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Advances in coronary intervention have increased the opportunity to intervene on complex lesions, resulting in an increase in PCI-related complication, including coronary artery perforation. However, treatment options for coronary perforation are limited, with delivery of devices to complex lesions being problematic. Balloon hemostasis is the usual bailout method, despite the risk of myocardial ischemia. In this report, we describe an over-the-wire balloon method to treat a patient with coronary perforation. Ischemia was avoided by injecting autologous blood through the catheter, while hemostasis was achieved by prolonged balloon inflation. This new technique is applicable when a perfusion balloon is not indicated.

Increase in cerebrospinal fluid (CSF) Na(+) concentration ([Na(+)]) precedes hypertension and is a key step in the development of salt-induced hypertension. In the choroid plexus (CP), epithelial Na(+) channels (ENaCs) have an important role in Na(+) transport from the blood into the CSF. However, it remains unknown whether the mineralocorticoid receptors (MR)/ENaCs pathway in the CP of stroke-prone spontaneously hypertensive rats (SHRSP) is involved in neural mechanisms of hypertension. Therefore, we examined the role of the MR/ENaCs pathway in the CP in the development of hypertension in SHRSP associated with an increase in CSF [Na(+)]. As a marker of MR activation, serum/glucocorticoid-inducible kinase 1 (Sgk1) expression levels in the CP were measured and found to be greater in SHRSP than in Wistar-Kyoto (WKY) rats. CSF [Na(+)] levels were also higher in SHRSP than in WKY rats. In SHRSP, high-salt intake (8%) increased blood pressure and urinary norepinephrine excretion compared with those in animals fed a regular salt diet (0.5%) for 2 weeks. Furthermore, the expression levels of MR, Sgk1 and ENaCs in the CP and the increase in CSF [Na(+)] were greater in SHRSP fed a high-salt diet than in those fed a regular salt diet. These alterations were attenuated by intracerebroventricular infusion of eplerenone (10 μg kg(-1) per day), except for α-ENaC and β-ENaC. We conclude that activation of the MR/ENaCs pathway in the CP contributes to hypertension via an increase in CSF [Na(+)], thereby exaggerating salt-induced hypertension with sympathetic hyperactivation in SHRSP.

Mineralocorticoid receptor (MR) is recognized as a target for therapeutic intervention in hypertension and heart failure. MRs in the central nervous system are thought to have an important role in blood pressure regulation. Thus, we examined whether activation of the MR pathway in the rostral ventrolateral medulla (RVLM) of the brainstem contributes to the neural mechanism of hypertension in stroke-prone spontaneously hypertensive rats (SHRSPs). We microinjected eplerenone, aldosterone or Na(+)-rich artificial cerebrospinal fluid (aCSF) into the RVLM of anesthetized Wistar-Kyoto (WKY) rats and SHRSPs. Arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded. The expressions of the MR protein and the serum- and glucocorticoid-regulated kinase protein (Sgk1), which is a marker of MR activity, in the RVLM were measured by western blot analysis. Bilateral microinjection of eplerenone into the RVLM decreased AP and RSNA in WKY rats and SHRSPs, and the decreases in those variables were significantly greater in SHRSPs than WKY rats. Microinjection of aldosterone or Na(+)-rich aCSF into the RVLM increased AP and RSNA dose-dependently. The increases in those variables were significantly greater in SHRSPs than in WKY rats. The pressor responses of aldosterone or Na(+)-rich aCSF were attenuated by the prior injection of eplerenone in SHRSPs. Sgk1 expression levels in the RVLM were significantly greater in SHRSPs than in WKY rats. These findings suggest that activation of MRs in the RVLM enhances sympathetic activity, thereby contributing to the neural mechanism of hypertension in the SHRSP.

An 80-year-old woman was admitted to our emergency department with ongoing dyspnea for 2 weeks. The patient was immediately intubated endotracheally because of the hypoxia with flush pulmonary edema. Electrocardiogram showed ST depression and echocardiogram showed hypokinesis of anterior left ventricular wall with poor systolic function. Also her cardiac enzymes were elevated, emergency coronary angiogram was performed from radial artery because both femoral arteries were not fully palpable. Coronary angiogram showed three vessels disease including chronic total occlusion of right coronary artery and left main bifurcation lesion. Also blood flow of left anterior descending coronary artery was delayed. Acute coronary syndrome was the cause of acute heart failure and revascularization was needed but aortography revealed total occlusion of infrarenal aorta. Patient was relatively hemodynamically stable; we planned treating total occlusion of infrarenal aorta with endovascular therapy to maintain a rout for cardiopulmonary support system. With bi-directional approach from both femoral artery and left brachial artery, occlusion site with heavy calcification was finally passed through by guide wire from retrograde approach. After pull-through technique, self-expanding nitinol stent was implanted after pre dilation with small balloon. Considering her EURO score, supposed perioperative mortality was high, percutaneous coronary intervention was performed. A 7 fr sheath was inserted from right femoral artery and intra-aortic balloon pump was inserted from left femoral artery. Sirolimus-eluting stent was implanted to left circumflex artery and also from ostium of left main to mid left anterior descending coronary artery after using an atherectomy device. After successful revascularization, patient became hemodynamically stable and weaning off the respirator was successful. Reporting case achieved successful revascularization to severe coronary artery disease after endovascular recanalization with infrarenal aortic occlusion.

This paper presents a closed-form solution to the sag of the Cartesian oval and an alternate iterative method for obtaining the sag. The emphasis is in providing a methodology for determining the sag and derivatives of a Cartesian surface for optical design, ray-tracing purposes. We verify our results by comparison of our solutions and by real ray tracing.

To investigate the long-term outcome of Percutaneous transluminal intervention (PCI) for chronic total occlusion (CTO). The subjects were 606 patients (1,145 lesions) who were treated for CTO between January 1996 and December 2003 at our institution. Among them, 436 patients with early success and confirmed patency at the CTO by follow-up coronary angiography after 6 months were classified as the patent group (Group P), while 170 patients without early success or with occlusion on follow-up angiography were classified as the occluded group (Group O). In April 2006 (mean: 660 ± 602 days), the outcome of CTO was investigated and the major adverse cardiac events (MACE)-free rate was calculated. Multivariate analysis was performed to identify determinants of death. The early success rate was 76.4% before 2003 when Conquest guidewires were not available. However, it subsequently showed significant improvement to 89%. The cumulative survival rate was significantly higher for Group P (92%) than for Group O (64%) and the MACE-free rate (free from, death, bypass surgery, myocardial infarction, and revascularization) showed a similar trend. The cumulative survival rate of patients without myocardial viability in the territory of the vessel with CTO was significantly higher for Group P (88%) than for Group O (55%). The outcome was significantly worse for patients with occlusion of other vessels (90%) than for patients without additional occlusion (42%). It was significantly better when the left ventricular ejection fraction (LVEF) was ≥40% than when the LVEF was ≤40% (90 vs. 68%). Multivariate analysis identified occluded CTO, other vessel occlusion, low ejection fraction (EF), unimproved EF, and old age as determinants of death from CTO. If early success is obtained and patency is maintained, the long-term outcome after PCI for CTO is significantly better than when failure occurs Occluded CTO, other vessel occlusion, low EF, unimproved EF, and old age are important determinants of the outcome.