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Acute Coronary

Syndrome

Chairman : Dr.Venkataramanappa

Moderator : Dr. Vinay

Presentor : Dr. Rahul.P.J


Acute coronary syndrome (ACS) :
 is a set of signs and symptoms suggestive
of sudden cardiac ischemia.

 usually caused by disruption of


atherosclerotic plaque in an epicardial
coronary artery.
include:
 Unstable Angina (UA)
 Non-ST Segment Elevation
Myocardial Infarction (NSTEMI),
&
 ST Segment Elevation
Myocardial Infarction (STEMI),
commonly referred to as a heart
attack.
Spectrum of Acute Coronary
Syndromes
Presentation Ischemic Discomfort
at Rest

Emergency No ST-Segment ST-Segment


Department Elevation Elevation

+ +
+ +
In-Hospital

Unstable Non-Q-wave MI Q-wave MI


Angina
(⊕ : positive cardiac biomarker)
• New Terminology in ACS
Plaque
Rupture

Stable Unstable Non– Q-wave


Old term Angina Angina Q-wave MI MI

New term Atherothrombosis UA/NSTEMI STEMI


Days- Minutes-
weeks hours

Antithrombotic Thrombolysis
Therapy Primary PCI

ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation
myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention.
Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
 ACS should be distinguished from stable
angina,develops during exertion and
resolves at rest. In contrast ,unstable
angina- occurs suddenly, often at rest or
with minimal exertion, or at lesser degrees
of exertion than the individual's previous
angina ("crescendo angina").
 New onset angina is also considered
unstable angina, since it suggests a new
pathophysiologic process in the coronary
artery.
Angina
• Chest pain and
related symptoms
which are caused
by inadequate
blood flow and
oxygen supply to
the myocardial
cells of the heart.
Unstable Angina

• Symptoms of
angina at rest
• New onset of
exertional angina
• Increase in
severity of
previously “stable”
angina
NSTEMI

• Similar to UA
except that
ischemia is severe
enough to cause
myocardial
damage resulting
in the release of
cardiac enzymes
Who’s at risk ?
• Classical: Male > Females
until age 60
• Gender Difference
• Symptom Presentation:
– Males – primarily chest
discomfort
– Females
» Shortness of Breath 55%
» Weakness 52%
» Fatigue 40%
» No Chest Pain 40%
• Risk Factors
Gender
Cigarette smoking
Cholesterol – LDL
Hypertension
Diabetes – vascular
disease more than
blood sugar level
Activity level
Stress
PATHOPHYSIOLOGY
 Decrease in O2 supply &/ increase myocardial O2 demand,
superimposed on coronary obstruction.
 4 pathophysiological processes contribute to this-
(a) plaque rupture/erosion with superimposed non
occlusive thrombus.
(b) dynamic obstruction {eg: coronary spasm}
(c) progressive mechanical obstruction.
(d) secondary to other systemic conditions{ anaemia}

AMONG UA/ NSTEMI-


 5% - left main vessel stenosis
 15%- 3 vessel CAD
 30%- 2 vessel disease
 40%- single vessel disease
 10%- no critical coronary stenosis
Unstable Angina
pathogenesis

• Plaque disruption

• Acute thrombosis

• Vasoconstriction
 Plaque disruption
– Passive plaque disruption
soft plaque with high concentration of cholesteryl esters and a thin
fibrous cap
– Active plaque disruption
macrophage-rich area with enzymes that may degrade and weaken
the fibrous cap; predisposing it to rupture
 Acute Thrombosis
-- Vulnerable plaque
disrupted plaque with ulceration
occurring in 2/3 of unstable patients
exposed lipid-rich core abundant in cholesteryl ester-highly
thrombogenic
--Systemic Hypercoagulable State
disrupted plaque with erosion
occurring in 1/3 of unstable patients
 Vasoconstriction
--the culprit lesion in response to arterial damage/plaque
disruption
--area of dysfunctional endothelium near the culprit lesion
--platelet-dependent and thrombin-dependent vasoconstriction,
-- --mediated by serotonin &
Process of resolution
– spontaneous thrombolysis
– vasoconstriction resolution
– presence of collateral circulation
Delayed or absence of resolution
may lead to non-Q-wave or Q-wave
myocardial infarction
The signs and symptoms may include:
• chest pain
• shortness of breath
• nausea
• vomiting
• diaphoresis (sweating)
• palpitations
• anxiety or sense of impending doom
• a feeling of being acutely ill
Chest Pain vs. Discomfort
Quality:
Heaviness Pressure
Constriction Tightness
Strangulation Indigestion
Burning Aching
Choking

