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38 Chapter 2: Cardiovascular system

Table 2.6 Patterns of acute myocardial infarction 12–24 hours: Infarcted area appears pale with inter-
cellular oedema.
Artery occluded Pattern of infarction
24–72 hours: Cellular inflammation visible.

Right coronary artery Inferior MI (and posterior MI, if
Weeks to months: White scar tissue develops through
the circumflex artery is small)
Left anterior descending Anteroseptal MI the process of repair.
(LAD)
Left circumflex artery Posterior MI (sometimes inferior, Immediate complications
if the right coronary artery Sudden death, one third of patients who suffer an MI die
is small)
Left main stem Extensive anterolateral MI within the first hour, most before admission to hospital.
Early complications (1 day to 2 weeks)
Cardiac arrhythmias: Particularly ventricular fibrilla-

Pathophysiology tion and ventricular tachycardia. If the atrioventricu-
Acute myocardial infarction is caused by the occlusion lar node is involved bradyarrhythmias are common,
of a coronary artery, usually as the result of rupture of although any arrhythmia is possible.
an atherosclerotic plaque with subsequent development Left ventricular failure is common with very large ar-
of thrombus. The myocardium supplied by that artery eas of infarction, which cause contractile dysfunction.
initially becomes ischaemic and if the occlusion does Cardiogenicshockmayresultfromlowcardiacoutput
not resolve leads to infarction. Myocardial infarctions due to extensive myocardial damage, rupture of the
occur more commonly in the early morning possibly ventricular septum or papillary muscle leading to mi-
due to increased coronary artery tone, increased platelet tral regurgitation. The latter present with worsening
aggregatability and decreased fibrinolytic activity. The refractory heart failure and a loud pansystolic mur-
extent and distribution of the infarct is dependent on the mur. If left untreated this has a very poor prognosis,
coronary artery affected, but also on individual variation and early surgical correction should be considered.
due to variable anatomy and presence of collaterals (see Ventricular wall rupture usually occurs 2–10 days af-
Table 2.6). tera large transmural infarct. A haemopericardium
develops due to exsanguination into the pericardial
cavity resulting in tamponade and rapid death. This
Clinical features
complication tends to affect older hypertensive pa-
Patients typically present with central crushing chest
tients, females more than males and the left ventricle
pain worse than stable angina, radiating to the jaw and
more than the right.
arms (especially the left), which occurs at rest and lasts
Thrombosis may occur on the inflamed endocardium
for some hours. It may provoke fear of imminent death
over the infarction with resulting risk of embolism.
(angor animi), but it may be less severe or even asymp-
tomatic (especially diabetics, hypertensives and in the
Long-term complications
elderly). It is often associated with restlessness, breath-
Recurrent ischaemia or myocardial infarction may oc-
lessness, sweating, nausea and vomiting. Signs may in-
cur due to thrombus formation within the same or
clude pallor, sweating, hypotension, tachycardia, raised
other coronary arteries.
venous pressure and bibasal crepitations.
Impaired left ventricular function leading to chronic
cardiac failure.
Macroscopy/microscopy Ventricular aneurysms may form as the collagen scar
In the infarct-related artery, there is nearly always evi- that replaces the infarcted tissue formation does not
dence of plaque rupture/erosion and thrombotic occlu- contract and is non-elastic. Ventricular aneurysms are
sion. In the infarct zone a sequence of changes occurs: frequently complicated by thrombus formation but
0–12hours:Notvisiblemacroscopically,thereislossof embolism is rare. They may worsen cardiac failure.

oxidative enzymes shown with nitroblue tetrazolium Dressler’s syndrome is a form of autoimmune-medi-
(NBT) stain. ated pericarditis and pericardial effusion associated