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Biomedical subjects

Hirokuni Arai

Publications and source records attributed to Hirokuni Arai.

7 recordsLinked to original sources

Double-patch technique for postinfarction ventricular septal perforation.

A modified infarct-exclusion technique for postinfarction ventricular septal perforation is presented. The perforation is closed directly by a small patch next to the conventional patch, and biological glue is applied between the patches to induce stable polymerization. The patch stuck to the infarcted septum, and no residual shunt was observed in any patient because the wide adhesion prevents excessive pressure on the suture line. Seven of 9 patients in whom this method was used had good results. This technique appears suited for repair of ventricular septal perforations, especially those with extensive fresh infarction.

Cardiac Surgical Procedures↗

Biventricular pacing with coronary bypass and Dor's ventriculoplasty.

We applied biventricular pacing to a patient with severe ischemic dilated cardiomyopathy (left ventricular [LV] ejection fraction 19%, LV end-diastolic volume 360 mL, and complete left bundle branch block). An epicardial LV lead was surgically implanted concomitant with on-pump beating coronary artery bypass grafting and Dor's endoventricular circular patch plasty. Biventricular pacing immediately achieved the resynchronization of the LV contraction, and improved cardiac function as well as reducing mitral regurgitation. Biventricular pacing combined with cardiac surgery for patients with cardiomyopathy and complete left bundle branch block may produce beneficial effects on LV function.

Aged↗

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↗

Biventricular pacing in a patient with severe congestive heart failure.

We report a case of dilated cardiomyopathy with severe congestive heart failure (ejection fraction: 19%) and complete left bundle branch block (QRS duration: 240 ms) 13 years after aortic valve replacement. Permanent biventricular pacing was implanted by inserting a left ventricular lead thorough a small left thoracotomy following intravenous insertion of right atrial and ventricular endocardial leads. Biventricular pacing increased hemodynamic parameters such as blood pressure, cardiac output and decreased mitral regurgitation. Symptoms and exercise tolerance improved dramatically. Left ventricular epicardial lead insertion via a small thoracotomy is thus useful in selected patients.

Aortic Valve↗

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↗

One piece ultracompact totally implantable electromechanical total artificial heart for permanent use.

An ultracompact, one piece, totally implantable electromechanical total artificial heart (TAH) has been developed as a permanent replacement for failing hearts. It consists of left and right pusher plate blood pumps (stroke volume 55 ml) made of titanium alloy (Ti-6Al-7Nb) sandwiching a miniaturized electromechanical actuator between them. The diameter of the TAH is 90 mm, with a thickness of 70 mm, yielding an overall volume of 400 ml. It weighs 450 g. Although it is miniaturized, it provided a maximum pump output of 8 L/min against a left afterload of 100 mm Hg. It required approximately 12 watts to provide a pump output of 6.5 L/min with maximum efficiency of 13.5%. To balance left and right flow, the right stroke length was made 10% shorter than the left, and an auxiliary compliance chamber was used to compensate for additional flow differences between them. Motor commutation pulses and a Hall effect pusher plate sensor signal were used in the controller to implement the left master alternate variable rate mode. The calf fitting study revealed excellent anatomic compatibility, and the first successful survivor was obtained in December 2001. Studies of system endurance and biocompatibility are required to ensure long-term reliability. This TAH is promising for permanent replacement of the failing heart as well as for bridge to heart transplantation for the smaller size group of end-stage cardiac patients.

Animals↗