Since myocardial perfusion by MDCT is based on the myocardial signal density (SD), it is pivotal to determine the normal values of myocardial SD and to identify potential mechanisms of misinterpretation of perfusion defects. In routine MDCT acquisitions, we commonly visualize a considerable SD drop at the posterobasal wall resembling perfusion defects, being attributed to beam hardening artifacts. Consecutive asymptomatic patients without history of coronary artery disease (CAD) and low probability of CAD who were referred for MDCT evaluation at our institution due to inconclusive or discordant functional tests constituted the study population. Perfusion defects were defined as a myocardial segment having a SD two standard deviations below the average myocardial SD for the 16 left ventricular American Heart Association (AHA) segments. Thirty six asymptomatic patients constituted the study population. Myocardial SD was evaluated in 576 American Heart Association (AHA) segments and 36 posterobasal segments. The mean myocardial SD at the posterobasal segment was 53.5 +/- 35.1 HU, whereas the mean myocardial SD at the basal, mid and apical myocardium was 97.4 +/- 17.3, with significant differences (p < 0.001) between posterobasal and all AHA segments. Posterobasal "perfusion defects" were identified in 26 (72%) patients. The only variable associated to the presence of posterobasal SD deficit was the heart rate (61.8 +/- 6.2 bpm vs. 56.3 +/- 8.1 bpm, p = 0.04), whereas body mass index, blood SD of the left and right ventricles, contrast-to-noise ratio, and the extent of atherosclerosis were not related to the presence of "perfusion defects". In an asymptomatic population with no history of coronary artery disease, a myocardial signal density deficit mimicking a perfusion defect is a common finding in the posterobasal wall and is not related to body mass index or scan quality.

The aim of the study was to explore the differences in plaque burden at different segments of the left main bifurcation and its relationship with the bifurcation angle using high-resolution multislice CT coronary angiography (MSCT). Patients were evaluated using a 40-row MSCT scanner. One observer assessed the localization, severity and distribution of plaques within the left main (LMCA) bifurcation, whereas another observer defined the angle. Fifty patients were included. The mean heart rate was 59.8 +/- 7.1. Seventeen (34%) patients presented at least wall irregularities in the LMCA and in the ostial LCx, whereas the ostial LAD was affected in 32 (64%) patients. More than 90% of plaques were located opposite to the flow divider. The median bifurcation angle was 88.5 degrees (IQR 68.8 degrees, 101.4 degrees). Of the 18 patients with a normal ostial LAD, 13 (72%) had a bifurcation angle < 88.5 degrees , whereas the 63% of the patients with any LAD disease had an angle >or= 88.5 degrees (P = 0.018). In conclusion, at the left main bifurcation, atherosclerotic plaques are commonly located at the ostial LAD and opposite to the flow divider. The angle of the left main bifurcation and the presence of plaques within the bifurcation are closely related.

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Early detection of myocardial viability immediately after primary PCI by the use of DE-MDCT is related to clinical and angiographic parameters of myocardial reperfusion.

The activity of olpadronate labelled with technetium-99m(99mTc) was monitored in plasma and urine samples after single oral (925 MBq 99mTc/10 mg, coadministered with 50 mg cold drug) and intravenous (925 MBq 99mTc/5 mg) administrations to two groups of patients with different rates of bone turnover. The first group comprised high bone turnover (HBTO) patients suffering from Paget's bone disease; the second group comprised patients with normal to low bone turnover (NBTO) having the diagnosis of rheumatoid arthritis and secondary osteoporosis. Kinetic variables were correlated with anthropomorphometric variables, biological markers of bone metabolism and plasma proteins. Data were also obtained after repeatedly dosing the HBTO patients. Additionally, Paget's bone and healthy bone (PB/HB) uptake before and after low-dose oral treatment were assessed by means of scintigraphy. Results showed that most of the kinetic variables did not differ between the two groups of patients, except for a greater Vss and smaller blood area under the curve AUC in the patients with HBTO. After a repeated-dose administration period, the blood AUC activity and Whole Body Retention (WBR) of the HBTO patients tended to be similar to those of the NBTO patients. In both groups, after oral dosing, the Cmax was 20 times lower than the C0.5 after i.v. injection, and the oral bioavailability ranged from 3% to 4%. Finally, the plasma t1/2 beta ranged from 9 to 14 h. Correlation coefficients were obtained from multiple regression analysis; kinetic variables showed very low correlations with anthropomorphometric measurements. In contrast the Vss and WBR were significantly correlated with serum alkaline phosphatase levels and the Vss also with urine hydroxyproline levels. Plasma protein concentration was also correlated with excretion parameters such as CLP and plasma t1/2 beta after an oral dose. Scintigraphic studies in the HBTO group allowed bone selectivity to be seen through skeletal drug uptake. The 15 Pagetic lesions analysed in the HBTO group showed a decrease in PB/HB ratio from 3.8 in the basal study to 2.7 after olpadronate administration for 30 days at the rate of 50 mg/day. In conclusion, the kinetic profile of 99mTc-labelled olpadronate, mainly AUC and WBR, showed a dependence upon bone metabolism and seemed unrelated to body size variables. HBTO patients showed a lower blood AUC but a higher Vss. Both variables may have been reflecting the fact that the drug binds selectively with calcified tissues and, in turn, with the target compartment. Scintigraphy confirmed the labelled-compound bone selectivity as a desirable feature for a bone-scanning agent.