Patel, Nikhil A.

In this case report, a patient with schizophrenia experienced recurrent priapism while undergoing treatment of acute psychosis. This necessitated a review of the emergent treatment of priapism and discussion of the difficulties in treating priapism in a patient with acute psychosis. Therefore, this case report explores multiple possible etiologies of priapism within the realm of psychiatric care, reviews the proposed mechanisms of medication-induced priapism, and considers the psychopharmacological concepts that pertain to antipsychotic selection in the context of antipsychotic-induced priapism.

Dynamic QT Interval Monitoring Post‐LCSDBackgroundVideoscopic left cardiac sympathetic denervation (LCSD) is an adjunct therapy for reduction of arrhythmia‐induced events in patients with long‐QT syndrome (LQTS). LCSD reduces LQTS‐triggered breakthrough cardiac events. The temporal effects of QTc changes post‐LCSD have not been studied.MethodsWe utilized continuous QTc monitoring on 72 patients with LQTS. We evaluated acute and long‐term QTc changes in comparison to 12‐lead ECG‐derived QTc values prior to surgery, 24 hours postsurgery, and at follow up ≥3 months.ResultsSeventy‐two patients underwent LCSD at our institution (46% male, mean age at LCSD was 14 ± 10 years). The mean baseline, pre‐LCSD QTc was 505 ± 56 ms, which had decreased significantly at ≥3 months post‐LCSD to 491 ± 40 ms (P = 0.001). QTc monitoring revealed that the majority of the cohort (53/72; 74%) had a transient increase >30 ms in QTc from baseline, with an average maximum increase of 72 ± 30 ms. Resolution within 10 ms of baseline or less occurred in 57% (30/53) at 24 hours post‐LCSD.ConclusionsAlthough LQTS patients may have a paradoxically increased QTc post‐LCSD, the effects are transient in most patients. Importantly, no patients experienced any arrhythmias in the postoperative setting related to this transient rise in QTc.

Background— A patent foramen ovale (PFO) may permit arterial embolization of thrombi that accumulate on the leads of cardiac implantable electronic devices in the right-sided cardiac chambers. We sought to determine whether a PFO increases the risk of stroke/transient ischemic attack (TIA) in patients with endocardial leads. Methods and Results— We retrospectively evaluated all patients who had endocardial leads implanted between January 1, 2000, and October 25, 2010, at Mayo Clinic Rochester. Echocardiography was used to establish definite PFO and non-PFO cohorts. The primary end point of stroke/TIA consistent with a cardioembolic etiology and the secondary end point of mortality during postimplantation follow-up were compared in PFO versus non-PFO patients with the use of Cox proportional hazards models. We analyzed 6075 patients (364 with PFO) followed for a mean 4.7±3.1 years. The primary end point of stroke/TIA was met in 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard ratio, 3.49; 95% confidence interval, 2.33–5.25; P <0.0001). The association of PFO with stroke/TIA remained significant after multivariable adjustment for age, sex, history of stroke/TIA, atrial fibrillation, and baseline aspirin/warfarin use (hazard ratio, 3.30; 95% confidence interval, 2.19–4.96; P <0.0001). There was no significant difference in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confidence interval, 0.77–1.07; P =0.25). Conclusions— In patients with endocardial leads, the presence of a PFO on routine echocardiography is associated with a substantially increased risk of embolic stroke/TIA. This finding suggests a role of screening for PFOs in patients who require cardiac implantable electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvascular lead placement may be considered.