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The relationship between preexisting atherosclerotic lesion characteristics and neointimal thickness after second-generation drug-eluting stent (DES) placement is still unknown. Thus, we evaluated that relationship using optical coherence tomography (OCT).A single-center, retrospective, observational study was conducted. Patients with stable angina or asymptomatic myocardial ischemia who received percutaneous coronary intervention for a de novo lesion using a second-generation DES under frequency domain OCT guidance and underwent follow-up coronary angiography (CAG) and OCT between December 2010 and December 2015 were included. The relationship between the neointimal thickness on the stent strut and the plaque characteristics was retrospectively evaluated using OCT immediately after stent implantation and at the time of follow-up CAG.We analyzed 3459 struts from 20 stents in 15 patients. The mean follow-up period was 264 days. In the follow-up study, no angiographic in-stent restenosis was found. Of the 3459 struts, 3315 (95.8%) were covered with neointima. The median neointimal thicknesses of the stent struts on calcified, fibrous, and lipid-rich lesions were 20 μm (interquartile range [IQR], 10-50 μm), 70 μm (40-140 μm; P < .001), and 90 μm (50-170 μm; P < .001), respectively. These differences were observed regardless of the type of second-generation DES used.Most of the stent struts were covered with neointima. The neointimal thickness after the second-generation DES implantation had a close relationship with the preexisting atherosclerotic lesion characteristics. In this study, we found differences in arterial healing processes due to underlying plaque; therefore, evaluating the lesion characteristics by OCT may predict the risk for future restenosis and thrombosis.

Aims: Although right ventricular septal pacing is thought to be more effective in minimizing pacing-induced left ventricular dysfunction, the accurate way to anchor the lead to the right ventricular septum (RVS) has not been established. Our aim was to clarify the usefulness of right ventriculography (RVG) to aid accurate anchoring of the lead to the RVS., Methods and Results: Eighty-four patients who underwent pacemaker implantation were enrolled. We anchored the lead to the RVS by using an RVG image obtained at a 30° right anterior oblique view as a reference. We confirmed the actual lead position by performing computed tomography after the procedure and examined the characteristics of the paced QRS complex. Of the 81 patients, except 3 patients whose leads were anchored to the apex due to high pacing thresholds in the RVS, the leads were successfully anchored to the RVS in the 79 (98%) patients, and the number of leads placed in the high-, mid-, and low-RVS was 3 (4%), 58 (73%), and 18 (23%), respectively. The paced QRS duration in these 79 patients was 140 ± 13 ms. The paced QRS duration from mid-RVS was considerably narrower than that from high- or low-RVS (137 ± 12 ms vs. 146 ± 12 ms; P = 0.012)., Conclusion: Right ventriculography was very useful in aiding accurate anchoring of the lead to the RVS. Further, pacing from mid-RVS may be more effective in minimizing the QRS duration than pacing from other RVS sites.

Pheochromocytoma multisystem crisis is a rare and life-threatening disease that is associated with numerous symptoms and which is also difficult to diagnose. We herein report an autopsy case of a 61-year-old man who died due to pheochromocytoma multisystem crisis. The patient complained of vomiting and breathlessness. Computed tomography showed a shadow-like region with a similar appearance to interstitial pneumonia. The patient was diagnosed with takotsubo cardiomyopathy induced by severe lung disease based on the results of echocardiography and coronary angiography. The patient was treated for interstitial pneumonia. However, his condition rapidly deteriorated and he died 6 hours after arrival. We were later informed of his extremely high catecholamine serum levels. We found pheochromocytoma with hemorrhage at autopsy. The patient's lungs showed acute passive congestion with edema and extravasation.

Although SPE-39 is a binding protein to Vps33B that is one of the subunit in the mammalian HOPS complex, the elements of SPE-39 function remain unknown. Here, we show that tyrosine phosphorylation of SPE-39 following EGF stimulation plays a role in the stability of SPE-39 itself. Ubiquitination of the C-terminal region of SPE-39 was also elevated in response to EGF stimulation, and this process was regulated by the phosphorylation of Tyr-11 in SPE-39. However, association of Vps33B with SPE-39 inhibited the elevation of ubiquitination of SPE-39 following EGF stimulation, which might be responsible for the stabilization of SPE-39. Furthermore, an opposing functional relationship between SPE-39 and Vps33B on the downregulation of the EGF receptor was observed in EGF-stimulated COS-7 cells., (Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.)

