Angina Pectoris

ANGINA PECTORIS
Dr Sidra Tanwir
DEFINITION
A type of chest pain caused by reduced blood flow to
the heart.
 Angina pectoris is a clinical syndrome of IHD
resulting from transient myocardial ischemia.
 It is characterized by paroxysmal pain in the
substernal or precordial region of the chest which is
aggravated by an increase in the demand of the heart
and relieved by a decrease in the work of the heart.
 Often, the pain radiates to the left arm, neck, jaw or
right arm.
 It is more common in men past 5th decade of life.
CLASSIFICATION
Stable angina
Stable angina is the most common type of angina.

 It occurs when the heart is working harder than usual.
 Stable angina has a regular pattern. (“Pattern” refers
to how often the angina occurs, how severe it is, and
what factors trigger it.)
CLASSIFICATION
 The pain usually goes away a few minutes after you

rest or take your angina medicine.
 Stable angina isn't a heart attack, but it suggests that a
heart attack is more likely to happen in the future.
CLASSIFICATION
Unstable Angina
Unstable angina doesn't follow a pattern.

It may occur more often and be more severe than
stable angina.
 Unstable angina also can occur with or without
physical exertion, and rest or medicine may not relieve
the pain.
CLASSIFICATION
Unstable angina is very dangerous and requires

emergency treatment.
 This type of angina is a sign that a heart attack may
happen soon.
CLASSIFICATION
Variant (Prinzmetal's) Angina
Variant angina is rare.
 A spasm in a coronary artery causes this type of
angina.
 Variant angina usually occurs while you're at rest, and
the pain can be severe.
 It usually happens between midnight and early
morning.
 Medicine can relieve this type of angina.
SIGNS AND SYMPTOMS
 Chest discomfort rather than actual pain.
 The discomfort is usually described as
 pressure
Heaviness
Tightness
Squeezing
Burning
choking sensation
 Apart from chest discomfort, anginal pains may also be
experienced in the epigastrium (upper central abdomen),
back, neck area, jaw, or shoulders.
SIGNS AND SYMPTOMS
 It is exacerbated by having a full stomach and by cold
temperatures.
Pain may be accompanied by
Breathlessness
 sweating
 nausea in some cases
CAUSES
 Major Risk Factors:
 Smoking
 Diabetes
 Dyslipidemia
 Obesity
 Hypertension
 Stress
 Kidney Diseases
 Inactivity
CAUSES
Other Medical Problems
Hyperthyroidism
Hypoxemia
Profound anemia
Uncontrolled hypertension
CAUSES
Other Cardiac Problems
Tachyarrhythmia
Bradyarrhythmia
Valvular heart disease
Hypertrophic cardiomyopathy
PATHOPHYSIOLOGY
 Angina results when there is an imbalance between
the heart's oxygen demand and supply.
 This imbalance can result from an increase in demand
(e.g., during exercise) without a proportional increase
in supply (e.g., due to obstruction or atherosclerosis of
the coronary arteries).
 However, the pathophysiology of angina in females
varies significantly as compared to males Non-
obstructive coronary disease is more common in
females
DIAGNOSIS
Acute Chest Pain
ECG
ST↑ No ST↑
Troponins
15mins 15 mins Test +ve

Test –ve (unstable angina/AMI)
> 6 hours chest pain

<6hours chest
(low risk/ other
pain disease)
Troponins (+ 4 hrs)
15 mins Test –ve 15 mins Test +ve

(low risk/other disease) (unstable angina / AMI)
Most Commonly Used Drugs In Treating Angina
Pectoris
Cardiac
Vasodilato
Depressan
rs
ts
Calcium Calcium Beta

