CURRICULUM VITAE

PERSONAL INFORMATION

Full Name : Dr. Erwin Sukandi, SpPD, K-KV, FINASIM

Place/Date of Birth : Curup, November 24th, 1965
Address : Jalan Macan Kumbang VI No. 4501.B, RT 40 RT 11,
Demang Lebar Daun, IB I, Palembang, Indonesia,
Postal Code 30153
Mobile : +62 812 7834464
email : esukandi@gmail.com

EDUCATIONAL BACKGROUND

1. Post Graduate from University of Sriwijaya, Subspecialist in Cardiovascular

(2010)
2. Post Graduate from University of Sriwijaya, Specialist in Internal Medicine
(2002)
3. Graduate from Faculty of Medicine University of Sriwijaya (1991)
EMERGENCY MEDICINE OF ACUTE
MYOCARDIAL INFARCTION
Erwin Sukandi
Division of Cardiology, Department of Internal Medicine
Faculty of Medicine, University of Sriwijaya
Dr. Mohammad Hoesin General Hospital, Palembang
 Case 1

• 44y Male, Chinese

• Chest pain 2 hrs
• Refered from private hospital with STEMI
anteroseptal
• Smoking, Dyslipidemia
• Non hypertension, Non diabetes
• ECG: SR, ST elevation V1-4
• Echo: RWMA (anteroseptal wall), LVEF
48%
 Coronary Artery Disease
• CAD is caused by atherosclerosis of the
coronary arteries that leads to a restriction of
blood flow to the heart.
• Atherosclerosis is a process that develops
slowly over time.
• Typically, atherosclerosis begins in a person’s
teenage years or earlier, and the disease
worsens quietly for decades.
 Atherosclerosis
• Atherosclerosis is a chronic condition that
narrows arteries by building fat-filled bulges in
the arterial walls.
• These bulges are called atherosclerotic
plaques, or simply plaques.
• In some people, the plaques eventually break
open and the contents cause blood clots.
 Atherothrombosis: A Generalized and
Progressive Disease
Atherothrombosis

Unstable angina
MI ACS

Ischemic stroke/TIA
Critical leg ischemia
Intermittent
Atherosclerosis claudication
CV death

Stable angina/Intermittent claudication

From first decade From third decade From fourth decade

Smooth muscle Thrombosis,

Growth mainly by lipid accumulation haematoma
and collagen
Adapted from Libby P. Circulation 2001; 104: 365–372
 Cardiovascular Disease

• 63,400,000 Americans have one or more forms

of heart or blood vessel disease

• 50% of all deaths are cardiovascular disease

14
 Cardiovascular Disease
• Acute Myocardial Infarction (Heart Attack) - leading
cause of death in U.S.

• 1.5 million Americans will have AMI’s this year

– Of these 0.5 million will die!
– 350,000 will die in first two hours!

Temple College EMS Program 15

 Risk Factors for Coronary Artery Disease

Non- modifiable: Modifiable:

• History • Tobacco Smoking
• Advancing Age • Dyslipidemia
• Gender • Hypertension
• History of premature CAD • Obesity
in the family
• Sedentary Lifestyle
• Modifiable • Diabetes
• Emerging Risk Factors
 Classification
Coronary Artery
Disease

Asymptomatic Symptomatic

Stable Angina Acute Coronary

Syndrome

Unstable Non ST-Elevation ST-Elevation

Angina Myocardial Myocardial
Infarction Infarction
 Acute Coronary Syndromes

Presentation Ischemic Discomfort

ACS

Working Dx

ECG No ST Elevation ST Elevation

NSTE-ACS

Cardiac Biomarker UA NSTEMI * STEMI *

Unstable Angina Myocardial Infarction Noncardiac

Final Dx NQMI QwMI Etiologies
Unstable
NSTEMI STEMI
Angina
Non-occlusive
thrombus Complete thrombus
Non occlusive sufficient to cause occlusion
thrombus tissue damage & mild
myocardial necrosis ST elevations on
Non specific ECG or new LBBB
ECG ST depression +/-
T wave inversion on Elevated cardiac
Normal cardiac ECG enzymes
enzymes
Elevated cardiac More severe
enzymes symptoms
 Acute Coronary Syndrome
• Unstable Angina Pectoris (UAP)
• Non ST segment Elevation Myocardial
Infarction (NSTEMI)
• ST segment Elevation Myocardial
Infarction (STEMI)
 Diagnosis

