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Last edited: 10/21/2022

ANTIANGINAL DRUGS
Antianginal Drugs Medical Editor: Ana Guerra

OUTLINE
I) PATHOPHYSIOLOGY OF ANGINA III) CALCIUM CHANNEL BLOCKERS V) RANOLAZINE
II) BETA BLOCKERS (A) CALCIUM CHANNEL (A) RANOLAZINE TREATMENT
(A) BETA BLOCKERS TREATMENT BLOCKERS TREATMENT ALGORITHM
ALOGORITH ALGORITHM VI) REVIEW QUESTIONS
IV) NITRATES VII) REFERENCES
(A) NITRATES TREATMENT VIII) ANSWERS TO QUESTIONS
ALGORITHM

I) PATHOPHYSIOLOGY OF ANGINA

(1) Atherosclerotic plaque or spasms


Occlusion of coronary arteries by atherosclerotic plaques or an spasm

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(2) Increased O2 demand by myocardial cells (MVO2)


Because of the poor amount of O2 that myocardial cells are receiving

(i) Stable angina


(ii) Vasospastic angina (AKA Prinzmetal or Variant)
o Reduction of oxygen supply to the myocardium but
i. At rest
still enough to prevent an infarction.
ii. Younger females with history of tobacco
i. Lasts less than ten minutes
smocking.
ii. Relieved by nitrates or by
iii. Triggered by triptanes, cocaine or alcohol.
iii. Relieved by exercise
iv. Occur more commonly during the morning.

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(iv) Unstable angina (v) NSTEMI

▪ Ischemia to the myocardium without exertion.


o Release of troponins from the myocardial cells.
o Due to unstable plaques
▪ No need of O2 demand
▪ Severe chest pain
▪ Infarction only affects partially the myocardium
walls.

(vi) STEMI

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II) BETA BLOCKERS


First-line prophylactic medication

(i) Metoprolol
(ii) Atenolol
(iii) Propranolol (beta 1 and beta 2 activity)
(1) Mechanism of action (2) Adverse effects
Bradycardia
Hypotension or shock – Careful with patients with
1) Inhibition of nodal cells (chronotropic and decompensated heart failure.
dromotropic actions) Bronchoconstriction when using propranolol for its
▪ Decrease of HR effects on Beta 2 receptors.
1) Decrease of contractility
▪ Decrease of stroke volume
• Decrease of cardiac output

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Hypoglycemia unawareness

(B) BETA BLOCKERS TREATMENT ALOGORITHM


Patient with angina (i) Good for patients

(ii) Careful with patients with

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III) CALCIUM CHANNEL BLOCKERS


Second-line prophylactic medication
Preferred in patients with Prinzmetal or vasospastic angina
(1) Mechanism of Action
(i) Non-DHP CCB´s:
o Verapamil
o Diltiazem
1) Inhibition of nodal cells

2) Decrease of contractility

RECALL RECALL
Within the heart, Non-DHP calcium channels allow Ca++ to Within the arterial smooth muscle cells, DHP calcium
enter into the nodal cells and increase action potential channels allow Ca++ to enter into the cells and increase
action potential

(ii) DHP CCB´s: o Verapamil > diltiazem


o DHP CCB > Non-DHP CCB
o Amlodipine
o Nifedipine
1) Arterial smooth muscle cells relaxation
(2) Adverse Effects
Bradycardia
Decrease of contractility
2) Reduction of vasospasm on coronary artery DHP CCB: Reflex tachycardia due to decrease of SVR
cells Increase risk of mortality in post MI patients

(B) CALCIUM CHANNEL BLOCKERS TREATMENT ALGORITHM


Patient with angina

a. CCB: Either Non-DHP or DHP: Especially


if vasospasm or Prinzmetal; HTN,
COPD or DM
b. Nitrates

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IV) NITRATES

(1) Mechanism of Action


(i) On veins Tolerance:
Drug enters the venous smooth muscle cell

▪ Stimulation of guanylate cyclase


o Have a nitrate-free interval (10-12 hours)

o Inhibits contraction of the smooth cell


▪ Venodilation → Reduction of
preload → Reduction of CO
• Reduction of O2 demand

(ii) On arteries
Drugs enters the arterial smooth muscle cell

▪ Stimulation of guanylate cyclase

o Inhibits contraction of the smooth cell


▪ Coronary vasodilation → Increase
perfusion to the myocardium
(2) Drugs

(i) Short acting

▪ Sublingual or subdermal

(ii) Long acting

(B) NITRATES TREATMENT ALGORITHM

a. CCB: Either Non-DHP or DHP: Especially if vasospasm or Prinzmetal; HTN, COPD or DM


b. Nitrates: Long acting nitrates (ISDN, ISMN)
▪ More beneficial: Post MI, DM, COPD/ Asthma
▪ CI: HTN
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V) RANOLAZINE

(1) Mechanism of Action


(i) Ischemia without Ranolazine
(ii) Ischemia with Ranolazine
o Na+ influx into the cell → Increase of Na+/Ca++
o Inhibition of inward Na+ channel → No Ca++ influx
contratransporter
into the cell

(2) Adverse Effects


Drug interactions
Prolonged depolarization phase → QT interval → Increase risk of Torsades de Pointes

(B) RANOLAZINE TREATMENT ALGORITHM

a. CCB: Either Non-DHP or DHP: Especially


if vasospasm or Prinzmetal; HTN,
COPD or DM
b. Nitrates: Long acting nitrates (ISDN,
ISMN)
▪ More beneficial: Post MI, DM, COPD/
Asthma
▪ CI: HTN

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▪ Beneficial to patient with arrhythmias

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VI) REVIEW QUESTIONS


3) Sarin is a nerve gas that is an
organophosphate cholinesterase inhibitor.
Which agent could be used as an antidote to
sarin poisoning?
b. Pilocarpine
c. Carbachol
d. Atropine
e. Physostigmine.

4) A patient with asthma was prescribed a β2


agonist for acute relief of bronchospasm, but
did not respond to treatment. Which drug is the
most likely next option for this patient?
a. Benztropine
b. Ipratropium
c. Oxybutynin
d. Physostigmine

5) A 50-year-old male who is noncompliant with


medications was recently diagnosed with
COPD. His physician would like to prescribed
an inhaled anticholinergic that is dosed once or
twice daily. Which drug is most appropriate for
this patient?
a. Atropine
b. Ipratropium
c. Tiotropium
d. Trospium

6) Which is the most effective drug for motion


sickness for a person planning to go on a
cruise?
a. Atropine
b. Fesoterodine
c. Scopolamine
d. Tropicamide

7) Which drug is useful in treating sinus


bradycardia?
a. Atropine
b. Cisatracurium
c. Neostigmine
d. Succinylcholine

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