Fludrocortisone in Pediatric Vasovagal Syncope: A Retrospective,Single-Center Observational Study

Background and PurposeThe purpose of this study was to determine the effect of fludrocortisone in patients with pediatric vasovagal syncope (VVS).MethodsThis retrospective observational single-tertiary-center study based on chart reviews included 74 patients who were newly diagnosed with VVS in the head-up tilt-table test (HUTT). Some of the patients had been treated with fludrocortisone. All patients were assessed using a brain and cardiac workup before treatment to rule out the syncope being due to other causes, which resulted in seven of them being excluded: two for epilepsy and five for brain pathologies. The remaining 67 patients were analyzed. The effect of fludrocortisone was evaluated based on the results of a follow-up HUTT, with a response to the treatment considered to be present if there was a negative change at the follow-up HUTT. Univariate logistic regression were used for statistical analyses, with the criterion for significance being p<0.05.ResultsThere were no significant differences in the characteristic of the patients between the no-medication (n=39) and fludrocortisone (n=28) groups, including age, sex, and duration of treatment. The recurrence rate of syncopal or presyncopal events was significantly lower in the fludrocortisone group (39.3%, 11 of 28) than in the no-medication group (64.1%, 25 of 39) (p=0.044), as was the rate of negative change at the follow-up HUTT: 57.1% (16 of 28) and 28.2% (11 of 39), respectively (p=0.017).ConclusionsOur findings suggest that fludrocortisone is more effective than no medication in pediatric patients with VVS.     

Newly diagnosed arrhythmogenic right ventricular dysplasia in an octogenarian

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is thought to be a disease of the young, with the majority of newly diagnosed patients under 40 years of age. Establishing this diagnosis in elderly patients may be challenging, and a few reports exist of patients older than 70 years diagnosed with ARVD/C at autopsy. We report the case of an octogenarian with antemortem newly diagnosed ARVD/C. This case report represents the oldest patient to date to have a newly established diagnosis of ARVD/C and highlights the difficulty in making the diagnosis in the elderly.     

Changes in Plasma Epinephrine Concentration and in Heart Rate During Head-Up Tilt Testing in Patients with Neurocardiogenic Syncope:

Sympathetic Activation in Neurocardiogenic Syncope. Introduction : Tilt table testing is widely used in the management of patients with neurocardiogenic syncope. However, the exact pathophysiologic mechanism of this disorder is still under debate. Likewise, therapy of these patients continues to represent a challenge in many cases. Therefore, the present study aimed to gain further insight into the pathophysiology of this syndrome and to examine easily accessible clinical parameters that can improve therapy selection.
Methods and Results : In 16 patients with neurocardiogenic syncope, changes in endogenous catecholamine concentrations were determined during repeated tilt table testing before and during treatment with metoprolol. Tachycardia preceded syncope in 8 of 10 responders compared to only 1 of 6 nonresponders (P < 0.05). In responders, the relative increase in epinephrine levels averaged 197%± 51% during drug-free tilting and 75%± 33% during repeated testing while on β-blocker therapy (P < 0.05). In nonresponders, there was a smaller relative increase in epinephrine averaging 137%± 35% at baseline tilt. During repeated tilt testing, a similar increase was observed in these patients with recurrent syncope (156%± 104%; P = NS compared to baseline).
Conclusion : In patients with neurocardiogenic syncope who show both an increase in epinephrine concentration during tilt test and sinus tachycardia prior to the onset of symptoms, β-blocker treatment is very effective. These findings confirm the major role of sympathetic activation as a trigger of syncope. Particularly, heart rate changes at the onset of syncope may allow early identification of patients responding to antiadrenergic therapy.     

Transient electromechanical dissociation in hypertrophic cardiomyopathy

We describe a patient with hypertrophic cardiomyopathy who experienced several episodes of syncopal attacks, in whom the mechanism was transient electromechanical dissociation.     

Physical Training as Non-Pharmacological Treatment of Neurocardiogenic Syncope

Background

Characterized as a sudden and temporary loss of consciousness and postural tone, with quick and spontaneous recovery, syncope is caused by an acute reduction of systemic arterial pressure and, therefore, of cerebral blood flow. Unsatisfactory results with the use of drugs allowed the nonpharmacological treatment of neurocardiogenic syncope was contemplated as the first therapeutic option.

Objectives

To compare, in patients with neurocardiogenic syncope, the impact of a moderate intensity aerobic physical training (AFT) and a control intervention on the positivity of head-up tilting test (HUT) and orthostatic tolerance time.