– Expanding from within Or just “an


unpleasant sensation”
“Classic” Anginal chest pain!
• Location: central chest
• Quality: squeezing, pressure, heaviness
• Radiation: arm(s), neck, jaw
• Associated symptoms: dyspnea,
diaphoresis, nausea
• Eliciting factors: exertion
• Relieving factors: rest, nitroglycerin
Differential Diagnosis
• Musculoskeletal • Psychiatric
• Gastrointestinal • Pulmonary
• Cardiac • Other/unknown
Cardiovascular Chest Pain

• Coronary Heart • Myocarditis


Disease • Valvular Heart
– Stable angina pectoris
– Unstable angina Disease
– Myocardial infarction – Aortic stenosis
– Mitral stenosis
• Coronary – Hypertrophic
Vasomotor cardiomyopathy

Disease • Aortic Dissection


– Variant angina
– Microvascular angina
• Post-
pericardiotomy
• Pericarditis
• Severity of Symptoms, not necessarily
correlated with severity of illness.
 Physical Appearance:
• “Normal”
• Pallor cold, clammy skin
• pulse-strong
• weak or thready or absent
• regular or irregular
• Precordial palpitations
• Altered consciousness
• Examination- may be unremarkable.
• If large area of myocardial ischaemia/large
NSTEMI,a 3rd &/ 4th heart sound, bibasilar rales &
sometimes hypotension, resembling findings of
large STEMI.
LABORATORY FINDINGS-
 ELECTROCARDIOGRAM-
ST segnent depression
Trasient ST segment elevation
T wave inversion
CARDIAC BIOMARKERS-
• Elevated biomarkers of necrosis- CK-MB,troponins
used 2 distinguish UA from NSTEMI
• Performed at baseline, 4-6hrs & 12hrs
Risk Stratification

Low Risk
• new-onset exertional angina
• minor chest pain during
exercise
• pain relieved promptly by
nitroglycerine
Management
• can be managed safely as an
outpatient (assuming close
follow-up and rapid
investigation)
Intermediate Risk
• prolonged chest pain
• diagnosis of rule-out MI
Management
• observe in the ER or Chest Pain Unit
• monitor clinical status and ECG
• obtain cardiac enzymes every 8 to 12 hours

High Risk
•recurrent chest pain
• ST-segment change
•hemodynamic compromise
•elevation in cardiac enzymes
Management
•monitor in the Coronary Care Unit
Therapeutic Goals
• Reduce myocardial
ischemia
• Control of symptoms
• Prevention of MI and
death

Medical Management
• Anti-ischemic therapy
• Anti-thrombotic therapy
Medical Therapy
• Anti-ischemic therapy
– nitrates, beta blockers, calcium
antagonists
• Anti-thrombotic therapy
– Anti-platelet therapy
• aspirin, ticlopidine, clopidogrel,
GP IIb/IIIa inhibitors
– Anti-coagulant therapy
• heparin, low molecular weight
heparin (LMWH), warfarin, hirudin,
hirulog
Anti-ischemic Therapy
• restrict activities
• morphine
• oxygen
• nitroglycerine
– pain relief, prevent silent ischemia, control hypertension, improve
ventricular dysfunction
– nitrate free period recommended after the first 24-48 hours
• beta-blockers
-- lowering angina threshold
-- prevent ischemia and death after MI
-- particularly useful during high sympathetic tone

