Cardiovascular magnetic resonance (CVMR) is a reality. The author provides a discussion of myocardial viability and infarction detection using delayed hyperenhancement. 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.
is the Director of Cardiovascular MRI, Memorial Care MRI, Long
To avoid any apparent conflict of interest, she discloses
that she has received educational grants from GE Medical Systems
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.
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
Therefore, infarcted tissue is bright when imaged after Gd
administration when signal from the normal myocardium is nulled
using MR techniques.
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,
the temporal changes are due to infarct shrinkage,
the spatial extent of DHE equals acute myocyte necrosis,
and measurement of DHE size is reproducible.
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.
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).
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,
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%.
Combining both studies, the detection of small and large MI by DHE
Viability and recovery of wall motion
The excellent spatial resolution of MRI enables detection of the
transmural extent of DHE, which predicted viability
and recovery of wall motion (WM) in experimental and clinical MI.
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.
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).
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