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Anti- anginal drugs
Anti- anginal drugs

Anti- anginal drugs - Description

content Anti anginal drugs Angina pectoris Types Classification Nitrates Calcium channel blockers b blockers Combination therapy Antianginal drugs Antianginal drugs may relieve attacks of acute myocardial ID: 590107 Download Presentation


nitrates decrease angina blockers decrease nitrates blockers angina hrs oxygen myocardial effect heart channel amp coronary cardiac agents isosorbide load nitroglycerin hours

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Anti- anginal drugsSlide2


Anti anginal drugs

Angina pectoris


ClassificationNitratesCalcium channel blockersb blockersCombination therapySlide3

Anti-anginal drugs

Antianginal drugs may relieve attacks of acute myocardial

ischemia by increasing myocardial oxygen supply

or by decreasing myocardial oxygen demand

Three groups of pharmacological agents have been shown to be effective in reducing the frequency, severity, or both of primary or secondary angina. These agents include the nitrates, adrenoceptor antagonists, and calcium entry blockers. To understand the beneficial actions of these agents, it is important to be familiar with the major factors regulating the balance between myocardial oxygen supply and demand.Slide4

Angina pectoris

It is the principal symptoms of patient with ischemic heart disease.

Manifested by sudden, severe, pressing substernal pain that often radiates to the left shoulder and along the flexor surface of the left arm.

Usually precipitated by exercise, excitement or a heavy meal. Slide5

Types of angina pectorisSlide7


Classification of nitrates


Rapidly acting nitrates

* used to terminate acute attack of angina * e.g.- Nitroglycerin and Amyl nitrate * usually administered sublingually

Long acting nitrates

* used to prevent an attack of angina

* e.g. –

tetra nitrate, Iso sorbide di nitrate, Penta erythrytol tetra nitrate

* administered orally or topicallySlide11

Organic nitrates

Organic nitrates & nitrites are simple nitric & nitrous esters of glycerol.

These agents cause a rapid decrease in myocardial oxygen demand leading to rapid resolution of symptoms.

Nitrates are effective for all types of angina.

Activation of guanylate cyclase increases cGMP activating a cGMP kinase leading to dephosphorylation of myosin light chains decreasing contractile force.Slide12


mechanism of action

Coronary artery dilatation

Decrease coronary bed resistance

(Relieved coronary vasospasm)Increase coronary blood flowIncrease oxygen supplySlide14


mechanism of action

Reduction on peripheral resistance

(Secondary to dilatation of aorta)

Decrease blood pressureDecrease after load Decrease workload

Decrease oxygen consumptionSlide15


mechanism of action

Reduced venous return

(Due to dilatation of the veins)

Decrease left ventricular volumeDecrease preload Decrease workload

Decrease oxygen consumptionSlide16

Route of administration

1. Sublingual route

– rational and effective for the treatment of acute attacks of angina pectoris. Half-life depend only on the rate at which they are delivered to the liver.

2. Oral route

– to provide convenient and prolonged prophylaxis against attacks of angina3. Intravenous Route – useful in the treatment of coronary vasospasm and acute ischemic syndrome.4. Topical route

– used to provide gradual absorption of the drug for prolonged prophylactic purpose



Usual single dose

Route of administration

Duration of action

Short acting


0.15-1.2 mg


10 - 30 min

Isosorbide dinitrate

2.5-5 mg


10 – 60 min

Amyl nitrite

0.18 – 3 ml


3 – 5 min

Long acting

Nitroglycerin sustained action

6.5 – 13 mg q 6-8 hrs


6 – 8 hrs

Nitroglycerin 2% ointment

1 – 1.5 inches q hr


3 – 6 hrs

Niroglycerin slow released

1 –2 mg per 4 hrs

Buccal mucosa

3 – 6 hrs

Nitroglycerin slow released

10 – 25 mg /24hrs (one patch/day}


8 –10 hrs

Isosorbide dinitrate

2.5 – 10 mg per 2 hrs


1.5 – 2 hrs

Isosorbide dinitrate

10 –60 mg per 4-6 hrs


4 – 6 hrs

Isosorbide dinitrate chewable

5 – 10 mg per 2-4 hrs


2 – 3 hrs

Isosorbide mononitrate

20 mg per 12 hrs


6 –10 hrs



1. Coronary artery dilatation

2. Reduction of peripheral arterial resistance – decrease after load

3. Reduce venous return – decrease preloadSlide20


The difference between nitrate preparations is mainly in time of onset of action.

Nitroglycerin suffers marked 1st pass metabolism so administration is sublingual.

t1/2 ~10 minutes.

