Anti-anginal agents are used to treat angina pectoris, which is characterized by chest pain due to insufficient oxygen supply to the heart. There are several classes of anti-anginal agents that work by different mechanisms: nitrates increase oxygen supply by dilating coronary arteries and reducing blood pressure; beta blockers decrease oxygen demand by lowering heart rate and blood pressure; calcium channel blockers increase oxygen supply and decrease demand by dilating arteries and relaxing smooth muscle. Organic nitrates are commonly used anti-anginal agents that work by dilating coronary arteries and veins to increase blood flow and decrease workload, thereby relieving chest pain.
3. Angina pectoris – commonly known as angina – It occurs due to insufficient
oxygen supply to the myocardium i.e the sensation of chest pain
The term derives from the Latin angina ("infection of the throat") from
the Greek ἀγχόνη ankhonē ("strangling"), and the Latin pectus ("chest"), and
can, therefore, be translated as "a strangling feeling in the chest".
Angina pectoris is chronic disease affecting the coronary arteries which
supply oxygenated blood from the left ventricle to all heart tissues.
Angina is the primary symptom of oxygen deficient heart disease &
characteristic by the sudden pain originating in the chest , often regarding to
the left shoulder and down of left arm
4. There can be severe pain with little or no risk of a myocardial
infarction {commonly known as a heart attack}, and a heart attack can
occur without pain)
Based on electrophysiological changes observed during the attack
angina is result of advanced state of food, exercise, emotional factor.
Typical angina characterized by low ST
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 path physiology of angina in females varies significantly as
compared to males.[
Non-obstructive coronary disease is more common in females
5. 2. Major risk factors
Age (≥ 55 for men, ≥ 65 for
women)
Cigarette smoking
Diabetes mellitus (DM)
Family History
Hypertension (HTN)
Kidney disease
Obesity
Physical inactivity
Medications
Types of Angina
Typical Angina ( Classical Angina )
pain is commonly induced by exercise,
excitement or a heavy meal
secondary to advanced atherosclerosis of
the coronary vessels
associated with ST-segment depression
on ECG
Variant Angina ( Prinzmetal Angina)
pain is induced while at rest
associated with ST-segment elevation on
ECG
secondary to vasospasm of the coronary
vessels
Unstable angina
may involve coronary spasm and may also
have the component of atherosclerosis
the duration of manifestation is longer than
the first two and has the manifestation of
Myocardial infarction.
6. * Myocardial ischemia which produces angina results from
imbalances in myocardial oxygen supply & demand relationship
such as decreased oxygen supply and/or increased oxygen
demand.
Etiology
1. Decrease oxygen supply
2. Increase demand for oxygen
Treatment Plan/Approach to develop antianginal drugs include
A. decrease the risk factor like atherosclerosis, hypertension, smoking
B. increase oxygen supply
C. decrease oxygen demand
D- to decrease workload on heart
E- to prevent or inhibit vasospasm
7. Antianginal Agents
Nitrates
Beta blockers
Calcium channel blockers
I. AGENTS WHICH ↓ O2 DEMAND & ↑ O2 SUPPLY
A. NITRATES
B. CALCIUM CHANNEL BLOCKERS
II. AGENTS WHICH ↓ O2 DEMAND
C. BETA BLOCKERS
8. Classification of Antianginal Drugs
For the treatment of angina pectoris include
1- nitrates and nitrites
2- Xanthines
3 – nicotinic acid and derivative
4 – papavarine
5- B- Adrenergic Blockers
6- MAO inhibitors
7- miscellaneous
13. 1st mechanism of action
Coronary artery dilatation
Decrease coronary bed
resistance
(Relieved coronary
vasospasm)
Increase coronary blood flow
Increase oxygen supply
2nd mechanism of action
Reduction on peripheral resistance
(Secondary to dilatation of
aorta)
Decrease blood pressure
Decrease after load
Decrease workload
Decrease oxygen consumption
14. 3rd mechanism of action
Reduced venous return
(Due to dilatation of the veins)
Decrease left ventricular volume
Decrease preload
Decrease workload
Decrease oxygen consumption