• Cardiac Chest pain

• ECG changes
• Cardiac biomarker
 Symptoms
• Substernal chest pain
• Great anxiety/Fear
• Fixation of the body
• Pale, ashen, or livid face
• Dyspnea (SOB) may be associated
• Nausea
• Diaphoresis
• BP usually up during attack
• Dysrhythmia may be present
23
 Chest Pain
– Substernal
– Squeezing/Crushing/Heaviness
– May radiate to arms, shoulders, jaw,
upper back, upper abdomen back
– May be associated with shortness of
breath, nausea, sweating

24
 THE ELECTROCARDIOGRAM
• 12 lead EKG
• Cornerstone of initial evaluation
• Within 10 minutes of presentation
• Previous EKG tracings
• Compare
• Serial EKGs
• Essential
 THE ELECTROCARDIOGRAM
1. ST segment elevation 2mm (2 contiguous leads), new LBBB, true posterior
ischemia
STEMI

2. ST depression >1mm, marked symmetrical T wave inversions >2 mm or

Wellen’s pattern, dynamic ST-T changes with pain
UA/NSTEMI LIKELY

3. Non-diagnostic or normal ECG

ACS LESS LIKELY
 THE ELECTROCARDIOGRAM
INFARCT LOCATION

– II, III, AVF : Inferior

– V1 - V4 : Anteroseptal
– I, aVL : High lateral
– I, aVL, V5-V6 : Lateral
– I,aVL, V1-V6 : Extensive anterior
– V1-V2 tall R, ST depression : True posterior
ELECTROCARDIOGRAM
Anterior Myocardial Infarction
■ Occlusion of the left
coronary artery—left
anterior descending
branch
■ ECG changes: ST
segment elevation
with tall T waves and
taller-than-normal R
waves in leads V3 and
V4
Inferior Myocardial Infarction
■ Occlusion of the right
coronary artery—
posterior descending
branch
■ ECG changes: ST
segment elevation in
leads II, III, and aVF
Lateral Myocardial Infarction
■ Occlusion of the left
coronary artery—
circumflex branch
■ ECG changes: ST
segment elevation in
leads I, aVL, V5, and V6
Septal Myocardial Infarction
■ Occlusion of the left
coronary artery—left
anterior descending
branch
■ ECG changes:
pathological Q waves;
absence of normal R
waves in leads V1 and
V2
Posterior Myocardial Infarction
■ Occlusion of the right
coronary artery (posterior
descending branch) or the
left circumflex artery
■ Tall R waves and ST
segment depression
possible in leads V1, V2,
V3, and V4
■ ST segment elevation in
true posterior leads, V8
and V9
 Cardiac Biomarker

Cardiac Initial Mean time Time to

enzyme elevation to peak return to
Marker after AMI elevations baseline
Myoglobin 1-4hr 6-7hr 18-24hr
CTnI 3-12hr 10-24hr 3-10 day
CTnT 3-12hr 12-48hr 5-14 day

CKMB 4-12 hr 10-24hr 2-3day

TCK 2-6 hr 4.7hr(3-5) 72hr(50-96)
 Management of ACS
STEMI NSTEMI/Unstable Angina

Presumed prognosis: very Presumed prognosis: low risk of

high risk of in-hospital in-hospital death, unless MI develops
death
Treatment goal: stabilize with aspirin
Treatment goal: prevent heparin +/-GIIb/IIIa & monitor for MI
death by restoring development
coronary blood flow
+ Cardiac enzymes – Cardiac Enzymes

Scheduled High- Low -

Fibrinolytic Direct risk risk
PCI features features
therapy PCI

Manage
medically
Algorithm for Management of Patients With Definite or Likely NSTE-ACS
NSTE-ACS:
Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy Initiate DAPT and Anticoagulant Therapy
1. ASA (Class I; LOE: A) 1. ASA (Class I; LOE: A)

2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) : 2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):
· Clopidogrel or · Clopidogrel or
· Ticagrelor · Ticagrelor

