Tissue edema does not change gadolinium‐diethylenetriamine pentaacetic acid (Gd‐DTPA)‐enhanced T₁ relaxation times of viable myocardium

Abstract

Purpose:To determine whether tissue edema changes gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced T 1 relaxation times of the viable myocardium. Materials and Methods:A total of 16 isolated pig hearts were divided into four groups (N ϭ 4/group) and perfused in a Langendorff apparatus. Gd-DTPA was injected into the aortic perfusion line. Tissue edema was then induced by two hours of simultaneous arterial/venous perfusion (SAVP). Myocardial water content and T 1 relaxation times were monitored throughout SAVP. The volumes of the extracellular and intracellular compartments were assessed using 31 P MRS-detectable markers, phenylphosphonic acid (PPA) and dimethyl methylphosphonate (DMMP).Results: Tissue water content in both viable and infarcted myocardium increased significantly during two-hour SAVP. However, Gd-DTPA-enhanced T 1 relaxation times of the viable myocardium remained relatively unchanged. Infarcted myocardium, on the other hand, exhibited significant T 1 shortening during SAVP. Furthermore, SAVP resulted in significant expansions of both extracellular and intracellular compartments, but the ratio of the volumes of the two compartments remained relatively constant. Conclusion:Tissue edema in the viable myocardium does not increase the relative distribution volume of the contrast agent. As a result, edema does not change Gd-DTPA-enhanced T 1 relaxation times of the viable myocardium.

Retrospective Determination of the Area at Risk for Reperfused Acute Myocardial Infarction With T2-Weighted Cardiac Magnetic Resonance Imaging

“…30,31 Importantly, delayed-enhancement imaging shows the relative sizes of the extracellular and intracellular volumes, ie, the volume of distribution. 32,33 For edematous viable myocardium, this ratio has not been substantially altered 28 ; therefore, the peri-infarct zone does not exhibit significant contrast enhancement. On the other hand, the acute infarct demonstrates delayed contrast enhancement as a result of the disproportionately increased apparent extracellular space.…”

“…27 In acute MI, edema in the peri-infarct zone results from balanced water content increases in both the extracellular and intracellular compartment volumes of viable myocardium. 28 Within acutely infarcted myocardium, there is a conversion of intracellular space into extracellular space as a result of cell lysis. 28 Because of the increased total water content and increased water mobility, both the peri-infarct and the infarcted zones appear hyperintense on T2W images.…”

“…28 Within acutely infarcted myocardium, there is a conversion of intracellular space into extracellular space as a result of cell lysis. 28 Because of the increased total water content and increased water mobility, both the peri-infarct and the infarcted zones appear hyperintense on T2W images.…”

Myocardial Salvage

“…The lack of increased gadolinium signal in the border zone indicates that its partition coefficient must be similar to normal myocardium and less than within the area of necrosis, which is in accordance with experimental evidence. 21 This can be reconciled if there is balanced intracellular and extracellular edema occurring in the border zone. [21][22][23] CMR is not the only technique that can identify ischemia in retrospect.…”

“…21 This can be reconciled if there is balanced intracellular and extracellular edema occurring in the border zone. [21][22][23] CMR is not the only technique that can identify ischemia in retrospect. In nuclear cardiology, the fatty acid tracer 123 I-␤-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) also has similar properties, and the mechanism appears to be due mainly to a metabolic imprint related to a persistent decrease in ␤-oxidation with increased shunt retention of BMIPP in the triglyceride pool.…”