Summary: Rest-stress perfusion and viability cardiac magnetic resonance imaging
(CMRI) tests are performed on a 60-year-old male with known coronary
arterial atherosclerotic disease (CAD) (Figures 1-6). Previously, the
patient sustained a right coronary artery (RCA) territory myocardial
infarction (MI) and underwent successful RCA stent placement. No
intervention was performed for left circumflex (LCX) 40% and first
obtuse marginal (OM1) 50% stenoses. While the patient is currently
asymptomatic, a recent surveillance echocardiography demonstrated
worsening global left ventricular function with regional wall-motion
abnormalities in the inferior and lateral walls.
Left circumflex coronary artery stress-induced ischemia
CMRI short axis (SAX) (Figure 1), two-chamber (2CH) (Figure 2),
three-chamber (3CH) (Figure 3), and four–chamber (4CH) (Figure 4) CINE
imaging confirm global mild hypokinesis with proximal apical-inferior
wall thinning and akinesis, and mid- and basilar-inferior septum,
inferior wall, and posterior-lateral wall myocardial thinning with mild
hypokinesis. The best preserved function during rest is
in the true apex, most distal apex, and the anterior septum, anterior
wall and anterior-lateral wall (apex to base). (Click here to view Figure 4 in our DICOM viewer.)
echo-gradient rest-perfusion images (Figure 5) are remarkable for
subendocardial hypoenhancement in the apical-inferior wall and mid- and
basilar-inferior septum, inferior wall, and posterior lateral wall.
Adenosine fast-field echo-gradient stress imaging (Figure 5) reveals
similar decreased subendocardial perfusion, with exception to stress
induced subendocardial hypoenhancement in the apical-anterior lateral
wall, extending to the junction with the midchamber myocardium (Figure
Inversion-recovery delayed short-axis images (Figure 6) are
remarkable for apical-inferior wall (Figure 6) transmural (> 50%)
delayed hyperenhancement (DHE), extending into the posterior-lateral
wall, confirming the presence of myocardial scar and focal myocardial
nonviability in the RCA territory. In the mid- and basilar-inferior
septum, inferior wall, and posterior-lateral wall RCA territory (Figure
6), thin linear < 50% subendocardial DHE is demonstrated, consistent
with subendocardial myocardial scar, but with viable myocardium. Of
significance, images reveal absence of DHE in the apical-anterior
lateral wall (Figure 6), confirming viability and corroborating the
presence of stress-induced ischemia in the LCX/OM territory.
CMR myocardial perfusion and viability imaging has become a useful
approach to evaluate coronary artery disease. When acquisitions are
acquired using current stress and rest perfusion techniques, moderate to
high sensitivity (84-100%) and specificity (80-100%) can be achieved
for the detection of hemodynamically significant (> 70% stenosis)
coronary artery lesions.1 As illustrated in Figures 1-6,
accurate diagnoses can be made to determine the extent and location of
myocardial scar and stress induced ischemia, in addition to evaluating
cardiac morphology and function. Regions of scar are further
characterized as having residual viable myocardium (eg, < 50% of
myocardium) or having no viable myocardium (eg, > 50% of myocardium),
by determining the burden of scar relative to the myocardium. In
patients with known ischemic cardiomyopathy and myocardial scar, CMR
stress-rest perfusion and viability imaging can be used to predict
future risk for adverse cardiovascular events.2 In this
regard, CMR imaging can be utilized to plan effective therapy for
minimizing cardiovascular morbidity and mortality, including medical
management, percutaneous coronary intervention (PCI), and coronary
artery bypass grafting.
In summary, this patient’s perfusion-viability CMR imaging
demonstrates a small focal area of apical-inferior wall transmural, >
50% myocardial DHE with corresponding akinesis and fixed-perfusion
rest-stress defects, corresponding to RCA territory scar with nonviable
myocardium, related to the patient’s prior MI. In the mid- and
basilar-inferior septum, inferior wall, and posterior-lateral wall, <
50% subendocardial DHE with corresponding mild hypokinesis and
fixed-perfusion rest-stress defects, corresponds to RCA scar, but viable
myocardium, related to the prior MI.
At the apex, with extension
to the junction with the midchamber myocardium, stress-induced ischemia
in the LCX/OM territory corresponds to hemodynamically significant CAD.
As residual nonhemodynamically significant LCX/OM disease was known
from the patient’s prior coronary catheterization, CMR imaging suggests
progression of disease and supports the need for maximizing CAD medical
management and possible coronary catheterization with PCI. The patient
ultimately underwent coronary catheterization, which confirmed
obstructive LCX disease with no significant change in the OM1 lesion.
PCI-LCX stent placement was performed with subsequent improved left
ventricular global function on a post-PCI echocardiography.
- Coelho-Filho OR, Rickers C, Kwong RY, Jerosch-Herold M. MR myocardial perfusion imaging. Radiology. 2013; 266:701-715.
- Tsukiji M, Nguyen P, Narayan G, et al. Peri-infarct ischemia
determined by cardiovascular magnetic resonance evaluation of myocardial
viability and stress perfusion predicts future cardiovascular events in
patients with severe ischemic cardiomyopathy. J Cardiovasc Magn Reson. 2006;8:773-779.