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J Am Coll Cardiol, 2004; 44:561-563, doi:10.1016/j.jacc.2004.05.007 © 2004 by the American College of Cardiology Foundation |
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
* Reprint requests and correspondence: Dr. Andrew E. Arai, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Building 10, Room B1D416, MSC 1061, 10 Center Drive, Bethesda, Maryland 20892-1061, USA.
araia{at}nih.gov
In practice, the immediate evaluation and triage of patients with possible or probable acute coronary syndrome begins with a 12-lead electrocardiogram (ECG) to look for ST-segment elevation. ST-segment elevation in the appropriate clinical setting triggers percutaneous intervention, if feasible, or thrombolytic therapy if not contraindicated (2,3). Even before the use of high-sensitivity troponin assays, ST-segment elevation on an ECG had a relatively poor sensitivity (<50%) for acute MI (4). One might wonder why a test with such a low sensitivity plays such a central role in patient management when new tests with such low sensitivity would have trouble getting published. The answer is in the high specificity of ST-segment elevation for acute MI, low cost, simplicity, and near-universal availability. The resulting high positive predictive value allows us to safely institute therapies that are either expensive, are labor intensive, or have undesirable potential adverse effects. Furthermore, large infarcts are the most likely to demonstrate ST-segment elevation and are the most likely to benefit from emergency interventions.
The distinction between QWMI and NQWMI continues to have clinical value because this ECG finding reflects the underlying pathology (5). The CMR study by Moon et al. (6) in the current issue of the Journal demonstrates that Q-waves are indicative of larger MIs but are not particularly useful in determining the transmural extent of infarction. The authors graphically demonstrate that even the classification of an infarct as transmural or subendocardial is overly simplistic. Moon et al. (6) found that 99% of patients with QWMI had a least a portion of that infarction in a subendocardial distribution, whereas 28% of patients with a NQWMI had regions of infarction that were transmural.
The NQWMIs have a better in-hospital prognosis, but long-term prognosis is similar or worse than QWMI. The intermediate- and long-term prognosis data for NQWMI probably represent two determining factors. Early after infarction, the patient with a NQWMI is more likely to have residual viable but ischemic myocardium than the patient with a QWMI (7) and is more vulnerable to recurrent infarction or ischemia. Late prognosis is probably determined by the consequences of having ischemic heart disease.
What role do Q-waves play in our current clinical algorithms? The natural history of the Q-wave takes time to develop—often well after the important initial diagnostic and therapeutic interventions have taken place. Thus, the Q-wave does not figure strongly in our acute-management decisions. Although early data from Thrombolysis in Myocardial Infarction IIIB (8) and Veterans Affairs Non–Q-Wave Infarction Strategies in Hospital (9) trials did not support an early aggressive interventional approach to NQWMI, more recent clinical trials, such as the Treat Angina With Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy (10) and Fragmin and Fast Revascularization During Instability in Coronary Artery Disease Investigators II (11) trials, support the modern invasive strategy of non–ST-segment elevation acute coronary syndrome. In the latter studies, an invasive strategy demonstrated improved mortality, reduced rates of recurrent infarction, improved symptoms, and lower readmission rates compared with a conservative strategy. This is particularly true for the patient with non–ST-segment elevation MI, a group that most commonly has a NQWMI. During the chronic phase of the disease, the Q-wave remains the most specific ECG finding for MI.
Many cardiologists wonder what impact CMR and other new technologies will have on the practice of cardiology. Many also question whether CMR is more than an academic or research tool. In short, CMR is a very powerful technique, particularly for characterization of patients with ischemic heart disease. Cine magnetic resonance imaging (MRI) methods provide exquisite views of cardiac anatomy and function (12). Even under the most difficult diagnostic conditions of induced myocardial ischemia at the high heart rates of dobutamine stress testing, CMR is at least as sensitive and specific as dobutamine stress echocardiography for the detection of coronary artery disease (13,14), is feasible on a large scale at a few centers, and provides results that have prognostic significance (15).
