Acute coronary syndrome

1 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)
Acute coronary syndrome
Acute coronary syndrome is a myocardial ischemia due to :
1- myocardial infarction (NSTEMI or STEMI)
2- unstable angina
NSTEMI = non-ST elevation myocardial infarction
STEMI = ST elevation myocardial infarction
• Unstable angina : is defined as angina at rest, new onset exertional angina
(<2 months), recent acceleration of angina (<2 months), or post
revascularization angina.
Acute myocardial infarction (MI) remains a leading cause of morbidity and
mortality worldwide. Myocardial infarction occurs when myocardial ischemia, a
diminished blood supply to the heart, exceeds a critical threshold and
overwhelms myocardial cellular repair mechanisms designed to maintain normal
operating function and homeostasis. Ischemia at this critical threshold level for
an extended period results in irreversible myocardial cell damage or death.
(Critical imbalance between oxygen supply and demand to the myocardium)
ACUTE CORONARY SYNDROME
No ST Elevation ST Elevation
Unstable Angina NQMI QwMI
Myocardial Infarction
NSTEMI

Classification
Anatomic or morphologic
Transmural= Full thickness
Non-transmural= Partial thickness
ECG
Q wave MI
Non Q wave MI
Does not distinguish transmural from a non-transmural MI .
DEFINITION:
Myocardial infarction ((acute, evolving, recent))
Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of
biochemical markers of myocardial necrosis with at least one of the following:
– a) Ischemic symptoms;
– b) Development of pathologic Q waves on the ECG;
– c) ECG changes indicative of ischemia (ST segment elevation or
depression);( dynamic T wave changes) or
– d) Coronary artery intervention (e.g., coronary angio-plasty).
NSTEMI is an acute process of myocardial ischemia with sufficient severity and
duration to result in myocardial necrosis.
– The initial ECG in patients with NSTEMI does not show ST-segment
elevation.
– NSTEMI is distinguished from UA by the detection of cardiac markers
indicative of myocardial necrosis in NSTEMI .

Unstable angina—an acute process of myocardial ischemia that is not of
sufficient severity and duration to result in myocardial necrosis.
Prevalence
Incidence of 600 per 100,000 people
The survival rate for U.S. pts hospitalized with MI is approximately 90%
This represents a significant improvement in survival and is related to
improvements in emergency medical response and treatment strategies.
Increase in the proportion of NSTEMI compared to STEMI
Approximately 500,000 to 700,000 deaths are caused by heart disease
annually in the United States.
PATHOPHYSIOLOGY:
The severity of an MI depends on three factors: 1.the level of the occlusion in
the coronary artery 2. the length of time of the occlusion, and 3. the presence
or absence of collateral circulation.
Generally, the more proximal the coronary occlusion, the more extensive the
amount of myocardium that will be at risk of necrosis. The larger the myocardial
infarction, the greater the chance of death because of a mechanical
complication or pump failure. The longer the period of vessel occlusion, the
greater the chances of irreversible myocardial damage distal to the occlusion.
STEMI is usually the result of complete coronary occlusion after plaque rupture.
This arises most often from a plaque that previously caused less than 50%
occlusion of the lumen. NSTEMI is
usually associated with greater plaque
burden without complete occlusion.
This difference contributes to the
increased early mortality seen in
STEMI and the eventual equalization

of mortality between STEMI and NSTEMI after 1 year.
Most myocardial infarctions are caused by a disruption in the vascular
endothelium associated with an unstable atherosclerotic plaque that stimulates
the formation of an intracoronary thrombus, which results in coronary artery
blood flow occlusion. If such an occlusion persists for more than 20 minutes,
irreversible myocardial cell damage and cell death will occur.
The atherosclerotic plaque occurs over a period of years to decades. The plaque
has a fibromuscular cap and an underlying lipid-rich core. Plaque erosion can
occur because of the actions of matrix metalloproteases and the release of
other collagenases and proteases in the plaque, which result in thinning of the
overlying fibromuscular cap. The action of proteases, in addition to
hemodynamic forces applied to the arterial segment, can lead to a disruption of
the endothelium and fissuring or rupture of the fibromuscular cap. The loss of
structural stability of a plaque often occurs at the juncture of the fibromuscular
cap and the vessel wall, a site otherwise known as the shoulder region.
Disruption of the endothelial surface can cause the formation of thrombus via
platelet-mediated activation of the coagulation cascade. If a thrombus is large
enough to occlude coronary blood flow, an MI can result.

