Comparison of 320-row computed tomography coronary angiography with conventional angiography for the assessment of coronary artery disease with different atherosclerotic plaque characteristics.

OBJECTIVE: The objective of this study was to compare the accuracy of 320-row computed tomography angiography (CTA) with conventional coronary angiography. METHODS: Two hundred seventy-four patients with coronary artery disease who received both invasive coronary angiography and 320-row CTA were included. Stenosis of 50% or greater was considered obstructive. RESULTS: In patient-based analysis, accuracy of CTA was 89.4%, with sensitivity of 94.6% and specificity of 54.3%. In segment-based analysis, the overall (4110 segments) accuracy of CTA was 90.7%, with sensitivity of 66.5% and specificity of 95.8%. For the segments with plaques (1191 segments), accuracy of CTA was 80.1%, with sensitivity of 83.5% and specificity of 77.0%. For segments with no plaque (2919 segments), accuracy of CTA was 95.0%, with sensitivity of 0.7% and specificity of 100.0%. For the segments with stents (110 segments), the accuracy of CTA was 86.4%. CONCLUSIONS: A 320-row CTA has potential to detect coronary lesions with soft and intermediate plaques.

Cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate and nordihydroguaiaretic acid inhibit human Kv1.5 currents independently of lipoxygenase.

In humans, Kv1.5 (hKv1.5) channels conduct the ultra-rapid delayed rectifier K(+) current (I(Kur)) that is important for the repolarization of cardiac action potentials. We aimed at examining the effect of lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (CDC), nordihydroguaiaretic acid (NDGA), and gossypol on hKv1.5 wild-type and mutant channels heterologously expressed in Chinese hamster ovary (CHO) cells, by use of the site-directed mutagenesis and whole-cell patch-clamp method. CDC and NDGA, but not gossypol, a structurally dissimilar inhibitor, reversibly inhibited hKv1.5 current in a concentration-dependent manner with IC(50) of 5.7 microM and 16.4 microM, respectively. The blockade evoked by both drugs was voltage-dependent between -20 and +10 mV (voltage range of channel opening). Moreover, this blocking action was found to progress with time during depolarizing voltage steps with a more rapid block at higher concentrations. CDC induced slight but significant delay of the deactivation rate. However, NDGA markedly slowed the deactivation time course, resulting in a tail crossover phenomenon. The recovery time constants from current block at repolarizing potentials for CDC and NDGA were 60.9 ms and 129.7 ms, respectively. Mutation of arginine 487 to valine (R487V) in the outer pore region of the channel significantly reduced the CDC action. These results demonstrate for the first time that CDC and NDGA block hKv1.5 channels by binding to the open state of the channels, independently of their effects on lipoxygenase activity. The putative binding site for CDC appears to be related to arginine 487 located in the outer pore region.