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A high resolution, noninvasive approach to quantify atherosclerotic plaque in the peripheral vasculature could have significant clinical and research utility. Seventeen patients with peripheral arterial disease (PAD) were studied in a 1.5T CMR scanner. Atherosclerotic plaque volume in the superficial femoral artery was measured and interobserver, intraobserver, and test-retest variability determined. Nineteen vessels were studied with mean acquisition time of 13.1 minutes per vessel. Mean plaque volume was 7.27 ± 3.73 cm3. Intra-observer intraclass correlation was R = 0.997, inter-observer was R = 0.987, and test-retest reproducibility was R = 0.996. Thus, high resolution measurement of plaque volume in PAD is reliable and reproducible. [ABSTRACT FROM AUTHOR]

Angiotensin II type 2 receptor (AT 2 -R) overexpression in the mouse heart preserves left ventricular (LV) size and global LV function during post-MI remodeling. We hypothesized that CMR tagging would localize regional improvements in myocardial function during post-MI remodeling in AT 2 -R cardiac overexpressed transgenic mice (TG), which could explain the preservation of global LV function post-MI. Six male wild-type (WT) C57BL/6 mice and 10 TG mice were studied by CMR at baseline (day 0) and days 1, 7, and 28 post-MI. MI was induced by 1 hour occlusion of the LAD followed by reperfusion. On day 1 post-MI, gadolinium-DTPA was injected to assess infarct size. LV size and function was assessed by cine CMR. Mean % circumferential shortening (%CS) was calculated within infarcted, adjacent, and remote regions at each time point in WT and TG mice. Quantitative interstitial collagen and mean myocyte cross-sectional area was measured postmortem at day 28 post-MI. LV end-systolic volume was lower and ejection fraction higher at baseline in the TG group and these differences were maintained post-MI. Within infarcted and remote zones, although %CS was higher in TG mice at day 0, there was no difference by day 28 between groups. Within adjacent regions, while there was no difference at day 0 or 1 in TG vs. WT, %CS was significantly higher in TG mice by day 7, and these changes persisted out to day 28 post-MI. Regional interstitial collagen and myocyte size were similar between groups. Thus, myocardial tagging can detect regional differences in contractile function post-MI in TG mice, and AT 2 -R overexpression is associated with improved contractile function in adjacent noninfarcted myocardium. [ABSTRACT FROM AUTHOR]

Delayed contrast-enhanced cardiac magnetic resonance imaging (ceCMR) delineates infarct size. The presence of hypoenhancement consistent with microvascular obstruction (MO) signifies larger infarcts with a worse prognosis. We hypothesized that the size of the contrast defect (CD) on ceCMR in acutely infarcted myocardium may change during infarct healing and depend upon the presence of MO. Twenty-five patients underwent CMR on weeks 1 and 8 after reperfused myocardial infarction. After short-axis cine CMR was performed, gadolinium was infused and ceCMR images and matched tagged cine MR images were obtained in the three most dysfunctional short-axis slices on cine CMR. The area and transmural extent of hyperenhancement (HE) with or without MO representing total CD size were planimetered. Between week I and week 8, the CD area fell from 1729 ± 970 mm2 at week 1 to 1270±706 mm2 (p<0.001), as did the transmural extent of infarction (7 1±22% to 63±24%, p<0.001). The decline in CD trended to be higher in patients with MO (840± 807 mm2) than in HE (3 12±485 mm2, p<0.07). In the patient group as a whole, ejection fraction (Eli improved (56±9% to 60± 10%, p=0.002) between weeks I and 8, but patients with MO showed no increase in EF. Segments with some HE demonstrated partial functional improvement whereas no improvement was seen in HE+MO segments. In patients 8 weeks after reperfused myocardial infarction (MI), the size of infarction by ceCMR decreases compared to week 1 post-MI, especially in those with microvascular obstruction in whom there is little improvement in regional or global function. [ABSTRACT FROM AUTHOR]