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Angina pectoris is the name for a
clinical syndrome rather than a disease. It is characterized by paroxysmal substernal or precordial pain or discomfort resulting from ischemia
without frank infarction.
Assessment of Ischaemic Myocardial Damage: CLICK
Clinical
presentation:
The typical patient with
angina is a 50 to 60 year old man who seeks medical help for
troublesome chest discomfort, usually described as heaviness,
pressure, squeezing, smothering or choking and only rarely frank pain.
This symptom usually lasts from 15 seconds to 15 minutes.
There are three distinct patterns
of angina clinically based on provocation and severity of pain.
1. Stable (typical) ;
2. Prinzmetal’s variety :3. Unstable
(crescendo)
Cause of angina
pectoris :
Coronary atheroma is the
commonest cause.
Factors which increase
myocardial oxygen requirement include any which add to the ventricular
preload such as exercise , anaemia or hyperthyroidism and those which
increase afterload such as hypertension, aortic stenosis or
cardiomyopathy .
Increased tension of the
ventricular wall as occurs in dilatation or hypertrophy may also
reduce coronary flow. Tachycardia increases cardiac work and often
brings on pain.
Other factors causing angina
include fixed stenosing plaques, disrupted plaques, vasospasm,
thrombosis, platelet aggregation and embolization.
1.Stable or typical angina :
Most common form of angina.
Ischemia is most intense in the poorly perfused subendocardial region
of the left ventricular myocardium.
Pathogenesis:
Reduction of coronary perfusion to a critical level by chronic
stenosing coronary atherosclerosis (greater than 75% stenoses in major
coronary arteries).
Pain is relieved by rest (decrease
demand) or by coronary dilator - nitroglycerine (increasing supply).
2.Prinzmetal’s variant angina :
Pattern of episodic angina that occurs at rest.
Pathogenesis: It
is caused due to coronary artery spasm. Patients with this form of
angina may have coronary atherosclerosis, but the attacks are usually
unrelated to physical activity, heart rate or blood pressure.
Patients respond
prompty to vasodilator-nitroglycerine
and calcium channel blockers.
3.Unstable
or crescendo
angina : Pattern is
characterized by an
increased frequency of anginal pain .
It is precipitated with
progressively less effort, often occurs at rest and tends to be of
prolonged duration ;
Pathogenesis: It is induced
by fissuring, ulceration, or rupture of an atherosclerotic plaque with
superimposed partial (mural) thrombosis and possibly embolization or
vasospasm (or both).
This pattern
forewarns of the possibility of subsequent
Acute Myocardial Infarction
and is also referred to as
preinfarction angina or acute coronary insufficiency.
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