ACUTE CORONARY SYNDROME

Acute coronary syndromes (ACSs) include all

syndromes resulting from imbalance between
myocardial oxygen demand and supply.
ACSs are classified according to electrocardiographic
(ECG) changes into
ü ST-segment-elevation MI (STEMI) or
ü Non–ST-segment elevation MI (NSTEMI), Unstable
Angina (UA).
 MYOCARDIAL
MYOCARDIAL INFARCTION
INFARCTION (MI) results
from a sudden interruption of blood supply to
an area of myocardium because of complete,
or near complete, occlusion of coronary
artery.

The occlusion persists long enough to

compromise myocardial function and lead to
myocardial necrosis.
 CLASSIFICATION
There are two basic types of acute myocardial infarction
based on pathology:
1. Transmural infarction: Characterized by ishchemic
necrosis of the full thickness of affected muscle
segment(s), extending from endocardium through the
myocardium to the epicardium. (STEMI)
2. Subendocardial infarction: Involves the innermost
layer and, in some cases, parts of the middle layer of the
myocardium but does not extend the epicardium.
(NSTEMI)
RISK FACTORS
Older age
Male gender
Cigarette smoking
Hypercholesterolemia (more accurately hyperproteinemia,
especially high LDL and low HDL.)
Diabetes
High blood pressure
Obesity
Types of Stress Tests
 Dobutamine or Adenosine Stress Test:
 used in people who are unable to exercise.
 heart respond as if the person were exercising.
 no exercise is required.
 Stress echocardiogram:
 An echocardiogram (often called "echo") is a graphic outline of
the heart's movement.
 accurately visualize the motion of the heart's walls and pumping
action when the heart is stressed
 Nuclear stress test:
 determine which parts of the heart are healthy and function
normally and which are not.
 radioactive substance is injected into the patient.
PATHOPHYSIOLOGY
CAD is the primary underlying process that leads to MI.
Fatty streaks deposited on coronary artery endothelium
may progress to form atherosclerotic plaque.
The earliest visible lesion
of atherosclerosis is the fatty
streak, which is due to an
accumulation of lipid-laden
foam cells in the intimal layer
of the artery. With time, the
fatty streak evolves into a
fibrous plaque, the hallmark of
established atherosclerosis.
Atherosclerosis results in a prothrombotic endothelial
surface and causes endothelial dysfunction, inflammation
and further contribute to development of atherosclerotic
coronary artery plaques.

The cause of ACS in more than 90% of patients is rupture,

fissuring, or erosion of an unstable atheromatous plaque and
platelet activation, which precipitate an acute MI.

After the onset of ischemia, cell death occurs within several

hours.
Development of fatty streaks
q LDL in blood plasma invades the endothelium and becomes
oxidized(free radicals in the endothelium)
q Inflammatory response.
o Monocytes enter the artery wall from the bloodstream, with platelets
adhering to the area with the help of VCAM-1 (Vascular Cell
Adhesion Molecule-1)
 Monocytes differentiate into macrophages which ingest oxidized LDL,
slowly turning into large "foam cells
PATHOPHYSIOLOGY :Atherogenesis
 Foam cells eventually die, and further propagate the inflammatory
process.
 smooth muscle proliferation and migration from tunica media to intima
 formation of a fibrous capsule covering the fatty streak.
Calcification and lipids
 Intracellular microcalcifications form within vascular smooth
muscle: leads to extracellular calcium deposits
 Cholesterol is delivered into the vessel wall by cholesterol-
containing LDL particles.
 These capped fatty deposits (now called atheromas), produce
enzymes that cause the artery to enlarge over time.
 leukocytes such as monocytes or basophils begin to attack the
endothelium
 inflammation leads to formation of atheromatous plaques in the
arterial intima
Rupture and stenosis
 Stenosis is often the result of repeated plaque rupture and healing
responses
 Platelets adhere to the plaque, become activated, release their
granule contents and aggregate to form microthrombi.
 Vasospasm is stimulated by mediators released from platelets.