• calcium antagonists
-- particularly the rate-limiting agents
-- nifedipine is not recommended without concomitant ß-blockade
Anti Thrombotic therapy
Anti-platelet Therapy
• aspirin is the “gold standard”
– irreversible inhibition of the cyclooxygenase pathway in platelets,
blocking formation of thromboxane A2, and platelet aggregation.
– in UA, ASPRIN reduced the risk of fatal or nonfatal MI by 71%
during the acute phase, 60% at 3 months, and 52% at 2 years
– bolus dose of 160-325 mg, followed by maintenance dose of 80-160
mg/d

• Thienopyridines
-- Ticlopidine (Ticlid )
-- clopidogrel (Plavix )

{ block platelet aggregation induced by ADP and the transformation of


GP IIb/IIIa into its high affinity state }
• GP IIb/IIIa inhibitors
– abciximab (monoclonal antibody)
– eptifibatide (peptidic inhibitor)
– lamifiban and tirofiban (non-peptides)

{direct occupancy of the GP IIb/IIIa receptor by a monoclonal antibody or by


synthetic compounds mimicking the RGD sequence for fibrinogen binding
prevents platelet aggregation }
Anti-coagulant Therapy
• Heparin
-- trials showed a 33% risk reduction in MI and death, but with a two fold
increase in major bleeding
– titrate PTT to 2x the upper limits of normal

•Low-molecular-weight heparin
-- advantages over heparin:
-- better bio-availability
-- higher ratio (3:1) of anti-Xa to anti-IIa activity
-- longer anti-Xa activity, avoid rebound
-- induces less platelet activation
-- ease of use (subcutaneous - qd or bid)
-- no need for monitoring

1. Circulation 1994;89:81-88
2. JAMA 1996;276:811-815
Coronary Interventions

– early intervention vs conservative strategy


(coronary angiography within 24-48 hrs,
followed by angioplasty {PCI} or bypass surgery
{CABG} )
LONG TERM MANAGEMENT
Risk factor modification, optimal wt :, diet
Cessation of smokeing, daily exercise, BP
control, tight control of hyperglycemia
Lipid management
Drugs { B-blockers, statins, ACE inhibitors etc}
Circulation 1994;89:1545-1556
STEMI

Acute, evolving or recent MI


• Requires 1 of 2:
1. Typical rise and gradual fall (troponin) or more
rapid rise and fall (CK-MB) of markers of
myocardial necrosis with >= 1 of:
- Symptoms
- Q waves
- ECG c/w ischemia
- S/p coronary artery intervention
2. Pathologic findings of AMI
Symptoms of STEMI
• Chest, epigastric, arm, wrist, jaw pain or
discomfort w/ exertion or at rest
• Pain-is deep & visceral {heavy, squeezing & crushing,
stabbing or burning} IIar in charc: of angina pectoris;
but more severe & lasts longer.
• Associated sx: dsypnea, diaphoresis, nausea,
vomiting, light-headedness,anxiety,weakness &
sense of impending doom.
• Other presentation-sudden loss of consciousness
confusional state.
• Substernal pain(>30min)+diaphoresis– strongly
suggests STEMI
• O/E-
• 25% with ant: infarction—sympathetic sys:
hyperactivity {tachycardia}
• 50% of inf: infarction– parasympathetic
hyperactivity{bradycardia &/hypotension}
• Raise in temp upto 38’ C
• Arterial press:-variable
• PRECORDIUM-quite..
• Apical impulse- diff: 2 palpate.
• S1-dec in intensity, S2-paradoxical splitting, Audible S3 &
S4.
• Trasient midsystolic/late systolic murmur in apical
area {dysfunction of mitral valve apparatus}
Laboratory findings
Electrocardiogram-
• ST segment elevation- in 2 or more contiguous leads
{corresponding to wall supplied by epicardial artery}
• 75%- presence of Q waves
• Gradually ST segment elevation dec: & T wave
inversion develops
• T wave inversion-persist 4 wks to mnths.
• Q waves-persist 4 mnths to yrs,sometimes lifelong
Cardiac markers-
• CK-rises within 4-8hrs,returns to normal by 48-
72hrs {lacks specificity for STEMI}
• CK-MB{more specific}-rises 6-10hrs aft onset of infarc-
-tion,{in absence of reperfusion/thrombolysis},peaks-24hrs, &
returns to normal- 36-72hrs
• Troponins{cTnT & cTnI}-rises 3-6hrs & peak-
24hrs,remain elevated for 7-10 days
• Myoglobin: for rapid diagnosis