Occasionally as nitroglycerin is metabolized anginal symptoms will return. Transdermal administration either as patch or paste provides a depot of agent for a steady availability. Nitro-Bid is an oral or topical preparation which saturates the hepatic catabolic pathways allowing a prolonged level of nitroglycerine. Isosorbide mono nitrate & Isosorbide di nitrate are long acting nitrates that are relatively resistant to hepatic catabolism ……t1/2 ~ 1 hour. Slide21

Adverse effects

1. Throbbing headache

2. Flushing of the face

3. Dizziness – especially at the beginning of treatment

4. Postural Hypotension – due to pooling of blood in the dependent portion of the bodySlide22


1. Renal ischemia

2. Acute myocardial infarction

3. Patients receiving other antihypertensive agentSlide23

Beta- blockers

β-Blockers decrease oxygen demands of the myocardium by lowering the heart rate and contractility (decrease CO) particularly the increased demand associated with exercise.

They also reduce PVR by direct vasodilatations of both arterial & venous vessels reducing both pre- and after load.

These effects are caused by blocking β

1 receptors, selective β1 antagonists (atenolol, metoprolol ) lose their selectivity at high doses and at least partially block β2 receptors. Slide24



antagonists reduce the frequency and severity of anginal episodes particularly when used in combination with nitrates.


1 antagonists have been shown to improve survival in post MI patients and decrease the risk of subsequent cardiac events & complications. There are a number of contraindications for β blockers: asthma, diabetes, bradycardia, PVD & COPD. β-Blockers in combination with nitrates can be quite effectiveSlide25

Hemodynamic effect


Decrease heart rate

2. Reduced blood pressure and cardiac contractility without appreciable decrease in cardiac outputSlide26

Mechanism of action

Decrease heart rate & Contractility

Increase duration of diastole

Decrease workload

Increase coronary blood flow Decrease oxy.consumptionIncrease oxygen supplySlide27


1. Congestive heart failure

2. Asthma

3. Complete heart blockSlide28

Calcium channel blockers



channel blockers protect tissue by inhibiting the entrance of Ca

+2 into cardiac and smooth muscle cells of the coronary and systemic arterial beds. All Ca+2 channel blockers produce some vasodilation (↓ PVR) and (-) inotropes. Some agents also show cardiac conduction particularly through the AV node thus serving to control cardiac rhythm.

Some agents have more effect on cardiac muscle than others but all serve to lower blood pressure.

CHF patients may suffer exacerbation of their failure as these are (-) inotropes.

They are useful in Prinzmetal angina in conjunction with nitrates.Slide29



This Ca+2 channel blocker works mainly on the arteriolar vasculature decreasing after load it has minimal effect of conduction or HR.

It is metabolized in the liver and excreted in both the urine & the feces. It causes flushing, headache, hypotension and peripheral edema. It also has some slowing effect on the GI musculature resulting in constipation. A reflex tachycardia associated with the vasodilatation may elicit myocardial ischemia in tenuous patients, as such it is generally avoided in non-hypertensive coronary artery disease.Slide30


The agents has its main effect on cardiac conduction decreasing HR and thereby O2 demand.

It also has much more (-) inotropic effect than other Ca+2 channel blockers

It is a weak vasodilator.

Because of its focused myocardial effects it is not used as an antianginal unless there is a tachyarrhythmia. It is metabolized in the liver. It interferes with digoxin levels causing elevated plasma levels; caution and monitoring of drug levels are necessary wit concomitant use.Slide31


This agent function similarly to Verapamil however it is more effective against Prinzmetal angina.

It has less effect on HR.

It has similar metabolism and side effects as Verapamil.Slide32


Onset of action

Peak of action



20 minutes

1 hour

3-4 hours


1-2 hours

5 hours

8-10 hours


15 minutes

30 minutes

3-4 hours


20 minutes

45 minutes

2-4 hours


2-5 hours

6-7 hours

11-16 hour


Adverse effect

Nausea and vomiting


Flushing of the face

Tachycardia – due to hypotensionSlide34


Cardiogenic shock

Recent myocardial infarction

Heart failure

Atria-ventricular blockSlide35

Combination therapy

1. Nitrates and B-blockers

The additive efficacy

is primarily a result of one drug blocking the adverse effect of the other agent on net myocardial oxygen consumption

B-blockers – blocks the reflex tachycardia associated with nitrates Nitrates – attenuate the increase in the left ventricular end diastolic volume associated with B-lockers by increasing venous capacitanceSlide36

Calcium channel blockers +beta blockers

Useful in the treatment of exertional angina that is not controlled adequately with nitrates and B-blockers

B-blockers – attenuate

reflex tachycardia produce by nifedipine

These two drugs produce decrease blood pressure Slide37

Calcium channel



in severe vasospastic or exertional angina (particularly in patient with exertional angina with congestive heart failure and sick sinus syndrome)

Nitrates reduce preload and after loadCa channels reduces the after loadNet effect is on reduction of oxygen demand Slide38

Triple drugs:-




blockerUseful in patients with exertional angina not controlled by the administration of two types of anti-anginal agent Nifidipine – decrease after load

Nitrates – decrease preload

B-blockers – decrease heart rate & myocardial contractilitySlide39

Anjali kotwal




b.pharmacyshoolini university

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