3. Anticoagulant: 3. Anticoagulant:
· UFH (Class I; LOE: B) or · UFH (Class I; LOE: B) or
· Enoxaparin (Class I; LOE: A) or · Enoxaparin (Class I; LOE: A) or
· Fondaparinux (Class I; LOE: B) · Fondaparinux† (Class I; LOE: B) or
· Bivalirudin (Class I; LOE: B)
Can consider GPI in addition to ASA and P2Y12 inhibitor
in high-risk (e.g., troponin positive) pts
(Class IIb; LOE: B)
· Eptifibatide
· Tirofiban

Medical therapy
chosen based on cath
findings

Therapy Therapy
Effective Ineffective
 Therapy Therapy
Effective Ineffective
PCI With Stenting
Initiate/continue antiplatelet and anticoagulant
therapy
1. ASA (Class I; LOE: B)
2. P2Y12 Inhibitor (in addition to ASA) :
· Clopidogrel (Class I; LOE: B) or
· Prasugrel (Class I; LOE: B) or
· Ticagrelor (Class I; LOE: B)
3. GPI (if not treated with bivalirudin at time of PCI)
· High-risk features, not adequately pretreated
with clopidogrel (Class I; LOE: A)
· High-risk features adequately pretreated with
clopidogrel (Class IIa; LOE: B)
4. Anticoagulant:
· Enoxaparin (Class I; LOE: A) or
· Bivalirudin (Class I; LOE: B) or
· Fondaparinux† as the sole anticoagulant (Class
III: Harm; LOE: B) or
· UFH (Class I; LOE: B)
†Inpatients who have been treated with fondaparinux (as upfront therapy) who are
undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at
the time of PCI because of the risk of catheter thrombosis.
CABG
Initiate/continue ASA therapy and
discontinue P2Y12 and/or GPI therapy
1. ASA (Class I; LOE: B)
2. Discontinue clopidogrel/ticagrelor 5 d
before, and prasugrel at least 7 d before
elective CABG
3. Discontinue clopidogrel/ticagrelor up to
24 h before urgent CABG (Class I; LOE: B).
May perform urgent CABG <5 d after
clopidogrel/ticagrelor and <7 d after
prasugrel discontinued
4. Discontinue eptifibatide/tirofiban at
least 2-4 h before, and abciximab ≥12 h
before CABG (Class I; LOE: B)
Late Hospital/Posthospital Care
1. ASA indefinitely (Class I; LOE: A)
2. P2Y12 inhibitor (clopidogrel or
ticagrelor), in addition to ASA, up
to 12 mo if medically treated
(Class I; LOE: B)
3. P2Y12 inhibitor (clopidogrel,
prasugrel, or ticagrelor), in
addition to ASA, at least 12 mo if
treated with coronary stenting
(Class I; LOE: B)
 Early Hospital Care

Standard Medical Therapies

 Oxygen

Recommendation COR LOE

Supplemental oxygen should be administered to patients with
NSTE-ACS with arterial oxygen saturation less than 90%,
I C
respiratory distress, or other high-risk features of hypoxemia.
 Anti-Ischemic and Analgesic Medications:
Nitrates
Recommendations COR LOE
Patients with NSTE-ACS with continuing ischemic pain
should receive sublingual nitroglycerin (0.3 mg to 0.4 mg)
every 5 minutes for up to 3 doses, after which an I C
assessment should be made about the need for intravenous
nitroglycerin if not contraindicated.
Intravenous nitroglycerin is indicated for patients with
NSTE-ACS for the treatment of persistent ischemia, HF, or I B
hypertension.
Nitrates should not be administered to patients with NSTE-
ACS who recently received a phosphodiesterase inhibitor, III:
B
especially within 24 hours of sildenafil or vardenafil, or Harm
within 48 hours of tadalafil.
 Anti-Ischemic and Analgesic Medications:
Analgesic Therapy
Recommendations COR LOE
In the absence of contraindications, it may be reasonable to
administer morphine sulfate intravenously to patients with NSTE-
ACS if there is continued ischemic chest pain despite treatment IIb B
with maximally tolerated anti-ischemic medications.

