Angina Drugs

Question 1

Angina is caused by what?

Answer 1

CORONARY ISCHAEMIA which is the result of atherosclerosis by
Sudden ischemia is usually caused by
thrombosis and may result in infarction

Question 2

-. Ca2+ overload results from

Answer 2

from ischemia
May be responsible for cell death, arrhythmias, diastolic dysfunction

Question 3

ANGINA occurs when

Answer 3

the oxygen supply to the myocardium is insufficient for its needs

Question 4

Three types of angina

Answer 4

1)Stable: predictable chest pain on exertion
Produced by increased demand on the heart usually caused by atheroma of coronary vessels or aortic stenosis
2) Unstable angina: pain that occurs with less and less exertion, culminating in pain at rest
Pathology is similar to myocardial infarction (MI)
but without complete occlusion of the vessel
3) Variant angina: relatively uncommon
Occurs at rest
Caused by coronary artery spasm, often in
association with atheromatous disease

Question 5

TREATMENT APPROACH for angina
(inc./dec.)

Answer 5

•Decrease oxygen requirements
-Decrease total peripheral resistance (TPR)
-Decrease cardiac output (CO)
-Nitrates, calcium channel blockers (CCBs), beta-blockers

● Increase oxygen delivery
-Coronary artery vasodilation
-Opposes coronary spasm in variant angina -Nitrates and CCBs

Question 6

Treatment for underlying atheromatous
disease

Answer 6

-Statins
-Prophylaxis against thrombosis with
antiplatelet drugs

Question 7

BETA-BLOCKERS MoA

Answer 7

-SNS stimulation increases CO
Ventricle:
● Increased force of contraction
● Increased SV

SA and AV node: increases HR

-Reduce cardiac work and thus oxygen consumption of the heart

Question 8

BETA BLOCKERS Clinical Use:

Answer 8

Clinical Use: Prophylaxis of stable angina (first- line) and treatment of unstable angina

Coronary diameter effects should be minor
Avoided in variant angina due to theoretical risk of
increasing coronary spasm

Question 9

an alternative for patients that cannot use beta-blockers

Answer 9

Ivabradine

Question 10

Three main L-type CCBs
For angina

Answer 10

Verapamil (heart)
Diltiazem (heart and smooth muscle vasculature)
Nifedipine (smooth muscle vasculature)

Question 11

What do CCBs do in angina

Answer 11

•Dilate coronary vessels (effect on smooth muscle
vasculature)
•Decrease metabolic demands (effect on TPR and heart)= DECREASES TPR

Question 12

Nitrates examples

Answer 12

•Glyceryl trinitrate (GTN): acute HF
•Isosorbide mononitrate: chronic HF

Question 13

Clinical Use
Of CCBs

Answer 13

May be used in combination with beta-blockers (dihydropyridines;CCB), when monotherapy is insufficient, or as alternative in stable angina

Dihydropyridines: vasospastic angina
(DIHYDROPYRIDINES= vasodilation drug)

Question 14

Therapeutic goal in angina
Of NITRATES

Answer 14

Improve perfusion of the myocardium
Reduce metabolic demands

Question 15

NITRATES: MOA

Answer 15

•Venorelaxation -> central venous pressure (CVP) reduction i.e. reduced preload, reduced SV
•Effects on arteries: reduce afterload
-Myocardial oxygen consumption falls due to reduced afteload and preload
•Direct coronary vessel dilation increases oxygen content in coronary sinus blood

Question 16

ADVERSE EFFECTS
Of nitrates

Answer 16

•(You build) Tolerance: d/t Depletion of –SH groups
Tolerance wears off after a brief nitrate-free interval
•Pronounced with long-acting nitrates or prolonged/frequent administration (IV infusion, transdermal patch)
•Postural hypotension- Contraindicated in hypotension
•Headache
•Reflex tachycardia

Question 17

NITRATES
Clinical use in angina

Answer 17

•Stable: May be used in combination with beta-
blockers/CCBs
•Variant: May be used in combination with CCBs
•Unstable: In combination with other drugs e.g. anti-platelets

Question 18

Nicorandil MoA
+ Adverse effects

Answer 18

•Potassium channel activator with nitrovasodilator activity
•Sometimes combined with other anti-anginal treatments in refractory angina resistant cases
•Both arterial and venous dilator
Adverse effects: headache, flushing, dizziness, hypotension

Question 19

POTASSIUM CHANNEL ACTIVATION
Works how

Answer 19

•Relax smooth muscle
-Open KATP channels
-Hyperpolarization
-Switching off of VDCC

•Antagonize the action of intracellular ATP on these channels

Question 20

RANOLAZINE MOA

Answer 20

-Ischemia causes increased Na+
-Prevents Ca2+ exit via Na+/Ca2+ exchanger (NCX)
!-Ranolazine inhibits late sodium current
!-Indirectly reduces intracellular Ca2+
!-Decreased EDP and thus improvement of diastolic coronary flow

Question 21

Ranolazine Adverse effects

Answer 21

-Adjunct to other anti-anginal drugs

•Adverse effects: constipation, headache, dizziness, nausea, increased QT interval

-!Does not reduce blood pressure or heart rate

Question 22

Ranolazine CI

Answer 22

Contraindicated in long QT syndrome or drugs which prolong the QT interval
Anti-psychotics, class Ia & III anti-arrhythmic drugs
Ex. Haloperidol

Question 23

Stable angina: first-line+ alternative/ combination therapy

Answer 23

1.Beta blocker
2. CCB / long acting nitrates

Question 24

Unstable angina tx

Answer 24

Anticoagulation, antiplatelets, β-blockers, ACE inhibitors,
statins Symptom control: nitroglycerin and morphine

Question 25

Variant angina:
1, first line
2. Alternator monotherapy / in combo

Answer 25

1.CCB (e.g.
amlodipine, diltiazem)

2.Long-acting nitrates