Magnetocardiography at rest predicts cardiac death in patients with acute chest pain.

Introduction: Sudden cardiac arrest is a major cause of morbidity and mortality worldwide and remains a major public health problem for which better non-invasive prediction tools are needed. Primary preventive therapies, such as implantable cardioverter defibrillators, are not personalized and not predictive. Most of these devices do not deliver life-saving therapy during their lifetime. The individual relationship between fatal arrhythmias and cardiac function abnormalities in predicting cardiac death risk has rarely been explored. Methods: We retrospectively analyzed the measurements at rest for 191 patients with acute chest pain (ACP) magnetocardiographically. Our recently introduced analyses are able to detect inhomogeneities of the depolarization and repolarization. Moreover, electrically silent phenomena-intracellular ionic currents as well as vortex currents-can be measured and quantified. All included ACP patients were recruited in 2009 at Yonsei University Hospital and were followed up until 2022. Results: During half of the follow-up period (6.5 years), 11 patients died. Out of all the included nine clinical, eight magnetocardiographical, and nine newly introduced magnetoionographical parameters we tested in this study, three parameters revealed themselves to be outstanding at predicting death: heart rate-corrected QT (QTc) prolongation, depression of repolarization current IKr + IKs, and serum creatinine (all significant in Cox regression, p < 0.05). They clearly predicted cardiac death over the 6.5 years duration (sensitivity 90.9%, specificity 85.6%, negative predictive accuracy 99.4%). Cardiac death risk was more than ninefold higher in patients with low repolarization reserve and QTc prolongation in comparison with the remaining patients with ACP (p < 0.001). The non-parametric Kaplan-Meier statistics estimated significantly lower survival functions from their lifetime data (p < 0.001). Discussion: To the best of our knowledge, these are the first data linking magnetocardiographical and magnetoionographical parameters and subsequent significant fatal events in people, suggesting structural and functional components to clinical life-threatening ventricular arrhythmogenesis. The findings support investigation of new prevention strategies and herald those new non-invasive techniques as complementary risk stratification tools.

Cimetropium bromide does not improve polyp and adenoma detection during colonoscope withdrawal: A randomized, double-blind, placebo-controlled study.

BACKGROUND: Endoscopic inspection of colonic mucosa is disturbed by colonic folds and peristalsis, which may result in missed polyps. Cimetropium bromide, an antispasmodic agent, inhibits peristalsis and colonic spasms, which may improve polyp detection. The purpose of this randomized, double-blind, placebo-controlled study was to investigate whether cimetropium bromide could improve polyp and adenoma detection in the colorectum and right colon. METHODS: Patients undergoing screening or diagnostic colonoscopy were randomized to receive intravenous cimetropium bromide (5 mg) or placebo after cecal intubation. The primary outcomes were the number of polyps per patient (PPP) and adenomas per patient (APP); secondary outcomes were the polyp detection rate (PDR), adenoma detection rate (ADR), and advanced neoplasm detection rate (ANDR). RESULTS: A total of 181 patients were analyzed; 91 patients received cimetropium bromide and 90 patients received placebo. Cimetropium bromide and placebo groups did not significantly differ in the PPP and APP for the colorectum (1.38 ±â€Š1.58 vs 1.69 ±â€Š2.28, P = .298; 0.96 ±â€Š1.27 vs 1.11 ±â€Š1.89, P = .517, respectively) and right colon (0.70 ±â€Š0.95 vs 0.78 ±â€Š1.21, P = .645; 0.47 ±â€Š0.81 vs 0.51 ±â€Š0.81, P = .757, respectively). Two groups also did not significantly differ in the PDR, ADR, and ANDR for the colorectum and right colon. Furthermore, there were no difference between groups in the PPP, APP, PDR, ADR, and ADNR in a sub-analysis of expert and non-expert endoscopists. CONCLUSIONS: Cimetropium bromide did not improve polyp and adenoma detection in the colorectum and right colon during colonoscope withdrawal, regardless of the expertness of the endoscopist. However, its use may be helpful in patients with active peristalsis or for beginning endoscopists during standard colonoscopy without a transparent cap.

Heparin bridging in warfarin anticoagulation therapy initiation could increase bleeding in non-valvular atrial fibrillation patients: a multicenter propensity-matched analysis.

BACKGROUND: The efficacy of heparin-bridging therapy during the initiation of oral anticoagulation therapy (OAC) in non-valvular atrial fibrillation (NVAF) is unclear. OBJECTIVES: To evaluate the efficacy and the safety of heparin-bridging therapy during OAC initiation in NVAF patients. PATIENTS/METHODS: This study included 5327 consecutive warfarin-naïve NVAF patients who received OAC that was initiated with (n = 1053) or without (n = 4274) heparin bridging at four tertiary hospitals. Stroke and bleeding events within 30 days of OAC were evaluated. RESULTS: While there was no difference in the incidence of stroke (0.5% vs. 0.3%, P = 0.381), major bleeding rate (0.9% vs. 0.3%, P = 0.004) was higher in heparin-bridged than in non-bridged patients. This trend remained in the propensity score-matched population (stroke 0.5% vs. 0.6%, P = 0.762; major bleeding 0.8% vs. 0.1%, P = 0.019). A high CHA2 DS2 -VASc score was an independent predictor for stroke, whereas bridging therapy had no beneficial effect in preventing stroke regardless of CHADS2 or CHA2 DS2 -VASc scores. The HAS-BLED score had a predictive value for major bleeding (odds ratio 1.80, 95% confidence interval 1.11-2.92, P = 0.018), and heparin-bridging therapy was associated with a higher major bleeding rate (odds ratio 4.44, 95% confidence interval 1.68-11.72, P = 0.003), especially in patients with a HAS-BLED score of ≥ 1. CONCLUSIONS: The heparin-bridging therapy increased bleeding without the benefit of preventing stroke at the initiation of OAC in NVAF. Our data suggest that heparin bridging should not be considered at the initiation of OAC in NVAF patients.