Summary
Summary pharmacological treatment of angina
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- Biomedical Science
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Summary of pharmacological treatment of angina
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Pharmacological Treatment of AnginaSession Description. Topics Covered:
Definition and types of angina pectoris
Signs and symptoms associated with angina pectoris
Factors affecting cardiac work and myocardial oxygen demand
Cardiovascular risk factors: modifiable and non-modifiable
Mechanisms of actions of drugs used in the treatment of angina
pectoris and for secondary prevention of cardiovascular disease
Key Points
Definition of angina
Types of angina
Reasons for treatment
Pharmacological treatments
Angina Pectoris
Angina pectoris means “strangulation in the chest” and is ultimately caused by local
myocardial ischemia caused when O2 demand exceeds supply (i.e. a small area of the
heart is being restricted/not receiving enough of O2).
The ischaemic (metabolic) products (e.g. lactate, K +, H+) then stimulate sympathetic
nociceptive afferents (sense pain). This leads to a crushing chest pain, pain also may
be experienced in jaw, shoulders and arms (due to viscera-somatic convergence,
referred pain, due to nociceptive fibres synapsing at same place with normal sensory
fibres).
Angina may also be associated with shortness of breath, sweating (caused by
sympathetic activity) and nausea (by vagal afferents). It is typically precipitated by
exertion and reversible on rest.
There are 2 million sufferers in the UK (a lot), with an annual risk of death of MI at 4-
6%.
Why are there increases in myocardial O2 demand? What are the risk factors for an
angina attack ->
Increased systolic blood pressure – If you have hypertension this produces stress on
the wall of the heart – increased afterload - so when it tries to eject blood it has to
overcome this stress and thus use more energy to do so (hence consume more O 2) –
Increased heart rate – If your heart works faster you need more oxygen, but as well
as this there will be decreased coronary perfusion as you only get coronary perfusion
during diastole, if heart rate is faster diastole may be slightly shorter
Increased force of contractility – If you stimulate sympathetic system due to stresses
(e.g. exercise, emotion, cold weather) this will increase force of contraction.
, There are also various other forces that affect contractility such as: having a large
meal, anaemia, aortic valve stenosis and arrhythmias.
Types of Angina
There are three types of angina:
Stable angina – Exercise induced, is predictable and caused by increased O 2 demand
not being supplied due to atheroma
Unstable angina – is exercise induced but minimal exertion is needed to precipitate
symptoms (e.g. getting out of chair), this is due to increased O 2 demand not being
supplied due to decreased O2 supply due to thrombosis (because of a plaque rupture)
– unpredictable – could very well lead to an MI as getting closer to being occluded
Variant (prinzmetal) angina – Much more random, where symptoms occur at rest
due to decreased O2 supply due to vasospasm downstream of an occlusion caused by
an atheroma (atheroma releases substances causing vasospasm)
As you go to greater severity you begin to get a stronger link to acute coronary
syndromes (where you have coronary thrombosis and get an MI). This is why this
needs to be treated.
Angina: Why a problem only during activity?
The reason can be explained using the cartoons below.
Firstly though it is important to remember that with arterioles and arteries,
resistance is in series so resistance adds up.
Normal coronary
artery and arteriole at rest
So our coronary artery here at rest ^^ is nice and large and only has a resistance of 1,
further downstream in the arteriole, it is more contracted and much smaller so has a
higher resistance of 19. The total resistance is therefore 20.
During exercise, the large coronary artery doesn’t change much, but the arterioles
will vasodilate due to the adenosine release etc.
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