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The partition coefficient of Gd-DTPA (lambda) is elevated in infarcted relative to normal myocardium. Although MRI following an infusion of Gd-DTPA allows for the quantification of lambda, infarct imaging is more routinely performed using a bolus. In this study we sought to determine how image delay time and time postinfarction influence the estimation of lambda by the bolus strategy. Both infusion and bolus imaging were performed twice in the same group of patients (N = 9): once at 3-4 weeks and again 6 months after reperfusion therapy for myocardial infarction (MI). Bolus estimates of lambda were compared with those calculated after 60 min infusion, and comparisons were repeated at 6 months. The lambda of infarcted myocardium was significantly greater than that of normal tissue, irrespective of either the technique used or the time postinfarction (P0.0001, for each). The concordance (Rc) between bolus and infusion estimates of lambda was0.83 for all image delays4 min postinjection, and Rc at 2 min (0.78 +/- 0.04) was significantly less than Rc determined for longer image delay times (P = 0.009). Rc did not change with time postinfarction (P = 0.604). Thus, the bolus strategy can be used to provide estimates of lambda that are stable from 1-6 months postinfarction and independent of image delay time.

It has previously been shown that the distribution volume of Gd-DTPA (λ) in infarcted, canine myocardium is higher than that of normal tissue. The purpose of this study was to determine whether stunned myocardium exhibits increased λ. Stunning was produced in beagles by means of 30 min LAD occlusion followed by 3 weeks (n = 4) reperfusion. Gd-DTPA was infused at each imaging session and λ determined in vivo using a saturation recovery turboFLASH sequence; cine imaging was used to assess ventricular wall thickening (%WT). 201Tl uptake was used as an independent assessment of viability. %WT data confirmed that the brief insult caused prolonged, yet reversible, regional contractile dysfunction in each animal. %WT was not significantly different from baseline values by 3 weeks post-reflow. Normal 201Tl uptake confirmed the absence of infarction. The λ of stunned tissue (λ = 0.381 ± 0.030 ml/g) was not elevated above that of normal tissue (λ = 0.398 ± 0.027 ml/g, P = NS), at any time point studied, in vivo. These data suggest that an increase in λ is a specific indicator of irreversible damage. Magn Reson Med 45:864–871, 2001. © 2001 Wiley-Liss, Inc.

It was previously shown in a canine model of ischemia/reperfusion injury that the partition coefficient of gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA) (λ) increases in infarcted tissue. That previous study used a non-magnetic resonance imaging (MRI) method to measure λ and only investigated reperfusion times from 2 hr to 3 weeks. This study presents evidence suggesting that λ starts to increase as early as 1 min after reperfusion of a 2 hr occlusion and continues to rise for up to 2 hr or more; λ stays increased as late as 8 weeks, reaching peak values at 1–11 days and subsequently decreasing. It was also demonstrated that λ can be accurately measured in vivo using a saturation recovery turbo fast low-angle shot (FLASH) sequence. The results of this study show that MRI during a constant infusion of Gd-DTPA has great potential for the non-invasive determination of myocardial viability as early as 1 min to as late as 8 weeks following reperfusion of acute myocardial infarction. Magn Reson Med 42:60–68, 1999. © 1999 Wiley-Liss, Inc.

We have developed a closed chest animal model that allows noninvasive monitoring of cardiac high energy phosphate metabolism before, during, and for at least 3 weeks after a myocardial infarction. Ten beagles underwent 2 h of coronary occlusion followed by 3 weeks of reperfusion. Myocardial high energy phosphates from 12-ml voxels were noninvasively tracked using 31P two-dimensional chemical shift imaging. Gadolinium enhanced 1H MRI identified the zone at risk, and radioactive microspheres assessed regional blood flow and partition coefficients. Occlusion of the left anterior descending coronary artery produced infarcts that were 13.7+/-8.8% (mean+/-SD) of the left ventricular volume. Rapid changes in the phosphocreatine and inorganic phosphate levels were observed during occlusion, whereas adenosine triphosphate levels decreased more slowly. All metabolites recovered to base-line levels 2 weeks after occluder release. Multiple inorganic phosphate peaks in the infarct voxel spectra indicated that more than one metabolically compromised tissue zone developed during occlusion and reperfusion. Microsphere data indicating three distinct blood flow zones during ischemia and reperfusion (0.3, 0.3-0.75, and0.75 ml/min/g) supported the grouping of pH values into three distinct metabolic distributions.