Risk factors for atherosclerosis:
Age
Male gender
Smoking
Hypercholesterolemia and triglyceridemia
Diabetes Mellitus
Poorly controlled hypertension
Family History
Sedentary lifestyle
Type A personality
Signs and symptoms:
The history is critical in making the diagnosis of MI and sometimes provide only
the only clues that lead to the diagnosis in the initial phase of presentation.
Acute MI can have unique manifestations in individual patients. The degree of
symptoms ranges from none at all to sudden cardiac death. An asymptomatic
MI is not necessarily less severe than a symptomatic event, but patients who
experience asymptomatic MIs ((SILENT)) are more likely to be diabetic. Despite
the diversity of manifesting symptoms of MI, there are some characteristic
symptoms.
TYPICAL SYMPTOM-chest pain or discomfort. You have to ask the patient about
onset as the vascular insult is acute and ask about duration , aggravating or
relieving symptoms ,site , character, radiation, severity ,course and association.
ONSET-all of a sudden , for first time in most of cases , awake pt
SITE-anterior precordium , central , right or left sided ,interscapular
DURATION- minutes to hours to days according to severity.

CHARACTER- pressure sensation, fullness, or squeezing in the midportion
of the thorax, burning , heaviness, stabbing , piercing, heart burn, pins
and needles, colicky, tightness ,ANY TYPE .
RADIATION-may radiate to jaw OR teeth, tip of shoulder, arm to the inner
sit of the upper limb more left or both limbs, and/or back ,anterior neck
and epigastrium up and down to the jaw.
AGGREVATING FACTORS- 60% no factors, others can be related to
stressful event or exercise or heavy work or walking in windy weather or
sudden heavy work or bad news.
ASSOCITED SYMPTOMS
 Nausea with and without vomiting
 Diaphoresis or sweating
 Syncope or near syncope
 Dyspnea- angina equivalent, poor LV function
 Nausea
SEVERITY-awake the patient from sleeping , fear of death, abstinence
from work , can’t sleep or eat , interfere with daily activities , chest
discomfort that is not relieved in any posture.
ATYPICAL SYMPTOMS
As many as half of MI are clinically silent((DIABETICS AND ELDERY))
Epigastric discomfort with or without nausea and vomiting.
All of sudden epigastric pain in a patient above 40years wither heart burn
or colicy abdominal pain or radiating up to the neck.
Sudden dyspnea with out lung diseases.
Syncope or near syncope without other cause
Palpitation all of sudden with fear of death in elder pt.
Impairment of cognitive function without other cause.
Profuse sweating all of sudden in diabetic with out hypoglycemia.
Jaw pain all of sudden in elder patient.
Fatigability al of sudden
MI can occur at any time of the day, but most appear to be clustered
around the early hours of the morning or are associated with demanding
physical activity, or both.

Physical signs:
Most of the patients has no signs on presentation(completely normal).
Others , they may present with left ventricular failure (dyspnea) or sweating
and cold extremities in others.
The physical exam can often be unremarkable
Hypertension , Hypotension
Tachycardia , bradycardia.
Sweating , dyspnea , apprehensive
Acute valvular dysfunction may be present
Rales on chest examination
Neck vein distention
Third heart sound may be present
A fourth heart sound--- poor LV compliance
Dysrhythmias
Low grade fever( fever in MI develop after a day of MI).
CAUSES OF MI OTHER THAN PLAQUE:
Coronary artery vasospasm
Ventricular hypertrophy
Hypoxia
Coronary artery emboli
Cocaine

Arteries
Coronary anomalies
Aortic dissection
Pediatrics Kawasaki disease, Takayasu arteritis
Increased afterload which increases myocardial demand
Acute coronary syndromes can also be due to secondary
causes:
– Thyrotoxicosis
– Anemia
– Tachycardia
– Hypotension
– Hypoxemia
– Arterial inflammation (infection, arteritis)
Differentials
4 IMPORTANT LIFE SAVING DIAGNOSIS NOT TO BE MISSED:
1. Acute coronary syndrome
2. Pulmonary embolism
3. Aortic Dissection
4. Pneumothorax
Other D/D
Endocarditis Myocarditis Pericarditis
Anxiety Aortic stenosis Asthma
Cholecystitis and biliary colic Cholethiasis
Esophagitis Pneumonia COPD

