Q. Write about etiopathogenesis of angina and its pharmacological management.
Answer:
Etiopathogenesis:
● Coronary artery disease: This is a buildup of plaque and cholesterol inside your
coronary arteries, which supply blood to your heart muscle. The buildup narrows
your artery so much that the oxygen-rich blood your heart needs can’t get
through, and your heart muscle becomes starved for oxygen. This causes ischemia
and angina. Atherosclerotic plaque causes 70% of fatal heart attacks.
● Blood clot: When plaque that forms in your narrow coronary artery breaks apart,
it can attract a blood clot. When a blood clot settles in a coronary artery that’s
already narrow, it can cause a blockage (thrombosis).
● Coronary artery spasm: This happens when the coronary arteries spasm, which
temporarily reduces or cuts off blood supply to your heart.
● Coronary artery dissection: This rare condition can keep blood from getting to
your heart.
● Ischemic heart disease like angina and myocardial infarction result due to the
effect on supply and demand of oxygen to myocardium.
● Coronary arteries attached to the aorta supply the oxygen to the heart muscle i.e.
myocardium.
● Problems can arise when there is a restriction of blood flow through coronary
arteries; this is commonly due to atherosclerosis, in which fatty material deposits
in arteries and restricts the blood flow to myocardium.
● When the luminal diameter is more than 70% blocked, stable angina arises.
● When oxygen demand of myocardium increased due to stress, coronary arteries
were unable to supply due to stenosis(narrowing).
● When coronary flow becomes zero this leads to ischemia and leads to angina and
it depends on demands of oxygen by myocardium.
The risk factors associated with angina pectoris and myocardial infarction are
dyslipidaemia with low high-density lipoprotein and elevated low-density lipoprotein
forms of cholesterol, hypertriglyceridemia, family history, age, premature menopause in
women, smoking, and disease conditions like hypertension, obesity, and diabetes
mellitus.
Pharmacological management
The drugs show their action by either increasing the amount of blood flow to the cardiac
muscles (oxygen supply) or decreasing the oxygen requirement (workload) of the heart.
The following classes of drugs are useful in the treatment of angina pectoris:
● Organic nitrates e.g., Glyceryl trinitrate, isosorbide dinitrate, pentaerythrityl
tetranitrate
● Beta adrenergic blockers e.g., metoprolol, atenolol
Calcium channel blockers e.g., verapamil, diltiazem, amlodipine
● Antiplatelet drugs e.g., aspirin, clopidogrel
● Potassium channel activators e g., nicorandil, minoxidil, diazoxide
Organic nitrates: They are available in multiple dosage forms like sublingual tablets,
sprays, ointments, transdermal patches, oral sustained release, and intravenous
preparations. The nitrates act as vasodilators, mainly as venodilators. Due to the dilation
of the veins, the venous return decreases, leading to a reduction in the preload. This helps
by reducing the myocardial oxygen demand. Also, they cause coronary vasodilation,
leading to increased blood supply and, in turn, oxygen supply to the myocardium, thus
relieving angina.
Beta adrenergic blockers: Beta blockers help in the treatment of angina pectoris by
reducing the myocardial oxygen demand.
Calcium channel blockers: These drugs inhibit the entry of calcium ions and cause
vasodilation and decreased heart rate.
Antiplatelet drugs: These drugs work by decreasing platelet aggregation and inhibiting
thrombus formation.
Potassium channel activators: These act as agonists on ATP-sensitive potassium
channels. It shows vasodilation both in arterial and venous vascular beds, leading to a
reduction in afterload and preload of the heart. It is used in patients with stable coronary
artery disease...
-----------------------------------------------------------------------
ONLY FOR EDITOR