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This study aimed to evaluate the efficacy of vascular intervention in percutaneous transluminal angioplasty (PTA) for the treatment of hepatic artery and hepatic vein stenosis after liver transplantation (LT), including thrombotic total occluded lesions.Percutaneous transluminal angioplasty after orthotopic liver transplantation was performed to re-open hepatic vessel lesions. We daily used routine Doppler ultrasound during admission for early detection of graft hepatic vessel lesions, including hepatic artery and vein lesions. In outpatients, Doppler ultrasound was performed every month. Urokinase was delivered with a dose of 150,000-300,000 IU by catheter before PTA for thrombotic total occlusion of the graft for hepatic artery patients. Laboratory data were collected to evaluate the effects of the PTA procedure.The study involved a total of seven patients, six of whom were successfully treated by a first PTA procedure. Thrombolysis use of urokinase in totally occluded donor hepatic arteries post-LT following stenting was successful in three patients. One complication occurred, an arterial dissection and perforation, finalizing the success rate at ~86% and the complication rate at ~14%. Therefore, our study has a primary patency rate of 100% at 1 and 3 months. Also, the graft survival rate was 100 % and 86 % in the first and third months, respectively.PTA with stenting is an effective treatment for hepatic vessel stenosis, including hepatic arteries and hepatic veins, after a liver transplantation without an increase in the complication rate. In addition, thrombolysis using urokinase intra-artery infusion in graft thrombotic total occluded patients is a good treatment strategy as well.Angioplasty; Complication; Liver transplantation.

Background: Whether connexin43 gap junctions (Cx43 GJs) and spatial heterogeneity of conduction velocity (CV) restitutions are altered in hearts during moderate (MH; 33°C) and severe (SH; 30°C) hypothermia remains unclear. Methods and Results: Using an optical mapping system, ventricular CV was evaluated by S1 pacing in 29 Langendorff-perfused isolated rabbit hearts at baseline (37°C, n=9), 30-min MH (n=6), 30-min SH (n=9), and rewarming (R, 30-min SH followed by 30-min 37°C, n=5). After CV evaluation, myocardium was collected to measure the level and distribution of non-phosphorylated (NP-Cx43) and total (T-Cx43) Cx43 by immunoblotting and immunoconfocal microscopy. In 6 additional hearts, Cx43 GJ remodeling was evaluated at 30-min SH with (n=3) or without (n=3) pretreatment of a protein kinase C (PKC) inhibitor. CV slowing and spatial heterogeneities of CV restitutions were enhanced in MH and SH hearts. NP-Cx43 was downregulated in MH (P=0.002) and SH (P

A 66-year-old male received an implant of a dual-chamber implantable cardioverter-defibrillator (ICD) and was prescribed amiodarone (400 mg/day). The intra-thoracic impedance monitor in the ICD antecedently detected amiodarone-induced acute fibrosing alveolitis >3 months prior to clinical symptoms.

BAPTA-AM and Repetitive Endocardial Focal Discharges. Introduction: In isolated rabbit hearts, repetitive endocardial focal discharges (REFDs) were consistently observed during ventricular fibrillation (VF) with prolonged (>5 minutes) global ischemia (GI). We hypothesized that BAPTA-AM, a calcium chelator, can suppress these REFDs. Methods and Results: Using a two-camera optical mapping system, we simultaneously mapped endocardial (left ventricle, LV) and epicardial (both ventricles) activations during ventricular arrhythmia with GI. In 5 hearts (protocol I), we infused Tyrode's solution (no BAPTA-AM) for ≥30 minutes before the onset of no-flow GI. In 7 additional hearts (protocol II), BAPTA-AM (20 μmol/L) was infused for ≥30 minutes before the initiation of GI. In protocol I, sustained VF (>30 seconds) was successfully induced in all 5 hearts with prolonged GI. REFDs were present in >85 % of recording time. In protocol II, however, ventricular arrhythmia was not inducible and REFDs were not observed after 5-minute GI in 5 hearts. Effects of BAPTA-AM on intracellular calcium (Cai) at the LV endocardium were also evaluated in 5 hearts (protocol III) using dual Cai/membrane potential mapping. GI, both without and with BAPTA-AM pretreatment, caused a decrease of Cai amplitude during S1 pacing. However, this effect was more pronounced in the hearts with BAPTA-AM pretreatment (P < 0.001). GI, without BAPTA-AM pretreatment, caused broadening of Cai transient. In contrast, GI, with BAPTA-AM pretreatment, caused narrowing of Cai transient. Conclusions: BAPTA-AM pretreatment attenuates Cai transient, suppressing the genesis of REFDs and pacing-induced ventricular arrhythmia during GI. These findings support the notion that Cai dynamics is important in the maintenance of REFDs. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1154-1162, October 2011)

