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ABSTRACT: A 78-year-old man who had been treated with maintenance hemodialysis for chronic renal failure was admitted with severe edema in left arm for 1 month. Venous angiography showed a severe stenosis in left innominate vein, then, he underwent percutaneous balloon angioplasty and venous stenting (Wall Stent RP). His arm edema soon improved after angioplasty, however, he complained of general fatigue and bradycardia 2 days after the venous angioplasty. Electrocardiogram showed complete atrioventricular block with 35 wide QRS complexes per minute. His echocardiogram showed a pipe-shaped structure with multiple slit and acoustic shadow in right ventricle. His radiographical right ventriculogram revealed the migrated venous stent from innominate vein to right ventricle. We tried to perform percutaneous transvenous stent extraction using Goose-Neck snare catheter, however, the wall stent stuck in the right external iliac vein, and contrast media leaked to the outside of the vascular wall. Therefore, we implanted this stent in the iliac vein with optimal-sized balloon inflation, and succeeded in stopping bleeding. Complete atrioventricular block was recovered to sinus rhythm with left bundle branch block just after the removal of the venous stent from right ventricle, and no cardiovascular events occurred after the treatment.
Journal of Cardiology 07/2009; 53(3):453-7. · 1.28 Impact Factor
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ABSTRACT: The restitution mechanism has been the focus of attention as the possible mechanism behind ventricular fibrillation (VF). However, its contribution in chronic ischemic heart has not been established.
We investigated chronic ischemic dogs with occlusion of left anterior descending artery. Sixty unipolar electrograms were simultaneously recorded from an entire cardiac surface. Activation-recovery intervals (ARIs) and QRST deflection area (AQRST) were measured during constant atrial pacing. The ischemic dogs were divided into two groups, five dogs in VF(+) group or seven dogs in VF(-) group, according to VF occurrence by programmed electrical stimulation.
When investigating ARI dispersions on an epicardium, there was no difference between VF(+) and VF(-) groups. The relationship between ARIs and diastolic intervals was quantified as an electrical restitution curve. The slopes of the ARI restitution curve for the anterior left ventricle in VF(+) dogs were significantly steeper than those of VF(-) dogs. The amplitude of AQRST alternans were significantly greater in VF(+) dogs than VF(-) dogs.
Combined observation of steep restitution slopes and increased electrical alternans supported the restitution mechanism as being involved in the arrhythmia. Dynamic restitution properties and not static single-beat ARI dispersion may play an important role in the VF arrhythmia in the chronic ischemic heart.
Cardiovascular Research 10/2004; 63(4):645-52. · 6.06 Impact Factor
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ABSTRACT: The aim of this study was to clarify the ventricular tachyarrhythmia mechanism induced by the I(Kr)-blocking agent E4031, simulating the LQT2 form. Electrophysiologic properties were examined in 13 canines before and after administration of E4031.
Thirty-six needle electrodes were inserted into the anterior left ventricular wall. From each needle, local unipolar electrograms were obtained from four intramural sites. Activation time (AT) and activation-recovery interval (ARI) were measured. To evaluate the susceptibility to ventricular arrhythmia, intramural ARI dispersions and the restitution relationship between ARI and diastolic interval were calculated. After E4031 administration, ARI prolonged uniformly in each myocardial layer. However, ARI dispersion was not augmented compared with control. The slope of the ARI restitution curve after E4031 was significantly steeper than control. A steep slope may result from augmented ARI alternans. In 11 of the 13 canines, ventricular tachyarrhythmia was induced by programmed stimulation after E4031, whereas no arrhythmia was induced by the same protocol in control.
Steepness of electrical restitution may play a major role in arrhythmogenicity in LQT2 hearts.
Journal of Cardiovascular Electrophysiology 10/2002; 13(9):910-4. · 3.06 Impact Factor
