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Biomedical subjects

Noriyuki Tabuchi

Publications and source records attributed to Noriyuki Tabuchi.

21 records · Page 2Linked to original sources

Temporary and permanent biventricular pacing via left ventricular epicardial leads implanted during primary cardiac surgery.

OBJECTIVES: Biventricular pacing (BVP) is a new strategy for treating patients with severe congestive heart failure (CHF) and intraventricular conduction delay, but its full potential and technicalities of BVP require further evaluation. We evaluated BVP benefits in 4 patients in whom we implanted a left ventricular lead during primary cardiac surgery. METHODS: Four CHF patients treated surgically between October 2000 and August 2001 underwent, at primary surgery, the implantation of leads in the right atrium, right ventricle, and left ventricle (LV) for postsurgical BVP. All patients had severe LV dysfunction and dilatation with intraventricular conduction delay. Surgeries involved CABG alone (n = 1), CABG + Dor's operation (n = 2), and tricuspid valve replacement + Maze procedure (n = 1). BVP was begun immediately after surgery in all 4 patients. Hemodynamic variables with BVP were compared to those without BVP for each patient, and the utility and technical aspects of implantation were evaluated. RESULTS: BVP increased mean systemic blood pressure by 11% and mean LV stroke work index by 19% in the acute postsurgery period, and reduced mitral regurgitation. Two of the patients were implanted with a generator for permanent BVP, one at 1 month and the other at 6 months after surgery. The threshold of the LV epicardial lead of these 2 patients was below 2 V during follow-up, and BVP was successful. CONCLUSIONS: Temporary BVP during the short-term after cardiac surgery improved cardiac function and decreased mitral regurgitation in all 4 of our patients. Epicardial lead implantation may thus be a useful option during surgical treatment of patients with CHF and intraventricular conduction delay if long-term permanent BVP is indicated.

Aged↗

Stented elephant trunk procedure combined with ascending aorta and arch replacement for acute type A aortic dissection.

OBJECTIVES: Despite steadily improving outcomes, surgery for acute type A aortic dissection has several unresolved problems such as expansion of the residual false lumen in the descending aorta. We performed transaortic stented graft implantation into the descending aorta combined with the ascending aorta and aortic arch replacement for acute type A aortic dissection. We review the efficacy and outcomes of this procedure with respect to the residual false lumen and postoperative neurologic complications we encountered. METHODS: Nine consecutive patients with acute type A aortic dissection underwent this procedure. The stented elephant trunk graft was implanted through the aortic arch under hypothermic circulatory arrest. The stented graft was 15 cm long in six patients, and 10 cm long in three patients. Enhanced computed tomography (CT) was performed 1 month after surgery and once each year after discharge to evaluate the postoperative time course of the residual false lumen. RESULTS: Cardiopulmonary bypass (CPB) time was quite long because of slow cooling and re-warming [352+/-92 (mean+/-SD) min], and average lower-body arrest time was 54+/-10min. The intima in one patient was injured at the time of implantation, and a small leak was created. One patient died of multiorgan failure postoperatively. One patient suffered cerebral injury, and two suffered spinal cord injury perioperatively. Average follow-up time was 40.4 months (range, 13-66 months). One patient died of cerebral infarction during follow up, and the other seven survived and remain well. Postoperative enhanced CT scans showed that the dissected descending aortas attached to the stented grafts and the aortas near the stented grafts returned to normal. In one patient with no re-entry, the false lumen completely closed with thrombi and the entire aorta returned to normal. The diameter of the descending aorta decreased or did not change in six of the seven patients (85.8%) and increased by only 2mm in one of them (14.2%) during follow up. CONCLUSIONS: Implantation of a stented elephant trunk into the descending aorta combined with replacement of the ascending aorta and total arch for acute type A aortic dissection is effective in closing the residual false lumen of the descending aorta and in preventing expansion of the descending aorta. However, further technical modifications, such as using a short stented elephant trunk, eliminating aortic clamping, shortening CPB and spinal cord ischemic time, and reconstruction of left subclavian artery, are needed to prevent neurologic complications.

Acute Disease↗

Lipopolysaccharide pretreatment attenuates myocardial infarct size: A possible mechanism involving heat shock protein 70-inhibitory kappaBalpha complex and attenuation of nuclear factor kappaB.

OBJECTIVE: Lipopolysaccharide pretreatment is known to reduce myocardial infarct size, but the mechanism has not been elucidated. We hypothesized that heat shock protein 70, induced by lipopolysaccharide pretreatment, formed complexes with inhibitory kappaBalpha, thereby inhibiting degradation and attenuating activation of nuclear factor kappaB and cellular injury in rat myocardium. METHODS: Fifteen Sprague-Dawley rats were given saline solution (control group) or lipopolysaccharide. After 48 hours, 5 hearts in each group were excised without ischemia for examination of heat shock protein 70 and inhibitory kappaBalpha levels and detection of heat shock protein 70-inhibitory kappaBalpha complexes. Myocardium from the remaining 10 rats in each group was exposed to 30 minutes of ischemia and 30 minutes of reperfusion (n = 5) to evaluate nuclear factor kappaB activity or to 24 hours of reperfusion (n = 5) to evaluate infarct size. RESULTS: Infarct size was reduced in the lipopolysaccharide group (P <.05). Nuclear factor kappaB was activated in the control ischemia group and attenuated in the lipopolysaccharide group (P <.05). Heat shock protein 70 levels were increased in the lipopolysaccharide group (P <.05), but inhibitory kappaBalpha levels were similar in both groups. Heat shock protein 70-inhibitory kappaBalpha complexes were detected only in the lipopolysaccharide group. Colocalization of the 2 proteins was observed in the lipopolysaccharide group. CONCLUSIONS: Heat shock protein 70, induced by lipopolysaccharide pretreatment, forms complexes with inhibitory kappaBalpha and attenuates activation of nuclear factor kappaB and myocardial infarct size. Our results suggest that attenuation of nuclear factor kappaB through a mechanism forming heat shock protein 70-inhibitory kappaBalpha complexes might protect the myocardium from ischemia-reperfusion injury.

Animals↗