#3 Acs 6 PDF

Al-Bayan University / College of Pharmacy
Pharmacology & Toxicology Dept. 2019-2020

Fourth stage / Clinical Pharmacy II - Lecture 3 / presented by
Dr. Atheer S. Alsabah
Ischemic Heart Disease "IHD" (ACS)

 Acute Coronary Syndrome (ACS)
- Is an umbrella term that includes pts who present with either unstable angina (UA)
or acute myocardial infarction (AMI) consisting of ST segment elevation
myocardial infarction (STEMI) or non–ST segment elevation myocardial
infarction (NSTEMI).
- Unstable angina is characterized by rapidly worsening angina, attack on minimal
exertion or at rest in the absence of myocardial damage.
- In contrast MI occurs when symptoms appear at rest & there is evidence of
myocardial necrosis, as demonstrated by an elevation in cardiac troponins (I or T)
or creatine kinase myocardial band (CK-MB).
ST segment elevation of cardiac biochemical markers
elevation
STEMI Yes Yes
NSTEMI No Yes
UA No No
• Pathophysiology:
1. Majority of ACS results from occlusion of a coronary artery secondary to
thrombus formation. The inciting event is rupture or fissuring of an atherosclerotic
plaque, which exposes the blood to thrombogenic lipids & leads to activation of
platelets & clotting factors leading to formation of a clot or thrombus as well as
ischemia in the myocardial area.
2. The coronary lesion demonstrates little thrombosis with UA, partial thrombotic
occlusion with NSTEMI, & total persistent thrombotic occlusion with STEMI.
1
• Risk factors:
1. Non-modifiable risk factors include age, male gender , and family history.
2. Modifiable risk factors include smoking, alcohol, physical inactivity,
hypertension, type II DM, dyslipidemias, & obesity.
• Clinical presentation:
1. Central chest pain similar to that occurring in angina is the most common
presenting symptoms .Unlike angina it is usually occurs at rest , is more severe
and last for longer duration e.g. some hours. Accompanying symptoms may
include nausea, vomiting, diaphoresis, or shortness of breath.
2. Elderly pts, diabetic pts, & women are less likely to present with classic
symptoms. They may have painless or silent MI. If syncope occurs, it is usually
due to an arrhythmia or profound hypotension.
• Diagnosis:
a. ECG: should be obtained within 10 min of pt presentation. The key findings
indicating myocardial ischemia or MI are ST segment elevation (in STEMI), ST-
segment depression, & T-wave inversion (in NSTEMI).
- An anterior wall infarction carries a worse prognosis than an inferior or lateral

wall infarction because it is more commonly associated with development of LVF
& cardiogenic shock.
2
b. Biochemical markers: when a cardiac cell is injured, enzymes are released into
the circulation & they are important for confirming diagnosis of MI. Troponins I
& T are highly specific for myocardial injury & preferred for diagnosis of acute
MI, while CK-MB are less specific for MI.
- Both troponins & CK-MB are detectable within 6hrs of MI. Troponins remain
elevated for 7 to 14 days, whereas CK-MB returns to normal within 48-72hrs.
Complications:
Myocardial infarction (MI) may cause two general classes of complications:
A-Electrical complications (arrhythmias):
Arrhythmias and conduction abnormalities may occurs after MI (like heart block, ventricular
fibrillation (VF) (VF cause sudden death), and atrial fibrillation (AF). The most dangerous
time after a myocardial infarction is the first few hours when ventricular fibrillation (VF) is
most likely to occur. If the patient survives this most critical stage, the liability to dangerous
arrhythmias remains, but diminishes as each hour goes by.
B-Mechanical complications (pump failure) [cardiogenic shock, and heart failure
(HF)]:
1. Cardiogenic shock (characterized by systemic hypotension )occurs in approximately 7%
of patients with MI and has a high mortality rate.
2. During a period of days to months after an AMI, ventricular remodeling may occurs. It is
characterized by left ventricular dilation and reduced pumping function of the left
ventricle, leading to cardiac failure.
3
B-Ventricular Remodeling Following an Acute MI:
#1-Ventricular remodeling is a process that occurs in several cardiovascular conditions
including heart failure (HF) and following an MI.
#2-It is characterized by left ventricular dilation and

reduced pumping function of the left ventricle, leading
to cardiac failure.
(As the ventricle dilates, it becomes less efficient and
heart failure may occurs).
#3-Because HF represents one of the principal causes of

mortality and morbidity following an MI, preventing
ventricular remodeling is an important therapeutic goal.
#4-ACE inhibitors, ARBs, β-blockers, and Aldosterone

antagonists are all agents that
slow down or reverse ventricular remodeling.
• Treatment:
- The primary strategy for pts with an occluded coronary artery (STEMI) is the
restoration of coronary flow with either a fibrinolytic agent or PCI.
- If the coronary artery is patent (UA & NSTEMI), then fibrinolysis is unnecessary
& probably harmful, although PCI may still be appropriate.
• Non-pharmacological therapy for STEMI

