Coronary circulation supplies oxygenated blood to the heart muscle through coronary arteries and drains deoxygenated blood away through cardiac veins. Interruptions in coronary circulation can cause heart attacks. Angina pectoris is chest pain that occurs when part of the heart doesn't get enough blood and oxygen, and can be a symptom of coronary artery disease. There are three types of angina pectoris: stable angina, unstable angina, and Prinzmetal angina. Treatment of angina aims to balance oxygen supply and demand through drugs like nitrates, beta-blockers, and calcium channel blockers.

1. BY ADHIL HASBULLA
119i4A

2. CORONARY CIRCULATION
 Coronary circulation is the circulation of blood in
the blood vessels that supply the heart
muscle (myocardium). Coronary
arteries supply oxygenated blood to the heart
muscle. Cardiac veins then drain away the blood after it has
been deoxygenated.
 Interruptions of coronary circulation quickly cause heart
attacks (myocardial infarctions).Such interruptions are
usually caused by coronary ischemia linked to coronary
artery disease, and sometimes to embolism from other
causes like obstruction in blood flow through vessels.

4. ANGINA PECTORIS
 Angina pectoris—or simply angina—is chest pain or
discomfort that keeps coming back. It happens when
some part of your heart doesn't get enough blood and
oxygen. Angina can be a symptom of coronary artery
disease (CAD).
 There are three types of angina pectoris:
1. Stable angina pectoris
2. Unstable angina pectoris
3. Prinzmetal angina pectoris

5. STABLE ANGINA:
It is characterised by episodes of chest pain
commonly associated with excertion. It is caused during
exercise or intensive work.

6. It is characterized
by angina at rest
or increased
frequency and
duration of
anginal attacks.

7. MYOCARDIAL INFARCTION
 A myocardial infarction, heart attack, caused by a lack of
blood flow to the heart muscle. The lack of blood flow can
occur because of many different factors but is usually
related to a blockage in one or more of heart arteries. It is
the necrosis from myocardial ischemia.

8. TREATMENT
 Treatment is aimed at maintaining the balance between oxygen
supply and demand.
 O2 supply.
- restore the coronary blood flow
- relieve the vasospasm by drugs: CCB/nitrates
- break the thrombi using thrombolytic agents
- prevent thrombus formation by using antiplatelet drugs.
 O2 demand.
- by reducing the work load of heart
- decrease preload: nitrates
- decrease afterload: CCB, K+ channel openers
- decrease the heart rate and contractability: β-Adrenergic
blockers

9. NITRATES: Nitroglycerin, isosorbide dinitrate,
isosorbide mononitrate.
Organic nitrates are prodrugs – they release nitric acid.
Nitrates are mainly vasodilators, also cause arteriolar dilation
thus reduce both preload and afterload. Nitrates have no direct
action on the heart.

10.  On vascular smooth muscle nitroglycerin quickly
relieves anginal pain by decreasing the O2
requirement and increasing O2 delivery to
myocardium.
 PHARMACOKINETICS:
 Organic nitrates are readily absorbed through the
buccal mucous membrane, skin and gastrointestinal
tract.
 Sublingual route produces rapid onset (2-5 mintues)
but short duration of action.
 Absorption through skin is slow; hence, transdermal
route is used for a prolonged effect
 The metabolites are excreted mainly in urine as
glucuronide derivatives.

11. • Headache
• Postural hypotension
• Tachycardia
• Weakness
• Rarely syncope
• Overdosage may cause
methaemoglobinaemia
ADVERSE
EFFECTS:
ISOSORBIDE DINITRATE:
• Used sublingually for acute anginal attack.
• Orally for chronic prophylaxis.
ISOSORBIDE MONONITRATE:
• Longer duration of action.
• High oral bioavailability.

12. β-ADRENERGIC BLOCKERS:
Propranolol, Metoprolol, Atenolol, Timolol.
The effects of this in exertional angina ae mainly
due to negative chronotropic and negative inotropic
effects.
•Bradycardia
•Heart block
•bronchospasm
Adverse
effects:
β-Blockers can increase
LV end-diastolic
volume.

13. CALCIUM CHANNEL BLOCKERS:
Verapamil, Diltiazem,
Dihydropyridines(DHPs): Nifedipine,
Amlodipine, Cilnidipine, Nicardipine.

14. 1. Verapamil:
 It is a phenylalkylamine.
 Predominant action on heart.
 Negative inotropic effect.
 Negative chronotropic effect
 It is a less potent coronary and peripheral vasodilators than DHPs.
2. Diltiazem:
 Its vasodilator property is less marked than DHPs and verpamil.
3. DHPs:
 These are potent arteriolar dilators.
 Reduce peripheral vascular resistance.
 Higher doses are required for significant cardiac effects.

15. (a) Nifedipine:
 It is the prototype drug.
 It has a predominant action on vascular smooth muscle.
 Reflex tachycardia and palpation are commonly seen with
nifedipine.
(b) Amlodipine:
 Palpitation and reflex tachycardia are less common.
 It is more potent.
 Has longer duration of action than nifedipine.
5. Cilnidipine:
 It blocks L-type and N-type calcium channels.
 Reflex tachycardia and ankle oedema is less.

16. •Constipation
•Sinus bradycardia
•Hypotension
•Peripheral Edema
•AV block occurs rarely
•Gingival hyperplasia
Adverse effect:
PHARMACOKINETICS:
All CCBs are well absorbed through GI tract but they undergo
varying degree. All are highly bound to plasma proteins,
metabolized in liver and excreted in urine

17. POTASSIUM CHANNEL OPENERS:
Nicorandil.
It is administered orally. It causes arteriolar and vasodilation
and also improves coronary blood flow.
ADVERSE EFFECT:
• Headache
• Hypotension
• Palpitation
• Nausea
• Ulcers in the
mouth etc.

18. OTHER DRUGS
ANTIPLATELET AGENTS:
 ASPIRIN is administered orally in patients with suspected
or definite MI. If the patient is allergic to aspirin,
clopidogrel is administered. Antiplatelet agent should be
continued once daily.
 RANOLAZINE It inhibits late inward sodium current and
decreases intracellular Ca+ overload in myocardium oxygen
consumption without altering heart rate and BP. It is also
an inhibitor of fatty acid oxidation.
 IVABRADINE site of action SA node-heart rate decreased
decreased oxygen demand. Can also be used in sinus
tachycardia.
 DIPYRIDAMOLE It dilates coronary blood vessels.
increases blood flow to non ischemic areas.

19. COMBINED DRUGS
 Nitrates × β-blockers (propranolol).
 Nifedipine (DHPs) × β-blockers.
 Β-blockers × verapamil/diltiazem
 CCBs × nitrates
 Nitrates × β-blockers × CCBs.

20. PHARMACOTHERAPY OF ACUTE
MYOCARDIAL INFARCTION
 Reperfusion therapy: primary percutaneous coronary
intervention or thrombolytic therapy- streptokinase,
alteplase, etc., to restore coronary patency and reperfusion
of infarcted area.
 Acidosis is treated with intravenous sodium bicarbonate.
 Antiplatelet agent – aspirin.
 Nitrates- intravenous nitroglucerin.
 Anticoagulants.
 ACE inhibitors – ramipril, captopril
 Statins – atrovastatin.
 β-blockers.

21. THANK YOU