●Pathophysiology 196
●Management of stable angina 196●Management of unstable coronary disease 198
●Drugs used in ischaemic heart disease 200CHAPTER 29
ISCHAEMIC HEART DISEASE
PATHOPHYSIOLOGY
Ischaemic heart disease is nearly always caused by atheroma
(Chapter 27) in one or more of the coronary arteries. Such
disease is very common in western societies and is often
asymptomatic. When the obstruction caused by an uncompli-
cated atheromatous plaque exceeds a critical value, myocar-
dial oxygen demand during exercise exceeds the ability of the
stenosed vessel to supply oxygenated blood, resulting in chest
pain brought on predictably by exertion and relieved within a
few minutes on resting (‘angina pectoris’). Drugs that alter
haemodynamics can reduce angina.
Most patients with angina pectoris experience attacks of pain
in a constant stable pattern, but in some patients attacks occur at
rest, or they may occur with increasing frequency and severity
on less and less exertion (‘unstable angina’). Unstable angina
may be a prelude to myocardial infarction, which can also occur
unheralded. Both unstable angina and myocardial infarction
occur as a result of fissuring of an atheromatous plaque in a coron-
ary artery. Platelets adhere to the underlying subendothelium
and white thrombus, consisting of platelet/fibrinogen/fibrin
aggregates, extends into the lumen of the artery. Myocardial
infarction results when thrombus occludes the coronary vessel.
In addition to mechanical obstruction caused by atheroma,
with or without adherent thrombus, spasm of smooth muscle
in the vascular media can contribute to ischaemia. The import-
ance of such vascular spasm varies both among different
patients and at different times in the same patient, and its con-
tribution is often difficult to define clinically. The mechanism
of spasm also probably varies and has been difficult to estab-
lish. A variety of vasoconstrictive mediators released from
formed elements of blood (e.g. platelets or white cells) or from
nerve terminals may contribute to coronary spasm. Its import-
ance or otherwise in the majority of patients with acute coron-
ary syndromes is a matter of considerable debate.
Treatment of patients with ischaemic heart disease is
directed at the three pathophysiological elements identified
above, namely atheroma, haemodynamics and thrombosis.
New onset of chest pain at rest or crescendo symptoms should
raise suspicion of unstable angina or myocardial infarction,
and emergency referral to a hospital with coronary care unit.
The general management of stable angina is illustrated in
Figure 29.1 and detailed further below.MANAGEMENT OF STABLE ANGINA
MODIFIABLE RISK FACTORSModifiable risk factors include smoking, hypertension, hyper-
cholesterolaemia, diabetes mellitus, obesity and lack of exer-
cise. The object of defining these factors is to improve them in
individual patients, thereby preventing progression (and
hopefully causing regression) of coronary atheroma. This is
discussed in Chapters 27, 28 and 37.PAIN RELIEFAn attack of angina is relieved by glyceryl trinitrate(GTN),
which is given by sublingual administration. However, in
patients with chronic stable angina, pain usually resolves
within a few minutes of stopping exercise even without treat-
ment, so prophylaxis is usually more important than relief of
an attack. In patients hospitalized with acute coronary syn-
drome, GTN is often administered by intravenous infusion; its
short half-life allows rapid titration, thus permitting effective
pain relief whilst promptly averting any adverse haemo-
dynamic consequences (in particular, hypotension).PROPHYLAXISFigure 29.2 outlines the drug treatment of stable angina.
Antithrombotic therapy with aspirinreduces the incidence of
myocardial infarction; its use and mechanism of action as
an antiplatelet agent are discussed further in Chapter 30.
Prophylaxis is also directed at reducing the frequency of
attacks of angina. In this context, GTNis best used for ‘acute’
prophylaxis. A dose is taken immediately before undertaking
activity that usually brings on pain (e.g. climbing a hill), in