DIAGNOSIS OF ACUTE CARDIAC ISCHEMIA
Chest pain is one of the most frequent presenting complaints of emergency department (ED) patients
and often misdiagnosed. Estimates of the incidence of missed diagnoses of acute myocardial infarction (MI) in the ED
range from 1 - 5%. A recent study found that one-quarter of these missed MI patients were discharged with an ED diagnosis
of ischemic heart disease! The morbidity and short-term mortality rates in patients sent home with MIs are significantly
higher than MI patients who are correctly admitted. On the other side of the coin, low thresholds for admission of
"rule-out" MI (ROMI) patients to coronary care units (CCU) result in fewer than 30% "rule-in" MI rates.
Over-triage not only drives up the cost of medical care at a time when managing health care costs seems
to be the preeminent goal but also limits the availability of intensive care beds for other ED patients. Physicians must
also become better diagnosticians because of the advent of social trends, such as cocaine-associated myocardial ischemia
and more elderly patients with silent MIs and because of the advent of time-dependent therapies such as thrombolytic agents.
Due to the difficulty of diagnosing acute MIs, thrombolytic therapy is administered to fewer than 20% of all MI patients.
While clinical research has yet to identify a diagnostic method superior to bedside judgment in determining which patients
to admit for possible MI, chest pain diagnostic testing is rapidly evolving to enhance the physician's ability to better
utilize resources and to more rapidly detect patients in need of acute intervention.
The bedside determination of whether to admit a patient to ROMI has traditionally been based upon
the history, supplemented by the electrocardiogram (ECG). The Multicenter Chest Pain Study Group has collected data on
over 10,000 ED visits of patients with acute chest pain. This group has determined that it is possible to use historical
data to stratify patients into groups with higher or lower MI probability, but there are no absolute factors in the history
or physical examination to ROMI.
For example a "burning" type of pain is experienced by as many as 15% of MI patients.
And chest pain accompanied by tenderness of the chest wall is also found in as many as 15% of MI patients.
Statistical predictive models have been developed using the Chest Pain Study data (history and physical exam and
ECG results) including a model derived by logistic regression analysis and another using recursive partitioning.
Compared with practicing physicians, all of these computerized models show a trend toward higher specificity
(i.e., fewer ROMI admits). The sensitivity of these computerized models at detecting MI is no better than that of
physician judgment (i.e., no fewer missed MIs) and may be worse. The most sensitive (97%) and specific (96%)
mathematical model reported to date for the prediction of MI is the artificial neural network developed by Baxt.
However all of the published reports using mathematical models have included patients
with ECGs diagnostic for acute MI which inflates their calculated accuracy. The sensitivity of Baxt's neural
network is only 80% in the subgroup of MI patients with nondiagnostic ECGS, the results would have been 11 missed MI
cases. More relevant to current bedside practice, risk management analyses reveal that the medical record
documentation of the history in particular is often inadequate. Authorities recommend computerized dictation
systems which prompt the physician to be complete.
Use of the ECG?
The ECG is the most widely used diagnostic study in the ED evaluation of chest pain. Recently
published studies question the accuracy of ECG interpretation by emergency physicians, although the actual percentage
of clinically significant misreads is probably low, especially when the emergency physician has specialty training or
board certification in emergency medicine. However, one study found that one-quarter of all missed MIs are attributable
to misinterpretation of the initial 12-lead ECG.
Unfortunately the initial ECG performed in the ED reveals ST-segment elevation or other ST-T
wave changes in only about half of all acute MIs. The sensitivity of the ECG for acute cardiac ischemia can be enhanced
by the use of serial ECGs, right-sided chest leads (15 leads) and even back leads (22 leads). Continuous 12-lead ECG
trend monitoring with computerized programs can detect beat-to-beat changes in QRS complex morphology and ST-segment
shifts suggestive of ischemia or infarction. But, until these refinements in electrocardiography become standard
practice, the best use of the 12-lead ECG remains two-fold: to detect acute MI patients meeting ECG criteria for
thrombolytic therapy and to risk stratify ROMI patients to the CCU or intermediate unit. Chest pain patients with
abnormal ECGs are at high risk for complications requiring critical care interventions.
