One-year clinical and angiographic outcome after BES implantation was noninferior to and not different from that after EES implantation in a mostly stable coronary artery disease population. One-year clinical outcome after both BES and EES use was excellent, with a low rate of TLR and extremely low rate of stent thrombosis.

Perindopril and losartan similarly augment BK-induced coronary vasodilation. Perindopril may have a greater potential to enhance the BK-induced coronary release of t-PA than losartan.

938ZHOU J et al. Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jpGenes encoding α-subunits of If channels have 4 members, the hyperpolarization-activated cyclic nucleotide-gated channels 1-4 (termed HCN1-HCN4). 3 HCN1, -2, and -4 are expressed in the heart and brain, and all have 6 transmembrane helices (S1-S6) and a cyclic nucleotide binding domain (cNBD) in the middle of the C-terminus. 3 Similar to other members of voltagegated cation channels, the 4 subunits of the HCN channels most likely form a tetramer. Compared to other HCN isoforms, HCN4 is known to be more abundant in the heart. 7,8 HCN4 mutations are reported to cause familial sick sinus syndrome 9-11 and sporadic cases of sinus nodal dysfunction; 12 however, their relationship with atrioventricular (AV) block remains unknown. We recently identified a novel HCN4 mutation (G1097W) in a Japanese patient with AV block. The functional characterization of reconstituted If channels shows that the HCN4 mutation could predispose to AV nodal dysfunction, which might provide an important insight into the genetic basis for the AV block.he automaticity of heart rhythm is determined by a concerted function of various ion channels, including at least 4 different types of cation channels: 1-4 T-and L-type Ca 2+ channels, K + channels, and the If channels that carries both K + and Na + ions under physiological conditions (relative permeability ratio: PNa/PK=0.2-0.4), 5 thereby producing a reversal potential of approximately -25 mV. If channels flow in an inward depolarizing current in pacemaker cells after the channels are repolarized by the activation of K + channels and they drive the cell membrane potential up to the threshold of Ca 2+ channel activation. The activation of If channels generates the "pacemaker potential" and determines the rate of automaticity in nodal cells. If channel currents are regulated by intracellular cyclic adenosine monophosphate (cAMP) levels. In addition to hyperpolarization, an increase in cAMP accelerates the pacemaker potential rise by shifting the voltage dependence of If channels to a more positive potential. Background: Loss-of-function mutations in the HCN4 gene have been shown to be associated with sinus dysfunction, but there are no reports on HCN4-mediated atrioventricular (AV) block. A novel missense HCN4 mutation G1097W was identified in a 69 year-old Japanese male with AV block, and we characterized the functional consequences of If-like channels reconstituted with the heterozygous HCN4 mutation.

The plasma level of oxLDL is an appropriate surrogate for assessing coronary endothelial-dependent vasomotor function as estimated by responses to BK compared with conventional risk factors for atherosclerosis.

Flow-mediated dilation (FMD) of brachial artery provides a noninvasive assessment of coronary endothelial dysfunction. Acetylcholine (ACh) has been used as an agent for estimating coronary endothelial function. In contrast to ACh, there is no evidence for a relationship between FMD and coronary vasodilation to bradykinin (BK). The aim of this study was to compare the flow-mediated vasodilation of brachial artery with coronary vasomotor responses to intracoronary ACh or BK in patients with an angiographically normal left anterior descending coronary artery. Ninety-one patients underwent the cardiac catheterization examination with coronary endothelial function testing and the brachial ultrasound study. BK (0.2, 0.6, 2.0 microg/min) and ACh (3, 10, 30 microg/min) were administered into the left coronary artery in a stepwise manner. Coronary blood flow was evaluated by the Doppler flow velocity measurement. Coronary diameters were measured by the quantitative coronary angiography. The assessment of endothelial function in the brachial artery was made in response to reactive hyperemia with high-resolution ultrasound. Bradykinin induced dose-dependent increases in epicardial coronary diameter and blood flow. There was a significant positive correlation between FMD- and BK-induced vasodilations of epicardial coronary arteries (0.2 microg/min: r = 0.30; 0.6 microg/min: r = 0.42; 2.0 microg/min: r = 0.44, P < 0.01, respectively) and resistance coronary arteries (0.2 microg/min: r = 0.40; 0.6 microg/min: r = 0.56; 2.0 microg/min: r = 0.59, P < 0.0001, respectively). FMD correlated with ACh-induced vasomotions of resistance but not epicardial coronary arteries. No correlation was seen between nitroglycerin-induced brachial artery vasodilation and BK-induced coronary vasodilation. The endothelial dysfunction of peripheral arteries correlated well with that of the coronary arteries especially vasomotor responses to BK.