Diagnosis
Dx of acute coronary syndrome is based on
 1- History,
 2- Physical exam,
 3- ECG,
 4- Cardiac enzymes

INVESTIGATION:
2 OF 3 ARE DIAGNOSTIC FOR MI:
1. CHEST PAIN
2. ECG
3. CARDIAC ENZYMES
1.Complete blood count:
CBC is indicated if anemia is suspected as precipitant
Leukocytosis may be observed within several hours after
myocardial injury and returns to levels within the reference
range within one week.
2.Renal function test and electrolytes:
Potassium and magnesium levels should be monitored and
corrected ( rhythmogenic).
Decrease cardiac output may lead to renal impairment .
Creatinine levels must be considered before using contrast dye
for coronary angiography and percutanous revascularization
3. Electrocardiogram
A normal ECG does not exclude ACS
The first diagnostic test is electrocardiography (ECG), which may
demonstrate that a MI is in progress or has already occurred
High probability include ST segment elevation in two contiguous
leads or presence of q waves
Intermediate probability ST depression

In addition to ST-segment elevation, 81% of electrocardiograms
during STEMI demonstrate reciprocal ST-segment depression as
well.
T wave inversions are less specific in NSTEMI
Localization of MI
ST elevation only
 Inferior wall- II, III, aVF
 Lateral wall_ I, aVL, V4-V6
 Anteroseptal- V1-V3
 Anterolateral- V1-V6
 Right ventricular- RV4, RV5
 Posterior- R/S ratio >1 in V1 and T wave inversion
4. Cardiac Biomarkers
Cardiac biomarkers are protein molecules released into the blood
stream from damaged heart muscle .
Living myocardial cells contain enzymes and proteins (e.g.,
creatine kinase, troponin I and T, myoglobin) associated with
specialized cellular functions. When a myocardial cell dies,
cellular membranes lose integrity, and intracellular enzymes and
proteins slowly leak into the blood stream. These enzymes and
proteins can be detected by a blood sample analysis. These
values vary depending on the assay used in each laboratory.
Given the acuity of a STEMI and the need for urgent intervention,
the laboratory tests are usually not available at the time of
diagnosis. Thus, good history taking and an ECG are used to
initiate therapy in the appropriate situations.

Since ECG can be inconclusive , biomarkers are frequently used to
evaluate for myocardial injury
These biomarkers have a characteristic rise and fall pattern.
a. Troponin T and I
• These isoforms are very specific for cardiac injury.
• Preferred markers for detecting myocardial cell injury.
• Rise 2-6 hours after injury
• Peak in 12-16 hours
• Stay elevated for 5-14 days
b. Creatinine Kinase ( CK-MB)
 Creatinine Kinase is found in heart muscle (MB), skeletal muscle
(MM), and brain (BB)
 Increased in over 90% of myocardial infraction
 However, it can be increased in muscle trauma, physical exertion,
post-op, convulsions, and other conditions
 Time sequence after myocardial infarction
 Begins to rise 4-6 hours
 Peaks 24 hours
 returns to normal in 2 days
 MB2 released from heart muscle and converted to MB1.
 A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates
myocardial injury

c. Myoglobin
Damage to skeletal or cardiac muscle release myoglobin into
circulation.
Time sequence after infarction
Rises fast 2hours Peaks at 6-8 hours
Returns to normal in 20-36 hours
Have false positives with skeletal muscle injury and renal failure
5. Chest X-Ray
 Chest radiography may provide clues to an alternative
diagnosis ( aortic dissection or pneumothorax)
 Chest radiography also reveals complications of myocardial
infarction such as heart failure(CONGESTED LUNG-WHITE).

