Background-Contrast medium-induced acute kidney injury is associated with substantial morbidity and mortality. The underlying mechanism has been attributed in part to ischemic kidney injury. The aim of this randomized, double-blind, sham-controlled trial was to assess the impact of remote ischemic preconditioning on contrast medium-induced acute kidney injury. Methods and Results-Patients with impaired renal function (serum creatinine Ͼ1.4 mg/dL or estimated glomerular filtration rate Ͻ60 mL ⅐ min Ϫ1 ⅐ 1.73 m Ϫ2 ) undergoing elective coronary angiography were randomized in a 1:1 ratio to standard care with (nϭ50) or without ischemic preconditioning (nϭ50; intermittent arm ischemia through 4 cycles of 5-minute inflation and 5-minute deflation of a blood pressure cuff). Overall, both study groups were at high risk of developing contrast medium-induced acute kidney injury according to the Mehran risk score. The primary end point was the incidence of contrast medium-induced kidney injury, defined as an increase in serum creatinine Ն25% or Ն0.5 mg/dL above baseline at 48 hours after contrast medium exposure. Contrast medium-induced acute kidney injury occurred in 26 patients (26%), 20 (40%) in the control group and 6 (12%) in the remote ischemic preconditioning group (odds ratio, 0.21; 95% confidence interval, 0.07-0.57; Pϭ0.002). No major adverse events were related to remote ischemic preconditioning. Conclusions-Remote ischemic preconditioning before contrast medium use prevents contrast medium-induced acute kidney injury in high-risk patients. Our findings merit a larger trial to establish the effect of remote ischemic preconditioning on clinical outcomes. Clinical Trial Registration-URL: http://www.germanctr.de. Unique identifier: U1111-1118-8098. (Circulation. 2012;126:296-303.)

Conclusion: In patients at high risk for contrast-induced nephropathy, remote ischemic preconditioning (rIPC) before contrast medium use prevents acute kidney injury (AKI). Summary: The main predictor of contrast-induced AKI (CI-AKI) is a decreased estimated glomerular filtration rate (eGFR) of <60 mL/min/ 1.73 m 2. The magnitude of decrease in eGFR correlates directly with CI

BackgroundHigh-density mapping of ventricular tachycardia (VT) with PentaRay® (Biosense-Webster) provides high resolution with discrimination of local abnormal electrograms and slow conducting channels. We evaluate the feasibility of PentaRay® to characterize the anatomical substrate and assume an influence of the outcome despite limitations.MethodsOver a 24-month period, 26 endocardial and four epicardial maps were obtained of 26 VT patients (18 ischemic cardiomyopathy (ICM, 69.2%) and 8 non-ischemic cardiomyopathy (NICM, 30.8%), age 65 ± 9 years). Catheter ablation (CA) was performed with the aim of transecting the isthmus. The endpoint was non-inducibility of any VT. Manual review of the maps was performed and focused on evaluating scarring, bipolar electrograms, and procedure times.ResultsIn 55.6 ± 34.4 min, 1,085.9 ± 726.2 points were created. The mean ablation time was 50.8 ± 30.1 min. The endpoint was achieved in 12 patients (46.2%). The mean dense scar area and the mean patchy scar area were 49.4 ± 51.8 cm2 (range 0 - 190 cm2) and 14.7 ± 14.9 cm2 (range 0 - 110 cm2), respectively. Analyzing the learning curve, we found a tendency in decreasing procedure times. During the course of follow-up treatment averaging a 14-month period, device interrogation showed that 17 patients (65.4%) had remained free of any arrhythmia recurrence.ConclusionThe high-density maps with PentaRay® were safely created in a short period of time. Our manual review of the maps reveals limitations of current annotation criteria; nevertheless, medium-term outcomes were encouraging. Further prospective studies are required to validate our findings in a larger cohort of patients.

