Angina pectoris

CONTENTS:
 INTRODUCTION
 PATHOPHYSIOLOGY
 SIGN & SYMPTOMS
 CAUSES
 DIAGNOSTIC TESTS
 DRUG THERAPY
NITRATES
BETA BLOCKERS
Ca CHANNEL BLOCKERS
OTHER DRUGS

 It is a common
presenting
symptom
(typically, chest
pain) among
patients with
coronary artery
disease.
Angina is the result of
myocardial ischemia
caused by an
imbalance between
myocardial blood
supply and oxygen
demand.

Chest discomfort rather than actual pain. The discomfort usually
described as:
Pressure
Heaviness
Tightness
Squeezing
Burning
Choking sensation

 Apart from chest discomfort, angina pain may also be experienced
in the :
Epigastrum (upper central abdomen),
Back
Neck area, jaw or shoulder
 It is exacerbated by having a full stomach & by cold temperatures
 Pain may be accompanied by
Breathlessness
Sweating and nausea in some cases.

CAUSES
1. MAJOR RISK FACTORS:
Diabetes
Hypertension
Obesity
Kidney disease
Stress
2. OTHER MEDICAL PROBLEMS:
Hyperthyroidism
Hypoxemia
Profound anemia
Uncontrolled hypertension

3. OTHER CARDIAC PROBLEMS :
 Tachyarrythmia
 Bradyarrythmia
 Valvular heart disease
INITIATING FACTORS OF AN ATTACK:
o Cold weather
o Emotions
o Heavy meals
o Pain & smoking.
o Hypoglycemic
EPIDEMIOLOGY:
Occurs in both men and women of any age but commonly middle age and
older adults.

It detects and records the electrical activity of the heart. Certain
electrical patterns that the ECG detects can suggest whether CAD is
likely.
During an attack there may be a transient ST segment depression.
 if the angina is provoked by exertion, an exercise stress ECG should
be performed.

Typically, this test involves taking an electrocardiogram (ECG)
before, during, and after exercise on a treadmill or stationary
bicycle. Patients who are at risk for a coronary event with exercise
are, instead, given a drug to increase the heart rate.

3. CORONARY ANGIOGRAM:
Is obtained by injecting contrast material into the bloodstream
and taking x-rays of the coronary arteries. This enables the
physician to see blockages, malformations, and stenosis in the
vessels.

4.BLOOD TEST
Blood tests check the levels of certain fats, cholesterol,
sugar, and proteins in blood.
Abnormal levels may indicate risk factors for CAD.

TREATMENT STRATEGIES
 The main goal is to restore the balance between oxygen demand &
supply
 Lifestyle changes
 Anti-anginal drug
 Surgery
Angioplasty
Coronary artery bypass grafting (CABG)

Avoid stress.
Avoid large meals.
Over-weight >> weight loss.
Safe exercise plan.
Stop smoking.

ANTI ANGINAL DRUGS
 These agents lower the oxygen demand of the heart by affecting the
blood pressure, venous return, heart rate & contractility.
Acute attacks: GTN & ISDN
First line drugs : Nitrates & Beta blockers
Second line drugs: Ca channel blockers & Potassium channel blockers.

They are first line drugs & effective in both treatment
& prophylaxis against angina attacks.
 All organic nitrates share the same action; differ only
in time course. The only major action is smooth
muscle relaxation.

RAPID ACTING
Used to terminate acute
attack of angina
E.g: Nitroglycerin and Amyl
nitrate
Usually administered
sublingually
LONG ACTING
Used to prevent an attack of
angina.
E.g: Erythrytyl tetranitrate,
Isosorbide dinitrate,
Pentaerythrytol tetranitrate.
Administered orally or
topically.

 Well absorbed from
buccal, intestine & skin
Metabolism: .Liver (90 %)
-extensive-->For dinitrate
& tetranitrate
(bioavailability->10%).
Mononitrate does not
undergo metabolism->
bioavailability is very high.
Excretion -- Renal.

 Headache – most common.
Transient episodes of dizziness – in the beginning of
treatment.
High doses of organic nitrates causes postural hypotension,
facial flushing, and tachycardia.
Prolonged therapy causes endothelial dysfunction.
Overdosage may cause methemoglobinemia.

