
̶

SUBJECTIVE
• C/C: “chest pain”
• HPI:
– RS is a 59 yrs old Philippino male with no prior cardiac history presented at the
emergency room at 22:04 after having retrosternal chest pain for ~1.5 hours
– Described chest pain as compressive in nature, radiating to both arms and
associated with sweating
– Denied any history of shortness of breath, nausea, and vomiting
• PMHx:
– Hypertension (x 3 years) on amlodipine 10 mg by mouth daily, and aspirin 81
mg by mouth daily
• SHx: KFSH employee; current smoker
• FHx: unknown
• Allergy: NKA

• On Admission:
– Vitals : BP: 123/70 mmHg; HR: 76 bpm; RR: 25 br/min; Temp: 36.6 0C;
O2 Sat: 98% 3L nasal cannula
– Physical Exams: unremarkable
• CVS: S1 + S2 + 0
• Chest: clear; equal air entry with normal breath sounds
• Ext: no significant changes, no JVD
• CNS: no abnormality detected
• Abd: not distended
• Height: 148 cm; Weight: 87 kg (standing)
– ECG: ST segment abnormalities in V2-V6, and anterior leads
– Chest X-Ray: mild increase in the interstitial marking but no definite
pneumonic infiltration or pleural effusion
OBJECTIVE

LABS (DAY OF ADMISSION)
• Chemistry:
• CBC with differential: unremarkable
• Enzymes:
Na: 136 Cl: 103 Urea: 4.9 Glucose: 8.60 Ca (t): 2.22
K: 4.2 CO2: 22 Cr: 104 Mg: 0.91 PO4: 1.09
CK: 294 TrT: <0.01 Pro-BNP: 25 ALT: 22 AST: 21.4 Alk phos: 59

ASSESSMENT/PLAN
• He was diagnosed with anteroseptal STEMI and was sent to the cath lab for PPCI
• Medication:
– Heparin 7000 units (80 units/kg) IV push once
• Plan:
– Immediate PCI
– Admit to CCU after PCI for routine medical care
• Catheterization (23:56): PCI
– LM: Normal
– LAD: mid 99% followed by diffuse 20% lesion
– LCx: Large dominant mild irregularities, OM-2 has Ostial 20% stenosis
– RCA: small non dominant proximal 20% stenosis
– Impression: single vessel coronary artery disease (LAD)
– PCI to Mid LAD:
• Resolute integrity (DES) deployed
• Post intervention angio showed excellent result with TIMI 3 flow

Mid LAD
Occlusion
LAD Occluded 99%

Stent
Deployment
Resolute Integrity

Reperfusion
following
stent
TIMI 3 Flow

POST PCI– DAY 1
• Vitals: unremarkable except tachypnea (RR:21-23 br/min)
• Labs:
• ECHO:
• LV is normal in size. Apex, anterior septum, and anterior wall are akinetic
with partial loss of wall thickness. LV systolic function moderately reduced;
EF 40-45%
• A/P:
• Started on Metoprolol 25 mg PO twice a day, Atorvastatin 40 mg PO daily,
and Isosorbide dinitrate 20 mg twice a day
• Continued aspirin and clopidogrel
CK: 2343 TrT: 6.930 ALT: 45.6 AST: 242.6
K: 4.5 CO2: 25 Cr: 99 Mg: 0.88 PO4: 1.09
Trig: 2.247 Chol: 4.757 HDL: 0.91 LDL: 3.0 HbA1c: 0.061

• Vitals:
• Labs:
• Plan:
• Patient is walking and doing well; plan to transfer to A4
• Discharge medications:
1. Aspirin 81 mg PO daily
2. Clopidogrel 75 mg PO daily
3. Metoprolol 25 mg PO twice a day
4. Isosorbide dinitrate 20 mg PO twice a day
5. Atorvastatin 40 mg PO daily
POST PCI– DAY 2
K: 4.4 CO2: 24 Cr: 104 Mg: 0.84 PO4: 0.98
CK: 902 TrT: 2.780
BP:120’s/70’s HR: 50’s-60’s RR: 15-18 Temp: 36.8 O2 Sat: 95% RA

SUMMARY
• ST segment elevation MI/STEMI is a medical emergency which is the result of
complete occlusion of the coronary artery causing myocardial infarction
• Since atherosclerotic disease is the most common cause of STEMI, the
pathophysiology is mainly due to the rupture of “vulnerable plaque”
• Clinical presentation of STEMI may differ by gender and age. However, in
general patient presents with midline anterior and/or retrosternal pain
• Diagnosis of STEMI is based on:
– Clinical symptoms, ECG changes, and release of cardiac biomarkers

• Goals of management is to restore blood flow to the infarct artery as
promptly as possible to minimize infarct size
• Recommended time frame for PPCI in a skilled PCI capable facilities is ≤ 90
minutes otherwise fibrinolysis is preferred
• DAPT is indicated irrespective of modes of reperfusion therapy
• For PCI, anticoagulation therapy is provided once before procedure, whereas,
the duration of therapy is longer in patients treated with fibrinolysis
– UFH: 48 h, then other modes of anticoagulation
– Enoxaparin: 8 days or until discharge
SUMMARY (CONT)

ST-Elevation Myocardial Infarction

ST-Elevation Myocardial Infarction

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