Angina pectoris and its
treatment
Definition
Angina pectoris is a Syndrome characterized by sudden severe
pressing chest pain or heaviness radiating to the neck, jaw, back
and arms. It is often associated with tachypnea and nausea.
Angina is the result of myocardial ischemia caused by an imbalance between
myocardial blood supply and oxygen demand.
It is a common presenting symptom (typically, chest pain) among patients
with coronary artery disease.
Type of chest pain: pressure or discomfort
Classification of angina
1. Exertional angina, Stable, Atherosclerotic,Classic,
Due to obstruction of coronaries by atheroma.
2. Variant, Vasospastic angina
due to Spasm of coronaries.
3- Unstable angina.
Due to spasm and partial obstruction of coronaries.
Angina can be:
 Stable
 Unstable caused by unstable
plaque, occurs at rest, unpredictable,
pain can increase for no obvious
reason
 Prinzmetal’s occurs without
provocation, usually at rest, as a
result of coronary artery spasm
Stable angina pectoris
Provoked by physical exertion, especially in cold weather, after meals and
commonly aggravated by anger or excitement
The pain fades quickly with rest
In some patients pain occurs predictably at a certain level of exertion
Etiology and pathogenesis
Symptoms are results of myocardial ischemia due to
insufficient blood flow through atherosclerotically
changed coronary vessels
Clinical symptoms
Patient history is a˝golden standard˝
Retrosternal pain
Dyspnea
Nausea
Arrhythmia
Restlessness
Levine sign
Pain eased after taking nitrates
Investigations
Laboratory tests (leukocytes, hemoglobin, thyroid hormones, troponin I
and T, MB-CPK)
Resting ECG
Excercise ECG
Cardiac scintigraphy
Echocardiography
Coronary angiography
Treatment
Prognostic therapy: Aspirin, lipid-lowering therapy
Symptomatic treatment: GTN, beta-blockers,
 long-acting nitrates, calcium-channel blockers, ACEI
ANTIANGINAL DRUGS
I. AGENTS WHICH ↓ O2 DEMAND & ↑ O2 SUPPLY
A. NITRATES
B. CALCIUM CHANNEL BLOCKERS
II. AGENTS WHICH ↓ O2 DEMAND
C. BETA BLOCKERS
Nitrates & Nitrites
Preparations :
1- Short acting:
A) Nitroglycerine (Glyceryl trinitrate)
Used as sublingual tablets.
B) Isosorbide dinitrate
As sublingual spray.
C) Amyl nitrite
Inhalation
2- Long acting
Nitroglycerine, Isosorbide dinitrate,
Isosorbide mononitrate,Erythrityl –
Tetranitrate.
◦ Action of all start withen hours and continue for hours .
They are given : Orally,Ointment,Buccal,Transdermal
patch,Parenteral.
Absorption
Well absorbed according to the route:
GIT for the long acting
short acting Sublingual
Transdermal for long acting.
Mechanism of action
Glutathione S-transferase
Nitroglycerine ———————— No.
guanylyl cyclase and NO activates increase c GMP
c GMP dephosphorylate myosin light chain to myosin- LC Causing
muscle relaxation.
Pharmacological actions
Nitrates relax all types of smooth muscles vascular
or non vascular .
Relax both arteries and veins but more effective on
veins.
NO released stimulate guanylyl cyclase
1- Angina of effort
A) Decrease venous return
B) Decrease ABP
Both A&B decrease myocardial oxygen requirement.
2-Variant angina
Relax smooth muscle of epicardial coronary artery and relief coronary
spasm.
Unstable angina
◦ Decrease myocardial oxygen
requirement.
◦Relief coronary spasm.
Decrease platelet aggregation.
Adverse effects
Orthostatic hypotension
Throbbing headache
Tachycardia
Facial or cutaneous flushing
Tolerance (Tachyphylaxis)
Salt and water retention
Carcinogenicity
Methaemoglobinemia only with nitrities
Contraindication
Nitrates are contraindicated in increase intracranial pressure.
Nitrates can be used safely in increase of intraocular pressure
(Glucoma).
Calcium channel blockers
1- They block calcium entry in myocardium causing ;
◦A) decrease myocardium contractility &
myocardium oxygen requirement.
B) decrease heart rate causing decrease in myocardium oxygen
requirement.
2-Block calcium entry in vascular smooth muscles (arterioles) causing
a)decrease in peripheral resistance( after load)------ decrease in
oxygen requirement.
◦b)Relief of coronary spasm.
β- blocking drugs
They are not vasodilators
They are used in treatment of angina :
They decrease both heart rate & myocardial contractility that
decrease in myocardial oxygen requirement at rest & in exercise so
improve exercise tolerance.
Potassium channel openers
(Nicorandil )
◦ Activation of potassium channels.
Nitric oxide release.
Arterio & venodilators.
Used as prophylactic therapy .
May cause : Headache,flushing,dizziness.
Drug treatment of angina
1- Acute attack :
Short acting nitrates or nitritis.
2- Prophylactic therapy ;
Long –acting nitrates.
Calcium channel blockers.
β- adrenoceptors blockers.
Potassium channel openers.

Angina pectoris Exertional angina Stable

  • 1.