Biochemical Markers II
Biochemical Markers III
Molecular First Duration of Sensit Specif
Protein mass (kD) detection detection ivity icity

Myoglobin 16 1.5–2 8–12 hours +++ +


hours
CK-MB 83 2–3 1–2 days +++ +++
hours
Troponin I 33 3–4 7–10 days ++++ ++++
hours
Troponin T 38 3–4 7–14 days ++++ ++++
hours
CK 96 4–6 2–3 days ++ ++
hours
Non MI Causes of Troponin
Elevation

• Tachycardia
• PE w/ Right Vent: infarct
• Cardiac failure w/ myonecrosis
• Cardiac surgery
• Myocarditis
• Renal failure
Coronary Angiogram
• Observer variability
• Discordance btw severity of lesion
and physiologic effects
– Greater stenosis vs more unstable
plaques?
• 2-D picture of a 3-D problem
– Diffuse disease may limit estimation of
“abnormal segments”
• Missed lesions
Prehospital Chest Pain Evaluation
and Treatment

Prehospital EMS providers should administer


162 to 325 mg of aspirin (chewed) to chest pain
patients suspected of having STEMI unless
contraindicated or already taken by the patient.
Although some trials have used enteric-coated
aspirin for initial dosing, more rapid buccal
absorption occurs with non–enteric-coated
formulations.
ED Evaluation of
Patients With STEMI

Brief Physical Examination in the ED


1. Airway, Breathing, Circulation (ABC)
2. Vital signs, general observation
3. Presence or absence of jugular venous distension
4. Pulmonary auscultation for rales
5. Cardiac auscultation for murmurs and gallops
6. Presence or absence of stroke
7. Presence or absence of pulses
8. Presence or absence of systemic hypoperfusion (cool, clammy,
pale, ashen)
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Life-Threatening

Aortic dissection Tension pneumothorax


Pulmonary embolus Boerhaave syndrome
Perforating ulcer (esophageal rupture with
mediastinitis)
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Other Cardiovascular and
Nonischemic

Pericarditis LV hypertrophy with strain


Atypical angina Brugada syndrome
Early repolarization
Wolff-Parkinson-White Myocarditis
syndrome Hyperkalemia
Deeply inverted T-waves Bundle-branch blocks
suggestive of a central
nervous system lesion Vasospastic angina
or apical hypertrophic Hypertrophic
cardiomyopathy cardiomyopathy
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Other Noncardiac

Gastroesophageal reflux Cervical disc or neuropathic


(GERD) and spasm pain
Chest-wall pain Biliary or pancreatic pain
Pleurisy Somatization and
psychogenic pain disorder
Peptic ulcer disease
Panic attack
Electrocardiogram

If the initial ECG is not diagnostic of STEMI, serial


ECGs or continuous ST-segment monitoring should
be performed in the patient who remains
symptomatic or if there is high clinical suspicion for
STEMI.
Electrocardiogram

Show 12-lead ECG results to emergency physician


within 10 minutes of ED arrival in all patients with
chest discomfort (or anginal equivalent) or other
symptoms of STEMI.

In patients with inferior STEMI, ECG leads should


also be obtained to screen for right ventricular
infarction.
Laboratory Examinations

Laboratory examinations should be performed as part of the


management of STEMI patients, but should not delay the
implementation of reperfusion therapy.