Cardiac enzymes, specifically the creatine kinase isoenzyme (CKMB), are the in-hospital gold
standard for making the diagnosis of MI. But their acceptance and applicability to the early evaluation of the ED
patient remains controversial, in part because of previous experience with the nonspecific (skeletal as well as
cardiac muscle) and insensitive (not elevated in 15% of all MIs) creatine kinase (CK). There are many factors
to consider when interpreting CKMB. Previously, CKMB, like CK was measured by electrophoresis, a cumbersome and
relatively insensitive assay technique.
Newer immunochemical assays have been developed which can detect early small increases in CKMB.
The multicenter Emergency Cardiac Research Group has published several studies suggesting that serial CKMB measurements
over the first 3 - 4 hours after presentation to the ED can significanlty improve the accuracy of diagnosing MI patients
with nondiagnostic ECGs. The rapid availability of serial CKMB results appeared to affect clinical decision making in
about one-third of ED patients with chest pain and nondiagnostic ECGs. Serical CKMB results were more accurate than
serial 12-lead ECGs in the ED diagnosis of MI.
The numbers of hours of chest pain is key to interpreting cardiac enzyme results.
MI patients with chest pain for 3, 6, 9 and 12 hours had elevated CKMB results in nearly half, >50%, >75% and in
100% of cases, respectively. Myoglobin is released earlier than CKMB from damaged myocardial cells (within 4 - 6 hours),
but it disappears with a few more hours (about 6 - 12 hours), about the time of the expected CKMB elevation. Myoglobin is
also nonspecific because it also arises from skeletal muscle.
New rapid assays for myoglobin utilizing latex agglutination,
radioimmunoassay and immunoturbidimetric measurements are promising, showing up to 100% sensitivity for detecting
MI with serial evaluations over a 4-hour period. Another report showed myoglobin to be significantly more sensitive
than either CKMB or CK in detecting MI within the first 6 hours after onset of chest pain. Other serum markers of
myocardial damage like CK-MM subtypes, light chain myosin fragments and the troponin proteins are currently under
investigation. Troponin appears to have similar early diagnostic characteristics as CKMB but it remains elevated
for at least a week. Troponin is more specific than either CKMB or myoglobin in patients with concomitant skeletal
muscle and cardiac muscle damage and it can detect about one-third of patients with unstable angina who are not
detected by CKMB.
Cardiac Emergency Centers:
A trend in the evaluation of chest pain patients is the introduction of cardiac emergency centers or
chest pain units usually within the confines of existing EDs. The goal is to administer thrombolytic agents and other
equally efficacious but less risky medications (eg, aspirin, IV nitroglycerin, beta-blockers and magnesium) as soon as
possible to patients with ECGs diagnostic for acute MI as well as to prepare MI patients for invasive procedures (eg,
angiograms and angioplasty) in the hospital's cath lab.
In other chest pain patients, the goal is to combine as many diagnostic tools described above as
well as those usually associated with non-ED cardiac workups, such as echocardiograms and treadmill stress tests, in
order to "rule-out" cardiac ischemia as soon as possible. The introduction of ED cardiac centers takes this concept
further by avoiding unnecessary CCU admits.
Static cardiac evaluation is being intensively studied as a diagnostic tool in the ED.
Echocardiography can reveal regional wall motion abnormalities within the first hour after onset of coronary artery
occlusion. While the presence of wall motion abnormalities cannot differentiate an old infarct from an evolving MI,
the presence of such changes may be diagnostic in certain patients. Echo can also be used to rule out other critical
pathology, such as aortic dissection or cardiac tamponade as a cause of chest pain. Thallium and technetium scintigraphy
can show areas of decreased myocardial perfusion with 4 - 6 hours of infarction but the dilemma of distinguishing new
from old infarct remains.
The results of recent studies of nuclear medicine studies in ED patients conflict as to their
diagnostic usefulness in determining which patients with nondiagnostic ECG are likely to have an MI. Dynamic cardiac
evaluation may be appropriate for many stable chest pain patients with otherwise negative initial workups.
The preliminary studies of treadmill exercise stress testing in ED patients with atypical chest pain suggest
that false positive results may be more likely in this population of patients at low risk for significant
coronary disease. Further study on higher risk patients is necessary to delineate the proper role of stress testing
in the ED.
With demands for more rapid and accurate diagnosis and for better resource utilization
the future evaluation of chest pain patients will most likely involve some type of outpatient holding area in the ED.