The PCr recovery time constant is prolonged in patients with symptomatic PAD compared with normal subjects. The method is reproducible and may be useful in the identification of disease. Further study of this parameter's ability to track response to therapy as well as its prognostic capability is warranted.
Purpose:To develop a contrast-enhanced magnetic resonance (MR) technique to measure skeletal muscle perfusion in peripheral arterial disease (PAD).
Materials and Methods:A total of 11 patients (age ϭ 61 Ϯ 11 years) with mild to moderate symptomatic PAD (anklebrachial index [ABI] ϭ 0.75 Ϯ 0.08) and 22 normals were studied using an MR-compatible ergometer. PAD and normal max (Nl max ; N ϭ 11) exercised to exhaustion. Nl low (N ϭ 11) exercised to the same workload achieved by PAD. At peak exercise, 0.1 mm/kg of gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) was infused at 3-4 cm 3 / second followed by a saline flush at the same rate. A dualcontrast gradient echo (GRE) sequence enabled simultaneous acquisition of muscle perfusion and arterial input function (AIF). The perfusion index (PI) was defined as the slope of the time-intensity curve (TIC) in muscle divided by the arterial TIC slope.
Results
Conclusion:Peak-exercise measurement of lower limb perfusion with dual-contrast, first-pass MR distinguishes PAD from normals. This method may be useful in the study of novel therapies for PAD.
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 cm 3 . 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.
BACKGROUND and OBJECTIVES-The study was designed to determine the prevalence of extracardiac findings discovered during multidetector computed tomography (MDCT) examinations prior to atrial fibrillation ablation. MDCT has become a valuable tool in detailing left atrial anatomy prior to catheter ablation. The incidence of extracardiac findings has been reported for electron beam CT calcium scoring (EBCT) and coronary MDCT, but no data exists for the prevalence of extracardiac findings discovered prior to atrial fibrillation ablation with MDCT.
Because of its safety, accuracy, ease of interpretation, and increasing availability, cardiac magnetic resonance-based assessment of myocardial viability has quickly transitioned from bench to bedside. Routine clinical implementation has prompted improved diagnostic capabilities and easier image interpretation. As a research tool, cardiac magnetic resonance continues to provide valuable insights into the fundamental nature of viability.
Angiotensin II type 2 receptor (AT(2)R) overexpression (AT(2)TG) attenuates left ventricular remodeling in a mouse model of anterior myocardial infarction (MI). We hypothesized that the beneficial effects of cardiac AT(2)TG are mediated via the bradykinin subtype 2 receptor (B(2)R). Fourteen transgenic mice overexpressing the AT(2)R (AT(2)TG mice), 10 mice with a B(2)R deletion (B(2)KO mice), 13 AT(2)TG mice with B(2)R deletion (AT(2)TG/B(2)KO mice), and 11 wild-type (WT) mice were studied. All mice were on a C57BL/6 background. Mice were studied by cardiac magnetic resonance imaging at baseline and days 1, 7, and 28 after MI induced by 1 h of occlusion of the left anterior descending artery followed by reperfusion. Short-axis images from apex to base were used to compare ventricular volumes and ejection fraction (EF). At baseline, end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) were lower and EF higher in AT(2)TG mice compared with the other three strains. Infarct size was similar between groups. No differences were observed in global remodeling parameters at day 28 between AT(2)TG and AT(2)TG/B(2)KO mice; however, EDVI and ESVI were lower and EF higher in both transgenic groups than in WT or B(2)KO mice. Both strains lacking B(2)R demonstrated increased collagen content and less hypertrophy in adjacent noninfarcted regions at day 28. Attenuation of postinfarct remodeling by overexpression of AT(2)R is not directly mediated via a B(2)R pathway. However, B(2)R does appear to have a role in the smaller cavity size and hyperdynamic function observed at baseline in AT(2)TG mice and in limiting collagen deposition during postinfarct remodeling.
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