Oral Magnesium Ion Shortens Prolonged QTc Interval

Abstract

Sir: Pathological crying after stroke is characterized by outbursts of weeping and tearfulness that are not related to an underlying emotional state, but that can be very distressing to the patient.1 Disturbed serotonergic transmission is believed to play a role.2 A number of treatments have been reported as successful, including sertraline, 3 amitriptyline, 9 and nortriptyline. 10 We report the first case of venlafaxine used to successfully treat poststroke pathological crying.Case report. Mr. A, a 67-year-old right-handed man, suffered a hypertensive stroke in 1999 manifested at first by slurred speech and collapse. Computed tomography scan of the head revealed hemorrhage in the left parietal lobe and basal ganglia, compressing the left lateral ventricle, with minimal edema and no midline shift. Also noted were old, small rightsided infarcts with no apparent clinical sequelae.Mr. A was transferred to the rehabilitation service approximately 2 weeks after his stroke. We were asked to evaluate him at that time for crying spells. He denied any past psychiatric history or past untreated mood symptoms. Since the stroke, he reported having between 5 and 20 crying spells daily that were not associated with any change in mood. He did report feeling distressed by these spells but did not endorse symptoms of depression. He denied episodes of pathological laughter. The Pathological Laughter and Crying Scale (PLACS) 10 was administered, on which the patient scored 14 points.After informed consent was obtained from the patient, venlafaxine was initiated at a dose of 37.5 mg twice daily. Within 24 hours, the patient reported complete resolution of his crying spells. Follow-up at 2 weeks revealed a score of 0 on the PLACS. We continued to see him at the rehabilitation service and during his stay in the nursing home care unit. Throughout that 6-month period, he remained symptom-free and did not require any increase in dose.Several tricyclic antidepressants and selective serotonin reuptake inhibitors, as well as other medications, have been reported to dramatically reduce the frequency and severity of pathological crying spells after stroke. Venlafaxine is a serotonin-norepinephrine reuptake inhibitor that may be particularly useful in older patients due to its relatively low protein binding, low anticholinergic effects, low sedation, low orthostatic hypotension, and relatively favorable cytochrome P450 profile. 11,12 While there is the possibility of hypertension with doses over 300 mg daily, 11 which would be a concern in a stroke patient, we found that a low dose of venlafaxine was effective in providing complete relief from this often distressing and embarrassing sequela of stroke.We considered the possibility that since the patient had a hemorrhagic stroke, he might have had seizures manifested by crying. It is known that seizures occur more commonly with hemorrhagic stroke than with ischemic stroke, particularly when the stroke is cortical in location.13 Additionally, we know that venlafaxine acts to increase catechol...

Serum magnesium and cardiovascular mortality in peritoneal dialysis patients: a 5-year prospective cohort study

“…Severe serum Mg deficiency has been correlated with torsade de pointes and certain ventricular tachycardia events; intravenous Mg is regarded as the treatment of choice in these cases, even if hypomagnesaemia is not present ( 32 , 33 ) . Moreover, the phenomenon that oral Mg shortens the prolonged QTc interval caused by medications also suggests that Mg may be an important regulator in the electrocardio physiological process ( 34 ) . As described above, the incidence of hypomagnesaemia is high among PD patients in whom a low-Mg dialysate is routinely used ( 9 , 35 , 36 ) .…”

Identifying the translational gap in the evaluation of drug‐induced QTc interval prolongation

“…A Bayesian adaptation of a model comprising of three components, i.e. an individual correction factor for RR interval (heart rate), an oscillatory component describing the circadian variation and a truncated E max model to capture drug effects , was used as presented in Equation1: where, QT 0 (ms) is the intercept of the QT–RR relationship (gender was included as a covariate for this parameter), RR (s) is the interval between successive R waves, α is the individual heart rate correction factor, A (ms) is the amplitude of circadian rhythm, t is the clock time, φ is the phase, slope (ms/concentration) is the linear pharmacodynamic relationship, and C is the predicted drug concentration at the time of QT measurements.…”

The Role of Magnesium in the Development of Cardiovascular Diseases and the Possibility of their Prevention and Correction with Magnesium Preparations (Part 1)

“…Одним из механизмов воздействия иона магния является блокирование саркоплазматической сети, что нормализует интервал QTc [55]. Прием препаратов магния нормализует удлиненный интервал QT [56]. При парентеральном введении магния антиаритмический…”