Nonsteroidal anti-inflammatory drugs (NSAIDs) (except aspirin)

should not be initiated and should be discontinued during III:
B
hospitalization for NSTE-ACS because of the increased risk of Harm
MACE associated with their use.
 Anti-Ischemic and Analgesic Medications:
Beta-Adrenergic Blockers
Recommendations COR LOE
Oral beta-blocker therapy should be initiated within the first
24 hours in patients who do not have any of the following: 1)
signs of HF, 2) evidence of low-output state, 3) increased
risk for cardiogenic shock, or 4) other contraindications to I A
beta blockade (e.g., PR interval >0.24 second, second- or
third-degree heart block without a cardiac pacemaker,
active asthma, or reactive airway disease).
In patients with concomitant NSTE-ACS, stabilized HF, and
reduced systolic function, it is recommended to continue
beta-blocker therapy with 1 of the 3 drugs proven to reduce I C
mortality in patients with HF: sustained-release metoprolol
succinate, carvedilol, or bisoprolol.
 Anti-Ischemic and Analgesic Medications:
Beta-Adrenergic Blockers (cont’d)
Recommendations COR LOE
Patients with documented contraindications to beta blockers in
the first 24 hours of NSTE-ACS should be re-evaluated to I C
determine their subsequent eligibility.
It is reasonable to continue beta-blocker therapy in patients with
IIa C
normal LV function with NSTE-ACS.
Administration of intravenous beta blockers is potentially harmful
III:
in patients with NSTE-ACS who have risk factors for shock. B
Harm
 Anti-Ischemic and Analgesic Medications:
Calcium Channel Blockers
Recommendations COR LOE
In patients with NSTE-ACS, continuing or frequently
recurring ischemia, and a contraindication to beta blockers,
a nondihydropyridine calcium channel blocker (CCB) (e.g.,
verapamil or diltiazem) should be given as initial therapy in
I B
the absence of clinically significant LV dysfunction,
increased risk for cardiogenic shock, PR interval greater
than 0.24 second, or second- or third-degree atrioventricular
block without a cardiac pacemaker.
Oral nondihydropyridine calcium antagonists are
recommended in patients with NSTE-ACS who have
I C
recurrent ischemia in the absence of contraindications, after
appropriate use of beta blockers and nitrates.
 Anti-Ischemic and Analgesic Medications:
Calcium Channel Blockers (cont’d)
Recommendations COR LOE
CCBs† are recommended for ischemic symptoms when
beta blockers are not successful, are contraindicated, or I C
cause unacceptable side effects.
Long-acting CCBs and nitrates are recommended in
I C
patients with coronary artery spasm.
Immediate-release nifedipine should not be administered to
III:
patients with NSTE-ACS in the absence of beta-blocker B
Harm
therapy.

†Short-acting dihydropyridine calcium channel antagonists should be avoided.

 Anti-Ischemic and Analgesic Medications:
Cholesterol Management
Recommendations COR LOE
High-intensity statin therapy should be initiated or continued in
all patients with NSTE-ACS and no contraindications to its use. I A

It is reasonable to obtain a fasting lipid profile in patients with

NSTE-ACS, preferably within 24 hours of presentation. IIa C
 Dosing of Parenteral Anticoagulants During PCI
Drug* In Patients Who Have Received In Patients Who
Prior Anticoagulant Therapy Have Not Received
Prior Anticoagulant
Therapy
Enoxaparin · · 0.5 mg/kg–0.75
For prior treatment with enoxaparin, if last
SC dose was administered 812 h earlier mg/kg IV loading
or if <2 therapeutic SC doses of dose
enoxaparin have been administered, an IV
dose of enoxaparin 0.3 mg/kg should be
given
· If the last SC dose was administered
within prior 8 h, no additional enoxaparin
should be given
Bivalirudin · For patients who have received UFH, wait · 0.75 mg/kg loading
30 min, then give 0.75 mg/kg IV loading dose, 1.75 mg/kg/h
dose, then 1.75 mg/kg/h IV infusion IV infusion
· For patients already receiving bivalirudin
infusion, give additional loading dose 0.5
mg/kg and increase infusion to 1.75
mg/kg/h during PCI
 Dosing of Parenteral Anticoagulants During PCI
Drug* In Patients Who Have Received In Patients Who Have Not
Prior Anticoagulant Therapy Received
Prior Anticoagulant Therapy
Fondaparinux · For prior treatment with N/A
fondaparinux, administer
additional IV treatment with
anticoagulant possessing anti-
IIa activity, considering whether
GPI receptor antagonists have
been administered
UFH · IV GPI planned: additional UFH · IV GPI planned: 50–70
as needed (e.g., 2,000–5,000 U/kg loading dose to
U) to achieve ACT of 200–250 s achieve ACT of 200–250 s
· No IV GPI planned: additional · No IV GPI planned: 70–100
UFH as needed (e.g., 2,000– U/kg loading dose to
5,000 U) to achieve ACT of achieve target ACT of 250–
250–300 s for HemoTec, 300– 300 s for HemoTec, 300–
350 s for Hemochron 350 s for Hemochron
*Drugs are presented in order by the COR then the LOE. When more than 1 drug
exists within the same LOE and there are no comparative data, then the drugs are
listed alphabetically.
Factors Associated With Appropriate Selection of Early Invasive Strategy
or Ischemia-Guided Strategy in Patients With NSTE-ACS

