26-11-2012, 06:12 PM
Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation
1Management of acute myocardial.pdf (Size: 920.21 KB / Downloads: 28)
Introduction
The definition of acute myocardial
infarction
Acute myocardial infarction can be defined from a number of different
perspectives related to clinical, electrocardiographic (ECG), biochemical,
and pathological characteristics.1 The present guidelines
pertain to patients presenting with ischaemic symptoms and persistent
ST-segment elevation on the ECG (STEMI). The great majority
of these patients will show a typical rise of biomarkers of myocardial
necrosis and progress to Q-wave myocardial infarction. Separate
guidelines2 have been developed by another Task Force of the
ESC for patients presenting with ischaemic symptoms but without
persistent ST-segment elevation.
The pathogenesis of ST-segment
elevation acute myocardial infarction
Most cases of STEMI are caused by an occlusion of a major coronary
artery. Coronary occlusion and reduction in coronary blood
flow are usually due to physical disruption of an atherosclerotic
plaque with subsequent formation of an occluding thrombus.
Concomitant coronary vasoconstriction and microembolization
may be involved to some extent. Less commonly a thrombus
may form from a superficial erosion of the endothelial surface.
The risk of plaque disruption depends on plaque composition
and vulnerability (plaque type) and degree of stenosis (plaque
size).3 As many as three-quarters of all infarct-related thrombi
appear to evolve over plaques causing only mild to moderate stenosis.
Even portions of the coronary arterial tree that appear
normal by angiographic criteria often harbour a substantial
burden of atherosclerosis. In particular, plaques with substantial
outward remodelling, or ‘compensatory enlargement’, can have
thin, fibrous caps and large lipid pools without encroachment of
the lumen.4 However, severe stenoses are as likely to undergo
plaque events leading to infarction as mild ones.5 There is frequently
a delay (up to 2 weeks) between the rupture of a
plaque and its clinical consequences.6 Inflammation plays an
important role in plaque instability, and therefore in the pathogenesis
of acute coronary syndromes. Circulating levels of inflammatory
markers such as C-reactive protein (CRP) and interleukin-6
are correlating with the clinical course and outcome of an acute
coronary syndrome.
The natural history of STEMI
The true natural history of STEMI is hard to establish for a
number of reasons: the common occurrence of silent infarction,
the frequency of sudden death outside the hospital, and the
varying methods and definitions used in the diagnosis of the
condition. Community studies have consistently shown that the
overall case fatality rate of patients with presumed myocardial
infarction or acute coronary syndrome in the first month is
50%, and of these deaths about half occur within the first
2 h.13 This high initial mortality seems to have altered little
over the last years in contrast to hospital mortality.14 In contrast
to community mortality, there has been a profound fall in the
fatality of patients treated in hospital. Prior to the introduction
of coronary care units in the 1960s, the in-hospital mortality
seems to have averaged 25–30%. A systematic review of mortality
studies in the pre-reperfusion era of the mid-1980s
showed an average in-hospital fatality of 16%. With the widespread
use of coronary interventions, fibrinolytic agents, antithrombotic
therapy, and secondary prevention, the overall
1-month mortality has since been reduced to 4–6%, at least
in those who participated in the latest randomized large-scale
trials and qualified for fibrinolysis and/or coronary interventions.
15,16 However, mortality rates in registry studies are
much higher, suggesting that the patients included in the randomized
studies17 are at a lower risk when compared with
those seen in the real world.
Initial diagnosis and early
risk stratification
Rapid diagnosis and early risk stratification of patients presenting
with acute chest pain are important to identify patients in whom
early interventions can improve outcome. On the other hand,
when the diagnosis of STEMI has been ruled out, attention can
be focused on the detection of other cardiac or non-cardiac
causes of the presenting symptoms such as aortic dissection,
pulmonary embolism, and pericarditis. A working diagnosis of
STEMI must first be made (Table 3). This is usually based on the
history of chest pain/discomfort lasting for 10–20 min or more
(not responding fully to nitroglycerine). Other locations such as
epigastric or interscapular are possible. Important clues are a previous
history of coronary artery disease and radiation of the pain to
the neck, lower jaw, or left arm. The pain may not be severe and, in
the elderly particularly, other presentations such as fatigue, dyspnoea,
faintness, or syncope are common. There are no individual
physical signs diagnostic of STEMI, but many patients have evidence
of autonomic nervous system activation (pallor, sweating) and
either hypotension or a narrow pulse pressure. Features may
also include irregularities of the pulse, bradycardia or tachycardia,
a third heart sound, and basal rales. An ECG should be obtained as
soon as possible. Even at an early stage, the ECG is seldom normal.
In the case of STEMI or new or presumed new left bundle-branch
block, reperfusion therapy needs to be given, and measures to
initiate this treatment must be taken as soon as possible.
However, the ECG can be equivocal in the early hours, and
even in proven infarction it may never show the classical features
of ST-segment elevation and new Q-waves.
Cardiac arrest
Many deaths occur in the very first hours after STEMI due to
ventricular fibrillation (VF). The implementation of an organization
to cope with out-of-hospital cardiac arrest is pivotal to provide
prompt cardiopulmonary resuscitation, early defibrillation if
needed, and effective advanced cardiac life support. Availability
of automated external defibrillators is a key factor in increasing
survival. Readers are referred to the latest guidelines on cardiopulmonary
resuscitation provided by the European Resuscitation
Council.