Background: Microvascular damage immediately after reperfusion therapy is an independent predictor of left ventricular function in patients with acute myocardial infarction (AMI). However, its recovery may vary among individuals and the relationship between convalescent stage microvasculature and late myocardial morphologic change is unclear., Methods and Results: Patients treated with coronary angioplasty within 12 h of their first anterior AMI were enrolled in this study. Coronary flow reserve (CFR) was measured 3 weeks post AMI, in both branches of the left coronary artery: culprit (left anterior descending artery: LAD) and non-culprit (left circumflex artery: LCX). Left ventriculography was performed at 3 weeks and 6 months post AMI and compared. Seventeen patients showed abnormal CFR in the LAD (Group 1: CFR<2), whereas 20 patients showed normal CFR (Group 2: CFR >/=2). Percent changes of end-diastolic volume tended to be higher in Group 1 than in Group 2 (11.8+/-21.6% vs -1.3+/-14.4%, p=0.056), and %changes of end-systolic volume was significantly smaller in Group 2 (11.8+/-22.1% vs -8.7+/-25.1%, p<0.05). A statistically significant correlation was found between absolute and relative CFR in the LAD and %change of end-systolic volume (r=-0.58: p<0.001, and r=0.40: p<0.05, respectively)., Conclusions: Microvascular function in the convalescent stage may be related to these favorable changes.

A 63-year-old man presented with subclavian steal syndrome associated with left internal mammary artery (IMA) bypass graft to a coronary artery. He was admitted with a history of oppressive sensation in the chest, dizziness, and light headedness on exertion for 2 weeks in March 2002. He had undergone myocardial revascularization consisting of a left IMA-to-left anterior descending coronary artery graft in April 1988. His blood pressure was 140/70 mmHg in the right arm and 80/64 mmHg in the left arm. Aortic arch arteriography revealed complete occlusion of the left subclavian artery proximal to the left IMA takeoff and subclavian steal with anterograde flow of the left IMA. Percutaneous angioplasty and stent placement with protection of the left IMA bypass graft using a balloon catheter was successfully performed without complication by cerebral or myocardial ischemia. Complete recanalization of the occluded left subclavian artery and anterograde flow of the left vertebral artery were achieved. His symptoms disappeared and blood pressure in the left arm recovered. This variant of coronary subclavian steal might require protection of the left IMA during angioplasty and stent placement.

Hepatocyte growth factor (HGF) is a well-known powerful proliferative factor of vascular endothelial cells and it has been reported that plasma HGF concentrations are increased in acute myocardial infarction (AMI), although the mechanisms are not yet well delineated. Serum HGF levels and C-reactive protein (CRP) were measured in 22 patients with unstable angina pectoris (UAP) (15 males, 7 females; class IIb or IIIb of the Braunwald classification), 60 patients with AMI (37 males, 23 females; average time from the onset of symptoms to admission 4.6+/-0.7h, range, 0.5-12h), and 20 normal subjects. Immediate angioplasties were performed in 51 patients with AMI, and the time course of the HGF levels were measured in 31 patients among them. Heparin dramatically increased the HGF level and it declined to the normal range 18h after heparin injection. Blood samples were taken before heparin treatment, or at least 24h after. Serum HGF levels on admission was significantly increased in UAP (mean+/-SE: 0.30+/-0.03ng/ml, p<0.01), and AMI (0.27+/-0.02ng/ml, p<0.01) compared with the normal subjects (0.19+/-0.01 ng/ml). Even in the early stage (within 3 h of onset of symptoms to admission, average time was 1.8+/-0.1 h), serum HGF levels were already elevated (0.25+/-0.02 ng/ml, p<0.05). There was no significant difference between the HGF levels in UAP and AMI. Fifty-one of the 60 patients with AMI underwent immediate percutaneous transluminal coronary angioplasty and blood samples were obtained from 31 of them on days 7, 14, and 21 after MI. Serum HGF levels peaked on day 7 (0.34+/-0.04ng/ml, p<0.01) and there was a weak relationship between peak creatine kinase and serum HGF levels at that time. A statistically significant correlation was found between peak CRP and serum HGF levels on day 7 (r=0.62: p<0.001). Serum HGF levels decreased to nearly normal by day 21 (0.22+/-0.01 ng/ml). The study shows that serum HGF levels during the early stage of AMI increased significantly and peaked by day 7 after the onset, at which time there was a strong correlation with peak CRP levels. These data suggest that HGF production may be related to the inflammatory response in AMI.