 Tissue factor activates the coagulation pathway, adding to the bulk

of the thrombus.
 Within minutes, the thrombus expands to completely occlude the
vessel wall.
Myocardial response
 Coronary artery obstruction diminishes blood flow to the region of
myocardium causing ischemia, myocardium dysfunction, and
eventually, with prolonged vascular compromise, myocyte death.
DIAGNOSIS
 Clinical Presentation
qThe classic symptom of MI is chest pain:
ü Retrosternal
ü Substernal pressure sensation that is also perceived as
squeezing, aching, burning, or even sharp.
ü Often radiates up to neck, shoulder, and jaws, and down to the
left arm. (Movement, deep breathing, or a change in position
does not affect the pain.
ü 15-25% patients with MI have no pain , particularly with
diabetes.
qOther symptoms may include:
ü Anxiety (sense of impending doom)
ü Lightheadedness
Pain zones in myocardial infarction (dark red = most
typical area, light red = other possible areas).
ECG Findings
qTransmural Infarction:
§ Hyperacute T waves

§ ST elevation

§ Pathologic Q wave

§ Loss of R wave

qSubendocardial infarction
§ ST segment depression

§ Inverted T waves
CHEST RADIOGRAPHY
Although it does not provide detailed information about internal
cardiac structures, it can provide information about the position and
size of the heart and its chambers as well as adjacent structures.

ECHOCARDIOGRAPHY
 Using echocardiography, one can evaluate cardiac function and
structure with images produced by ultrasound.
 Two-dimensional echocardiography employs multiple windows of
the heart, and each view provides a wedge-shaped image.These
views are processed to produce a motion picture of the beating heart.
TROPONIN
It is the most sensitive and tissue-specific biomarker
available.
Troponin I and T are contractile proteins found only in
cardiac myocytes.
 In the patient with myocardial infarction, cTn is
detectable in the blood 2 to 4 hours after the onset of
symptoms and remains detectable for 5 to 10 days.
In the patient with ischemic chest pain, the presence of an
elevated serum cTn concentration establishes the
diagnosis of myocardial infarction, and the absence of
such an elevation excludes it.
 CK-MB
When serum cTn measurements are not available, the best
alternative is the MB isoenzyme of creatine kinase (CK-MB),
which is a cytosolic carrier protein for high-energy
phosphates that is released into the blood when myonecrosis
occurs.
In the patient with an acute myocardial infarction, CK-MB
can be detected in the blood 6 to 8 hours after symptom onset
Its serum concentration peaks within 24 hours, and it remains
detectable in the blood for 48 to 72 hours.
CK-MB is known to be present in small amounts in skeletal
muscle; as a result, it may be detectable in the blood of
patients with massive muscle injury
Exercise Stress Test
A physician may recommend an exercise stress test for various
reasons:
 diagnose coronary artery disease
 diagnose a possible heart-related cause of symptoms
 To determine a safe level of exercise
 To check the effectiveness of procedures done
 To predict risk of dangerous heart-related conditions such as a heart
attack.
 effectiveness of medications to control angina and ischemia.
 Management
General Principles:
q Close monitoring of vital signs , symptoms and ECG (first 48
to72 hrs).
q Activity should be restricted for first 2 to 3 days and gradually
increased as tolerated.
q The diet should involve multiple small meals, sodium
restriction and reduced content of fats and cholesterol.
q A stool softener (docusate sodium, 100mg or docusate calcium,
240 mg once or twice a day) to avoid problems with
defecation.
q For first 2-3 hrs of therapy, supplemental nasal Oxygenation
should be administered because uncomplicated patients may be
hypoxic.
 Pharmacological Therapy
q
Fibrinolytic therapy
§
Alteplase (tPA): 15 mg IV bolus followed by 0.75mg/kg
infusion (not ˃ 50 mg) over 30 min. followed by 0.5mg/kg
infusion (not ˃ 50 mg) over 1 hr.
§
Streptokinase: 1.5 million units 50 ml of saline over 60
min.
§
Anistreplase: 30 units by IV push over 2 min.
§
Reteplase: 10 units by IV push over 2 min.
§
Tenecteplase: A single IV bolus dose given over 5
seconds based on patients weighr: 30 mg ˃60 kg; 35 mg if
60-69.9 kg; 40 mg if 70-79.9 kg; 45 mg if 80-89.9 kg.
The presence of more than one relative contraindication is
considered an absolute contraindication.
q
Analgesics
q
Morphine SO4: 2-5mg/IV dose every 5 to 15 minutes as
needed
§
Potent analgesic
§
Peripheral venous vasodilation
§
Reduces myocardial O2 demand.
§
Decrease systemic vascular resistance.
§
It also decreases circulating concentrations of
catecholamines, which may reduce ventricular
arrhythmias.

q
Tranquilizres
§
To decrease anxiety
§
Diazepam (5-10 mg per IV/orem)
Drugs to Limit Infarct Size
qNitrates (IV or Sublingual NTG) [10-20µg/min via
infusion pump.

