Nagel.qxp 16/7/08 10:05 Page 33
The Role of Magnetic Resonance Imaging in the Detection of Coronary Artery Disease
patients with acute chest pain, negative troponin-I test results, and non- infarct size—defined as spatial extent on contrast-enhanced MRI—was a
diagnostic ECG findings, adenosine-stress perfusion MR demonstrated a stronger predictor of all-cause mortality than LVEF and LV volumes.
30
In
sensitivity of 100% and a specificity of 93% for the detection of future addition, in patients with a prior MI the extent of the peri-infarct zone
adverse cardiac outcomes. In patients with a negative perfusion scan, characterized by cardiovascular MRI provides incremental prognostic value
no adverse cardiac outcomes occurred during the first year of follow-up. beyond LV systolic volume index or EF.
31
Conclusion Safety
Myocardial perfusion imaging produces accurate information on Recent reports have identified a possible link between a new
the presence of myocardial ischemia and will become an integral part of the scleroderma-like disorder, nephrogenic systemic fibrosis (NSF), and
assessment of cardiovascular patients. exposure to gadolinium-containing contrast agents in patients with end-
Late Gadolinium Enhancement
Late gadolinium enhancement (LGE) MRI by use of gadolinium-based
Myocardial perfusion imaging produces
contrast agents has become increasingly important for demonstrating MI
accurate information on the presence of
and detection of myocardial viability. Due to its high spatial resolution,
LGE-MR can clearly demarcate infarcted tissue and viable myocardium
myocardial ischemia and will become an
within the myocardium (see Figure 2).
17
integral part of the assessment of
Imaging Procedure
cardiovascular patients.
Usually, LGE-MR images are acquired 10–15 minutes after the contrast
injection.
24
The use of DE is based on the fact that in the equilibrium phase, stage renal disease.
32
The pharmacokinetic properties of gadolinium are
gadolinium-containing contrast agents distribute into the extracellular space. similar to those of iodinated X-ray contrast, but with less nephrotoxicity
In contrast to healthy myocardium, the distribution volume of the contrast and a lower anaphylaxis risk. A study in almost 700,000 patients showed
agent is substantially increased in infarcted tissue,
25
resulting in enhancement that the rate of adverse reactions was low and the rate of serious allergic
of necrotic areas in inversion recovery (IR)-prepared MR images.
24,26
Usually, a reactions was <0.01%.
33,34
Typically, gadolinium-containing agents are
dose of 0.1–0.2mmol/kg of an extracellular gadolinium contrast agent is given excreted rapidly and almost completely via glomerular filtration.
intravenously. To optimally suppress the signal of healthy myocardium to However, in renally diseased patients the clearance of gadolinium-
achieve the optimal contrast between infarcted and viable myocardium, the containing contrast agents is exceedingly prolonged compared with that
inversion time (TI) needs to be adapted to every patient. To differentiate seen in healthy humans.
35
The US Food and Drug Administration (FDA)
between acute and chronic MI, T2-weighted images allow infarct-related and European medicines agencies recommend that in patients with
myocardial edema to be depicted as a marker of acute MI.
27
severe renal impairment and neonates, gadolinium-containing agents
should be used only if clinically essential.
32
Prognostic Value
The assessment of the extent of myocardial necrosis on LGE-MR has been Conclusion
shown to be useful in predicting functional recovery of dysfunctional DSMR provides the opportunity to quantify the extent of myocardial
myocardium in patients after MI. The likelihood of a functional improvement necrosis and detect even small subendocardial MI. The evaluation of the
after revascularization was negatively correlated with the transmural extent transmural extent of scarred tissue is useful for predicting functional
of enhancement in both chronic
28
and acute MI.
29
A study showed that recovery of dysfunctional myocardium. ■
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US CARDIOLOGY 33
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