Influence of power setting on superior vena cava potential during right pulmonary vein isolation

Purpose

High-power short-duration (HP-SD) ablation could reduce collateral tissue damage by shortening the conductive heating phase. However, it is difficult to evaluate the transmural effect of ablation lesions during pulmonary vein isolation (PVI) procedures. The present study aimed to evaluate the change in superior vena cava (SVC) potential delay as a surrogate marker of collateral tissue damage during right PVI, which is adjacent to SVC.

Methods

Out of 250 consecutive patients who underwent PVI, 86 patients in whom SVC potential during sinus rhythm was recorded both before and after right PVI were analyzed. In 46 of the patients, an HP-SD setting of 45–50 W was used (HP-SD group). In the remaining 40 patients, a conventional power setting of 20–30 W was used (conventional group). We compared the change in SVC potential delay after right PVI, radiofrequency energy, and mean contact force in the anterior–superior right PVI line, which was close to the posterior aspect of SVC, between the two groups.

Results

Although the total delivered radiofrequency energy (2,924 J vs. 2,604 J) and the mean contact force (18.5 g vs. 16.0 g) in the SVC overlapping area did not differ, the change in SVC potential delay after right PVI was significantly longer in the conventional group compared to the HP-SD group (5.0 ms vs. 0.0 ms, p?<?0.001).

Conclusions

The changes in SVC potential delay after right PVI might be a surrogate marker of collateral tissue damage according to the used energy settings.

     

A case of juvenile pulmonary infarction associated with diet therapy]

A 31-year-old man experienced chest pain, fever, bloody sputum and cough after diet therapy. Chest radiography and chest CT showed infiltration in the right lower lung field and right pleural effusion. Pulmonary embolism and infarction was diagnosed using 99mTc-MAA perfusion scans and chest enhanced CT. The patient did not have a thrombotic disposition and deep vein thrombosis in the lower extremities. This case did not have an acute onset or dyspnea, and was not typical of pulmonary embolism. The diet therapy may have caused dehydration and acted as a predisposing cause of pulmonary embolism.     

Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor

OBJECTIVE: In the present study, we delivered vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) gene to a rabbit model of hind limb ischemia utilizing an ex vivo method of gene transfer, and evaluated the functional performance of the developed collateral vessels. METHOD: The left femoral artery of a male Japanese White rabbit was excised to induce limb ischemia, and a section of skin was resected for culture of auto-fibroblasts. Twenty days later, the VEGF gene, bFGF gene or beta-galactosidase gene (LacZ) was adenovirally transferred to the cultured auto-fibroblasts (5x10(6) cells), and the next day, a pair of specifically infected fibroblasts (total 1x10(7) cells) was injected via the left internal iliac artery of the same rabbit. Pairs of transferred genes into the fibroblasts were as follows: LacZ/LacZ (control group), VEGF/LacZ (VEGF group), bFGF/LacZ (FGF group) and VEGF/bFGF (combination group). Twenty-eight days after cell administration, collateral development and its function were evaluated. RESULTS: Calf blood pressure ratio, resting blood flow of the left iliac artery and capillary density of ischemic muscle showed similar degrees of angiogenic effects in the VEGF and FGF groups, which were significantly greater than those in the control group. On the contrary, angiographic score, collateral conductance and smooth muscle cell (SMC)-positive vessel density in the FGF group were significantly greater than those in the VEGF group. In the combination group, collateral conductance showed synergistic effects, and in vivo blood flow and smooth muscle cell-positive vessel density revealed additive effects of VEGF and bFGF. CONCLUSION: These findings suggested that bFGF-induced collateral development exceeded VEGF-induced collateral development in the induction of arteriogenesis, and that combined gene delivery of VEGF and bFGF produced additive or synergistic effects of collateral development as compared with the effects induced by transfer of each gene alone.     