Immediate Refractory angina

invasive Signs or symptoms of HF or new or worsening mitral regurgitation
(within 2 h) Hemodynamic instability
Recurrent angina or ischemia at rest or with low-level activities despite
intensive medical therapy
Sustained VT or VF
Ischemia- Low-risk score (e.g., TIMI [0 or 1], GRACE [<109])
guided Low-risk Tn-negative female patients
strategy Patient or clinician preference in the absence of high-risk features
Early None of the above, but GRACE risk score >140
invasive Temporal change in Tn (Section 3.4)
(within 24 h) New or presumably new ST depression
Delayed None of the above but diabetes mellitus
invasive Renal insufficiency (GFR <60 mL/min/1.73 m²)
(within Reduced LV systolic function (EF <0.40)
2572 h) Early postinfarction angina
PCI within 6 mo
Prior CABG
GRACE risk score 109–140; TIMI score ≥2
 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.
 Regional Systems of STEMI Care,
Reperfusion Therapy, and Time-to-Treatment
Goals
I IIa IIb III
All communities should create and maintain a regional system of
STEMI care that includes assessment and continuous quality
improvement of EMS and hospital-based activities. Performance
can be facilitated by participating in programs such as Mission:
Lifeline and the D2B Alliance.

I IIa IIb III

Performance of a 12-lead ECG by EMS personnel at the site of
FMC is recommended in patients with symptoms consistent with
STEMI.
 Regional Systems of STEMI Care,
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.

I IIa IIb III

EMS transport directly to a PCI-capable hospital for primary PCI is
the recommended triage strategy for patients with STEMI with an
ideal FMC-to-device time system goal of 90 minutes or less.*

*The proposed time windows are system goals. For any individual patient, every effort should be
made to provide reperfusion therapy as rapidly as possible.
 Regional Systems of STEMI Care,
Reperfusion Therapy, and Time-to-Treatment
Goals
I IIa IIb III
Immediate transfer to a PCI-capable hospital for primary PCI is the
recommended triage strategy for patients with STEMI who initially
arrive at or are transported to a non–PCI-capable hospital, with an
FMC-to-device time system goal of 120 minutes or less.*

I IIa IIb III

In the absence of contraindications, fibrinolytic therapy should be
administered to patients with STEMI at non–PCI-capable hospitals
when the anticipated FMC-to-device time at a PCI-capable hospital
exceeds 120 minutes because of unavoidable delays.

*The proposed time windows are system goals. For any individual patient, every effort should be
made to provide reperfusion therapy as rapidly as possible.
 Regional Systems of STEMI Care,
Reperfusion Therapy, and Time-to-Treatment
Goals

I IIa IIb III

When fibrinolytic therapy is indicated or chosen as the primary
reperfusion strategy, it should be administered within 30 minutes of
hospital arrival.*

I IIa IIb III

Reperfusion therapy is reasonable for patients with STEMI and
symptom onset within the prior 12 to 24 hours who have clinical
and/or ECG evidence of ongoing ischemia. Primary PCI is the
preferred strategy in this population.

*The proposed time windows are system goals. For any individual patient, every effort should be
made to provide reperfusion therapy as rapidly as possible.
Reperfusion at a PCI-Capable Hospital

Primary PCI in STEMI

 Primary PCI in STEMI

I IIa IIb III

Primary PCI should be performed in patients with STEMI and
ischemic symptoms of less than 12 hours’ duration.

