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Treatment of

Angina Pectoris

Bonniface Obura, BPharm, DPSCM, MSc.


Introduction

• Angina pectoris denotes chest pain caused by


accumulation of metabolites resulting from my-
ocardial ischemia

• Common causes of angina:

– Coronary artery disease

– Coronary artery spasms


Types of angina

• Classic angina (effort angina)

• Vasospastic angina (variant or Prinzmetal


angina)

• Further classification: stable and unstable


angina (acute coronary syndrome)
Pathophysiology of angina

• Primary derailment: imbalance between the


oxygen requirement of the heart and the oxy-
gen supply

• Determinants of myocardial oxygen demand;


wall stress, heart rate, contractility

• Determinants of coronary blood flow; perfusion


pressure, vascular resistance
Drugs used to treat angina

• Goal; decrease myocardial oxygen require-


ment and increase oxygen delivery

• Classes of drugs used to achieve the above


goal:

• Organic nitrates

• Calcium channel blockers

• Beta blockers
Nitrates and nitrite

• Examples: Nitroglycerin, isosorbide dinitrate,


nitroprusside, amyl nitrite

• Nitroglycerin, isosorbide dinitrate undergo sig-


nificant first pass effect; administer sublingual
route

• Mechanism of action: produce nitric oxide


which causes an increase in cGMP hence SM
relaxation
Nitrates and nitrite

• Toxicity

• Orthostatic hypotension

• Tachycardia

• Throbbing headache

• CI; increased intracranial pressure


Calcium channel blockers

• Examples: amlodipine, nifedipine, nicardipine,


verapamil, diltiazem

• Orally active agents; undergo high first-pass ef-


fect

• Verapamil and diltiazem are also used by the


intravenous route
Calcium channel blockers cont..

Mechanism of action

• Bind to and block the L-type calcium channel

• The drugs act from the inner side of the mem-


brane

• Bind more effectively to open channels and in-


activated channels
Calcium channel blockers cont..

• Vascular smooth muscle appears to be the


most sensitive; arterioles are more sensitive
than veins

• CCBs reduce cardiac contractility in a dose-


dependent fashion

• Toxicity: bradycardia, AV block, cardiac arrest,


and HF
Beta-blockers

• Examples; Bisoprolol, carvedilol, metoprolol,


and nebivolol etc

• Beneficial effects are related to their hemody-


namic effects—decreased heart rate, blood
pressure, and contractility

• Lower HR may increase coronary perfusion


Beta-blockers cont..

• Undesirable effects; increase in end-diastolic


volume, impaired exercise tolerance

• Contraindications: asthma, severe bradycardia,


AV blockade
THE END
THANK YOU

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