Pacing for neurally-mediated syncope: How to decide?

Neurally-mediated syncope has a broad clinical spectrum which ranges from typical vasovagal syncope on one hand, to those situations in which reflex syncope occurs with uncertain, or even apparently absent, triggers or prodromes, on the other hand. Overlap of clinical features is frequent in clinical practice and makes any classification difficult to apply when selecting patients for cardiac pacing. Typically, the reflex is both hypotensive and cardio-inhibitory. The rationale for efficacy of cardiac pacing is that the cardio-inhibitory reflex is dominant, since there is no role for pacing in preventing vasodilatation and hypotension. Establishing a relationship between symptoms and cardio-inhibitory reflex should be the goal of the clinical evaluation before embarking on permanent pacing. Similar efficacy has been observed in patients affected by dominant cardio-inhibitory reflex irrespective of the clinical form. In general, cardiac pacing should be considered last choice applied only in highly selected patients, i.e. those ≥ 40 years of age, affected by severe forms of reflex syncope with recurrences associated with frequent injury, often due to the lack of prodromes. Recurrence of syncope may still occur despite cardiac pacing in a minority of patients

Management of transient loss of consciousness in emergency department: what’s new from 2018 European Society of Cardiology guidelines?

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A very prolonged asystolic vasovagal syncope is suspended but not aborted by counterpressure manoeuvre

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The Higgs mass as a function of the compactification scale

We calculate to a few percent precision the Higgs potential in a model with supersymmetry broken by boundary conditions on an extra-dimension, compactified to a segment of length $L$, and a top quark quasi-localized on one of the two boundaries. 1/L alone, in the range 2-4 TeV, determines the Higgs mass, in the range 110-125 GeV, and the spectrum of gauginos, higgsinos and of the third-generation squarks. Lower values of 1/L cannot be excluded, with a progressive delocalization of the top quark.Comment: 22 pages, 6 figure

An abnormal neural reflex plays a role in causing syncope in sinus bradycardia

AbstractObjectives. This study Investigates the rote of an abnormal neural reflex in causing syncope in patients with sinus bradycardia.Background. Syncope is commonly considered an indication of severity in sinus bradycardia. However, the occurrence of syncope is unpredictable, and the prognosis appears to be similar in patients with and without syncope.Methods. Head-up tilt testing (60 ° for 60 min), carotid sinus massage in the supine and standing positions, 24-h Bolter ambulatory electrocardiographic (ECG) recording and etectrophysiologic study before and after pharmacologic autonomic blockade were performed in 25 patients with sinus bradycardia and syncope (group I, sinus rate <50 beats/min, age 71 ± 12 years) and 25 patients with sinus bradycardia and no neurologic symptoms (group II, sinus rate <50 beats/min, age 67 ± 16 years).Results. Clinical characteristics and ambulatory ECG monitoring data were similar in the two study groups. A positive response (induction of syncope or presyncope with hypotension and/or bradycardia) was obtained by head-up tilt testing in 15 group I (60%) and in 3 group II (12%) patients (p < 0.001) and by carotid sinus massage in 11 group I (44%) and 6 group II (24%) patients (p = NS). Results of at least one test (head-up tilt testing or carotid sinus massage, or both) were positive in 19 group I (76%) and 9 group II (36%) patients (p < 0.01). Basal and intrinsic corrected sinus node recovery time did not differ significantly between the two groups. An abnormal intrinsic heart rate was present in 66% of group I and 26% of group II patients (p < 0.01). The different percentage of positive findings on head-up tilt testing and carotid sinus massage in the two groups was independent of the presence of intrinsic sinus node dysfunction.Conclusions. These results indicate that an abnormal neural reflex plays a role in causing syncope in patients with sinus bradycardia. This reflex seems to be unrelated to the severity of sinus node dysfunction, even if the latter could enhance the cardioinhibitory response

Isometric arm counter-pressure maneuvers to abort impending vasovagal syncope

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