In order to clarify the relationship between coronary artery disease (including myocardial infarction) and image contrast in gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA-enhanced MRI it was decided to model the myocardial tissue distribution and clearance of Gd-DTPA using the modified Kety equation. Using a canine model, myocardial tissue Gd-DTPA concentrations ([Gd-DTPA]m) were measured 1 or 5 min after a bolus injection of Gd-DTPA or immediately after the end of a constant infusion of Gd-DTPA in a total of 35 dogs. It was found that within 5 min of a bolus injection [Gd-DTPA]m is determined primarily by myocardial blood flow (MBF) and after about 10 min primarily by myocardial extracellular volumes (MECV). This study suggests that repeat, rapid (every 2–4 s) measurements of myocardial T1 relaxation rates following the bolus injection of Gd-DTPA are required to calculate MBF (i.e., myocardial tissue perfusion) and MECV. © 1992 Academic Press, Inc.

MRI after a constant infusion (CI) of Gd-DTPA has been used to identify the extent of myocardial infarction (MI). However, Gd-DTPA-enhanced “viability” imaging is more commonly performed with a bolus (for “delayed-enhancement” (DE) imaging). This study sought to determine how image delay time and time postinfarction influence the assessment of necrosis by DE. Both infusion and DE imaging was performed in dogs with reperfused (N = 6) or unreperfused (N = 4) MI. Estimates of the partition-coefficient of Gd-DTPA (λ) with DE were compared with those calculated after 60 min of infusion, and the comparisons were repeated until 4 (reperfused) or 8 (unreperfused) weeks postinfarction. In reperfused animals, the concordance (Rc) between DE and infusion estimates of λ was > 0.90 for most image delays > 8 min postinjection, for day 0 through week 3, with Rc at day 0 greater than at week 4 (P = 0.022). In unreperfused animals, there was an interaction between image delay time and time postinfarction (P 0.90 corresponded to longer image delays at week 1 than at weeks 4–8. Therefore, when image delays are selected appropriately, DE images can strongly reflect λ and identify irreversibly injured myocardium. Magn Reson Med 52:1069–1079, 2004. © 2004 Wiley-Liss, Inc.

We have previously shown that the myocardial Gd-DTPA concentration ([Gd-DTPA]t(t)) after a bolus injection of Gd-DTPA can be predicted by the Modified Kety Equation (MKE). If [Gd-DTPA]t(t) can be determined by MRI and the data fit to the MKE, then the distribution volume (lambda) of Gd-DTPA and the myocardial flow (F) times the extraction efficiency (E), i.e., the FE product, can be determined. Therefore F can only be quantified if E is known. We measured the global E in vivo in normal canine myocardium, and measured E and lambda, in vitro, locally in normal, acute ischemic (n = 5; coronary artery occlusion4 h), infarcted (n = 4; coronary artery occlusion, 6 days) and reperfused (n = 4; coronary artery occlusion 2 h, and reperfusion 2 h and 6 days) myocardium. Results indicate that E differs with F and with individuals and consequently, F cannot be quantified using the MKE unless the local E is also determined in vivo.

Normally, cardiac triggering in MR spin-echo imaging restricts repetition times (TR) to integral values of the cardiac period (TC), and introduces irregularities in TR due to variations in TC. We have investigated how much these restrictions decrease the accuracy and precision of spin-lattice relaxation (T1) values of the myocardium calculated from two cardiac-triggered spin-echo images. By introducing additional excitation pulses, TR can effectively be reduced to a fractional value of TC and considerable improvement in T1 precision is possible. For TC = 800 ms, the improvement in T1 precision is 30% when two spin-echo images of TR = 1/2 X TC and TR = 2 X TC are used to calculate T1 instead of two images with TR = TC and TR = 2 X TC. The irregularities in TR decrease both T1 precision and accuracy. Irregularities of the order of 15% in a mean TR of 800 ms produce a fourfold decrease in precision. Since irregularities in TC easily exceed 15%, MRI data should be acquired when individual TR values are approximately within +/- 15% of the subject's mean TC.