 Serum biomarkers for cardiac damage


 Complete blood count (CBC) with platelets
 International normalized ratio (INR)
 Activated partial thromboplastin time (aPTT)
 Electrolytes and magnesium
 Blood urea nitrogen (BUN)
 Creatinine
 Glucose
 Complete lipid profile
Biomarkers of Cardiac Damage

Cardiac-specific troponins should be used as the


optimum biomarkers for the evaluation of patients
with STEMI who have coexistent skeletal muscle
injury.

For patients with ST elevation on the 12-lead ECG


and symptoms of STEMI, reperfusion therapy
should be initiated as soon as possible and is not
contingent on a biomarker assay.
Imaging

Patients with STEMI should have a portable chest


X-ray, but this should not delay implementation of
reperfusion therapy (unless a potential
contraindication is suspected, such as aortic
dissection).

Imaging studies such as a high quality portable chest


X-ray, transthoracic and/or transesophageal
echocardiography, and a contrast chest CT scan or
an MRI scan should be used for differentiating STEMI
from aortic dissection in patients for whom this
distinction is initially unclear.
Oxygen

Supplemental oxygen should be administered to


patients with arterial oxygen desaturation (SaO2
< 90%).

It is reasonable to administer supplemental


oxygen to all patients with uncomplicated STEMI
during the first 6 hours.
Nitroglycerin

Patients with ongoing ischemic discomfort should


receive sublingual NTG (0.4 mg) every 5 minutes for a
total of 3 doses, after which an assessment should be
made about the need for intravenous NTG.

Intravenous NTG is indicated for relief of ongoing


ischemic discomfort that responds to nitrate therapy,
control of hypertension, or management of pulmonary
congestion.
Nitroglycerin

Nitrates should not be administered to patients with:


• systolic pressure < 90 mm Hg or ≥ to 30 mm
Hg below baseline
• severe bradycardia (< 50 bpm)
• tachycardia (> 100 bpm) or
• suspected RV infarction.

Nitrates should not be administered to patients who


have received a phosphodiesterase inhibitor for
erectile dysfunction within the last 24 hours (48
hours for tadalafil).
Analgesia

Morphine sulfate (2 to 4 mg intravenously with


increments of 2 to 8 mg intravenously repeated at
5 to 15 minute intervals) is the analgesic of choice
for management of pain associated with STEMI.
Aspirin

Aspirin should be chewed by patients who have


not taken aspirin before presentation with STEMI.
The initial dose should be 162 mg to 325 mg

Although some trials have used enteric-coated aspirin for


initial dosing, more rapid buccal absorption occurs with
non–enteric-coated formulations.
Beta-Blockers

Oral beta-blocker therapy should be administered


promptly to those patients without a contraindication,
irrespective of concomitant fibrinolytic therapy or
performance of primary PCI.

It is reasonable to administer intravenous beta-


blockers promptly to STEMI patients without
contraindications, especially if a tachyarrhythmia or
hypertension is present.
Reperfusion

• Given the current literature, it is not possible to say


definitively that a particular reperfusion approach is
superior for all pts, in all clinical settings, at all times of
day

• The main point is that some type of reperfusion therapy


should be selected for all appropriate pts with suspected
STEMI

• The appropriate & timely use of some reperfusion


therapy is likely more important than the choice of
therapy
Treatment Delayed is Treatment Denied

Symptom Call to PreHospital ED Cath Lab


Recognition Medical System

Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy


Contraindications and Cautions
for Fibrinolysis in STEMI
• Any prior intracranial hemorrhage

