ABSTRACT
OBJECTIVE: To develop a new method for the cardiac MR (CMR) quantification of peri-infarct ischaemia using fused perfusion and delayed-enhanced images and to evaluate this method using quantitative single photon emission CT (SPECT) imaging as a reference. METHODS: 40 patients presenting with peri-infarct ischaemia on a routine stress (99m)Tc-SPECT imaging were recruited. Within 8 days of the SPECT study, myocardial perfusion was evaluated using stress adenosine CMR. Using fused perfusion and delayed-enhanced images, peri-infarct ischaemia was quantified as the percentage of myocardium with stress-induced perfusion defect that was adjacent to and larger than a scar. This parameter was compared with both the percent myocardium ischaemia (SD%) and the ischaemic total perfusion deficit (TPD). The diagnostic performance of CMR in detection of significant coronary artery stenosis (of ≥70%) was also determined. RESULTS: On SPECT imaging, in addition to peri-infarct ischaemia, reversible perfusion abnormalities were detected in a remote zone in seven patients. In the 33 patients presenting with only peri-infarct ischaemia, the agreement between CMR peri-infarct ischaemia and both SD% and ischaemic TPD was excellent [intraclass coefficient of correlation (ICC) = 0.969 and ICC = 0.877, respectively]. CMR-defined peri-infarct ischaemia for the detection of a significant coronary artery stenosis showed an areas under receiver-operating characteristic curve of 0.856 (95% confidence interval, 0.680-0.939). The best cut-off value was 8.1% and allowed a 72% sensitivity, 96% specificity, 60% negative predictive value and 97% positive predictive value. CONCLUSION: This proof-of-concept study shows that CMR imaging has the potential as a test for quantification of peri-infarct ischaemia. ADVANCES IN KNOWLEDGE: This study demonstrates the proof of concept of a commonly known intuitive idea, that is, evaluating the peri-infarct ischaemic burden by subtracting delayed enhancement from first-pass perfusion imaging on CMR.
Subject(s)
Magnetic Resonance Imaging/methods , Myocardial Ischemia/diagnosis , Myocardial Perfusion Imaging/methods , Tomography, Emission-Computed, Single-Photon/methods , Adult , Aged , Aged, 80 and over , Coronary Angiography , Female , Humans , Image Enhancement/methods , Male , Middle Aged , Myocardial Infarction/complications , Myocardial Ischemia/etiology , Prospective Studies , ROC Curve , Sensitivity and SpecificityABSTRACT
We have characterized a new gene, SWI1, involved in sister chromatid cohesion during both male and female meiosis in Arabidopsis thaliana. A first allele, swi1.1, was obtained as a T-DNA tagged mutant and was described previously as abnormal exclusively in female meiosis. We have isolated a new allele, swi1.2, which is defective for both male and female meiosis. In swi1.2 male meiosis, the classical steps of prophase were not observed, especially because homologs do not synapse. Chromatid arms and centromeres lost their cohesion in a stepwise manner before metaphase I, and 20 chromatids instead of five bivalents were seen at the metaphase plate, which was followed by an aberrant segregation. In contrast, swi1.2 female meiocytes performed a mitotic-like division instead of meiosis, indicating a distinct role for SWI1 or a different effect of the loss of SWI1 function in both processes. The SWI1 gene was cloned; the putative SWI1 protein did not show strong similarity to any known protein. Plants transformed with a SWI1-GFP fusion indicated that SWI1 protein is present in meiocyte nuclei, before meiosis and at a very early stage of prophase. Thus, SWI1 appears to be a novel protein involved in chromatid cohesion establishment and in chromosome structure during meiosis, but with clear differences between male and female meiosis.