Patients receiving other antihypertensive agent.
Patients with elevated intracranial pressure.
Drug Interaction: Sildenafil and other PDE-5 inhibitors can
potentiate the actions of nitrates because they inhibit the
breakdown of cGMP (they should not be taken within 6
hours of taking a nitrovasodilator)

Tolerance to the actions of nitrates develops rapidly and blood
vessels become desensitized to vasodilation.
Tolerance can be overcome by providing a daily “nitrate-free
interval” to restore sensitivity to the drug.
 Dependence: Sudden withdrawal after prolonged exposure
has resulted in spasm of coronary and peripheral blood vessels.
Withdrawal of nitrates should be gradual

Angina Pectoris All types.
Acute coronary syndrome preload as well as coronary
flow.
Myocardial infarction (MI).
Biliary colic.
Esophageal spasm.
Cyanide poisoning: Nitrates generate methaemoglobin which
has high affinity for cyanide radical and forms
cyanomethaemoglobin.

MECHANISM OF ACTION
Beta blockers reduce the heart rate, blood
pressure, and the force of contractions,
thereby decreasing the amount of oxygen
the heart requires to pump blood.

SIDE EFFECTS
 Cardiac effects
o Worsen heart failure
o Bradycardia
 Noncardiac effects
o Constriction of airways
o Circulatory problems
o Hallucinations
o Insomnia
o Fatigue

PRECAUTIONS AND MONITORING
EFFECTS:
 Doses should be increased until the anginal episodes have been
reduced or until un-acceptable side-effects occur.
 β- blockers should be avoided in Prinzmetal’s angina (caused by
coronary vasospasm) because they increase coronary resistance.
 Asthma is a relative contraindication because all β-blockers
increase airway resistance and have the potential to induce
bronchospasm in susceptible patients.

CONTD
 Sudden cessation of beta-blocker therapy may trigger a
withdrawal syndrome that can aggravate anginal
attacks(especially in patients with coronary artery
disease) or cause myocardial infarction.
 Diabetic patients and others predisposed to
hypoglycemia should be warned that beta-blockers mask
tachycardia, which is a key sign of developing
hypoglycemia.

CALCIUM CHANNEL BLOCKERS
 They dilate arteries & lower blood pressure. Which
decreases the force of contractions.
They also dilate veins, reduces the amount of blood
returning to the heart which reduces the work load of the
heart.

PHARMACOKINETICS
 All CCBs are well absorbed through GI tract but
they undergo varying degree of first pass
metabolism.
All are highly bound to plasma proteins,
metabolized in the liver and excreted in urine.

ADVERSE EFFECTS
 Constipation
 Peripheral edema
 Headache
 Reflex tachycardia
PRECAUTIONS:
DONOT STOP ABRUPTLY
INTERACTIONS:
Grape fruit juice Concentration.
Verapamil Plasma Concentration of digoxin

POTASSIUM CHANNEL OPENER
Potassium-channel openers are drugs that activate (open)
ATP-sensitive K+-channels in vascular smooth muscle.
Opening these channels hyperpolarizes the smooth
muscle, which closes voltage-gated calcium channels and
decreases intracellular calcium leading to relaxation and
vasodilation.
example
Nicorandil

ANTIPLATELET AGENTS
An antiplatelet drug decreases platelet aggregation and
inhibit thrombus formation.
 Antiplatelet drugs can reversibly or irreversibly inhibit the
process involved in platelet activation resulting in decreased
tendency of platelets to adhere to one another
Example
Aspirin

ANTICOAGULANTS
A medication used to prevent the formation of blood
clots and to maintain open blood vessels.
Anticoagulants are called blood "thinners," but they do not
thin the blood, they only prevent or reduce clots, or thrombi
Example
Heparin

LATE INWARD SODIUM CURRENT
BLOCKER
 It blocks late inward sodium currents in cardiomyocytes.
late inward sodium currents contribute to an elevation in
intracellular sodium, which leads to an increase in
intracellular calcium through the sodium-calcium exchanger
Example
ranolazine

Angina pectoris

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Angina pectoris