5. Echocardiography
 Use 2-dimentional and M mode echocardiography when
evaluating overall ventricular function and wall motion
abnormalities, intracardiac thrombus.
 Echocardiography can also identify complications of MI ( eg.
Valvular or pericardial effusion, VSD)
 The presence of wall motion abnormalities on the ECHO may be
the result of an acute MI or previous (old) MI or other myopathic
processes, limiting its overall diagnostic utility.
Complications of MI:
Arrhythmic Complications of MI
About 90% of patients who have an acute myocardial infarction (AMI)
develop some form of cardiac arrhythmia during or immediately after the
event. In 25% of patients, such rhythm abnormalities manifest within the first
24 hours. In this group of patients, the risk of serious arrhythmias, such as
ventricular fibrillation, is greatest in the first hour and declines thereafter.
The incidence of arrhythmia is higher with an ST-elevation myocardial
infarction (STEMI) and lower with a non–ST-elevation myocardial infarction.
The clinician must be aware of these arrhythmias, in addition to reperfusion
strategies, and must treat those that require intervention to avoid
exacerbation of ischemia and subsequent hemodynamic compromise. Most
peri-infarct arrhythmias are benign and self-limited. However, those that
result in hypotension, increase myocardial oxygen requirements, and/or
predispose the patient to develop additional malignant ventricular
arrhythmias should be aggressively monitored and treated.
Pathophysiology of arrhythmic complications
AMI is characterized by generalized autonomic dysfunction that results in
enhanced automaticity of the myocardium and conduction system. Electrolyte
imbalances (eg, hypokalemia and hypomagnesemia) and hypoxia further
contribute to the development of cardiac arrhythmia.

The damaged myocardium acts as substrate for re-entrant circuits, due to
changes in tissue refractoriness.
Enhanced efferent sympathetic activity, increased concentrations of circulating
catecholamines, and local release of catecholamines from nerve endings in the
heart muscle itself have been proposed to play roles in the development of peri-
infarction arrhythmias. Furthermore, transmural infarction can interrupt
afferent and efferent limbs of the sympathetic nervous system that innervates
myocardium distal to the area of infarction. The net result of this autonomic
imbalance is the promotion of arrhythmias.
Classification of peri-infarction arrhythmias
Supraventricular tachyarrhythmias, including sinus tachycardia,
premature atrial contractions, paroxysmal supraventricular tachycardia,
atrial flutter, and atrial fibrillation
Accelerated junctional rhythms
Bradyarrhythmias, including sinus bradycardia and junctional bradycardia
Atrioventricular (AV) blocks, including first-degree AV block, second-
degree AV block, and third-degree AV block
Intraventricular blocks, including left anterior fascicular block, right
bundle branch block (RBBB), and left bundle branch block (LBBB)
Ventricular arrhythmias, including premature ventricular contractions
(PVCs), accelerated idioventricular rhythm, ventricular tachycardia, and
ventricular fibrillation
Reperfusion arrhythmias
Mechanical Complications of MI:
Left ventricular failure due to
1. Ventricular free wall rupture (VFWR)
2.ventricular septal rupture (VSR)
3. papillary muscle rupture with severe mitral regurgitation (MR).

4.RV infarction
5.Infarct expansion, aneurysm, LV remodeling
6. Intracardiac Thrombus
Treatment of ACS:
The goals of therapy in acute MI are 1. the expedient restoration of normal coronary blood
flow and 2. the maximum salvage of functional myocardium. These goals can be met by a
number of medical interventions and adjunctive therapies. The primary obstacles to
achieving these goals are the patient's failure to recognize MI symptoms quickly and the
delay in seeking medical attention. When patients present to a hospital, there are a variety of
interventions to achieve treatment goals. “Time is muscle” guides the management
decisions in acute STEMI, and an early invasive approach is the standard of care for acute
NSTEMI
Treatment of STEMI ((6A))
ADMISSION & CANNULA
ASSURANCE
ANALGESIA
ANGESIED
ASPIRIN 600MG CRUSHED
AIR- OXYGEN
THROMBOLYSIS FOR STEMI & LBBB/NG &HEPARIN FOR NSTEMI
• ASA
• NTG (consider MSO4 if pain not relieved)
• Beta Blocker
• Heparin/LMWH
• ACE-I after 24 hrs
• +/-Clopidogrel
• +/- Statin
• Activate the Cath Lab!!!
Pain Control
Pain from MI is often intense and requires prompt and adequate analgesia.
The agent of choice is morphine sulfate, IV at 5 to 15 minute intervals at
doses of 2 to 4 mg OR pethidine 50mg-150mg. Reduction in myocardial
ischemia also serves to reduce pain, so oxygen therapy, nitrates, and beta
blockers remain the mainstay of therapy.