Absolute • Known structural cerebral vascular lesion


Contraindications (e.g., arteriovenous malformation)
• Known malignant intracranial neoplasm
(primary or metastatic)
• Ischemic stroke within 3 months EXCEPT
acute ischemic stroke within 3 hours
• Suspected aortic dissection
• Active bleeding/ bleeding diathesis
• Sig: closed head/ facial trauma{within 3 mths
NOTE: Age restriction for fibrinolysis has been removed
compared with prior guidelines.
Contraindications and Cautions
for Fibrinolysis in STEMI
Relative • History of chronic, severe, poorly controlled
Contraindications hypertension
• Severe uncontrolled hypertension on
presentation (SBP > 180 mm Hg or DBP >
110 mm Hg)
• History of prior ischemic stroke greater than
3 months, dementia, or known intracranial
pathology not covered in contraindications
• Traumatic or prolonged (> 10 minutes) CPR
or major surgery (< 3 weeks)
Contraindications and Cautions
for Fibrinolysis in STEMI

Relative • Recent (< 2 to 4 weeks) internal bleeding


Contraindications • Noncompressible vascular punctures
• For streptokinase/anistreplase: prior
exposure (> 5 days ago) or prior allergic
reaction to these agents
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher the
INR, the higher the risk of bleeding
Fibrinolysis

Fibrinolytic therapy should not be administered to


asymptomatic patients whose initial symptoms of
STEMI began more than 24 hours earlier.

Fibrinolytic therapy should not be administered to


patients whose 12-lead ECG shows only ST-
segment depression, except if a true posterior MI
is suspected.
Primary PCI for STEMI:
Specific Considerations
It is reasonable to perform primary PCI for
patients with onset of symptoms within the
prior 12 to 24 hours and 1 or more of the
following:

a. Severe CHF

b. Hemodynamic or electrical instability

c. Persistent ischemic symptoms.


Rescue PCI

Rescue PCI is reasonable for selected patients 75


years or older with ST elevation or LBBB or who
develop shock within 36 hours of MI and are suitable
for revascularization that can be performed within 18
hours of shock.

It is reasonable to perform rescue PCI for patients


with one or more of the following:

a. Hemodynamic or electrical instability

b. Persistent ischemic symptoms.


PCI After Fibrinolysis

In patients whose anatomy is suitable, PCI should be


performed for the following:

Objective evidence of recurrent MI

Moderate or severe spontaneous/provocable


myocardial ischemia during recovery from STEMI

Cardiogenic shock or hemodynamic instability.


Ancillary Therapy to Reperfusion

Unfractionated heparin (UFH) should be given


intravenously in:

 Patients undergoing PCI or surgical


revascularization

 After alteplase, reteplase, tenecteplase

 After streptokinase, anistreplase, urokinase in


patients at high risk for systemic emboli.
Aspirin

A daily dose of aspirin (initial dose of 162 to


325 mg orally; maintenance dose of 75 to 162
mg) should be given indefinitely after STEMI to
all patients without a true aspirin allergy.
Thienopyridines

In patients for whom PCI is planned, clopidogrel


should be started and continued:

• ≥ 1 month after bare-metal stent


• ≥ 3 months after sirolimus-eluting stent
• ≥ 6 months after paclitaxel-eluting stent
• Up to 12 months in absence of high risk for
bleeding.
Thienopyridines

In patients taking clopidogrel in whom CABG is


planned, the drug should be withheld for at
least 5 days, and preferably for 7 days, unless
the urgency for revascularization outweighs the
risk of excessive bleeding.
Glycoprotein IIb/IIIa Inhibitors

It is reasonable to start treatment with


abciximab as early as possible before primary
PCI (with or without stenting) in patients with
STEMI.

Treatment with tirofiban or eptifibatide may be


considered before primary PCI (with or
without stenting) in patients with STEMI.
Other Pharmacological Measures

Inhibition of Angiotensin converting enzyme (ACE)


the renin
inhibitors
-angiotensin
-aldosterone Angiotensin receptor blockers (ARB)
system
Aldosterone blockers
Glucose control
Magnesium
Calcium channel blockers
Strict Glucose Control During STEMI

An insulin infusion to normalize blood glucose


is recommended for patients and complicated
courses.

It is reasonable to administer an insulin


infusion to normalize blood glucose even in
patients with an uncomplicated course.
Secondary Prevention and Long Term Management

Goals Recommendations

Smoking • Assess tobacco use.