Nitrates
Blockers Blockers Blockers
Classification of Anti-anginal Agents
Nitrates
Organic nitrates are prodrugs and they release nitric
oxide.
 Nitrates are mainly venodilators also cause arteriolar
dilation and as a result reduces both preload and
afterload.
 These compounds cause a rapid reduction in
myocardial oxygen demand, followed by rapid relief
of symptoms.
Increased nitrates in the blood increase formation of
nitric oxide, increase cGMP formation and hence
increased dephosphorylation of myosin vascular
smooth muscle relaxation
 Smooth muscles of bronchi, oesophagus, biliary tract,
etc are also relaxed by nitrates.
The nitrates are inactivated in liver by glutathione or
ganic nitrate reductase.
Therefore their oral bioavailability is considerably less
due to their first-pass metabolism.
The sublingual route, which avoids first pass effect, is
therefore preferred.
Duration of action lasts for about 25-30min
pharmacokinetics
Pharmacological Action On Smooth Muscles
Venodilation Arterial dilation
Peripheral pooling
↓PVR
of blood
↓Venous return to
↓Afterload
the heart
↓Preload Relief of Pain
↓Left and right end-

diastolic volume and
pressure
↓Cardiac work
↓Oxygen requirement of
myocardium
Relief of Pain
 The most common adverse effect of nitroglycerin, as
well as of the other nitrates, is headache.
 High doses of organic nitrates can also cause postural
hypotension, facial flushing, and tachycardia.
Sildenafil potentiates the action of the nitrates.
 Over doses may cause methaemoglobinaemia.
Calcium channel blockers:
Nifedipine
 This drug has minimal effect on cardiac conduction or
heart rate.
 Nifedipine is administered orally, usually as extended-
release tablets.
It undergoes hepatic metabolism to products that are
eliminated in both urine and the feces.
The vasodilation effect of nifedipine is useful in the

treatment of variant angina caused by spontaneous
coronary spasm.
Nifedipine can cause flushing, headache, hypotension,
and peripheral edema
Verapamil
The diphenylalkylamine verapamil slows cardiac
atrioventricular (AV) conduction directly, and
decreases heart rate, contractility, blood pressure, and
oxygen demand.
Verapamil causes greater negative inotropic effects
than nifedipine, but it is a weaker vasodilator.
The drug is extensively metabolized by the liver;
therefore, care must be taken to adjust the dose in
patients with liver dysfunction.
Verapamil is contraindicated in patients with
preexisting depressed cardiac function or AV
conduction abnormalities.
It also causes constipation.
Verapamil should be used with caution in patients
taking digoxin, because verapamil increases digoxin
levels.
Diltiazem
It dilates peripheral and coronary arteries
 It also causes negative inotropic, chronotropic and
dromotropic effects.
It is used in the treatment of angina, hypertension and
supraventricular arrhythmias.
Verapamil or diltiazem should not be given with beta
blockers as SA nodal depression, conduction defects or
asystole may occur or be aggravated.
 These should not be used with other cardiac
depressants drugs like quinidine or disopyramide.
These drugs increase plasma digoxin levels by
decreasing its excretion.
Uses of CCBs
Angina pectoris
Variant angina
Unstable angina
Supraventricular arrhythmias
Hypertension
Hypertropic cardiomyopathy
Migraine
Raynaud’s phenomenon
Beta Blockers
• ↓ Heart rate
• ↓ Force of
• Propranolol
Β1 myocardial
Beta • Metoprolol
• receptors contraction
blockers Atenolol • ↓↓ Cardiac work
• of heart
Timolol • ↓ Myocardial oxygen
consumption
 They are, however, contraindicated in patients with
asthma, diabetes, severe bradycardia, peripheral
vascular disease, or chronic obstructive pulmonary
disease
 Adverse effects:
Bradycardia
Heart block
Bronchospasm
Hypoglycaemia
Combination therapy
Nitrates × beta blockers

Nifedipine × β-blockers
Β-blockers × verapamil/diltiazem
Calcium channel blockers × nitrates
Nitrates + β-blockers + CCBs
DRUGS COMMONLY USED IN
TREATING ANGINA
No Concomitant Disease
Long acting nitrate
Β Blockers
KEY
Calcium Channel
Commonly used
Blockers
Less effective
drugs drugs

Angina Pectoris

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ANGINA PECTORIS

Stable angina is the most common type of angina.

 The pain usually goes away a few minutes after you

Unstable angina doesn't follow a pattern.

Unstable angina is very dangerous and requires

15mins 15 mins Test +ve

> 6 hours chest pain

15 mins Test –ve 15 mins Test +ve

Calcium Calcium Beta

Venodilation Arterial dilation

↓Preload Relief of Pain

↓Left and right end-

The vasodilation effect of nifedipine is useful in the

Nitrates × beta blockers

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