Pharmacokinetic modeling demonstrated that the distinctive dark blood appearance of late gadolinium enhancement in cardiac amyloid is likely due to diffuse expansion of the extravascular extracellular space in both the reference myocardium and the body.
Pharmacokinetic modeling demonstrates that the distinctive 'dark blood' LGE appearance in cardiac amyloidosis is likely driven by diffuse expansion of the extravascular extracellular space in both the myocardium and the body.
BACKGROUND: Late gadolinium enhancement (LGE) is a valuable part of cardiac magnetic resonance imaging (CMR). In particular, inversion-recovery imaging of LGE, with nulling of the signal from reference areas of myocardium, can have a distinctive pattern in some patients with cardiac amyloid, including both diffuse (relatively faint) subendocardial LGE and a relatively dark appearance of the blood. However, the underlying reasons for this distinctive appearance have not previously been well investigated. Pharmacokinetic modeling of myocardial contrast enhancement kinetics can potentially provide insight into the mechanisms of the distinctive LGE appearance that can be seen in cardiac amyloid, as well as why it may be unreliable in some patients. METHODS: An interactive three-compartment pharmacokinetic model of the dynamics of myocardial contrast enhancement in CMR was implemented, and used to simulate LGE dynamics in normal, scar, and cardiac amyloid myocardium; the results were compared with previously published values. RESULTS: The three-compartment model is able to capture the qualitative features of LGE, in patients with cardiac amyloid. In particular, the characteristic "dark blood" appearance of PSIR images of LGE in cardiac amyloid is seen to likely primarily reflect expansion of the extravascular extracellular space (EES) by amyloid in the "reference" myocardium; the cardiac amyloid contrast enhancement dynamics also reflect expansion of the body EES. CONCLUSION: The distinctive appearance of LGE in cardiac amyloid is likely due to a combination of diffuse expansion by amyloid of the EES of the reference myocardium and of the body EES.
Leon Axel (Wed,) conducted a other in Cardiac amyloidosis. Pharmacokinetic modeling of Gd-DTPA kinetics vs. Normal myocardium and scar models was evaluated on Simulated T1 values and contrast agent kinetics. Pharmacokinetic modeling demonstrated that the distinctive dark blood appearance of late gadolinium enhancement in cardiac amyloid is likely due to diffuse expansion of the extravascular extracellular space in both the reference myocardium and the body.