Methods

Were studied 21 patients with a history of recurrent neurocardiogenic syncope and HUT. The patients were randomized into: trained group (TG), n = 11, and control group (CG), n = 10. The TG was submitted to 12 weeks of AFT supervised, in cycle ergometer, and the CG to a control procedure that consisted in 15 minutes of stretching and 15 minutes of light walk.

Results

The TG had a positive effect to physical training, with a significant increase in peak oxygen consumption. The CG did not show any statistically significant change before and after the intervention. After the intervention period, 72.7% of the TG sample had negative results to the HUT, not having syncope in the revaluation.

Conclusion

The program of supervised aerobic physical training for 12 weeks was able to reduce the number of positive HUT, as it was able to increase tolerance time in orthostatic position during the HUT after the intervention period.     

Vasodepressor cough syncope masked by sleep apnea-induced asystole

Vasodepressor Cough Syncope. Cough syncope is classified among the neural-reflex "situational" faints, but whether the clinical consequences in affected individuals result from reflex triggered bradyarrhythmia or vasodepressor-induced hypotension, or both, is often unknown. In this report we describe findings in a patient with a clinical history consistent with cough syncope, and in whom documented multiple asystolic spells were at first believed to be responsible for symptoms. However, pacemaker therapy initiated at an outside facility failed to suppress symptoms, and subsequent referral for more detailed autonomic study revealed the asystole to be due to sleep apnea, whereas cough-induced vasodepressor hypotension was the basis of syncope in this individual; the latter provided a pathophysiologic target for prevention of recurring symptoms. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1024-1027, September 2012).     

The predictive value of heart-type fatty acid-binding protein is independent from symptom duration in normotensive patients with pulmonary embolism

Background

Heart-type fatty acid-binding protein (H-FABP) is a useful biomarker for risk stratification of patients with pulmonary embolism (PE). In patients with acute myocardial infarction, H-FABP plasma concentrations rise after 30 minutes and return to normal within 20-24 hours. We tested whether the predictive value of H-FABP is affected by the duration of symptoms prior to diagnosis in patients with PE.

Material and Methods

We prospectively studied 257 consecutive normotensive patients with confirmed symptomatic PE.

Results

Patients with acute (< 24 hours; n = 150) symptom onset presented more often with syncope (28.7% vs. 6.5%; p < 0.001) compared to patients with symptoms ≥ 24 hours (n = 107); other baseline characteristics, comorbidities, and risk factors were distributed equally. Patients with an adverse 30-day outcome (6.6%) had higher H-FABP levels (11.84 [3.57-19.62] ng/ml) compared to patients with a favorable course (3.42 [1.92-5.42] ng/ml; p < 0.001). However, the proportion of patients with H-FABP levels ≥ 6 ng/ml did not differ among patients with acute symptom onset and late presentation (p = 0.104). Only tachycardia and elevation of H-FABP were associated with an increased risk of an adverse 30-day outcome both in patients with acute symptom onset (H-FABP: OR, 5.8; 95% CI, 1.4-24.5; p = 0.016; tachycardia: 7.0 [1.4-36.0]; p = 0.018) and late presentation (H-FABP: 9.3 [2.0-43.2]; p = 0.004 and tachycardia: 12.3 [1.5-103.6]; p = 0.021). The prognostic value could further be improved by the use of a simple H-FABP-based clinical prediction score.

Conclusions

Our findings indicate that H-FABP is a useful biomarker for risk stratification of normotensive patients with PE regardless of symptom duration prior to diagnosis.     

Inherited catecholaminergic polymorphic ventricular tachycardia due to RYR2 mutation

We report the case of an 11‐year‐old boy who was diagnosed with catecholaminergic polymorphic ventricular tachycardia (CPVT). The patient had a medical history of three episodes of syncope. The last episode was cardiac arrest while swimming. After resuscitation using automated external defibrillator, he was placed under cerebral hypothermia, examined for long QT syndrome, and underwent insertion of implantable cardioverter defibrillator. He was subsequently discharged from hospital without any adverse sequelae. The patient was diagnosed with CPVT after detection of ryanodine receptor 2 mutation. His father also carried the same mutation, although he did not have any symptoms nor did he have a history of syncope. We propose that CPVT should be included in the differential diagnosis in children with recurrent episodes of syncope.     

Permanent cardiac pacing for severe pallid breath-holding spells

We report the case of an infant affected by frequent episodes of loss of consciousness with the clinical features of pallid breath-holding attacks. Prolonged asystole, up to 26 seconds, was demonstrated by Holter monitoring. The patient was treated with permanent pacemaker implantation, followed by complete symptom resolution during a 26-month follow-up.