I IIa IIb III

Primary PCI should be performed in patients with STEMI and
ischemic symptoms of less than 12 hours’ duration who have
contraindications to fibrinolytic therapy, irrespective of the time
delay from FMC.

I IIa IIb III

Primary PCI should be performed in patients with STEMI and
cardiogenic shock or acute severe HF, irrespective of time delay
from MI onset.
 Primary PCI in STEMI

I IIa IIb III

Primary PCI is reasonable in patients with STEMI if there is clinical
and/or ECG evidence of ongoing ischemia between 12 and 24
hours after symptom onset.

I IIa IIb III

PCI should not be performed in a noninfarct artery at the time of
primary PCI in patients with STEMI who are hemodynamically
stable
Harm
Primary PCI in STEMI
Reperfusion at a Non–PCI-Capable
Hospital

Fibrinolytic Therapy When

There Is an Anticipated
Delay to Performing Primary
PCI Within 120 Minutes of
FMC
 Fibrinolytic Therapy When There Is an Anticipated
Delay to Performing Primary PCI Within 120 Minutes
of FMC
I IIa IIb III
In the absence of contraindications, fibrinolytic therapy should be
given to patients with STEMI and onset of ischemic symptoms
within the previous 12 hours when it is anticipated that primary
PCI cannot be performed within 120 minutes of FMC.
I IIa IIb III
In the absence of contraindications and when PCI is not
available, fibrinolytic therapy is reasonable for patients with
STEMI if there is clinical and/or ECG evidence of ongoing
ischemia within 12 to 24 hours of symptom onset and a large
area of myocardium at risk or hemodynamic instability.
I IIa IIb III
Fibrinolytic therapy should not be administered to patients with
ST depression except when a true posterior (inferobasal) MI is
suspected or when associated with ST elevation in lead aVR.
Harm
Indications for Fibrinolytic Therapy When There Is a
>120-Minute Delay From FMC to Primary PCI
Routine Medical Therapies

Beta Blockers
 Beta Blockers
I IIa IIb III
Oral beta blockers should be initiated in the first 24 hours in
patients with STEMI who do not have any of the following: signs
of HF, evidence of a low output state, increased risk for
cardiogenic shock,* or other contraindications to use of oral beta
blockers (PR interval >0.24 seconds, second- or third-degree
heart block, active asthma, or reactive airways disease).
I IIa IIb III
Beta blockers should be continued during and after
hospitalization for all patients with STEMI and with no
contraindications to their use.

*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the
risk of developing cardiogenic shock) are age >70 years, systolic BP <120 mm Hg, sinus
tachycardia >110 bpm or heart rate <60 bpm, and increased time since onset of symptoms of
STEMI.
 Beta Blockers

I IIa IIb III

Patients with initial contraindications to the use of beta blockers
in the first 24 hours after STEMI should be reevaluated to
determine their subsequent eligibility.

I IIa IIb III

It is reasonable to administer intravenous beta blockers at the
time of presentation to patients with STEMI and no
contraindications to their use who are hypertensive or have
ongoing ischemia.
Routine Medical Therapies

Renin-Angiotensin-
Aldosterone System
Inhibitors
 Renin-Angiotensin-Aldosterone System
Inhibitors
I IIa IIb III
An ACE inhibitor should be administered within the first 24 hours
to all patients with STEMI with anterior location, HF, or EF less
than or equal to 0.40, unless contraindicated.

I IIa IIb III

An ARB should be given to patients with STEMI who have
indications for but are intolerant of ACE inhibitors.
 Renin-Angiotensin-Aldosterone System
Inhibitors
I IIa IIb III
An aldosterone antagonist should be given to patients with
STEMI and no contraindications who are already receiving an
ACE inhibitor and beta blocker and who have an EF less than or
equal to 0.40 and either symptomatic HF or diabetes mellitus.

I IIa IIb III

ACE inhibitors are reasonable for all patients with STEMI and no
contraindications to their use.
Routine Medical Therapies

Lipid Management
 Lipid Management

I IIa IIb III

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

I IIa IIb III

It is reasonable to obtain a fasting lipid profile in patients with
STEMI, preferably within 24 hours of presentation.
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