04/03/2018

Pharmaceutical Care 5:
Clinical Pharmacy
CORONARY ARTERY DISEASE
Course Facilitators:
Bartolome, Michelle D., MSc, CPS, RPh
Maclan, Grace Marie A., MSc, CPS, RPh
Dela Cruz, Sharmaine Y, RPh

Learning Objectives:
• Define Coronary Artery Disease
• Identify the Risk Factors and pathophysiology of
Coronary Artery Disease
• Differentiate the types of Angina
• Identify manifestation of Acute Coronary Syndrome
• Identify the biomarkers associated with Myocardial
infarction
• Differentiate STEMI from NSTEMI based their etiology,
diagnostics and management
• Create a therapeutic plan for patients with coronary
artery disease

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Anatomy of the Coronary Artery

Coronary Artery Disease

• A condition in which the vascular supply to heart is
impeded by atheroma, thrombosis or spasm

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Atherosclerosis
• It is a condition in which patchy deposit of plaque
(atheromas or atherosclerotic plaque) develop in
the wall of the medium and large sized arteries,
leading to reduced or blocked blood flow

Atherosclerosis

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Atherosclerotic Plaque
• Atherosclerotic plaque is composed of
1. Lipid
2. Inflammatory cell
3. Smooth Muscle cell and connective tissue
4. Thrombi
5. Calcium deposit

Formation of Atherosclerotic
Plaque

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Fibrous Plaque
1. Stable plaque ( static grows slowly )
2. Unstable plaque ( rupture, causing thrombosis )

Myocardial Ischemia
• Occurs when oxygen demand exceeds the oxygen
supply

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Etiology of CAD
• Decrease blood flow to the myocardium
• Atherosclerosis
• Coronary spasm
• Traumatic Injury
• Embolic event

Etiology of CAD
• Increased oxygen demand
• Diastole
• Systole
• Contractile state of the heart
• Increase in systolic wall tension
• Lengthening of ejection time
• Change in the heart rate

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Pathophysiology

Angina
• Transient chest discomfort that are attributed to
insufficient myocardial oxygen
• Stable Angina
• Unstable Angina

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Stable Angina
• Characterized by chest pain and breathlessness on
exertion, symptoms are relieved promptly with rest
• Patient has a reproducible pattern of pain or other
symptoms

Symptoms of Stable Angina

• Pressure or burning sensation over the sternum but
not always radiating
• Pain usually lasting for 0.5 to 30 minutes
• Precipitating factors include exercise, cold
weather, emotional stress
• Relief occurs with rest and nitroglycerin

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Unstable Angina
• Rest Angina
• >20 minutes occurring within a week of presentation
• Increasing angina
• Previously diagnosed angina with distinctly more
frequency, longer duration or lower threshold
• Has decrease response to nitroglycerin

Angina Decubitus
• Nocturnal angina
• Occurs when patient is in a recumbent position
• Gravitational force shifts fluid within the body with
a resultant increase in ventricular volume

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Prinzmetal Angina
• Coronary artery spasm that reduces blood flow
• Due to a thrombi or plaque formation
• Occurs at rest rather than exertion
• ECG shows ST-elevation

Diagnostic Test
• Resting ECG
• Exercise test
• Myocardial scintigraphy
• Stress Echocardiography
• Coronary Angiography

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Treatment Goals for Angina

• Prevent MI and death, thereby improving the
patient’s quality of life

• Reduce symptomatology

• Remove or reduce risk factors

Chronic Stable Angina

• A – Aspirin and Antianginal Therapy
• B – Beta blocker and BP
• C – Cigarette smoking and Cholesterol
• D – Diet and Diabetes
• E – Education and Exercise

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Recommendations
• Weight reduction/ maintenance
• Physical activity for 30 - 60 minutes/day x 7 day
• LDL-C <100mg/dL
• BP < 130mmHg
• No smoking and no environmental exposure to
smoke
• Reduce intake of saturated fats
• If Diabetic HbA1c <7%

Management
• Anti-platelets/Anti-thrombotic
• ACEI’s and ARBS
• Statins
• Beta-blocker
• Calcium Channel Blocker
• Nitrates

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Anti-Thrombotic Agents

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Anti-Thrombotic Agents

ACE Inhibitor
• Proven beneficial for post MI

• Vasodilatory effect caused by the inhibition of the

production of Angiotensin II

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Statin
• Demonstrate the benefit of reducing cholesterol,
especially LDL-C, in patients with CHD

• Earlier studies focused on patients with “elevated”

cholesterol, but all patients with coronary risk
factors benefit from reduction of their serum
cholesterol level.

Statins
• No safe level for cholesterol for patients with CAD
and there is a continuum of risk down to very low
cholesterol level

• Level of LDL-C of <2mmol/L and total cholesterol

<4mmol/L are recommended for patients with
established CVD

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Beta-Blocker
• Considered first line agent in angina

• Reduce mortality both in patients who suffered

from previous MI and patients with HF

• Reduce myocardial oxygen demand by blocking β-

adrenergic receptor, there by decreasing the heart
rate and force of left ventricular contraction and
lowering blood pressure

Beta Blockers
• Useful in exertional angina
• Patients treated optimally should have a resting
heart rate of around 60 beats/minute
• Used in caution in patients with diabetes
• Tendency to cause bronchospasm and peripheral
vascular spasm

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Beta Blocker
• Should not be stopped abruptly