Irritant-induced cyclooxygenase-2 is involved in the defense mechanism of the gastric mucosa in mice

Background. Endogenous and exogenous prostaglandins (PGs) have been shown to contribute to reducing the gastric injury caused by irritants given subse-quently. The aim of this study was to clarify whether cyclooxygenase-2 (COX-2) protein induced by pretreatment was involved in the prevention of subsequent ethanol-caused gastric injury in mice. Methods. Mice were pretreated with acidified ethanol or saline and then COX-2 protein expression in the stomach was immunohistochemically determined every 8 h. Mice were administered 95% ethanol 24 h after the acidified ethanol pretreatment, and gastric mucosal damage was evaluated macroscopically and histologically. The effects of NS-398 or indomethacin on the 95% ethanol-caused damage were also examined. Results. Acidified ethanol pretreatment induced COX-2 protein expression in lamina propria macrophages of the gastric mucosa, with a peak level 24 h after the pretreatment. The 95% ethanol treatment caused gastric mucosal damage. The degree of the damage was not different between mice pretreated with acidified ethanol and those pretreated with saline. However, NS-398 aggravated the ethanol-caused damage only in mice pretreated with acidified ethanol, while indomethacin aggravated the damage, evaluated histologically, irrespective of the pretreatment. Conclusions. Pretreatment-induced COX-2, in addition to COX-1, seemed to be involved in the defense mechanism through minimizing the damage caused by a subsequent irritant. Received: October 16, 2000 / Accepted: September 14, 2001     

Infection of sabA-positive H. pylori does not induce anti-Lewis X antibody in host

BACKGROUND/AIMS: H. pylori uses the sialic acid-binding adhesin (SabA) to recognize Lewis X (LeX) antigen of gastric epithelial cells. SabA is associated with nonopsonic activation of human neutrophils. The aims of this study were to examine the association of bacterial sabA status to the presence of anti-LeX antibody in host and the grade of gastritis. METHODOLOGY: 44 H. pylori strains cultured from gastric biopsies were examined by PCR for presence of 23SrRNA, cagA, and sabA. Serum samples were obtained from all the patients to measure the level of anti-LeX antibody. Histological grade of gastritis was graded according to the updated Sydney System. RESULTS: 23SrRNA gene and the cagA gene were seen in all the samples while 21 strains were sabA positive. The mean titer of anti-LeX antibody was 0.09 and 0.18 in patients infected with sabA-positive and -negative strain, respectively (NS). The grade of inflammatory infiltration was not significantly different between groups in both the corpus and the antral mucosa. CONCLUSIONS: Possession of the sabA gene by infected H. pylori strain might not associate with the presence of anti-LeX antibody in the host. Possession of sabA gene by infected H. pylori might not associate with severity of gastric mucosal inflammation.     

Prevalence of total knee arthroplasty and its predictive factors in Japanese patients with rheumatoid arthritis: Analysis using the NinJa cohort

Objectives. The aim of this study was to clarify the prevalence and the predictive factors for undergoing total knee arthroplasty (TKA) among patients with rheumatoid arthritis (RA).

Methods. The data of 1,134 patients with RA who were enrolled in the Japanese nationwide cohort database NinJa in 2003 and consecutively followed up until 2009 were analyzed.

Results. Seventy-six patients underwent TKA during the observation period. The yearly progression of the modified Health Assessment Questionnaire or mHAQ score from 2003 to 2004, but not the yearly progression of the Disease Activity Score in 28 Joints or DAS28 or patient visual analog scale (VAS) score, was significantly higher in the patients who underwent TKA than those who did not.

Multivariate analysis showed that knee involvement in the disease, high Steinbrocker stage (III or IV), and high patient VAS score at the time of enrollment were powerful predictive factors, with hazard ratios of 4.01, 3.71, and 1.20, respectively.

According to survival analysis with TKA as an endpoint, patients with knee involvement in the disease at the time of enrollment had a significantly worse 5-year survival rate than did those without knee involvement (83.5% vs. 97.0%, respectively).

