Transcatheter closure of perimembranous ventricular septal defects with Amplatzer® duct occluder I; The first case report in Japan.

We report the first case of transcatheter perimembranous ventricular septal defect (pmVSD) closure in Japan where none of existing devices for VSD closure has been approved. The pmVSD was successfully closed with first generation Amplatzer® duct occluder (ADO-I; St Jude Medical, St Paul, MN, USA). The procedure was performed under general anesthesia with transesophageal echocardiographic and fluoroscopic guidance. The left ventricular volume overload after the procedure was remarkably improved and no major complications occurred. ADO-I can be a safe and effective option for transcatheter pmVSD closure. The incidence of heart block may be less than reported with the original device. .

Static balloon atrial septostomy for the purpose of left heart intervention in postoperative adult CHD.

Background and purposeStatic balloon atrial septostomy is a widely accepted intervention for children with CHD. Successful surgical palliation is creating increasing numbers of adult CHD patients who need subsequent left heart intervention requiring transseptal access. In these patients, the interatrial septum is usually thick and fibrotic because of a previous open heart surgery or catheter intervention, and conventional transseptal puncture may be unsuccessful. Static balloon atrial septostomy to access the left atrium may facilitate intervention via the interatrial septum in such situations. The purpose of this study was to investigate the usefulness and the safety of static balloon atrial septostomy, and the evolution of an iatrogenic atrial septal defect post procedure in adult CHD. METHODS: We retrospectively reviewed six procedures in five adults with CHD and collected demographic characteristics, details of the procedures, clinical outcome, and size changes of the iatrogenic atrial septal defect. RESULTS: The mean age at the time of the procedure was 35 years. The intended primary interventions were pulmonary vein isolation, stenting for pulmonary vein obstruction, and catheter ablation for focal atrial tachycardia. All static balloon atrial septostomies were effective, and the left heart interventions were successfully achieved via transseptal sheaths. There were no major complications associated with the static balloon atrial septostomy. There were no adverse clinical outcomes related to iatrogenic atrial septal defect, and the size of the defects regressed over time in all cases. CONCLUSIONS: Static balloon atrial septostomy can be a safe and useful technique in adult CHD patients needing left heart procedures. The thick interatrial septum found in postoperative patients may reduce the risk of persistent iatrogenic atrial septal defect.

Stent unzipping using an ultra-high-pressure balloon: in vitro and animal experiments.

As a child grows, limitations to the maximum dilatable stent diameter (MDD) will result in stenosis associated with size mismatch. If an implanted stent can be intentionally fractured along its length, a process called "unzipping," it may eventually be redilated to adult vessel size. Few studies have addressed how a stent can be unzipped using an ultra-high-pressure balloon (UHB) with the smallest balloon diameter. Eleven commercially available stents, three Liberté stents (LS), six genesis renal stents (GS), and two express vascular SD stents (ES), were tested for in vitro unzipping. In addition, using eight stents, we investigated whether a balloon that had unzipped the stent in vitro would work similarly in the vessel of a pig. Finally, we assessed the histological influence of the unzipped stent on the surrounding tissue. In a bench test, LS, GS, and ES were consistently unzipped by a balloon whose diameter was ≥ 1.5, 2.18, and 1.66 times that of MDD, respectively. In animal experiments, LS, GS, and ES were predictably unzipped with balloons of 1.50, 1.81, and 1.66 times the MDD, respectively. After unzipping, the unzipped strut did not damage the surrounding tissue histologically. Use of a UHB enabled unzipping of the stent with a balloon diameter less than two times the MDD enables implantation of a larger stent in the unzipped small stent by incremental steps.

Novel curved balloon catheter for dilating postoperative angled lesions associated with congenital heart disease.

OBJECTIVES: This study aimed to analyze the surface stress generated by a novel curved balloon and assess its efficacy for treating angular lesions associated with congenital heart disease. BACKGROUND: Obstructions at the anastomosis of aortopulmonary shunts and cavopulmonary connections may occur postoperatively. Catheter interventions are often performed for such lesions; however, acute angulation may cause balloon slippage or inappropriate stress on the vessel wall. METHODS: We dilated the curved balloon in a curved vessel model and measured the resultant wall stress and its distribution. Clinical evaluations were performed using this balloon in angled lesions. RESULTS: In the curved vessel model, curved balloons generated uniform stress on the lesser and greater curvatures (curved type, lesser/greater = 0.343 MPa/0.327 MPa; P = 0.61), whereas straight balloons caused disproportionate stress (straight type, lesser/greater = 0.358 MPa/0.254 MPa; P = 0.19). However, the difference in average stress was not statistically significant. Furthermore, the stress was uniform along the entire length of the curved balloon, but differed between the mid and end portions of the straight balloon. Curved balloon dilations were performed for 10 lesions in 7 patients. The curved balloon conformed well to the angulated lesion without slipping. The median percent change in the minimal lumen diameter (MLD) was 64% (range, 0-206%). In 5 lesions, MLD increased by ≥50%. Oxygen saturation increased by 5% (0-9%). CONCLUSIONS: Although further clinical evaluation is necessary, this novel curved balloon may be a reasonable alternative in angled lesions, providing better conformability and preventing excessive stress to the vessel wall adjacent to the stenosis.

