Magnetic resonance imaging in a patient with an implantable cardiac defibrillator

A 58-year-old man, in whom an implantable cardiac defibrillator (ICD) had been implanted for Brugada syndrome, suffered rapidly progressive general paralysis. Various diagnostic imaging techniques were performed, but the cause could not be determined. Magnetic resonance imaging (MRI) scanning was performed. A 1.5-Tesla MRI system was used, and the ICD was programmed to ODO mode and all tachycardia detection was turned off. MRI was performed safely under electrocardiogram and pulse oximeter monitoring, and appropriate precautions were taken in preparation for an emergency. ICD parameters did not change in post-imaging investigations. MRI revealed an apparent tumor in the patient's medulla and upper cervical spinal cord, which was diagnosed as high-grade astrocytoma. When performing MRI procedures in patients with an ICD under urgent conditions, it is necessary to have complete knowledge of the procedure and to make careful preparations

The Rho/Rho-kinase Systems Are Involved in Rapid Pacing-induced Changes of Atrial Refractory Period in a Canine Model

Introduction: The Rho/Rho-kinase pathway has been related to various physiological responses of the cardiovascular system. Previous reports have suggested a significant effect of Rho signals on the electrophysiological characteristics of the heart. We hypothesized that the Rho/Rho-kinase system would contribute to the rapid pacing-related change of atrial effective refractory period (AERP). Methods and Results: In 17 dogs, AERP was measured at the right atrial appendage (RAA) and posterior left atrium (LA) before, during, and after 6-hours rapid atrial pacing at 500 bpm. Saline control (n = 5), verapamil (n = 5), or fasudil (n = 7) were infused throughout the protocol. The shortening of AERP after rapid pacing was abrogated by the administration of verapamil, as reported in previous studies. Furthermore, fasudil (Rho/Rho-kinase inhibitor) influenced the change of AERP in a manner similar to the infusion of verapamil throughout the experiments. Conclusions: Since the AERP was attenuated by fasudil, rapid pacing-related atrial electrophysiological changes might involve the Rho/Rho-kinase pathway

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo