Synopsis
Clinical Background
Cardiovascular disease is a leading cause of
morbidity and mortality worldwide. Many novel imaging methods have been
developed to study atherosclerosis in patients suffering from coronary artery
disease (CAD). Imaging techniques that will allow identifying progressive
cardiac disease and prediction of future clinical risk are becoming of more and
more importance.
In addition
to echocardiography, cardiac magnetic resonance imaging (MRI) might be used for
the noninvasive assessment of LV volumes and LVEF in a heart failure setting. One
of the main advantages of cardiac MRI over other imaging modalities is its
ability to assess changes in tissue. For example by using contrast-enhanced pulse
sequences cardiac MRI can be used to assess myocardial viability. This
technique has displayed high diagnostic accuracy for acute inflammatory or
ischemic injury.
Nowadays,
late gadolinium enhancement (LGE) imaging has become the primary diagnostic
tool for assessment of myocardial viability in patients suffering from CAD. With
LGE, hypo- or akinetic but still viable myocardium can be identified as
dysfunctional myocardium without scar or significant remaining viable tissue
(<50% transmurality of scarring). In clinical practice this additional
information will help to decide whether or not the patient will recover after revascularization.
Basic principle of
late gadolinium enhancement (LGE)
The
mechanism of LGE in acute and chronic infarction is the increase in the
extracellular space caused by necrosis (loss of cell membrane integrity) with
the former and the larger extracellular space of scar compared to myocardium
with the latter. Magnetic resonance contrast agent that diffused to the
interstitial space will be resorbed into the capillary bed and undergo renal
excretion. However, when the tissue is damaged, for example, due to infarction,
diffuse fibrosis or even inflammation, the resorption rate of contrast agent
will be diminished. At 10-20 min after contrast injection, washout will
be complete in normal myocardium in contrast to infarcted or edematous tissue.
This phenomenon is the basis of “late gadolinium enhancement” imaging.
Various studies
have shown the relation between myocardial viability and the size of the area
displaying late gadolinium enhancement. In MR images, the presence of contrast
agent can be detected as a bright area on images acquired with T1-weighted MR images.
Moreover, a strong correlation between the transmural extent of LGE and
regional function recovery has been demonstrated in several studies, revealing LGE
imaging as a powerful predictor of myocardial damage after myocardial
infarction.
While the
distribution of LGE is invariably subendocardial for ischemic disease (either
acute or chronic myocardial infarction), the pattern of enhancement has a
variable transmural distribution in non-ischemic myocardial disease. In
ischemic heart disease LGE conforms to the distribution of one or more coronary
arteries.
Microvascular Obstruction (MO)
Microvascular
obstruction (MO) or the “no-reflow” phenomenon is an established complication
of coronary reperfusion therapy. It is increasingly recognized as a poor
prognostic indicator and can serve as an imaging marker of subsequent adverse
LV remodeling. Although MO can be assessed using various imaging modalities, evaluation
by cardiac MRI is particularly useful in enhancing its detection, diagnosis, and
quantification, as well as following its subsequent effects on infarct
evolution and healing. MO assessment has become a routine component of the MR
evaluation of acute myocardial infarction and will increasingly play a role in
therapeutic decision pathways.
MO is
characterized by a number of ultrastructural and functional changes at the
microvascular level. Understanding these histopathophysiologic changes can
inform the approach by MRI to detecting MO, to understand the results and their
subsequent clinical implications. It can also help potentially improve how MO
is assessed by CMR which has implications with regard to the understanding of
infarct evolution as well as the evaluation of the efficacy and mechanism of
reperfusion treatment.
MO has been
found to be predictive of clinical outcome, independently of or when adjusted
for other indices such as infarct size and LV ejection fraction (EF).Many of
these outcome studies showed a severe relationship between presence of MO and
adverse LV remodeling with reduced global systolic function and larger LV
volumes at follow-up exams, suggesting a possible mechanism for the poor
prognosis.
Acknowledgements
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