Pharmacotherapy of chronic stable angina modified

Pharmacotherapy of Ischemic Heart
Disease and Chronic Stable Angina
Prof. Dr. Ghada Suddek
Clinical Pharmacy Program

(2023-2024)
Pharmacotherapy of
cardiovascular diseases Course
The major goals for the treatment of IHD are to:
•Short-term goals are to reduce or prevent anginal
symptoms that limit exercise capability and impair quality of life.
•Long-term goals are to prevent CHD events such as MI,
arrhythmias, and HF and to extend the patient’s life.
Therapeutic Management of CHD
A. Antiplatelet Therapy
Aspirin: Clopidogrel
Indication all patients with CHD unless Decrease CV events by about one-
contraindicated third
Dose 75 - 162 mg/day 75 mg\day if aspirin absolutely

contraindicated
No benefit of dual antiplatelets in
setting of stable CAD.
B. Lipid-Lowering
Therapy "statins“
(Plaque stabilization)
High-intensity statin therapy if without contraindications, drug-drug
interactions, or history of statin intolerance (class I recommendation).
C. ACE
Inhibitors
I. Decrease CV events in patients with CHD (and no LV
dysfunction) at high risk of subsequent CV events .
II. Consider in all patients who also have an LVEF of ≤40% , HTN,
diabetes mellitus, and /or CKD (class I recommendation).
III. Consider using in lower-risk patients with a mildly reduced or

normal LVEF in whom CV risk factors are well controlled and
revascularization has been performed (class IIb recommendation).
D. ARBs
Recommended as an alternative to ACE inhibitors in patients who
also have an LVEF 40% , HTN, diabetes mellitus, and /or CKD or
who are unable to tolerate an ACE inhibitor (e.g. cough or
angioedema) (class IIa recommendation).
E. Additional Therapies for Chronic Stable Angina
Definition of Chronic Stable Angina: Predictable angina
symptoms with exertion
Goals:
• Reduce symptoms of ischemia
• Increase physical function
• Improve quality of life
In general , achieved by either:

• Decreasing myocardial oxygen demand or
• Increasing myocardial oxygen supply
b. Calcium channel
blockers
Place in therapy
Added to β-blocker therapy: to achieve HR goals
Instead of β-blocker therapy when: unacceptable adverse effects
emerge or if treating Prinzmetal angina (where β- blockers are
contraindicated)
Short-acting CCBs (nifedipine, nisoldipine) have been associated
with increased CV events; should be avoided (except in slow-
release formulations)
Contraindications for non-dihydropyridines:

Systolic HF, severe bradycardia, high-degree AV block (without
pacemaker), and sick sinus syndrome (without pacemaker)
Contraindications for dihydropyridines:
LV dysfunction (except amlodipine and felodipine)
c. Nitrates
Pharmacologic effects:
Increase oxygen supply:
vasodilation, Increase blood flow to the myocardial tissues
decrease oxygen demand:
Decreased LV volume because of decreased preload
Place in therapy
•A scheduled nitrate is useful in conjunction with a β- blocker
or non-dihydropyridine CCB (blunt the reflex sympathetic tone
with nitrate therapy).
•As-needed sublingual tablets or spray nitrate is necessary
to relieve effort or rest angina.
• In addition, as-needed nitrates can be used before exercise to
avoid ischemic episodes
d. Ranolazine
Pharmacologic effects
Inhibits late phase sodium channels
Reduction of calcium influx
Coronary vasodilation during ischemic
events
Place in therapy (Ideal role is
unclear)
• As a substitute for a β-blocker if:
initial treatment with β-blockers results in adverse effects or if β- blockers are
ineffective or contraindicated.
•Use in combination with β-blockers, CCBs, or nitrates when initial

management with these drugs is unsuccessful.
2 Metabolized by CYP3A:
a. Avoid in hepatic dysfunction.
b. Avoid use with strong CYP3A inhibitors, or CYP3A inducers
c. Limit the dose of simvastatin to 20 mg daily when administered with
Acute Coronary syndrome (ACS)
Definition:
ACS refers to a heterogeneous group of
thrombotic coronary artery diseases resulting primarily from
diminished myocardial blood flow secondary to an occlusive or
partially occlusive coronary artery thrombus
PATHOPHYSIOLOGY
• Endothelial dysfunction, inflammation, and formation of fatty
streaks 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.
• A clot forms on top of the ruptured plaque.
Clot Formation
• Exposure of collagen and tissue factor induces platelet adhesion and
activation, which promote release of ADP and thrombaxane A2
Promotes vasoconstriction and platelet activation
• GP IIb/IIIa receptors on platelets change conformation to induce platelet
cross linkage with fibrinogen
• Simultaneously, Extrinsic coagulation pathway activated
Produce thrombin
Convert fibrinogen to fibrin
Fibrin stabilizes the clot
Classification of ACS due to ECG changes
PATIENT PRESENTS WITH
SYMPTOMS OF ACUTE
CORONARY SYNDROME
1
Unstable angina Non-ST-segment ST-segment elevation
(UA) elevation myocardial infarction
myocardial (STEMI)
infarction (NSTEMI)
occlusion Partial occlusion of coronary artery Total occlusion
of coronary
artery
ECG changes
ST-segment elevation
ST-segment depression, ST-
segment inversion Or no specific
changes
Injury No myocardial injury Myocardial injury Myocardial necrosis
Biomarkers No positive Positive Positive

biomarkers for biomarkers biomarkers
myocardial necrosis Troponin I or T Troponin I or T
CK-MB ˃ 5% of CK-MB ˃ 5% of
total CK total CK
Initial Management of ACS (Emergent Treatment) –
“MONA” plus β-Blocker
•- Evaluate patient, diagnose type of ACS episode & deliver emergent drug therapy
•- All patients with STE MI and without contraindications should receive within the
first day of hospitalization and preferably in the emergency department:
M Morphine 2 - 4 mg IV prn chest pain (if not relieved by

NTG) as an analgesic and venodilator that lowers preload.
O Oxygen Intranasal:To maintain O2 sat > 90%
0.3-0.4 mg SL q5min prn x 3
N Nitroglycerin 1-2 sprays under tongue q5min x 3
(if no response 10 mcg/min IV)
A Aspirin 160-325 mg PO chew and swallow (non-enteric
coated)
Beta blocker 25 mg PO q6h
B Metoprolol 5 mg IV q2-5min x 3 doses (no IV if
high risk of cardiogenic shock)
Start an ACE inhibitor within 24 hours in patients who have either
anterior wall MI or LVEF of 40% or less and no contraindications.

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Pharmacotherapy of Ischemic Heart

Disease and Chronic Stable Angina

Prof. Dr. Ghada Suddek

Clinical Pharmacy Program

Dose 75 - 162 mg/day 75 mg\day if aspirin absolutely

III. Consider using in lower-risk patients with a mildly reduced or

In general , achieved by either:

Contraindications for non-dihydropyridines:

•Use in combination with β-blockers, CCBs, or nitrates when initial

Injury No myocardial injury Myocardial injury Myocardial necrosis

Biomarkers No positive Positive Positive

M Morphine 2 - 4 mg IV prn chest pain (if not relieved by

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