Fibrinolytics
Restoration of coronary blood flow in MI patients can be accomplished
pharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy is
indicated for patients who present with a STEMI within 12 hours of symptom
onset without a contraindication. These are streptokinase. Metalase , tissue
plasminogen activator.
Absolute contraindications to fibrinolytic therapy
1. Allergy to thrombolysis
2. History of intracranial hemorrhage
3. Ischemic stroke or closed head injury within the past 3 months
4. Presence of an intracranial malignancy
5. Signs of an aortic dissection
6. Active bleeding(duodenal ulcer,varices, haemophylia).
Fibrinolytic therapy is primarily used at facilities without access to an
experienced interventionalist within 90 minutes of presentation.
Cautions/Relative Contraindications
■ Severe uncontrolled hypertension on presentation (BP >180/110 mm Hg)
■ History of prior cerebrovascular accident or known intracerebral disease
not covered in contraindications
■ Current use of anticoagulants in therapeutic doses (international
normalized ratio [INR] ≥2:3); known bleeding diathesis
■ Recent trauma (within 2–4 weeks), including head trauma
or traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation
(CPR) or major surgery (<3 weeks)
As a class, the plasminogen activators have been shown to restore normal
coronary blood flow in 50% to 60% of STEMI patients. The successful use of
fibrinolytic agents provides a definite survival benefit that is maintained for

years. The most critical variable in achieving successful fibrinolysis is time from
symptom onset to drug administration. A fibrinolytic is most effective within
the first hour of symptom onset and when the door-to-needle time is 30
minutes or less
Supplemental Oxygen
Oxygen should be administered to patients with symptoms or signs of
pulmonary edema or with pulse oximetry less than 90% saturation.
AIM- the erythrocytes will be saturated to maximum carrying capacity.
Because MI impairs the circulatory function of the heart, oxygen extraction by
the heart and by other tissues may be diminished. In some cases, elevated
pulmonary capillary pressure and pulmonary edema can decrease oxygen
uptake as a result of impaired pulmonary alveolar-capillary diffusion.
Supplemental oxygen increases the driving gradient for oxygen uptake.
Arterial blood that is at its maximum oxygen-carrying capacity can potentially
deliver oxygen to myocardium in jeopardy during an MI via collateral coronary
circulation. The recommended duration of supplemental oxygen administration
in a MI is 2 to 6 hours, longer if congestive heart failure occurs or arterial oxygen
saturation is less than 90%
Aspirin
• Aspirin is an antiplatelet agent that initiates the irreversible inhibition of
cyclooxygenase, thereby preventing platelet production of thromboxane A2
and decreasing platelet aggregation
• Administration of ASA in ACS reduces cardiac endpoints
 The nidus of an occlusive coronary thrombus is the adhesion of activated
platelets at the site of intimal disruption in an unstable atherosclerotic plaque.
 Its beneficial effect is observed early in therapy and persists for years with
continued use. The long-term benefit is sustained, even at doses as low as
75 mg/day
ACC/AHA Guidelines for Aspirin Therapy
Aspirin should be given in a dose of 75-325 mg/day to all
patients with ACS unless there is a contraindication (in which
case, clopidogrel should be given)

Nitrates
Nitroglycerin is considered a cornerstone of anti-anginal therapy,
despite little objective evidence for its benefit.
Mechanism of Action
-Relaxes vascular smooth muscle
- Benefit is thought to occur via reduction in myocardial O2 demand
secondary to venodilation induced reduction in preload as well as
coronary vasodilation and afterload reduction.
Titrate to relief of chest pain; chest pain = death of myocardial cells
No documented mortality benefit
Contraindications :
1.BP<100mm Hg
2.Pt. Has already taken maximum dose of three doses (1.2mg)
Dose
– .4mg sublingual Tablet or Metered-dose Spray
– .4mg Trans-dermal patch May repeat at 5 minute intervals up to 3 .
If tablet form - Protect potency
Store in original brown bottle,Keep tightly sealed
Protect from light, air, heat, Secure new supply every 4 - 6 months
Intravenous nitroglycerin in patients with persistent chest pain after
three sublingual nitroglycerin tablets, as well as in patients with
hypertension or HF. However, nitrates must be used with caution or
avoided in settings in which hypotension is likely or could result in serious
hemodynamic decompensation, such as right ventricular infarction or
severe aortic stenosis. In addition, nitrates are contraindicated in patients
who have taken a phosphodiesterase inhibitor for erectile dysfunction (or
pulmonary hypertension) within the previous 24 hours