§ NTG relieves MI via coronary and peripheral

vasodilatation.
§ It is used to manage ischemia for the first 24-48 hrs.
§ Used beyond 48 hrs should be reserved for patients with
large MI, persistent chest discomfort, heart failure and
hypertension.
§ Sublingual NTG (0.4 mg) is often given to determine
whether chest pain is due to MI or ischemia.
§ NTG associated headache is common; decreasing the
infusion rate and/or administering acetaminophen may be
effective.
q Beta Blockers
§ Propranolol: 0.03-0.05 mg/kg slow IV push every 10 min.
§ Metoprolol: 5 mg every 5 min for 3 doses; total dose 15mg
§ Atenolol: 2.5-5.0 mg every 5-10 minutes; total dose 10 mg

§ Reduce myocardial oxygen consumption by decreasing:

 Cardiac index
 Stroke index
 Heart rate
 Blood pressure
An oral regimen can be initiated 6 to 12 hours after last IV dose.
§ Propranolol: 40-60 mg four times per day
§ Metoprolol: 100 mg twice daily.
q Antithrombotic Therapy
q Aspirin, clopidrogel and ticlopidine
§ Aspirin (60-325 mg) has been shown to decrease mortality and
re-infarction rates
§ Administer aspirin immediately
§ Continue aspirin indefinitely
§ Clopidogrel (300 mg orally loading dose followed by 75 mg
daily) may be used as an alternative (GI intolerance or allergy to
aspirin)

q Administer a platelet glycoprotein (GP) IIb/IIIa-receptor

antagonist
§ continuing ischemia or with other high-risk features and to
patients in whom a percutaneous coronary intervention (PCI) is
planned.
§ Eptifibatide and tirofiban are approved for this use.
§
q Unfractionated Heparin (UFH)

Heparin (and other anticoagulant agents)

established role as an adjunctive agent in patients

receiving t-PA but not with streptokinase.

Heparin is also indicated in patients undergoing primary

angioplasty.

Low–molecular-weight heparins (LMWHs) have been

shown to be superior to UFHs in patients with unstable

angina or NSTEMI.
Administer a platelet glycoprotein (GP) IIb/IIIa-receptor
antagonist

Abciximab, eptifibatide and tirofiban

§ continuing ischemia or with other high-risk features and to

patients in whom a percutaneous coronary intervention (PCI)

is planned.

§ Eptifibatide and tirofiban are approved for this use.

§ Abciximab also can be used for 12-24 hours in patients with

.
qACE inhibitors
§ reduce mortality rates after MI.
§ Administer ACE inhibitors as soon as possible
§ ACE inhibitors have the greatest benefit in patients with
ventricular dysfunction.
§ Continue ACE inhibitors indefinitely after MI.
§ Angiotensin-receptor blockers (ARBs) may be used as an
alternative.
Reperfusion
ST segment elevation (STEMI) or
new bundle branch block on the 12 lead ECG
presumed to have an occlusive thrombosis in an epicardial
coronary artery.
candidates for immediate reperfusion,

§ Thrombolytic therapy

§ Percutaneous coronary intervention

§ CABG
The effectiveness:
highest in the first 2 hours

After 12 hours, the risk associated with thrombolytic

therapy outweighs any benefit
Contraindicated
 unstable angina and NSTEMI
 and for the treatment of individuals with evidence of cardiogenic
shock
Examples: streptokinase, urokinase, and alteplase
(recombinant tissue plasminogen activator, rtPA), reteplase,
tenecteplase
Surgical Care
 Percutaneous coronary intervention
 treatment of choice
 STEMI, (door to needle time of less than 90 minutes.)
 PCI provides greater coronary patency
 lower risk of bleeding
 and instant knowledge about the extent of the underlying disease.
 The widespread use of stenting and adjunctive IIb/IIIa therapy are
improving the results of primary PCI.
Coronary artery bypass grafting: Emergent or urgent
coronary artery graft bypass surgery is indicated when
angioplasty fails
develop mechanical complications such as a VSD, LV, or