Reentrant Ventricular Outflow Tract Tachycardia Arising from Focal Scar Detected by Delayed Enhancement Magnetic Resonance Imaging

A 58‐year‐old man was referred to our emergency room with hemodynamically unstable sustained ventricular tachycardia (VT). The morphology of the VT exhibited a left bundle branch block and inferior axis deviation. He had no past history of cardiovascular disease. Echocardiography, cardiac catheterization, cardiac biopsy, gallium scintigram, myocardial scintigram, T1,T2‐weighted magnetic resonance imaging (MRI), and gadolinium‐enhanced cine MRI did not detect any structural heart disease or abnormal cardiac function. However, delayed‐enhancement MRI (DE‐MRI) detected a focal intramural scar within the septal ventricular outflow tract. An electrophysiological study revealed a sustained VT with several morphologies and the entrainment phenomenon. Radiofrequency catheter ablation to the site corresponding to the focal scar detected by DE‐MRI successfully eliminated the VT. (PACE 2012;35:e349–e352)     

Incremental Value of Objective Frailty Assessment to Predict Mortality in Elderly Patients Hospitalized for Heart Failure

Background

The impact of frailty on long-term prognosis in patients with heart failure (HF) remains unclear, and there is no simple and objective assessment for it. This study was performed to examine the association between frailty score and clinical outcome in elderly patients hospitalized for HF.

Prediction of Optimal Atrioventricular Delay in Patients with Implanted DDD Pacemakers

In patients with an implanted DDD pacemaker (PM), the atrial contribution may be interrupted by too short an atrioventricular (AV) delay, and filling time may be shortened by too long an AV delay. The AV delay at which the end of the A wave on transmitral flow coincides with complete closure of the mitral valve may be optimal. The subjects were 15 patients [70.3+/-12.3 (SD) years old] with an implanted DDD PM. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan-Ganz catheter. Transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 msc. When the AV delay was set at 155+/-26 ms, the end of the A wave coincided with complete closure of the mitral valve. When the AV delay was prolonged 25, 50, 75, and 100 ms from this AV delay, the interval between the end of the A wave and complete closure of mitral the valve was prolonged 16+/-5, 39+/-6, 65+/-4 and 88+/-5 ms, respectively (r = 0.97, P<0.0001) and diastolic mitral regurgitation was observed during this period. Thus, the optimal AV delay may be predicted as follows: the slightly prolonged AV delay minus the interval between the end of the A wave and complete closure of the mitral valve. When the AV delay was set at 215 ms, there was a significant positive correlation between the predicted optimal AV delay (166+/-23 ms) and the optimal AV delay (CO: 161+/-26 msec, r = 0.93, P<0.0001, PCWP: 161+/-28 msec, r = 0.95, P<0.0001). In conclusion, optimal AV delay can be predicted by this simple formula: slightly prolonged AV delay minus the interval between end of A wave and complete closure of mitral valve at the AV delay setting.     

Renoprotective effects of asialoerythropoietin in diabetic mice against ischaemia–reperfusion-induced acute kidney injury

Aim: Diabetic patients are at higher risk of failure to recover after acute kidney injury, however, the mechanism and therapeutic strategies remain unclear. Erythropoietin is cytoprotective in a variety of non‐haematopoietic cells. The aim of the present study was to clarify the mechanism of diabetes‐related acceleration of renal damage after ischaemia–reperfusion injury and to examine the therapeutic potential of asialoerythropoietin, a non‐haematopoietic erythropoietin derivative, against ischaemia–reperfusion‐induced acute kidney injury in diabetic mice. Methods: C57BL/6J mice with and without streptozotocin‐induced diabetes were subjected to 30 min unilateral renal ischaemia–reperfusion injury at 1 week after induction of diabetes. They were divided into four group: (i) non‐diabetic plus ischaemia–reperfusion injury; (ii) non‐diabetic plus ischaemia–reperfusion injury plus asialoerythropoietin (3000 IU/kg bodyweight); (iii) diabetic plus ischaemia–reperfusion injury; and (iv) diabetic plus ischemia–reperfusion injury plus asialoerythropoietin. Experiments were conducted at the indicated time periods after ischaemia–reperfusion injury. Results: Ischaemia–reperfusion injury of diabetic kidney resulted in significantly low protein expression levels of bcl‐2, an anti‐apoptotic molecule, and bone morphogenetic protein‐7 (BMP‐7), an anti‐fibrotic and pro‐regenerative factor, compared with non‐diabetic kidneys. Diabetic kidney subsequently showed severe damage including increased tubular cell apoptosis, tubulointerstitial fibrosis and decreased tubular proliferation, compared with non‐diabetic kidney. Treatment with asialoerythropoietin induced bcl‐2 and BMP‐7 expression in diabetic kidney and decreased tubular cell apoptosis, tubulointerstitial fibrosis and accelerated tubular proliferation. Conclusion: Reduced induction bcl‐2 and BMP‐7 may play a role in the acceleration of renal damage after ischaemia–reperfusion injury in diabetic kidney. The renoprotective effects of asialoerythropoietin on acute kidney injury may be mediated through the induction of bcl‐2 and BMP‐7.     

30%双氧水浸泡后对牙本质中钙/磷含量的影响

目的针对临床型漂白剂在使用中直接接触牙颈部暴露的牙本质和通过牙釉质渗透到牙本质的特点,观察30%双氧水对牙本质中的Ca/P的影响.方法实验组7颗离体牙浸泡在30%双氧水24小时后,对照组5颗离体牙浸泡在生理盐水中24小时后,两组使用OCPC法对浸泡液中的Ca离子含量进行测定,同时运用Fiske-Subbarow法对浸泡液中的磷酸根含量进行测定.然后两组进行统计学比较分析.结果实验组30%双氧水浸泡液中Ca/P含量明显高于对照组(P<0.01).说明在30%双氧水浸泡过程中发生了明显脱矿现象.结论 30%双氧水对牙本质有脱矿作用,建议在使用临床型漂白治疗后应加以再矿化和防龋措施.     

Possible correlation between polymorphism in the tumor necrosis factor-beta gene and the clinicopathological features of bladder cancer in Japanese patients

OBJECTIVES: In a variety of cancers, several polymorphisms of the tumor necrosis factor (TNF) genes have been reported to result in different clinical outcomes. We investigated whether a polymorphism of the TNF gene is associated with a susceptibility to bladder cancer and its disease status. METHODS: Polymorphisms in the TNF-alpha gene promoter (-308 bp) and the NcoI site in the first intron of the TNF-beta gene were analyzed in 141 Japanese patients with bladder cancer and 173 Japanese controls by polymerase chain reaction-restriction fragment length polymorphism. The correlations between the polymorphisms of the TNF genes and the clinicopathological features were analyzed. RESULTS: The number of cases and controls with TNF-alpha2 was too small to be assessable. In contrast, the TNF-beta1/2 genotype at the NcoI site in the first intron conferred a 1.71-fold increased risk of bladder cancer compared to the TNF-beta2/2 genotype. In the bladder cancer group, patients with the TNF-beta1 allele had a significantly higher risk for a high-grade tumor (grade 3) or carcinoma in situ (CIS) than those without the TNF-beta1 allele. Moreover, in the superficial bladder cancers, patients with the TNF-beta1 allele showed a significantly higher intravesical recurrence rate than those without the TNF-beta1 allele. CONCLUSION: This polymorphism in the TNF-beta gene appears to be associated with tumor occurrence and disease status, such as the tumor grade and the presence of CIS. Further study with an increased sample size is warranted.