Dr. Grover-McKay is the Director of Cardiovascular MRI, Memorial Care MRI, Long Beach, CA.

To avoid any apparent conflict of interest, she discloses that she has received educational grants from GE Medical Systems and Siemens.

Cardiovascular magnetic resonance (CVMR) is a clinical reality. A previous article discussed both the technology that has made CVMR feasible and CVMR techniques, and gave an overview of clinical issues that can be addressed using CVMR. ¹ This article will provide an in-depth discussion of myocardial viability and infarction detection using a phenomenon called delayed hyperenhancement (DHE).

Detection of myocardial infarction

Standard imaging signs of myocardial infarction (MI) have included a thin myocardial wall, wall motion abnormality, fixed perfusion defect, and lack of metabolic activity. The use of CVMR with intravenous gadolinium (Gd) yields high-resolution images that reproducibly provide the transmural extent of necrotic tissue, thereby identifying viable myocardium. Thus, comprehensive information can be obtained with a single test. The practitioner must be aware that despite the clinical utility of DHE, this use of Gd has not been approved by the Food and Drug Administration.

Gadolinium is a paramagnetic contrast agent that shortens T1 relaxation time, thereby providing tissue contrast. When delayed CVMR images are obtained in both acute and chronic MI, the infarcted myocardium contains more Gd than normal myocardium, likely due to impaired washout of Gd in MI compared with normal myocardium. ² Therefore, infarcted tissue is bright when imaged after Gd administration when signal from the normal myocardium is nulled using MR techniques. ³ This increased signal in MI is known as DHE (Figure1). The mechanism of Gd retention is probably different in acute and chronic infarcted myocardium. In acute infarction, Gd is thought to enter damaged myocytes, whereas in chronic infarction, the Gd may be retained in the expanded extracellular space.

Experimental and clinical studies have demonstrated that DHE does not occur in reversibly injured myocardium, ^4,5 the temporal changes are due to infarct shrinkage, ⁴ the spatial extent of DHE equals acute myocyte necrosis, ^4,6 and measurement of DHE size is reproducible. ⁷

Several studies have found that DHE imaging has the ability to detect both small and large areas of myocardial necrosis. The area of DHE accurately reflects experimental MI size. ⁸ In patients, very small areas of infarction with a median creatine kinase of the myocardial band (CK-MB) of 21 ng/mL (estimated 2 g of necrosis) were detected following percutaneous transluminal coronary angioplasty (PTCA). ⁹ In a study of 14 patients who had PTCA and CK-MB elevation, all had DHE detected by MRI, and of the 5 patients with diabetes mellitus (DM), 4 had CK-MB elevation, ⁹ suggesting increased risk of small infarctions after PTCA in DM patients. In a study of healed MI, 29 of 32 (91%) had DHE at 3 months and 19 of 19 at 14 months for an overall sensitivity of 94%. ¹⁰ Combining both studies, the detection of small and large MI by DHE is 95%.

Viability and recovery of wall motion

The excellent spatial resolution of MRI enables detection of the transmural extent of DHE, which predicted viability ¹¹ and recovery of wall motion (WM) in experimental and clinical MI. ^12-14 If <25% of the myocardial wall demonstrated DHE, then WM improved after revascularization in 60% to 85% of these segments. However, if DHE was transmural or nearly transmural (ie, 100% of the wall involved), then WM did not improve in >95% of these segments. The best predictor of global improvement in cardiac function was the amount of myocardium with abnormal function and DHE comprising <25% of the wall thickness. ¹⁵ Thus, since the goal of the clinician is to identify dysfunctional myocardium that will demonstrate improved WM after revascularization, CVMR can provide a simple, reliable method to identify these regions (Table 1).

Conclusion

Delayed hyperenhancement is just one application of CVMR that has tremendous potential for improving patient care and for providing the necessary imaging techniques to perform clinical and experimental investigative studies. This is an endeavor that needs to be undertaken by those who have experience and expertise with the technology and the clinical and scientific questions to be answered. We must be willing to break down the barriers (perhaps most importantly, the financial barriers) between radiologists and cardiologists, thereby combining their expertise to optimally meet the needs of referring clinicians and their patients. This likely will require creative arrangements for interpretation and reimbursement to rapidly disseminate CVMR and techniques such as DHE. AR