[Early Results of Complex Fractionated Atrial Electrogram Mapping Guided Atrial Fibrillation Surgery].

OBJECTIVE: Although the Cox-maze operation is the standard surgical procedure for permanent atrial fibrillation(AF), conversion to sinus rhythm is limited by patient characteristics, including the duration of AF, atrial size, and voltage of fibrillation waves. A surgical strategy based on structural alteration of the electrical substrates of AF is required to achieve better outcomes of AF surgery. Complex fractionated atrial electrogram (CFAE) plays an important role in the electrical substrate of AF. We performed AF surgery guided by preoperative CFAE mapping using a 3-dimensional (3D) mapping system. This study evaluated the early results of our procedure. METHODS: From January 2015 to August 2016, 8 patients (mean age:66.5±6.4 years) underwent CFAE mapping-guided AF surgery. In the preoperative electrophysiological study using 3D mapping, CFAE was defined by a low voltage electrogram (0.05~0.25 mV) with a highly fractionated potential (short cycle length <120 msec). First, right atrial CFAE sites were ablated by using a catheter ablation system. Several days after right-sided CFAE ablation, a modified Cox-maze operation was performed with additional cryoablation of CFAE sites. RESULTS: There were 1~3 (mean:2.5 ±0.8) CFAE sites in the right atrium and 2~4 (mean:2.4±0.7) sites in the left atrium. Mean CFAE mapping time was 87.6±24.6 minutes, fluoroscopy time was 53.1±22.2 minutes, and volume of contrast agent was 44±3 ml. Concomitant cardiac surgery included mitral valve plasty in 6 patients, and aortic valve replacement and mitral valve replacement in 1 patient each. The mean time for CFAE mapping-guided AF surgery was 25.7±5.6 minutes. At discharge, 7 patients were in sinus rhythm and 1 patient still had AF, but sinus rhythm recovered at 3 months postoperatively without anti-arrhythmic medication. After a mean follow-up of 11.7±8.5 months, all patients remained in sinus rhythm. CONCLUSIONS: Early results suggest that CFAE mapping-guided atrial fibrillation surgery is feasible and effective. Although the long-term effect of CFAE ablation on maintenance of sinus rhythm and atrial function should be evaluated, this novel method could provide an alternative strategy for the surgical treatment of AF.

Reduced carnitine level causes death from hypoglycemia: possible involvement of suppression of hypothalamic orexin expression during weaning period.

The mechanism of onset of hypoglycemia in patients with carnitine deficiency has yet to be determined. Using mice with systemic carnitine deficiency (JVS mice), we examined this mechanism, focusing on the weaning period (days 14-28 postpartum). For normal mice, the survival rate was 100%, and no hypoglycemia was observed at all. Gastric lactose began to decrease on day 17, and cellulose increased sharply in amount thereafter. For JVS mice, the survival rate was 77% on day 14 and 28% on day 28. From day 21 on, hypoglycemia was noted. Gastric lactose had disappeared almost completely by day 17, and cellulose was almost undetectable from days 14 to 28. Expression of orexin mRNA in the hypothalamus did not differ between JVS and normal mice on day 14, but was suppressed in JVS mice on days 21 and 28. When JVS mice were fed a carnitine-rich diet, suppression of expression of orexin mRNA in hypothalamus was eliminated, and on day 28 lactose and cellulose were detected in the stomach without hypoglycemia. In conclusion, the suppression of the expression of orexin in the hypothalamus during the weaning period may be involved in the marked anorexia in JVS mice, which eventually leads to death from hypoglycemia.

22-Oxacalcitriol prevents progressive glomerulosclerosis without adversely affecting calcium and phosphorus metabolism in subtotally nephrectomized rats.

BACKGROUND: 22-Oxacalcitriol (OCT), an analogue of vitamin D, has been shown to inhibit cell proliferation in cultured mesangial cells. OCT also prevented albuminuria and glomerular injury in an acute model of anti-Thy1 glomerulonephritis. However, potential side effects, including calcaemic actions and tubular dysfunction, of chronic OCT treatment remain unclear. In the present study, we evaluated the effect of OCT in a chronic model of progressive glomerulosclerosis in subtotally nephrectomized (SNX) rats. METHODS: At one week after subtotal nephrectomy, SNX rats were divided into 3 groups having equivalent serum creatinine levels and body weight. OCT (0.08 or 0.4 micro g/kg body weight) was administered intravenously three times per week for 8 weeks to SNX rats. We evaluated effects of OCT on renal function during treatment and on morphologic parameters in glomeruli at 8 weeks. We additionally measured calcium and phosphate levels in serum and urine, and tubular dysfunction markers, including beta(2)-microgloblin (beta(2)m) and N-acetyl-beta-D-glycosaminidase (NAG) levels in urine. RESULTS: OCT treatment significantly suppressed urinary albumin excretion, prevented increases in serum creatinine and serum urea nitrogen, and inhibited glomerular cell number, glomerulosclerosis ratio and glomerular volume in SNX rats at 8 weeks. At that time, OCT-treated groups did not show hypercalcaemia, hypercalciuria or hyperphosphaturia. Furthermore, OCT treatment did not affect beta(2)m or NAG levels in urine, and did not induce histological changes in tubular or interstitial regions. CONCLUSIONS: These findings suggest that OCT may provide a clinically useful agent for preventing the progression of glomerulosclerosis without adversely affecting calcium and phosphorus metabolism or causing subsequent tubular dysfunction.