- For pts with STEMI, primary percutaneous coronary intervention "PCI" (with
either balloon angioplasty or stent placement) is the treatment of choice for
reestablishing coronary artery blood flow .
- Primary PCI may be associated with a lower mortality rate than fibrinolytic drugs,
possibly because PCI opens >90% of coronary arteries compared with <60%
opened with fibrinolytics . The risks of major bleeding are also lower with PCI
than with fibrinolysis.
4
• Non-pharmacological therapy for NSTEMI
- In pts with NSTEMI, it is recommended either PCI or coronary artery bypass
grafting (CABG) revascularization as an early treatment.
• Early pharmacotherapy for STEMI

1. Oxygen.
2. Morphine is administered to pts with refractory angina as an analgesic &
venodilator.
3. Sublingual followed by IV nitroglycerin (NTG):
- Immediately upon presentation, one sublingual NTG tablet should be administered
every 5min for up to 3 doses.
- IV NTG should be initiated in all pts with an ACS who have persistent ischemic
symptoms, heart failure, or uncontrolled high blood pressure.
4. Fibrinolytic therapy:
- In the absence of C/Is, a fibrinolytic agent should be given to pts with STEMI
presenting within 12hrs of the onset of chest discomfort when it is anticipated that
primary PCI cannot be performed .
- Fibrin-specific agents e.g. alteplase, reteplase, tenecteplase, are preferred over the
non-fibrin-specific agent e.g. streptokinase. Fibrin-specific agents open a greater
percentage of infarct arteries.
5. Antiplatelet & anticoagulant therapy:

a. Aspirin: should be administered within the first 24hrs of hospital admission. In pts
experiencing an ACS, non-enteric-coated aspirin (to enhance absorption), should
be chewed & swallowed as soon as possible. A daily maintenance dose is
recommended thereafter and should be continued indefinitely.
b. P2Y12 receptor inhibitors e.g. clopidogrel, prasugrel, ticagrelor: should be given
for all pts with STEMI in addition to aspirin .
c. Anticoagulants: either unfractionated heparin (UFH) or bivalirudin is preferred for
pts undergoing primary PCI, whereas enoxaparin is preferred when fibrinolysis
reperfusion therapy is chosen for STEMI
d. Glycoprotein IIb/IIIa receptor inhibitors e.g. abciximab, eptifibatide, tirofiban: in
pt undergoing PCI in STEMI & receive UFH as anticoagulant, a GP IIb/IIIa
inhibitor (usually abciximab or eptifibatide) should be added to UFH.
6. β-Blockers: an I.V bolus or oral doses of a β-blocker should be administered early

for pts with STEMI (within the first 24hrs), & then an oral β-blocker should be
continued indefinitely.
7. ACEIs & ARBs: an ACEIs should be started within 24hrs of presentation.
5
• Early pharmacotherapy for NSTEMI
- Is similar to that for STEMI except that:
1. Fibrinolytic therapy is never administered to NSTEMI.
2. The risk of death from MI is lower in these pts, & the hemorrhagic risks of
fibrinolytic therapy outweigh the benefits.
• Long term therapy after MI

1. Aspirin: All pts should receive aspirin indefinitely or clopidogrel if aspirin is C/I.
2. ACEIs & ARBs: should be initiated in all pts after MI to prevent HF development.
3. β-Blockers: after an ACS, pts should receive a β-blocker indefinitely. A calcium
channel blocker can be used in pts who cannot tolerate or have a C/I to β-blockers.
4. Nitrates: all pts should be prescribed a short-acting sublingual NTG or lingual
NTG spray to relieve anginal symptoms when necessary.
5. P2Y12 receptor inhibitors e.g. clopidogrel, prasugrel, ticagrelor: should be
prescribed to all pts with MI (STEMI or NSTEMI).
6. Aldosterone antagonist e.g. eplerenone & spironolactone: should be considered
within the first 2wks after MI to reduce mortality in all pts with MI and have
LVEF ≤40%. The drugs are continued indefinitely.
7. Lipid lowering agents: all pts with CAD should receive dietary counseling &
pharmacotherapy in order to reach an LDL cholesterol concentration <100 mg/dl
(optional LDL goal of <70 mg/dl).
- Statins are the preferred agents for lowering LDL cholesterol & should be
prescribed in most pts .
- Recent data indicate that all pts with CAD benefit from statins, regardless of
baseline LDL. Beyond their lipid-lowering properties, statins are believed to
exhibit pleiotropic effects, which include plaque stabilization, anti-inflammatory
effect, antithrombotic effect, & modulation of endothelial function.

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Al-Bayan University / College of Pharmacy

Pharmacology & Toxicology Dept. 2019-2020

Ischemic Heart Disease "IHD" (ACS)

- An anterior wall infarction carries a worse prognosis than an inferior or lateral

#2-It is characterized by left ventricular dilation and

#3-Because HF represents one of the principal causes of

#4-ACE inhibitors, ARBs, β-blockers, and Aldosterone

• Non-pharmacological therapy for STEMI

• Early pharmacotherapy for STEMI

5. Antiplatelet & anticoagulant therapy:

6. β-Blockers: an I.V bolus or oral doses of a β-blocker should be administered early

• Long term therapy after MI

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