ACS ST Elevation
ACS ST Elevation
ACS ST Elevation
com
CLINICAL REVIEW
1
Department of Cardiology, The diagnosis and management of acute coronary syn- necrosis. Whether myocardial infarction (that is,
Academic Medical Center, dromes have been evolving rapidly in recent years. necrosis of cardiac muscle) is present usually becomes
PO Box 22660, Amsterdam 1100, New antithrombotic agents have improved the results clear at a later stage, on the basis of laboratory tests
Netherlands
2 of medical treatment, and new methods of estimating a (elevation of markers such as creatine kinase MB or
Department of Medicine,
McMaster University and patient’s risk of an adverse outcome help clinicians to cardiac troponins) or on the electrocardiogram (loss
Population Health Research decide who may benefit from invasive treatment—that of QRS voltage or development of pathological Q
Institute, Hamilton Health is, coronary angiography and subsequent revasculari- waves). Because of the therapeutic decisions that
Sciences, Hamilton,
ON L8L 2X2, Canada sation (percutaneous coronary intervention or coron- need to be made on admission of patients with acute
Correspondence to: R J G Peters ary bypass surgery). As these therapeutic decisions chest pain, before myocardial necrosis may be
r.j.peters@amc.uva.nl need to be made soon after admission, the classification detected, new terms for the admission diagnosis have
BMJ 2007;334:1265-9
of acute coronary syndromes is now based on the infor- been introduced. These are based primarily on the
doi:10.1136/bmj.39220.618646.AE mation that is available on admission. findings on the admission electrocardiogram (table).
In the United Kingdom, about 114 000 patients with If ST segment elevation (suggestive of transmural
acute coronary syndromes are admitted to hospital ischaemia) is present, a diagnosis of ST segment eleva-
each year.1 More than 5.5 million patients present to tion acute coronary syndrome is made. These patients
a US emergency department with chest pain and other have an indication for urgent reperfusion treatment,
symptoms related to acute coronary syndrome each either by percutaneous coronary intervention or by
year.2 Acute coronary syndrome is seen in people of administration of a thrombolytic agent. If no ST seg-
all ages, races, and socioeconomic backgrounds. ment elevations are present (normal or depressed ST
segments or T wave inversion), a diagnosis of non-ST
Pathology segment elevation acute coronary syndrome is made.
Acute coronary syndromes generally represent acute If myocardial necrosis is documented, as indicated
complications of chronic atherosclerotic disease of the above, a discharge diagnosis of ST segment elevation
coronary arteries. The progressive accumulation of myocardial infarction or non-ST segment elevation
inflammatory materials and lipids over the years can myocardial infarction is made. According to current
ultimately lead to erosions of the intima or rupture of guidelines, any elevation of cardiac markers qualifies
lipid rich plaques. Both events are strongly thrombo- as a myocardial infarction.3 Depending on the devel-
genic, and a blood clot often forms. Many of these clots opment of the electrocardiogram after admission,
remain clinically undetected but contribute to the pro- myocardial infarction may be subclassified as Q wave
gressive thickening of the arterial wall and the narrow- or non-Q wave myocardial infarction. If no evidence of
ing of the vessel. Thrombi may lead to acute reductions myocardial necrosis exists, a discharge diagnosis of
in vessel patency, resulting either in sudden onset or acute coronary syndrome or unstable angina is gener-
worsening of angina; they may also acutely occlude ally used. In this review, we focus on non-ST segment
the vessel, causing acute myocardial infarction. Inter- elevation acute coronary syndrome.
mediate presentations also occur, with incomplete
occlusion leading to myocardial damage or, conver- Sources and selection criteria
sely, with complete occlusion that does not lead to Acute coronary syndromes represent one of the most
necrosis. The last of these may be the case if adequate intensively studied topics in clinical research. Current
collaterals have been formed in the preceding weeks or guidelines and practice are based on a very large body
months as a response to chronic recurrent ischaemia. of evidence, a summary of which is beyond the scope
of this review. Our information came from personal
How are acute coronary syndromes classified? archives and searches of Medline with the key words
Until recently, the two typical clinical presentations “acute coronary syndrome” and “unstable angina”.
were generally referred to as unstable angina and We used current guidelines on the management of
acute myocardial infarction. A diagnosis of acute myo- acute coronary syndromes and searched for relevant
cardial infarction requires evidence of myocardial Cochrane reviews.
Classification of discharge diagnoses How can we stratify risk in patients with acute coronary
syndrome?
