RESUMO
Exposure to critical incidents and hence potentially traumatic events is endemic in law enforcement. The study of law enforcement officers' experience of moral injury and their exposure to potentially morally injurious incidents, and research on moral injury's relationship with different forms of traumatization (e.g. compassion fatigue, post-traumatic stress disorder) are in their infancy. The present study aims to build on prior research and explores the role of moral injury in predicting post-traumatic stress disorder (PTSD) and its clusters thereof. To this end, a sample of law enforcement officers (N = 370) from the National Police of Finland was recruited to participate in the current study. Results showed that moral injury significantly predicted PTSD as well as its diagnostic clusters (i.e., avoidance, hyperarousal, re-experiencing). The aforementioned role of moral injury to significantly predict PTSD and its clusters were unequivocal even when compassion fatigue was incorporated into the path model. Clinical, research, and law enforcement practice implications are discussed.
RESUMO
BACKGROUND: The ventricular tachycardia (VT) circuit is often assumed to be located in the endocardium or epicardium. The plateauing success rate of VT ablation warrants reevaluation of this mapping paradigm. OBJECTIVE: The purpose of this study was to resolve the intramural components of VT circuits by mapping in human hearts. METHODS: Panoramic simultaneous endocardial-epicardial mapping (SEEM) during intraoperative mapping (IOM) was performed in human subjects. In explanted hearts (EH), SEEM and intramural multielectrode plunge needle mapping (NM) of the left ventricle were performed. Overall, 37 VTs (26 ischemic cardiomyopathy [ICM], 11 nonischemic cardiomyopathy [NICM]) were studied in 32 patients. Intraoperative SEEM was performed in 16 patients (16 ICM). Additionally, 16 explanted myopathic human hearts (9 NICM, 7 ICM) were studied in a Langendorff setup. Predominant intramural location of the VT was imputed by the absence of significant endocardial-epicardial activation during IOM (using SEEM and no NM) or by the presence of intramural activation spanning the entire cycle length (including mid-diastole) in EH (SEEM and NM). RESULTS: By IOM (SEEM), predominant endocardial activation (entire tachycardia cycle length including mid-diastolic activation) was present in 10 of 18 VTs (55%). In 8 of 18 VTs (44%), the VT circuit was presumed to be intramural due to incomplete diastolic activation in endocardium and epicardium. In EH (SEEM and NM), VT location was predominantly intramural, endocardial, and epicardial in 8 of 19 (42%), 5 of 19 (26%), and 1 of 19 VTs (5%), respectively. CONCLUSION: In a significant proportion of both ischemic and nonischemic ventricular tachycardias, the predominant activation was located in the intramural space.
