Angina Pectoris

 

·        Pathophysiology.

·        Principles of drug therapy.

·        Individual drugs.

 

Pathophysiology

 

1.       Cause:

 

a.       Angina pectoris is a symptoms of ischaemic heart disease caused by a relative insufficiency of coronary blood flow.

 

b.       Develops when the blood supply is inadequate to meet myocardial demand.

 

2.       Stable angina:

 

a.       Characterized by predictable precipitating factors (e.g. exercise, emotion or heavy meal) causing retrosternal chest pain and usually lasting no more than a few minutes following rest.

 

b.       Cause is usually due to atherosclerotic obstruction to coronary blood flow.

 

3.       Unstable angina:

 

a.    New or sudden worsening of previous angina occurring at rest or minimal effort.

 

b.       Symptoms frequently herald the onset of myocardial infarction.

 

4.       Variant angina: symptoms are due to coronary vasopasm and can occur at rest, often during the night.

 

 

Principles of drug therapy

 

1.       Treatment objective is to unload the heart or to prevent / relax spasm of the coronary arteries so that oxygen need is adequately met.

 

2.       Determinants of oxygen consumption:

 

a.       Preload: the venous filling and stretching of the heart and its muscle fibers, which evokes the contractility.

 

b.       Afterload: the peripheral arteriolar resistance against which the heart must eject blood.

 

c.       Heart rate: determines the duration of diastole during which intramyocardial pressure is low enough to allow myocardial perfusion to occur via the coronary arteries.

 

3.    The heart can be unloaded by:

 

a.       halting the provocative exercise (physical or emotional).

 

b.       reducing the preload (venous return).

 

c.       reducing the afterload (arteriolar resistance).

 

d.       reducing the rate.

 

e.       dilating the coronary arteries.

 

4.       Summary of treatment:

 

a.    Any contributory cause is treated when possible, e.g. anaemia, dysrhythmia.

 

b.    Life style is changed so as to reduce the number of attacks, e.g. weight reduction, quit smoking.

 

c.    For immediate pre-exertional prophylaxis: glyceryl trinitrate sublingually or nifedipine.

 

d.    For an acute attack: glyceryl trinitrate (sublingual) or nifedipine (bite capsule).

 

e.    For long-term prophylaxis: propranolol, nifedipine or diltiazeim, isosorbide dinitrate or mononitrate and antiplatelet therapy with aspirin.  

 

5.       Individualization of drug therapy:

 

a.       Variant angina: calcium channel blockers, avoid beta-blockers.

 

b.       Beta-blockers should not be used in patients with history of asthma, incipient heart failure, diabetes or bradyarrhythmias.

 

c.       Nitrates and calcium channel blockers are preferred in chronic obstructive pulmonary disease.

 

d.       Hypertension with tendency to tachyarrhythmias: beta-blockers or calcium channel blockers.

 

Individual drugs

 

1.       Organic nitrates reduce preload and afterload and dilate the main coronary arteries.

 

2.       Beta-adrenoceptor blocking drugs reduce myocardial contractility and slow the heart rate.

 

3.       Calcium channel blockers reduce cardiac contractility, dilate the coronary arteries and reduce afterload.

 

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