Anti anginal drugs. Dr.V.V.Gouripur. Ischaemic Heart Disease,. ALSO known as Coronary Artery Disease Angina pectoris Myocardial infarction (Acute coronary syndrome). Ischaemic Heart Disease,. A condition that affects the supply of blood to the heart.
(Acute coronary syndrome)
-new onset angina with frequent attacks (greater than or equal to 3 episodes/day),
-rest angina, and
May be associated with an unstable plaque of the coronary arteries that can initiate thrombus formation and total occlusion very quickly.
Also cause occlusion by flap dissection or by dislodging & becoming wedged in a smaller diameter artery.
Is a medical emergency and does not follow the predictable pattern of exertional pain alleviated with rest that is often seen with stable angina.
Organic nitrates ---- Glyceryl trinitrite (GTN)
Beta blockers- ------Atenalol
Calcium channel blockers- Verapamil
NO is capable of dilating all blood vessels, however, there is a greater effect on large arteries and veins compared to arterioles.
This means that low concentrations of GTN dilates veins first. In order to dilate arterioles, larger concentrations are needed.
However, the main target to reduce preload is the effects on the veins
GTN dilates the veins, which causes increased venous pooling (increased venous capacitance)
This reduces venous return (preload) and hence reduces the amount of blood the heart has to pump, thus making it work less (thus reducing the O2 demand)
In normal individuals, GTN will also act to dilate the coronary arterioles, thus allowing increased perfusion to the heart.
However, this is not the case in people with classic angina because the arterioles are already maximally dilated, therefore there will be no increase in cardiac blood flow
Develops with all nitrates coronary arterioles, thus allowing increased perfusion to the heart.
Disappears in 24 h. after stopping the drug
Tolerance can be avoided
- Using the least effective dose
- Creating discontinuous plasma levels
" Decrease in the effect of a drug
when administered in a long-acting form"
Tolerance occurs because the enzyme required to break down GTN (the tissue thiols) are depleted, and so there is lack of conversion of GTN to NO.
After a drug free period, the enzymes regenerate, and are ableto convert GTN to NO again.
The best way to overcome the tolerance is to have a drug free period - the patient puts on a patch in the morning and takes it off at night (so that nighttime is their drug free period)
NITRATES GTN (the tissue thiols) are depleted, and so there is lack of conversion of GTN to NO.
In anticipation of an attack
The CCBs have little effect on preload GTN (the tissue thiols) are depleted, and so there is lack of conversion of GTN to NO.
CCBs may inhibit platelet aggregation
The desired therapeutic effects of CCBs in treating angina are to:
Reduce myocardial oxygen consumption by reducing afterload
Reduce myocardial oxygen consumption by reducing heart rate and contractility (except for the dihydropyridines which have minimal effects on contractility)
Improve oxygen delivery to ischemic myocardium by vasodilating coronary arteries and by reducing heart rate (increased time spent in diastole)
May also inhibit platelet aggregation
ß-ADRENERGIC BLOCKERS GTN (the tissue thiols) are depleted, and so there is lack of conversion of GTN to NO.
Hypotension: BP < 100 mmHg
Bradycardia: HR < 50 bpm
Chronic bronchitis, ASTHMA
Severe chronic renal insufficiency
GTN relieves the spasm
(Reduce Ca2+ entry into the smooth muscle around the coronary vessels, hence preventing theirconstriction)
THE END GTN (the tissue thiols) are depleted, and so there is lack of conversion of GTN to NO.