• Contraindicated in the rare Prinzmetal’s angina

where coronary spasm is a major factor

Calcium Channel Blocker

• Acts on a variety of smooth muscle and cardiac
tissue
• Short acting dihydropyridine CCBs have been
implicated in the exacerbation of angina

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Nitrates
• Organic nitrates are valuable in angina
• Dilate vein → decrease preload
• Dilate arteries to a lesser extent → decrease afterload
• Promote flow in collateral coronary vessel, diverting
blood from the epicardium to the endocardium
• Relax vascular smooth muscle by releasing nitric oxide

• Tolerance is one of the main limitation

Nitrates
• Nitrate preparation
• IV infusion
• Tablet / capsule
• Transdermal patch
• Sublingual tablet
• Spray

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Acute Coronary Syndrome

• Group of condition similar to symptoms of chest
pain which is not, or only partially relieved by GTN
• Conditions include
• Acute myocardial infarction (AMI)
• UA
• NSTEMI
• STEMI

Acute Coronary Syndrome

• Arise from the rupture of an unstable atheromatous
plaque

• Volume of the eventual thrombus and the time the

vessel is occluded determine the degree of
myocardial necrosis that occurs

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Acute Coronary Syndrome

• Unstable Angina
• Chest pain that often occurs at rest, can occur suddenly,
may worsen suddenly or may be stuttering, recurring
over days to weeks
• Non-ST- Elevation Myocardial Infarction
• Symptoms similar to unstable angina but differentiated
on the basis of markers and ECG
• ST-Elevation Myocardial Ischemia
• A condition that requires immediate reperfusion therapy,
through either thrombolysis or percutaneous coronary
intervention (PCI)

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Acute Coronary Syndrome

Manifestation
1. Severe chest pain and discomfort
2. Irreversible cellular injury
3. Release of myocardial enzymes - (Troponin I and
T, CK-MB, CPK, LDH)
4. Electrocardiogram changes- (ST elevation, T wave
inversion, pronounced Q waves)
5. Inflammatory response from the injured
myocardium
6. Coagulative necrosis

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• Myocardial Ischemia -
Results from decreased
oxygen and nutrient
delivery To myocardium

• Myocardial Injury - Results

if ischemia progresses
unresolved or untreated

• Myocardial Infarction -
Death of myocardial cells

12 – Lead ECG

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Cardiac Markers
• Troponin
• Troponin T – found in cardiac and skeletal muscle
• Troponin I – found only in cardiac muscle
• Troponin C – found in cardiac and skeletal muscles

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Cardiac Markers
• Creatinine kinase
• Found primarily in the heart muscle, skeletal muscle and
brain tissue
• Aids in the diagnosis of acute myocardial or skeletal
muscle damage
• CK- BB – Brain tissues
• CK- MM – Skeletal muscles
• CK-MB – Heart muscle

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Overall Treatment Goals for ACS

1. Reduce chest pain and anxiety
2. Reduce cardiac workload and stabilize cardiac
rhythm
3. Prevent / reduce myocardial damage by limiting
the area affected and preserving the pump
function
4. Prevent or arrest complications
5. Reopen ( reperfuse ) closed coronary vessel with
thrombolytic drug and/or PCI

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Thombosis in Myocardial
Infarction (TIMI) Score

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Management for UA/NSTEMI

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Morphine
• MOA: Causes venous pooling and reduces preload,
cardiac workload and oxygen consumption
• For myocardial pain and anxiety
• Precaution:
• May cause orthostatic hypotension and fainting
• Can produce bradyarrhythmia

Oxygen
• Administered in patients with arterial saturation
less than 90%, respiratory distress or high risk
features of hypoxemia

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Nitroglycerin
• Nitrates causes venous dilation which reduces left
ventricular volume (preload) and myocardial wall
tension, decreasing oxygen demand

• It also reduce arteriolar resistance, helping reduce

afterload, which decrease myocardial oxygen
demand

Antiplatelet
• Antiplatelet therapy should be initiated promptly
• Aspirin should be administered as soon as possible
after presentation and continued indefinitely

• Clopidogrel should be administered to patients who

cannot tolerate GI effect and those who are
hypersensitive to ASA

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Management STEMI

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Percutaneous Coronary
Intervention

Coronary Bypass Graft

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Management for STEMI

• Fibrinolytics
• Administration of thrombolytic agents causes the
thrombus clot to be lysed when administered early after
symptom onset (6 to 12 hrs) and to restore blood flow.
The conversion of plasminogen to plasmin promotes
fibrinolysis and breakdown of the clot.

• Therapy of choice when PCI is not available.

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Fibrinolytics
• t-PA is relatively fibrin specific and is able to lyse
clots without depleting fibrinogen, and Tnkase has
a greater fibrin specificity.

• When used early, can reopen (reperfuse) occluded

coronary arteries and reduce mortality by up to
30% from STEMI.

References
• Schwinghammer, T., Wells, B. G., Malone, P. M., Kolesar, J. M., &
DiPiro, J. T. (2016). Pharmacotherapy: Principles & practice. McGraw-
Hill Education.
• Shargel, L. (2009). Comprehensive pharmacy review. Lippincott
Williams & Wilkins.
• WALKER, R., & EDWARDS, C. (2003). Clinical pharmacy and
therapeutics. Churchill Livingstone.
• https://www.acls.net/acute-coronary-syndromes-algorithm.htm
• https://www.youtube.com/watch?v=3Nf6Q2skGOM
• https://www.youtube.com/watch?v=gvRtP3wl_AY

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