Pharmacological characteristics and clinical applications of K201.

K201 is a 1,4-benzothiazepine derivative that is a promising new drug with a strong cardioprotective effect. We initially discovered K201 as an effective suppressant of sudden cardiac cell death due to calcium overload. K201 is a non-specific blocker of sodium, potassium and calcium channels, and its cardioprotective effect is more marked than those of nicorandil, prazosine, propranolol, verapamil and diltiazem. Recently, K201 has also been shown to have activities indicated for treatment of atrial fibrillation, ventricular fibrillation, heart failure and ischemic heart disease, including action as a multiple-channel blocker, inhibition of diastolic Ca(2+) release from the sarcoplasmic reticulum, suppression of spontaneous Ca(2+) sparks and Ca(2+) waves, blockage of annexin V and provision of myocardial protection, and improvement of norepinephrine-induced diastolic dysfunction. Here, we describe the pharmacological characteristics and clinical applications of K201.

Risk of heart failure due to a combination of mild mitral regurgitation and impaired distensibility of the left ventricle in patients with old myocardial infarction.

BACKGROUND: Ischemic mitral regurgitation (MR) is a serious complication after myocardial infarction, and the incidence of heart failure (HF) increases as the severity of MR increases. However, little is known about the relationship between mild MR and HF in the patients with old myocardial infarction (OMI) and a normal ejection fraction (EF). HYPOTHESIS: We hypothesized that a combination of mild MR and impaired distensibility of the left ventricle may increase the risk of diastolic HF in the patients with OMI and a normal EF. METHODS: The relationship between HF and mild MR was retrospectively investigated in 62 patients with OMI and EF of > 50% on echocardiography. RESULTS: Of the 62 patients, 47 (76%) did not have HF and 15 (24%) had HF. There was a significant difference in the incidence of mild MR between the patients with and without HF (p < 0.0001): of the 47 patients without HF, mild MR was detected in 19, but all 15 patients with HF had mild MR. However, there were no significant differences in age, gender, infarct sites, diseased coronary vessels, peak CK level, and observation period between the 2 groups. An increased E-wave and the ratio of the E-wave to the A-wave (E/A), a reduction of the E-wave deceleration time, and an increased brain natriuretic peptide (BNP) level were significantly noted in HF patients with mild MR compared with patients without HF. CONCLUSIONS: Even a mild MR may cause diastolic HF in patients with impaired distensibility of the left ventricle due to ischemic heart disease.

K201, a multi-channel blocker, inhibits clofilium-induced torsades de pointes and attenuates an increase in repolarization.

K201 (JTV519) is a 1,4-benzothiazepine derivative that exhibits a strong cardioprotective action and acts as a multiple-channel blocker, including as a K+ channel blocker. An experimental model of prolongation of the QT interval and torsades de pointes can be induced in rabbits by treatment with clofilium in the presence of the alpha1-adrenoreceptor agonist methoxamine. In this study we examined the effects of K201 with and without methoxamine on the QT and QTc intervals, and determined whether K201 inhibits clofilium-induced torsades de pointes in the presence of methoxamine (15 microg/kg/min) in rabbits (n=74). Administration of K201 (0, 40, 100, 200 and 400 microg/kg/min) with and without methoxamine prolonged the QT interval in a dose-dependent manner, and torsades de pointes did not occur in any animals. However, clofilium (50 microg/kg/min) with methoxamine induced torsades de pointes in all animals (6/6). Torsades de pointes occurred at rates of 100%, 67%, 40% and 0% at K201 concentrations of 0, 50, 200 and 400 microg/kg/min, respectively, in the clofilium-infused torsades de pointes model. Therefore, 400 microg/kg/min of K201 completely inhibited clofilium-induced torsades de pointes and attenuated the increase of repolarization caused by clofilium; the inhibitory effects of K201 may be related to its pharmacological properties as an alpha1-adrenoceptor blocker. Overall, our results show that K201 causes prolongation of the QT and QTc intervals, but does not induce torsades de pointes, with and without alpha1-adrenoceptor stimulation. Furthermore, K201 inhibits clofilium-induced torsades de pointes, despite QT prolongation, suggesting that QT prolongation alone is not a proarrhythmic signal.