Angina pectoris is a pain syndrome that occurs when coronary blood flow is inadequate to supply the oxygen required by the heart in a portion of the myocardium.
The primary cause of angina pectoris is an imbalance between the demand and supply of oxygen.
1. FACULTY OF PHARMACEUTICAL SCIENCE
PHARMACOTHERAPEUTICS ER20-24T
Chapter 2.1: Cardiovascular System
Topic 2.1.2. Angina Pectoris
FACULTY OF PHARMACEUTICAL SCIENCE
RAMA UNIVERSITY, UTTAR PRADESH
KANPUR, INDIA
2023-2024
Presented by- Ms. ALKA
Assistant Professor
2. Definition
Angina pectoris is defined as severe chest pain that occurs
when coronary blood flow is inadequate to supply the
oxygen required by the heart.
Anti-anginal drugs are those drugs that prevent or
terminate the attack of angina pectoris.
The primary cause of angina pectoris is an
imbalance between the oxygen requirement of
the heart and the oxygen supplied to it.
FACULTY OF PHARMACEUTICAL SCIENCE
3. Types of angina
There are three types of angina:
Classic (stable) angina: (atherosclerotic angina) occurs with stress and
exertion and is caused by atheromatous obstruction of the large
coronary vessels.
Unstable angina: occurs over the course of a day with progressive
severity, frequency and is caused by the narrowing or partial occlusion
of coronary arteries by thrombi/platelets aggregation.
Variant (Prinzmetal, vasospastic) Oxygen delivery decreases as a
result of reversible coronary vasospasm.
FACULTY OF PHARMACEUTICAL SCIENCE
5. 1. Fatigue: Feeling excessively tired or fatigued can be associated with hypertension.
2. Dyspnoea (Shortness of Breath): Difficulty breathing or shortness of breath,
especially during physical activity, can be a sign of hypertension-related complications.
3. Chest Pain: Chest pain or angina can occur due to the increased workload on the heart
caused by high blood pressure.
4. Palpitation (Raise in Pulse rate): Rapid pulsations or abnormally rapid or irregular
beating of the heart.
5. Chest pain radiates to the shoulders, arms, and back.
6. Increase sweating.
7. Weakness
Clinical manifestations
FACULTY OF PHARMACEUTICAL SCIENCE
6. Atherosclerosis
Coronary artery spasm
Vasoconstriction
Blockage of coronary arteries due to blood clot or thrombus
Inflammation in coronary arteries.
Injury of coronary arteries.
Diseases (arrhythmia, obesity, kidney failure)
Smoking
Etiology
FACULTY OF PHARMACEUTICAL SCIENCE
8. Diet and nutrients
Salt restriction
Avoid alcohol intake
Smoking cessation
Lifestyle modification
Non-Pharmacological management
FACULTY OF PHARMACEUTICAL SCIENCE
9. Pharmacological management
Act as a vasodilator
1. Nitrates: Increase blood flow, and oxygen supply, reduce venous pressure,
preload, and cardiac workload.
2. Calcium channel blocker: it reduces the demand of the heart by reducing the
contraction of the heart which reduces afterload. It also acts on blood vessels and
prevents the contraction of blood vessels which helps in dilations and ultimately
gets relief from angina.
3. Beta-blockers: only selective beta blockers are used (β1 blockers)- it helps in
the reduction of heart rate, contractility rate, cardiac output, and blood pressure.
FACULTY OF PHARMACEUTICAL SCIENCE
10. 4. K+ channel openers: The most prominent action is hyperpolarization and relaxation
of vascular as well as visceral smooth muscle.
5. Others (Voltage-gated sodium channel blockers):
Ranolazine inhibits a late Na+ current (late Na) in the myocardium which indirectly
facilitates Ca2+ entry through Na+ /Ca2+ exchanger. Reduction in Ca2+ overload in the
myocardium during ischaemia decreases contractility and has a cardioprotective effect.
Selective blockade of If current by ivabradine results in heart rate reduction without
any other electro-physiological or negative inotropic (slowing of myocardial relaxation)
effect. Heart rate reduction decreases cardiac O2 demand and prolongation of diastole
tends to improve myocardial perfusion (O2 supply).
FACULTY OF PHARMACEUTICAL SCIENCE
