An Underrecognized Cause of Recurrent Nocturnal Syncope with a Pacemaker: Sleep Rate Mode.

BACKGROUND: Nocturnal syncope is a common presentation in the emergency department, often related to orthostatic hypotension and subsequent loss of cerebral perfusion when patients get up from sleep to use the restroom faster than their cardiac output and vascular tone can accommodate. Poor hydration status and antihypertensive medications can increase this risk. Patients with syncope who present to the emergency department with a pacemaker are usually evaluated with a pacemaker interrogation to evaluate for runs of nonperfusing rhythms (e.g., ventricular tachycardia or fibrillation). Sleep rate mode (SRM) is a relatively new feature of modern pacemakers and is not currently recognized by emergency physicians. It was implemented to accommodate more physiologic fluctuations in heart rate during rapid eye movement sleep. There is a paucity of evidence supporting the clinical benefit of SRM and similarly no documentation of prior complications of SRM in the current literature. CASE REPORT: We report the case of a 92-year-old woman with a Medtronic Avisa pacemaker presenting with recurrent nocturnal syncope and bradycardia resulting in multiple emergency department visits. These episodes ultimately resolved by turning off SRM on her pacemaker. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: SRM is not currently flagged on interrogation report summaries provided to emergency physicians. This report highlights the importance of recognizing this mode as a potential etiology of nocturnal syncope related to chronotropic incompetence in patients with pacemakers.

A Great Heist: Subclavian Steal Syndrome Causing Posterior Transient Ischemic Attack and Stroke.

Introduction Subclavian steal syndrome is a phenomenon of arterial flow reversal secondary to occlusive disease in proximal subclavian arteries, occasionally resulting in neurologic sequelae. Case Presentation The authors present the case of a 67-year-old man with stroke risk factors and a history of receiving head and neck radiation therapy who developed subclavian steal physiology leading to a transient ischemic attack and posterior circulation stroke. He was medically optimized without substantial progression or recurrence of disease. Conclusion This case illustrates a case of vertebrobasilar transient ischemic attack and posterior circulation stroke from subclavian steal syndrome in the setting of prior radiation therapy manifesting as extremity weakness and discoordination. Further research on therapeutic radiation dosages and subsequent incidence of arterial disease which could contribute to subclavian steal syndrome is necessary.

Protective effects of the mechanistic target of rapamycin against excess iron and ferroptosis in cardiomyocytes.

Clinical studies have suggested that myocardial iron is a risk factor for left ventricular remodeling in patients after myocardial infarction. Ferroptosis has recently been reported as a mechanism of iron-dependent nonapoptotic cell death. However, ferroptosis in the heart is not well understood. Mechanistic target of rapamycin (mTOR) protects the heart against pathological stimuli such as ischemia. To define the role of cardiac mTOR on cell survival in iron-mediated cell death, we examined cardiomyocyte (CM) cell viability under excess iron and ferroptosis conditions. Adult mouse CMs were isolated from cardiac-specific mTOR transgenic mice, cardiac-specific mTOR knockout mice, or control mice. CMs were treated with ferric iron [Fe(III)]-citrate, erastin, a class 1 ferroptosis inducer, or Ras-selective lethal 3 (RSL3), a class 2 ferroptosis inducer. Live/dead cell viability assays revealed that Fe(III)-citrate, erastin, and RSL3 induced cell death. Cotreatment with ferrostatin-1, a ferroptosis inhibitor, inhibited cell death in all conditions. mTOR overexpression suppressed Fe(III)-citrate, erastin, and RSL3-induced cell death, whereas mTOR deletion exaggerated cell death in these conditions. 2',7'-Dichlorodihydrofluorescein diacetate measurement of reactive oxygen species (ROS) production showed that erastin-induced ROS production was significantly lower in mTOR transgenic versus control CMs. These findings suggest that ferroptosis is a significant type of cell death in CMs and that mTOR plays an important role in protecting CMs against excess iron and ferroptosis, at least in part, by regulating ROS production. Understanding the effects of mTOR in preventing iron-mediated cell death will provide a new therapy for patients with myocardial infarction. NEW & NOTEWORTHY Ferroptosis has recently been reported as a new form of iron-dependent nonapoptotic cell death. However, ferroptosis in the heart is not well characterized. Using cultured adult mouse cardiomyocytes, we demonstrated that the mechanistic target of rapamycin plays an important role in protecting cardiomyocytes against excess iron and ferroptosis.