Beta Blockers
• Beta Blockers reduce myocardial oxygen demand by reducing heart rate,
contractility, and ventricular wall tension
• Administration of beta blockers in ACS reduces cardiac endpoints
AHA/ACC Guidelines for Beta Blocker Therapy
• Intravenous beta blockers should be used
initially in all patients (without contraindication)
followed by oral beta blockers with the goal being
decrease in heart rate to 60 beats per minute
• A combination of beta blockers and nitrates can
be viewed as first line therapy in all patients with
ACS
Heparin
• Heparin (unfractionated heparin or UFH) has traditionally been
the mainstay of therapy in acute coronary syndromes as its efficacy
has been documented in several large, randomized trials
LMWH
• More recent studies indicate that low molecular weight heparin
is also effective in the reduction of end points such as myocardial infarction
or death, DVT ,INTRACARDIAC THROMBUS OR PE.
• Some studies report that LMWH, when used in combination with ASA,
may be superior to continuous infusion of Heparin.
ACC/AHA Guidelines for Heparin Therapy
• All patients with acute coronary syndromes should
be treated with a combination of ASA (325 mg/day)
and low molecular weight heparin unless one of the
drugs is contraindicated

Enoxaparin 1mg/Kg bd
• UFH if primary PCI
• After thrombolysis continue until hospital discharge?
ACE-I
To reduce ventricular remodeling over days to weeks after myocardial
damage.
However, there is data that a mortality benefit exists when
these agents are used early in the course of ACS.
• Administration of ACE-I in ACS reduces cardiac endpoints
AHA/ACC Guidelines for ACE-I Therapy
• ACE-I should be administered to all patients
in the first 24 hours of ACS provided hypotension
and other clear cut contraindications are absent
Statins
• Statins may be of benefit in ACS
• Mechanisms ---plaque stabilization, reversal of endothelial dysfunction,
decreased thrombogenicity, and reduction of inflammation.
IIBIIIA Inhibitors
• More potent inhibition of platelet aggregation may be of importance
in patients with ACS that is associated with unstable coronary lesion
and thrombus formation.
This can be achieved by the use of GP IIBIIIA inhibitors
• Administration of IIBIIIA inhibitors reduces cardiac endpoints

AHA/ACC Guidelines for use of IIBIIIA inhibitors
• A IIBIIIA inhibitor should be administered to all patients in whom a
percutaneous intervention is planned (in addition to heparin/ASA)
• Eptifibatide or Tirofiban should be administered to patients with
ACS in whom PCI is not planned if other high risk features are
present (TIMI risk score >3)
Score of 3 or less = low risk
Score of 4-5 = intermediate risk (use IIBIIIA)
Score of 6-7 = high risk (use IIBIIIA)
Clopidogrel
• Clopidogrel is a potent antiplatelet agent
• It should be administered to all patients who cannot take ASA
• The CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin in
patients going for PCI,STEMI ,NSTEMI.
• Give 300 mg loading dose followed by 75mg/day
TIMI Risk Score
• Age >65 yrs
• Daily ASA Therapy (>7 days prior to event)
• Symptoms of Unstable Angina
• Documented CAD (stenosis > 50%)
• 3 or more traditional cardiac risk factors
• Elevated cardiac enzymes
• ECG changes

AHA/ACC Guidelines for Clopidogrel
• Clopidogrel should be administered to patients who cannot
take ASA because of hypersensitivity or gastrointestinal intolerance
• In hospitalized patients in whom an early, noninterventional approach is
planned, clopidogrel should be added to ASA as soon as possible on
admission and administered for at least 1 month and up to 9 months.
Do not use clopidogrel if there is any possibility patient may be candidate
for CABG
Emergent Revascularization
• In the setting of STEMI primary PCI is associated with better outcomes than
thrombolysis
• Emergent PCI is also indicated in the setting of a new LBBB
PCI = percutaneous coronary intervention
AHA/ACC Guidelines for Primary PCI
• Primary PCI is indicated as an alternative to thrombolysis when
the following criteria are met:
– STEMI or new LBBB
– Can undergo PCI within 12 hours of the onset of symptoms
– The MD doing the intervention does more than 75 PCI’s/yr
– The procedure is done in a center that does more than 200 PCI’s/yr
and has surgical backup
Treatment of NSTEMI/USA
• ASA
• NTG (consider MSO4 if pain not relieved)
• Beta Blocker
• Heparin/LMWH
• ACE-I
• +/- Statin
• +/- Clopidogrel (don’t give if CABG is a possibility)
• +/- IIBIIIA inhibitors (based on TIMI risk score)
ANTIAARYTHMIC FOR ARRTHMIA AND DIURETIC FOR FAILURE
DILTIAZEM (CCB) FOR CORONARY SPASM

Acute coronary syndrome

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