Goal:
Complete • Strongly encourage patient and family to
Cessation stop smoking and to avoid secondhand
smoke.

• Provide counseling, pharmacological


therapy (including nicotine replacement and
bupropion), and formal smoking cessation
programs as appropriate.
Secondary Prevention and Long Term Management

Goals Recommendations
If blood pressure is 120/80 mm Hg or greater:
Blood
pressure • Initiate lifestyle modification (weight control, physical
control: activity, alcohol moderation, moderate sodium
Goal: < 140/90 restriction, and emphasis on fruits, vegetables, and low-
mm Hg or fat dairy products) in all patients.
<130/80 mm Hg
if chronic If blood pressure is 140/90 mm Hg or greater or
kidney disease 130/80 mm Hg or greater for individuals with
or diabetes chronic kidney disease or diabetes:

• Add blood pressure-reducing medications,


emphasizing the use of beta-blockers and inhibitors of
the renin-angiotensin-aldosterone system.
Secondary Prevention and Long Term Management

Goals Recommendations

Physical • Assess risk, preferably with exercise test, to


activity: guide prescription.
Minimum goal:
30 minutes 3 to 4
days per week; • Encourage minimum of 30 to 60 minutes of
Optimal daily
activity, preferably daily but at least 3 or 4 times
weekly (walking, jogging, cycling, or other
aerobic activity) supplemented by an increase in
daily lifestyle activities (e.g., walking breaks at
work, gardening, household work).

• Cardiac rehabilitation programs are


recommended for patients with STEMI.
Secondary Prevention and Long Term Management
Goals Recommendations
Lipid
• Start dietary therapy in all patients (< 7% of total
management:
calories as saturated fat and < 200 mg/d cholesterol).
(TG less than
Promote physical activity and weight management.
200 mg/dL)
Encourage increased consumption of omega-3 fatty
Primary goal:
acids.
LDL-C << than
100 mg/dL
• Assess fasting lipid profile in all patients, preferably
within 24 hours of STEMI. Add drug therapy according to
the following guide:

LDL-C < 100 mg/dL (baseline or on treatment):


Statins should be used to lower LDL-C.

LDL-C ≥ 100 mg/dL (baseline or on


treatment):
Intensify LDL-C–lowering therapy with drug
treatment,giving preference to statins.
Secondary Prevention and Long Term Management

Goals Recommendations

Antiplatelet • In the absence of contraindications, start aspirin


agents/
75 to 162 mg/d and continue indefinitely.
anticoagulants
• If aspirin is contraindicated, consider clopidogrel
75 mg/day or warfarin.
• Manage warfarin to INR 2.5 to 3.5 in post-
STEMI patients when clinically indicated or for
those not able to take aspirin or clopidogrel.
Secondary Prevention and Long Term Management

Goals Recommendations

Renin- ACE inhibitors in all patients indefinitely; start early in


Angiotensin- stable, high-risk patients (ant. MI, previous MI, Killip
Aldosterone class ≥ 2 [S3 gallop, rales, radiographic CHF], LVEF <
System 0.40).
Blockers
Angiotensin receptor blockers in patients who are
intolerant of ACE inhibitors and with either clinical or
radiological signs of heart failure or LVEF < 0.40.

Aldosterone blockade in patients without significant renal


dysfunction or hyperkalemia who are already receiving
therapeutic doses of an ACE inhibitor, have LVEF ≤ 0.40,
and have either diabetes or heart failure.
Secondary Prevention and Long Term Management

Goals Recommendations

Beta- Start in all patients. Continue indefinitely.


Blockers Observe usual contraindications.
Cardiac Rehabilitation

Cardiac rehabilitation/secondary prevention


programs, when available, are recommended
for patients with STEMI, particularly those
with multiple modifiable risk factors and/or
those moderate- to high-risk patients in whom
supervised exercise training is warranted.
THANK U