ST elevation on Myocardial necrosis
The in-hospital management of patients with chest
admission ECG Yes No
pain is determined by the risk of complications and
Yes ST segment elevation myocardial infarction ST segment elevation acute coronary
syndrome
death. Indicators of high risk include typical com-
No Non-ST segment elevation myocardial Non-ST segment elevation acute coronary
plaints, documented coronary artery disease, and
infarction syndrome advanced age. On physical examination, new mitral
Collective terms (Acute) myocardial infarction Acute coronary syndrome or unstable angina regurgitation, hypotension, excessive sweating, pul-
ECG=electrocardiogram. monary oedema, and rales are all associated with high
risk.6 On the electrocardiogram, new Q waves, new ST
segment deviation, or new T wave inversion with
How is acute coronary syndrome diagnosed? symptoms indicate high risk. Raised cardiac troponin
The main initial diagnostic challenge is to differentiate T, troponin I, or creatine kinase MB in the serum indi-
acute coronary syndromes from non-cardiac chest cates myocardial necrosis and a high risk of an adverse
pain. The assessment requires a thorough history outcome. In addition, markers of congestive heart fail-
(including analysis of risk factors), a physical examina- ure, particularly plasma B-type natriuretic peptide,
tion, and, often, an electrocardiogram and determina- have been shown to be independent predictors of
tion of serum cardiac “markers” (troponin T, troponin death in patients with non-ST segment elevation
I, creatine kinase MB isoenzyme). The most important acute coronary syndrome.
determinant is the patient’s history.4 Symptoms of For patients admitted with this diagnosis, several risk
acute coronary syndrome include substernal chest scores have been developed from clinical trials and
pain, radiating to the arms, the jaw, the neck, the registries.7-10 These can help to identify patients who
back, or even the abdomen, which may be accompa- are most likely to benefit from “invasive” treatment
nied by nausea, vomiting, dyspnoea, and diaphoresis. (coronary angiography and revascularisation). As
Some patients may present without chest pain, and patients included in trials represent a selected group of
dyspnoea may be the only complaint.5 Typical chest patients, risk models derived from unselected registries
pain that occurs suddenly at rest, particularly in a are probably more reliable in clinical practice (box).
young patient, may suggest acute coronary spasm,
which is sometimes associated with the use of cocaine How are patients managed in hospital?
or methamphetamine. Abnormalities on physical The treatment of patients with non-ST segment eleva-
examination are usually absent but may include signs tion acute coronary syndrome, according to current
of heart failure, such as rales or oedema, hypotension, guidelines, consists of two components: to alleviate
excessive sweating, or new mitral regurgitation. the patient’s complaints of pain and anxiety and to pre-
Patients suspected of having acute coronary vent recurrences of ischaemia and progression to (or to
syndrome should be referred to a hospital for observa- limit) myocardial infarction.11 12 This requires inten-
tion, electrocardiography, and blood testing (cardiac sive antithrombotic treatment, and often an invasive
markers). Importantly, a normal electrocardiogram strategy with coronary angiography followed by revas-
does not rule out acute coronary syndrome (although it cularisation if appropriate.
does make it less likely), particularly if documented after Drug treatment routinely includes β blockers, which
relief of symptoms. In addition, normal concentrations reduce myocardial oxygen demand by reducing heart
of cardiac markers do not rule out acute coronary rate and blood pressure and reduce the risk of arrhyth-
syndrome, particularly if measured shortly after the mias and recurrent ischaemia. Sedatives and analgesics
onset of complaints. Elevation of these markers takes may be used with the same goals, by reducing anxiety
four to six hours after myocardial necrosis, and six to and pain. Vasodilators, such as nitrates and calcium chan-
eight hours are needed before markers of necrosis nel blockers, are used to reduce the dynamic (spastic)
appear in peripheral blood. If an initial blood test is component of coronary obstruction, and to lower blood
normal, and the history is highly suggestive, most pressure, but none of these drugs has been shown to
clinicians do a second test after eight to 12 hours. If this reduce the risk of myocardial infarction or death.
is also normal, and the electrocardiogram is normal or
shows little acute evolution, then the patient is at very
low risk and may be discharged. However, such patients Predictors of death in patients with acute coronary
should have an early stress test to document whether syndromes, according to the GRACE registry
Age
provoked ischaemia is present. If the cardiac biomarkers
are raised or the electrocardiogram shows evolutionary Killip class (heart failure)
changes, admission to hospital is indicated. Heart rate
Imaging techniques may support the diagnostic Blood pressure
process by showing wall motion abnormalities (echo- ST deviation on electrocardiogram
cardiography, magnetic resonance imaging), ischaemia Cardiac arrest
(nuclear perfusion scanning), or coronary pathology Raised creatinine
(multislice computed tomography scanning). However, Raised creatine kinase MB or troponin
their role has not been firmly established.