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Commentary |
1
Radiology Service, Mail Code 114, VA North Texas Healthcare System, 4500 S.
Lancaster Rd., Dallas, TX 75216.
2
Department of Radiology, University of Texas Southwestern Medical Center, 5323
Harry Hines Blvd., Dallas, TX 75235-8896.
Received November 19, 1999;
accepted after revision November 19, 1999.
This article is a commentary on the preceding article by Sandstede et
al.
Introduction
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For a variety of reasons, most practitioners and imagers are reluctant to use cardiac MR imaging in the routine workup of patients with ischemic heart disease. In general, reluctant physicians lack exposure to and training in cardiac MR imaging. Furthermore, these examinations are technically difficult and require cardiac gating, which lengthens the duration of the MR study setup time. Large clinical studies that may prove the usefulness of MR imaging for ischemic heart disease are only now being performed or planned. However, as pointed out by Dr. Higgins [4], a key component of the MR evaluation of ischemic heart disease, namely coronary MR angiography, has not yet reached a sufficient level of technical maturity. Unfortunately, cardiac MR imaging technology is evolving so fast that most clinical trials cannot be completed before a technique becomes obsolete, thus creating the perception that the technology is not mature. Coronary MR angiography is one of the best examples of such recent technologic evolutions in cardiac MR imaging. The first coronary MR angiographic techniques appeared very promising [6] but never gained widespread acceptance because they acquired only one image per breath-hold, were limited to two-dimensional acquisitions, and required operator skills [7,8,9]. Improved coronary MR angiographic techniques using navigator echoes, also referred to as second generation coronary MR angiography techniques, allowed free breathing and increased spatial resolution [10,11,12,13]. Recently, third generation techniques have allowed the acquisition of a three-dimensional volume within one breath-hold [14]. Although these newer coronary MR angiographic techniques are nearly as easy to use as a conventional CT scanner, many practitioners are not comfortable with this constant change and evolution in MR techniques.
The use of cardiac MR imaging for the direct evaluation of myocardial viability and myocardial ischemia has seen a similar dramatic evolution. Early research was focused on first-pass perfusion and detection of myocardial wall motion abnormalities. Many investigators used myocardial tagging schemes, extensive postprocessing and data analysis, and three-dimensional rendering. The importance and potential of dobutamine stress testing in an MR unit have been shown by Zoghbi et al. [15]. However, these techniques are complex and not easily reproduced outside specialized research centers. Simpler concepts, such as delayed hyperenhancement of a subacute myocardial infarction, have been described [16]. This simple concept was recently reinvented and shown to apply to subacute and chronic infarcts [17,18,19,20,21]. The concept that delayed hyperenhancement equals dead myocardium suddenly became popular again. Most importantly, this type of MR imaging study is easy to perform on most existing clinical MR scanners. It has even been suggested that this test might be better than the existing gold standard of positron emission tomography. Therefore, given this great potential for widespread clinical use, one has to carefully consider the arguments of the detractors and weigh the value of their objections against the potential overall good of such a simple noninvasive imaging test.
Delayed myocardial hyperenhancement after injection of gadolinium-labeled MR contrast material has been shown to delineate areas of myocardial infarction in several human and animal studies [17,18,19]. Ramani et al. [19] showed that delayed (3-15 min) hyperenhancement of gadopentetate dimeglumine contrast-enhanced MR images occurs frequently in dysfunctional areas of the left ventricle in patients with stable coronary artery disease. Hyperenhancement is associated with nonviability by rest-redistribution 201-Tl-weighted scintigraphy and dobutamine echocardiography, particularly in regions exhibiting resting akinesis or dyskinesis. The absence of hyperenhancement correlates with radionuclide and echocardiographic determinations of viability, regardless of resting contractile function. The report by Sandstede et al. [20] in this issue of the AJR addresses a similar finding. Sandstede et al. conclude that delayed hyperenhancement of dysfunctional myocardium predicts lack of mechanical improvement or nonviability, whereas the lack of hyperenhancement predicts improvement of regional contractility or viability after revascularization. Kim et al. [21] also reported, on the basis of a study in dogs, that both acute and chronic myocardial infarcts hyperenhance. They showed infarct resorption and viable tissue hypertrophy over an 8-week period. Their work suggests that contrast-enhanced MR imaging may allow noninvasive regional evaluation of ventricular remodeling after ischemic injury with high spatial resolution and full ventricular coverage. These reports are exciting because they propose a general clinical approach to the MR imaging examination of patients after myocardial infarction. If shown to be reliable, this algorithm could be used by most MR imaging practitioners; thus, these reports deserve great attention.
Unfortunately, no such algorithm is without controversy and detractors [1]. Within the infarct zone exhibiting delayed hyperenhancement, central areas of microvascular obstruction (the no-reflow or low-reflow region of an infarct) exhibit decreased first-pass perfusion. Thus, the infarct zone is not always histologically homogeneous and may contain "dead" and "more dead" myocardium. Furthermore, some investigators claim they can see the peripheral zone of potentially salvageable myocardium and others claim it does not exist. The fate of tissue exhibiting delayed hyperenhancement is an even greater controversy among some investigators, with some studies showing "recovery from death." In particular, in a study of 17 patients with reperfused myocardial infarction Rogers et al. [22] described a subgroup of 13 patients in whom segments with normal contrast-enhanced first-pass signal and hyperenhanced signal on delayed images (HYPER) had partially reversible dysfunction and, thus, represented predominantly viable myocardium. Only one such segment was found in the study by Sandstede et al. [20]. However, both studies had many segments with both absence of normal first-pass enhancement and delayed hyperenhancement (COMB). Rogers et al. concluded that these latter (COMB) segments show borderline improvement and likely contain an admixture of viable and necrotic myocardium. Sandstede et al. conclude that most (24/25) of their segments with delayed hyperenhancement (COMB) are nonviable. The conclusions of these two studies appear, on the surface, to be in contradiction. These discrepant findings may result from differences in patient groups, differences in the definition of "partially reversible dysfunction," differences in sensitivity to wall motion abnormalities using cine MR imaging with or without tagging, limited spatial resolution and accuracy of the cine MR imaging studies used to evaluate function, hyperenhancement in surrounding reversibly injured regions, and partial volume effects. Wu et al. [23] established a relationship between MR imaging contrast defects during first-pass perfusion and long-term prognosis after infarction. They postulated that first-pass hypoperfusion most likely corresponds to areas of microvascular obstruction. They found that patients with microvascular obstruction had more cardiovascular events than those without. However, the zone of delayed hyperenhancement extended beyond this area of microvascular obstruction. Saeed et al. [24] have shown in an animal study that the delayed hyperenhanced zone includes a peripheral zone of potentially salvageable myocardium, which contradicts the work by Kim et al. [21], in which no such peripheral zone was detected. Certain diffuse myocardial diseases, such as myocarditis, can also cause diffuse hyperenhancement.
The work reported in this issue of AJR by Sandstede et al. [20] holds great promise, but should still be considered an active area of research. If future studies confirm, in certain clinical settings, the conclusion that delayed hyperenhanced myocardium equals dead myocardium, then we will indeed have an easy-to-perform noninvasive MR imaging test with a great clinical impact. Such a simple noninvasive MR imaging test may soon become part of the routine clinical workup of many patients with ischemic heart disease.
Acknowledgments
I thank the many people who, via discussions and feedback, have helped me
shape these opinions and better understand all the nuances of this important
controversy: Lawrence Boxt, Arthur Stillman, Orlando Simonetti, Joao Lima,
Raymond Kim, Robert Judd, Walter Rogers, and Christopher Kramer.
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