A prospective study approved by the local ethics committee was performed to establish the normal range and reproducibility of myocardial T1 values as assessed with single-breath-hold T1 mapping with high spatial resolution. With a 1.5-T magnetic resonance (MR) imaging system, baseline and contrast material-enhanced modified Look-Locker inversion recovery, or MOLLI, imaging was performed in 15 healthy volunteers who had given written informed consent. Image quality scores and myocardial T1 values were derived for standard short-axis segments and sections. Results were compared with those from a second MR imaging study performed on the same day (baseline only) and those from a third study performed on a different day (baseline and contrast enhanced; eight volunteers). Intra- and interobserver agreement were determined. Myocardial T1 maps were obtained rapidly in a reproducible fashion. A normal range for baseline and postcontrast myocardial T1 was established (baseline mean T1 in short-axis sections, 980 msec +/- 53 [standard deviation]; 95% confidence interval: 964, 997; number of sections, 43). This technique could enable direct quantification of changes in tissue characteristics in ischemic and inflammatory myocardial diseases.

Homologous recombination (HR) deficient cells are sensitive to methyl methanesulfonate (MMS). HR is usually involved in the repair of DNA double-strand breaks (DSBs) in Saccharomyces cerevisiae implying that MMS somehow induces DSBs in vivo. Indeed there is evidence, based on pulsed-field gel electrophoresis (PFGE), that MMS causes DNA fragmentation. However, the mechanism through which MMS induces DSBs has not been demonstrated. Here, we show that DNA fragmentation following MMS treatment, and detected by PFGE is not the consequence of production of cellular DSBs. Instead, DSBs seen following MMS treatment are produced during sample preparation where heat-labile methylated DNA is converted into DSBs. Furthermore, we show that the repair of MMS-induced heat-labile damage requires the base excision repair protein XRCC1, and is independent of HR in both S.cerevisiae and mammalian cells. We speculate that the reason for recombination-deficient cells being sensitive to MMS is due to the role of HR in repair of MMS-induced stalled replication forks, rather than for repair of cellular DSBs or heat-labile damage.

T 1 maps obtained with modified Look-Locker inversion recovery (MOLLI) can be used to measure myocardial T 1 . We aimed to evaluate the potential of MOLLI T 1 mapping for the assessment of acute and chronic myocardial infarction (MI). A total of 24 patients with a first MI underwent MRI within 8 days and after 6 months. T 1 mapping was performed at baseline and at selected intervals between 2-20 min following administration of gadopentetate dimeglumine (Gd-DTPA). Delayed-enhancement (DE) imaging served as the reference standard for delineation of the infarct zone. On T 1 maps the myocardial T 1 relaxation time was assessed in hyperenhanced areas, hypoenhanced infarct cores, and remote myocardium. The planimetric size of myocardial areas with standardized T 1 threshold values was measured. Acute and chronic MI exhibited different T 1 changes. Precontrast threshold T 1 maps detected segmental abnormalities caused by acute MI with 96% sensitivity and 91% specificity. Agreement between measurements of infarct size from T 1 mapping and DE imaging was higher in chronic than in acute infarcts. Precontrast In present imaging techniques for in vivo infarct sizing, such as cardiac magnetic resonance (CMR) and singlephoton emission computed tomography (SPECT), the viewing window (i.e., the range of gray/color values to be selected for viewing) is determined arbitrarily before reporting, and thus requires a subjective preassessment of the images.In CMR the delayed-enhancement (DE) method produces high contrast between infarcted and noninfarcted myocardium (bright ϭ dead). The observable high contrast is reliant upon the imaging strategy employed. A preparatory inversion-recovery pulse in a T 1 -weighted gradientecho sequence nulls signal from noninfarcted myocardium, while infarcted myocardium, which retains a higher concentration of a gadolinium (Gd)-based extracellular contrast agent, returns higher signal due to its reduced spin-lattice relaxation time (T 1 time) (1). The contrast between infarcted and noninfarcted areas on the resulting images is therefore enhanced over and above the underlying physical differences in T 1 relaxation properties between these areas. The apparent degree of enhancement is dependent on the effectiveness of the nulling process, which is a function of the inversion time (TI) selected for the preparation pulse. Incomplete nulling will cause reduced contrast and create significant variation in the signal of remote myocardium, which is used as the reference to determine the threshold between infarcted and noninfarcted myocardium (2). The choice of TI therefore ultimately influences the infarct size as measured with DE techniques.T 1 -mapping CMR techniques circumvent the influences of windowing and variations in signal enhancement by directly measuring the underlying T 1 relaxation times of the different areas of the myocardium. At a given magnetic field strength, each tissue has a normal range for spinlattice T 1 relaxation time (3,4), much like the normal ranges of tissue X-ray attenuation in c...

Abstract-ECG criteria for left ventricular hypertrophy (LVH) were mostly validated using left ventricular mass (LVM) as measured by M-mode echocardiography. LVM as measured by cardiac MRI has been demonstrated to be much more accurate and reproducible. We reevaluated the sensitivity and specificity of 4 ECG criteria of LVH against LVM as measured by cardiac MRI. Patients with systemic hypertension (nϭ288) and 60 normal volunteers had their LVM measured using a 1.5-Tesla MRI system. A 12-lead ECG was recorded, and 4 ECG criteria were evaluated: Sokolow-Lyon voltage, Cornell voltage, Cornell product, and Sokolow-Lyon product. Based on a cardiac MRI normal range, 39.9% of the hypertensive males and 36.7% of the hypertensive females had elevated LVM index. At a specificity of 95%, the Sokolow-Lyon product criterion had the highest sensitivity in females (26.2%), the Cornell criterion had the highest sensitivity in males (26.2%), and the Cornell product criteria had a relatively high sensitivity in both males and females (25.0% and 23.8%). Receiver operating characteristic curves showed the Cornell and Cornell product criteria to be superior for males whereas the Sokolow-Lyon product criterion was superior for females. Comparing the mean LVM index values of the subjects who were ECG LVH positive to the normal volunteers indicated that the ECG LVH criteria detect individuals with an LVM index substantially above the normal range. We have redefined the partition values for 4 different ECG LVH criteria, according to gender, and found that they detect subjects with markedly elevated LVM index.