Intramyocardial hematoma is a rare sequela of percutaneous coronary intervention after acute myocardial infarction. Clinical outcomes of intramyocardial hematoma vary from asymptomatic remission to cardiac death. Close follow-up is imperative. Herein, we report the case of a 69-year-old man who had sustained an acute inferior myocardial infarction. During primary percutaneous coronary intervention to the occluded right coronary artery, an intramyocardial hematoma developed and immediately ruptured into the right ventricle. Because the patient remained hemodynamically stable, a conservative approach was taken. Follow-up with serial multidetector computed tomographic imaging elucidated the course and extent of the hematoma and clearly revealed the healing process. After 1 year, this method of imaging showed complete remission of the hematoma. To the best of our knowledge, this is the 1st use of serial multidetector computed tomography to document the remission of an intramyocardial hematoma that ruptured after complicated percutaneous coronary intervention. We believe that multidetector computed tomography is useful in tracing the natural history of intramyocardial hematomas.

Background: Therapeutic hypothermia (TH, 30°C) protects the brain from hypoxic injury. However, TH may potentiate the occurrence of lethal ventricular fibrillation (VF), although the mechanism remains unclear. The present study explored the hypothesis that TH enhances wavebreaks during VF and S1 pacing, facilitates pacing-induced spatially discordant alternans (SDA), and increases the vulnerability of pacing-induced VF. Methods and Results: Using an optical mapping system, epicardial activations of VF were studied in 7 Langendorff-perfused isolated rabbit hearts at baseline (37°C), TH (30°C), and rewarming (37°C). Action potential duration (APD)/conduction velocity (CV) restitution and APD alternans (n=6 hearts) were determined by S1 pacing at these 3 stages. During TH, there was a higher percentage of VF duration containing epicardial repetitive activities (spatiotemporal periodicity) (P

On the basis of the ESVEM trial, d,l-sotalol has been approved for the treatment of life-threatening ventricular tachycardia (VT) and ventricular fibrillation (VF).1,2 Previous studies have shown that d,l-sotalol reduced the complexity of epicardial activation patterns and prolonged wavelength (WL) during VF in isolated rabbit hearts.3 Recently, Pak et al. reported that d,l-sotalol at therapeutic doses (≤10 mg/L) effectively terminated VF/VT by flattening action potential duration restitution (APDR) in isolated swine ventricles.4 However, the effects of d,l-sotalol at therapeutic concentrations on the wavefront characteristics of VF and the genesis of electrophysiological heterogeneity (such as APD dispersion and spatial heterogeneity of restitutions) are still not completely understood. We have previously demonstrated that 2 types of VF exist in the same isolated rabbit heart.5 As APDR was flattened by low dose methoxyverapamil (D600), the multiple-wavelet type 1 VF was converted to VT. A further increase of D600 concentration converted VT to a slower (type 2) VF with a stationary or slow drifting mother rotor. During type 2 VF, the anatomical structure, papillary muscle (PM), always served as an anchoring site for the mother rotor.6 We hypothesized that d,l-sotalol at therapeutic concentrations, with both the effects of APDR flattening and WL prolongation, can also convert a pre-existing type 1 VF into a regular rhythm, finally leading to the termination of ventricular tachyarrhythmia. To test this hypothesis, an optical mapping system was used to record epicardial activation patterns during d,l-sotalol infusion. The aims of this study were to determine (1) whether or not acute administration of d,l-sotalol can effectively convert a pre-existing VF into VT before its termination, and (2) the wavefront characteristics of VF and the electrophysiological heterogeneity during d,l-sotalol infusion with therapeutic concentrations in isolated rabbit hearts.

A 41-year-old man received an electrophysiological study (EPS) and radiofrequency catheter ablation (RFCA) for atrioventricular reentrant tachycardia (AVRT) in our hospital. Massive pulmonary embolism (PE) with hypotension developed 9 hours after these procedures. After emergent pulmonary angiography and catheter-directed intrathrombus urokinase infusion and clot breaking, the patient recovered well. This case suggests that life-threatening PE may occur in patients who receive EPS, RFCA, or both. An adequate observation time after RFCA and clinical alertness are necessary for immediate diagnosis and treatment. Emergent catheter-directed therapy may be of benefit in some patients with acute massive PE.