    Angina pectoris andits treatment
  • 2.
    Definition Angina pectoris isa Syndrome characterized by sudden severe pressing chest pain or heaviness radiating to the neck, jaw, back and arms. It is often associated with tachypnea and nausea. Angina is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand. It is a common presenting symptom (typically, chest pain) among patients with coronary artery disease. Type of chest pain: pressure or discomfort
  • 3.
    Classification of angina 1.Exertional angina, Stable, Atherosclerotic,Classic, Due to obstruction of coronaries by atheroma. 2. Variant, Vasospastic angina due to Spasm of coronaries. 3- Unstable angina. Due to spasm and partial obstruction of coronaries.
  • 4.
    Angina can be: Stable  Unstable caused by unstable plaque, occurs at rest, unpredictable, pain can increase for no obvious reason  Prinzmetal’s occurs without provocation, usually at rest, as a result of coronary artery spasm
  • 5.
    Stable angina pectoris Provokedby physical exertion, especially in cold weather, after meals and commonly aggravated by anger or excitement The pain fades quickly with rest In some patients pain occurs predictably at a certain level of exertion
  • 6.
    Etiology and pathogenesis Symptomsare results of myocardial ischemia due to insufficient blood flow through atherosclerotically changed coronary vessels
  • 8.
    Clinical symptoms Patient historyis a˝golden standard˝ Retrosternal pain Dyspnea Nausea Arrhythmia Restlessness Levine sign Pain eased after taking nitrates
  • 9.
    Investigations Laboratory tests (leukocytes,hemoglobin, thyroid hormones, troponin I and T, MB-CPK) Resting ECG Excercise ECG Cardiac scintigraphy Echocardiography Coronary angiography
  • 10.
    Treatment Prognostic therapy: Aspirin,lipid-lowering therapy Symptomatic treatment: GTN, beta-blockers,  long-acting nitrates, calcium-channel blockers, ACEI
  • 11.
    ANTIANGINAL DRUGS I. AGENTSWHICH ↓ O2 DEMAND & ↑ O2 SUPPLY A. NITRATES B. CALCIUM CHANNEL BLOCKERS II. AGENTS WHICH ↓ O2 DEMAND C. BETA BLOCKERS
  • 12.
    Nitrates & Nitrites Preparations: 1- Short acting: A) Nitroglycerine (Glyceryl trinitrate) Used as sublingual tablets. B) Isosorbide dinitrate As sublingual spray. C) Amyl nitrite Inhalation
  • 13.
    2- Long acting Nitroglycerine,Isosorbide dinitrate, Isosorbide mononitrate,Erythrityl – Tetranitrate. ◦ Action of all start withen hours and continue for hours . They are given : Orally,Ointment,Buccal,Transdermal patch,Parenteral.
  • 14.
    Absorption Well absorbed accordingto the route: GIT for the long acting short acting Sublingual Transdermal for long acting.
  • 15.
    Mechanism of action GlutathioneS-transferase Nitroglycerine ———————— No. guanylyl cyclase and NO activates increase c GMP c GMP dephosphorylate myosin light chain to myosin- LC Causing muscle relaxation.
  • 16.
    Pharmacological actions Nitrates relaxall types of smooth muscles vascular or non vascular . Relax both arteries and veins but more effective on veins. NO released stimulate guanylyl cyclase
  • 17.
    1- Angina ofeffort A) Decrease venous return B) Decrease ABP Both A&B decrease myocardial oxygen requirement.
  • 18.
    2-Variant angina Relax smoothmuscle of epicardial coronary artery and relief coronary spasm.
  • 19.
    Unstable angina ◦ Decreasemyocardial oxygen requirement. ◦Relief coronary spasm. Decrease platelet aggregation.
  • 20.
    Adverse effects Orthostatic hypotension Throbbingheadache Tachycardia Facial or cutaneous flushing Tolerance (Tachyphylaxis) Salt and water retention Carcinogenicity Methaemoglobinemia only with nitrities
  • 21.
    Contraindication Nitrates are contraindicatedin increase intracranial pressure. Nitrates can be used safely in increase of intraocular pressure (Glucoma).
  • 22.
    Calcium channel blockers 1-They block calcium entry in myocardium causing ; ◦A) decrease myocardium contractility & myocardium oxygen requirement. B) decrease heart rate causing decrease in myocardium oxygen requirement. 2-Block calcium entry in vascular smooth muscles (arterioles) causing a)decrease in peripheral resistance( after load)------ decrease in oxygen requirement. ◦b)Relief of coronary spasm.
  • 23.
    β- blocking drugs Theyare not vasodilators They are used in treatment of angina : They decrease both heart rate & myocardial contractility that decrease in myocardial oxygen requirement at rest & in exercise so improve exercise tolerance.
  • 24.
    Potassium channel openers (Nicorandil) ◦ Activation of potassium channels. Nitric oxide release. Arterio & venodilators. Used as prophylactic therapy . May cause : Headache,flushing,dizziness.
  • 25.
    Drug treatment ofangina 1- Acute attack : Short acting nitrates or nitritis. 2- Prophylactic therapy ; Long –acting nitrates. Calcium channel blockers. β- adrenoceptors blockers. Potassium channel openers.