In a single-center observational study, both conventional and high-density mapping approaches in VT patients are comparable in terms of procedure duration and outcome. Mapping time when using a multi-electrode catheter seems to have the tendency of being shorter. We should be encouraged to recruit more patients comparing the benefit of different catheter types.

We thank the authors for their interest in our study on the impact of remote ischemic preconditioning on contrast medium-induced acute kidney injury (CI-AKI). 1 The incidence of CI-AKI varies substantially among several studies because of the lack of a uniform definition of CI-AKI. 2 Rates of CI-AKI may be as high as 50% or even higher, depending on the presence of risk factors such as chronic renal insufficiency and diabetes mellitus. Although the definition of CI-AKI varies across the trials, the most commonly used definition includes an absolute increase in serum creatinine of 0.5 mg/dL or a 25% relative increase in serum creatinine from the baseline value at 48 hours after exposure to contrast agent in the absence of alternative causes of acute kidney injury. This definition of CI-AKI was used consistently in our study. ), patients with a calculated risk score of 13 have an ≈40% risk of developing CI-AKI. Considering that the RenPro cohort displayed a mean risk score of 13, the CI-AKI rate of 40% in our control arm coincides exactly with the predicted risk for CI-AKI development. Calculation of the incidence of CI-AKI by combining a serum creatinine increase >25% and >0.5 mg/dL over the baseline did not change the reported outcomes significantly (34% in the control group versus 12% in the remote ischemic preconditioning arm; P=0.016).The different rates of CI-AKI in our study and in the trials cited by Drs Mehta-Oza and Raman 5,6 can be explained solely by the differences in the mean Mehran risk score, since our study group included predominantly high-risk patients with a higher-integer risk score. Furthermore, a different definition of CI-AKI (eg, the glomerular filtration rate-based definition in the report by Brar et al 5 ) along with the use of the different types and volumes of contrast media, population size, planned nature of the interventional procedure, and the different length of patient follow-up, may explain the varying CI-AKI rates.Nevertheless, the relevant difference in incidences among studies reveals the need for a uniform definition of CI-AKI to be used in clinical practice. In this respect, serum creatinine, although simple to obtain in clinical routine, is not reliable enough for identification of patients at risk for CI-AKI development. To evaluate renal function accurately, assessment of other renal markers, such as neutrophil gelatinase-associated lipocalin or cystatin C, might be a better choice. DisclosuresNone.

Zusammenfassung Anamnese und klinischer Befund Wir berichten über einen 79-jährigen Patienten, der während der Visite durch lageabhängige Dyspnoe und Lippenzyanose auffiel. Untersuchungen In liegender Position bestand eine normale Sauerstoffsättigung von > 95 %, welche in aufrechter Position reproduzierbar auf SpO2-Werte von 76–85 % abfiel. Echokardiografisch konnte ein großes persistierendes Foramen ovale (PFO) mit spontanem Rechts-Links-Shunt nachgewiesen werden. Nebenbefundlich fiel ein Aneurysma der thorakalen Aorta auf. Diagnose Aufgrund der typischen Befundkonstellation aus lageabhängiger Dyspnoe und Sauerstoffsättigungsabfall bei persistierendem Foramen ovale und begleitendem Aortenaneurysma stellten wir die Diagnose eines Platypnoe-Orthodeoxie-Syndroms. Therapie und Verlauf Nach perkutanem PFO-Verschluss war der Patient beschwerdefrei und die Sauerstoffsättigung blieb lageunabhängig bei > 95 %. Ein relevanter Rechts-Links-Shunt ließ sich echokardiografisch nicht mehr nachweisen. Folgerung Die Kombination aus lageabhängiger Dyspnoe und objektivierbarem Sauerstoffsättigungsabfall sollte immer an ein mögliches Platypnoe-Orthodeoxie-Syndrom denken lassen. Hierbei sind die ursächlichen Befundkonstellationen vielfaltig und nicht nur kardiologischer Genese.

In case of incongruent findings, the BNP-level seems to be a useful additional diagnostic tool in the diagnosis of pericarditis constrictiva.