Conclusion. Several factors were elucidated as predictive factors for undergoing TKA among patients with RA.     

Evaluation of the usefulness of recording the ECG in the 3rd intercostal space and prevalence of Brugada-type ECG in accordance with recently established electrocardiographic criteria.

BACKGROUND: It has been reported that recording electrocardiograms (ECGs) in the 3rd intercostal space (ICS) is one method that can be used for detecting Brugada syndrome; however, the prevalence of Brugada-type ECGs recorded in the 3rd ICS and the usefulness of recording the ECG in the 3rd ICS in accordance with recently established electrocardiographic criteria is unknown. METHODS AND RESULTS: ECGs were recorded in both the 4th and 3rd ICS in 17 Brugada-type ECG patients (group A) and in 206 consecutive male subjects (group B). Brugada-type ECGs were divided into 3 types. In group A, the prevalence of type 1 ECG, which is a coved-type ECG with ST-segment elevation of >/=2 mm, increased from 23.5% to 64.7% when ECG was recorded in the 3rd ICS. The conversion to type 1 ECG was found to be related to induction of ventricular arrhythmia. In group B, the prevalence of Brugada-type ECG increased from 1.5% to 5.8% when the ECG was recorded in the 3rd ICS. CONCLUSIONS: Recording the ECG in the 3rd ICS is useful for identifying high-risk patients with Brugada-type ECG and for detecting concealed Brugada-type ECG.     

R353Q polymorphism, activated factor VII, and risk of premature myocardial infarction in Japanese men.

BACKGROUND: The association between myocardial infarction (MI) and the R353Q polymorphism of the Factor VII (FVII) gene, which reportedly influences FVII concentrations, activated Factor VII (FVIIa), or FVII antigen (FVIIag), remains controversial. METHODS AND RESULTS: The present case - control study in 127 Japanese men with their first MI at or before 45 years of age and 150 matched healthy controls was designed to clarify this association in premature MI. R353Q polymorphism was determined by polymerase chain reaction, and plasma concentrations of FVIIa and FVIIag were assayed. The distribution of the RR, RQ, and QQ genotypes with respect to R353Q polymorphism was 117, 10, and 0 in the patients, and 131, 17, and 2 in the controls. The Q allele was negatively associated with premature MI (odds ratio =0.41, p=0.038). The plasma concentration of FVIIa was slightly higher in patients (55.1+/-40.9 U/L) than in controls (44.8+/-20.2 U/L), but not significantly (p=0.078); the plasma concentration of FVIIag did not differ between patients (88.7+/-15.7%) and controls (87.0+/-9.0%) (p=0.557). Plasma FVIIa concentrations were influenced by R353Q polymorphism (p<0.001). CONCLUSIONS: The Q allele may be protective against premature MI.     

Indication of aortocoronary by-pass for coronary arterial obstruction due to Kawasaki disease

Summary Six patients with coronary arterial lesions due to Kawasaki disease underwent aortocoronary by-pass grafting at our institute. Before surgery, all of them had been closely monitored for some years by means of selective coronary arteriography, thallium myocardial imaging, electrocardiography (treadmill and/or Holter), and two-dimensional echo cardiography. Based on this experience, we propose the following guidelines as an indication for aortocoronary by-pass in such patients. First, the following three conditions should be satisfied: 1) The progress of coronary arterial lesions has been documented by serial selective coronary arteriography; 2) redistribution to the perfusion defect has been detected on the delayed image in myocardial imaging; 3) no coronary arterial lesions distal to the graft site have been detected by coronary angiography. When these three conditions are satisfied, at least one of the following conditions must apply: 1) Localized stenosis in the left main trunk has progressed to critical stenosis; 2) there is occlusion of two or more vessels; 3) collateral vessels connecting to the peripheral portion of an occluded coronary artery arise from the peripheral part of a vessel with progressive localized stenosis; 4) progressive localized stenosis or critical stenosis has developed in the left anterior descending artery, in addition to significant stenosis in the right coronary artery.