Interventricular Septal Hematoma after Retrograde Intervention for a Chronic Total Occlusion of a Right Coronary Artery: Echocardiographic and Magnetic Resonance Imaging—Diagnosis and Follow-Up

The reverse CART technique provides the potential to modify the retrograde procedure by improving the controlled movement of the retrograde wire and improve the success rates of percutaneous coronary intervention (PCI) of chronic total occlusion (CTO). Development of interventricular hematoma is a rare complication of CTO PCI. A 63-year-old man with effort angina with a right coronary artery CTO lesion underwent PCI by retrograde approach from the LAD to a septal branch. A contrast “stain” was demonstrated surrounding the septal collateral channel used for the retrograde approach at the end of the procedure without symptom. Echocardiography indicated an increased interventricular septum thickness with low echo signals region and decreased contractility. Cardiac magnetic resonance (CMR) imaging using gadolinium showed a diffusely thickened septum with a low signal fusiform neocavitation delimited by an enhanced-signal ring suggesting intraventricular septal dissecting hematoma. After conservative treatment, follow-up echocardiogram and CMR showed the resolution of the hematoma without clinical events. This case highlights the potentially lethal complication of septal perforator dissection and hematoma that may cause severe myocardial injury caused by retrograde approach for CTO PCI

Amyloid beta induces neuronal cell death through ROS-mediated ASK1 activation

Amyloid beta (Abeta) is a main component of senile plaques in Alzheimer\u27s disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in Abeta-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in Abeta-induced neuronal cell death. Abeta activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly, ASK1-/- neurons were defective in Abeta-induced JNK activation and cell death. These results indicate that ROS-mediated ASK1 activation is a key mechanism for Abeta-induced neurotoxicity, which plays a central role in Alzheimer\u27s disease

Peeled Guidewire Coating with Debulked Plaque Obtained by Directional Coronary Atherectomy

Percutaneous directional coronary atherectomy (DCA) is a plaque debulking method performed in Japan, and recently a renewed DCA device has been launched. We present a case with a tight left anterior descending lesion undergoing percutaneous coronary intervention with application of DCA. After several sessions of DCA, white plaques accompanied by green, stringed materials were obtained from the device; some materials were considerably long (approximately 15 mm in length). A drug-eluting stent was subsequently implanted, and the procedure was completed successfully without any complications. The extracted plaques and artificial materials were pathologically examined, and no inflammatory changes were detected on plaques adjacent to the material. Assessing pathological findings and structure of the DCA catheter, the obtained artificial materials were considered as peeled guidewire, possibly resulting from the friction between the guidewire and metallic bearing in the housing of DCA catheter. Of note, this phenomenon has been recognized even in other DCA cases in which guidewires of the other kind are used. We report this phenomenon for the first time, warning of theoretically possible distal embolization of artificial materials caused by any debulking devices

Low-intensity pulsed ultrasound enhances angiogenesis and ameliorates contractile dysfunction of pressure-overloaded heart in mice

<div><p>Introduction</p><p>Chronic left ventricular (LV) pressure overload causes relative ischemia with resultant LV dysfunction. We have recently demonstrated that low-intensity pulsed ultrasound (LIPUS) improves myocardial ischemia in a pig model of chronic myocardial ischemia through enhanced myocardial angiogenesis. In the present study, we thus examined whether LIPUS also ameliorates contractile dysfunction in LV pressure-overloaded hearts.</p><p>Methods and results</p><p>Chronic LV pressure overload was induced with transverse aortic constriction (TAC) in mice. LIPUS was applied to the whole heart three times in the first week after TAC and was repeated once a week for 7 weeks thereafter (n = 22). Animals in the control groups received the sham treatment without LIPUS (n = 23). At 8 weeks after TAC, LV fractional shortening was depressed in the TAC-Control group, which was significantly ameliorated in the TAC-LIPUS group (30.4±0.5 vs. 36.2±3.8%, P<0.05). Capillary density was higher and perivascular fibrosis was less in the LV in the TAC-LIPUS group than in the TAC-Control group. Myocardial relative ischemia evaluated with hypoxyprobe was noted in the TAC-Control group, which was significantly attenuated in the TAC-LIPUS group. In the TAC-LIPUS group, as compared with the control group, mRNA expressions of BNP and collagen III were significantly lower (both P<0.05) and protein expressions of VEGF and eNOS were significantly up-regulated associated with Akt activation (all P<0.05). No adverse effect related to the LIPUS therapy was noted.</p><p>Conclusions</p><p>These results indicate that the LIPUS therapy ameliorates contractile dysfunction in chronically pressure-overloaded hearts through enhanced myocardial angiogenesis and attenuated perivascular fibrosis. Thus, the LIPUS therapy may be a promising, non-invasive treatment for cardiac dysfunction due to chronic pressure overload.</p></div

Intracellular signaling pathways for the beneficial effects of the LIPUS.

<p>The LIPUS therapy ameliorates cardiac contractile dysfunction by enhancing angiogenesis through up-regulation of VEGF, eNOS and p-Akt and attenuating perivascular fibrosis through down-regulation of collagen III in the LV, suppressing the transition from compensated LVH to decompensated HF.</p

The LIPUS therapy ameliorates cardiac contractile dysfunction.

<p>(A) Representative echocardiographic images at 8 weeks after TAC. (B~G) Graphs showing the time course of anterior wall thickness (AWT) and posterior wall thickness (PWT) of the LV, LV dimension at end-diastole (LVDd), LVD at end-systole (LVDs), LV fractional shortening (LVFS), and LV ejection fraction (LVEF). Results are expressed as mean±SD. n.s., not statistically significant. Statistical analysis was performed at 8 weeks after TAC.</p

Study protocol.

<p>(A) Study protocol. LIPUS was applied to the whole heart three times in the first week after TAC and was thereafter repeated once a week for 7 weeks in the LIPUS group, while the control group underwent the same procedures but without the LIPUS therapy. (B) Study setup. (C) Peak flow velocity at TAC. (D) Heart weight/body weight (HW/BW). (E) Lung weight /body weight (LW/BW). Results are expressed as mean±SD.</p

The LIPUS therapy activates the angiogenic signaling pathways.

<p>Protein levels of VEGF and eNOS, phosphorylation state of eNOS (Ser1177), Akt and ERK1/2, and protein levels of CD31 (n = 3, 3, 6, 6 for each group). Results are expressed as mean±SD.</p