Cardiac magnetic resonance viability techniques have generated high interest in the field and are ready for widespread clinical dissemination. Searching the literature published before 1999 will show a range of confusing and contradictory results. A major technical breakthrough around 1999 greatly improved CMR imaging of MI (16). This method has been validated in animal models of acute and chronic MI (17). The method is directly applicable to humans and able to predict the recovery of regional contractile function in patients with coronary artery disease based on the transmural extent of infarction (18). The presence or absence of Q-waves should not be used to determine viability. Although techniques such as positron emission tomography (PET), dobutamine echocardiography, and thallium scans can evaluate viability clinically, CMR has the unique ability to define the transmural extent of infarction.
Because there are many clinical tools available for imaging viable myocardium, one might ask, "Why bother with CMR?" This can be answered simply by considering the following characteristics of CMR viability imaging: accuracy, resolution, and simplicity. Human studies have confirmed the accuracy of CMR by the strong correlation between CMR and PET (19). However, these authors note that 47% of CMR scans showing only subendocardial infarction were read as normal on the PET scan. Similarly, Wagner et al. (20) reported that single photon emission computed tomography scans routinely miss subendocardial infarction in animals and in humans. The high image resolution has allowed the detection of infarction associated with recognized side-branch occlusions during percutaneous coronary interventions and the effects of distal embolization (21) and may explain why lower-resolution tests miss small infarctions. Using gadolinium-enhanced CMR, viability can be assessed without a stress test, which facilitates its use in the acutely ill patients.
The skeptic may wonder whether the tiny areas of MI that may be found have any clinical significance. Although long-term studies remain to be completed, the literature on troponin indicates that even the smallest recognized MIs (1) have important prognostic significance (22). Because CMR studies can detect smaller infarcts than other imaging modalities, one can extrapolate that prognostic studies will ultimately demonstrate that CMR viability imaging carries similar prognostic value.
Clinicians also wonder about the general feasibility of CMR. Is it safe to perform a CMR scan on acutely ill patients? Ultimately, the safety and feasibility of CMR is going to be determined by the degree of responsibility accepted by the physicians supervising the study. This statement is no different than quality assurance standards for performing stress testing, transesophageal echocardiography, cardiac catheterization, and percutaneous coronary interventions. When performed by well-trained and conscientious physicians, it is safe to do procedures that were frankly contraindicated 20 to 30 years ago. As an indication of feasibility, we were able to safely study patients with possible or probable acute coronary syndrome within 6 h of presentation to a community hospital emergency department and to achieve higher diagnostic accuracy than a conventional clinical assessment (23).
What are the disadvantages of the CMR technique? The greatest problems limiting widespread dissemination of this technology revolve around reimbursement issues, patient contraindications, physician education, rapidly changing technology, and control of MRI scanners. As of 2003, patients with pacemakers, defibrillators, ferromagnetic brain aneurysm clips, and certain other medical devices should not undergo a CMR scan (24). Although the technology is expensive, MRI scanners can be profitable devices in the treatment of neurological diseases and orthopedics, so it is reasonable to believe the systems could be profitable for cardiovascular diseases, particularly in light of the wide range of cardiovascular applications and the large number of patients requiring evaluation for ischemic heart disease. Other barriers to the widespread implementation of CMR include some significant training issues and the limited number of training centers. Many clinicians find MRI physics to be relatively complicated, and this is further complicated by rapid innovations and technical developments in the field. Finally, disappointing "turf" battles remain between cardiologists and radiologists at many centers.
In a time when medicine relies increasingly on high technology, it is reassuring to recognize the continued positive impact of simple and inexpensive tests such as the ECG. Electrocardiographic abnormalities associated with MI were first reported in 1920 (25). More than 80 years later, the widespread reliance of physicians on the ECG for triage and diagnosis of patients helps put in perspective why this invention warranted awarding a Nobel Prize to Willem Einthoven in 1924. Hopefully, CMR will continue to develop and provide useful diagnostic information for an equally long history beyond the 2003 Nobel Prize awarded to Paul Lauterbur and Sir Peter Mansfield for their discoveries concerning MRI.
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