Daniel Kosinski

The Postural Orthostatic Tachycardia Syndrome: A Neurocardiogenic Variant Identified During Head‐Up Tilt Table Testing

Head upright tilt table testing has emerged as an accepted modality for identifying an Individuals predisposition to episodes of autonomically mediated hypotension and bradycardia that are sufficiently profound so that transient loss of consciousness ensues (neurocardiogenic syncope). However it has also become apparent that less dramatic falls in blood pressure, while not sufficient to cause full syncope, may produce symptoms such as near syncope, vertigo, dizziness, and TIA‐like episodes. We have identified a subgroup of individuals with a mild form ofautonomic dysfunction with symptoms of postural tachycardia and lightheadedness, disabling fatigue, exercise intolerance, dizziness, and near syncope. During baseline tilt table testing these patients demonstrated a heart rate increase of ± 30 beats/min (or a maximum heart rate of 120 beats/min) within the first 10 minutes upright (unassociated with profound hypotension), which reproduced their symptom complex. In addition these patients exhibit an exaggerated response to isoproterenol infusions. Similar observations have been made by others who have dubbed this entity the Postural Orthostatic Tachycardia Syndrome (POTS). We conclude that POTS represents a mild (and potentially treatable) form of autonomic dysfunction that can be readily diagnosed during head upright tilt table testing.

Use of sertraline hydrochloride in the treatment of refractory neurocardiogenic syncope in children and adolescents

OBJECTIVES The purpose of our study was to determine whether the serotonin reuptake inhibitor sertraline hydrochloride could prevent neurocardiogenic syncope in children and adolescents resistant to or intolerant of other therapies. BACKGROUND The serotonin reuptake inhibitor fluoxetine hydrochloride has been reported to be effective in preventing neurocardiogenic syncope in adults. METHODS Seventeen consecutive young patients (mean age 15 years, range 10 to 18; 7 male, 10 female) with recurrent syncope and a positive head-upright tilt table test, and in whom standard therapies (fludrocortisone, transdermal scopolamine, beta-adrenergic blocking agents, disopyramide) were ineffectual, poorly tolerated or contraindicated, were referred for study. Sertraline was administered orally at 50 mg daily for 4 to 6 weeks. A head-upright tilt table test was then reperformed, and the clinical effect was noted. RESULTS Three patients (18%, 95% confidence interval [CI] 1 to 44) were intolerant of the drug, and it was discontinued. Nine patients became asymptomatic and tilt negative (53%, 95% CI 26 to 76), and five remained tilt positive (36%, 95% CI 15 to 65). Over a mean follow-up period of 12 +/- 5 months, the tilt-negative patients remained symptom free while taking sertraline. CONCLUSIONS The serotonin reuptake inhibitor sertraline hydrochloride can be effective in preventing recurrent neurocardiogenic syncope in selected patients unresponsive to or intolerant of other therapeutic modalities.

Tilt Table Testing: Concepts and Limitations

Recurrent unexplained syncope is a common and often frustrating clinical problem. Over the last decade, bead upright tilt table testing bas emerged as an important diagnostic metbod far the identification of individuals whose syncope is likely to be neurocardiogenic in origin. At the same time, tilt table testing, by providing syncopal episodes in a controlled setting, has allowed for a much greater understanding of these disorders. This article reviews the concepts behind tilt table testing, as well as the uses and limitations of the evolving diagnostic modality.

Pathophysiological Aspects of Neurocardiogenic Syncope: Current Concepts and New Perspectives

Neurocardiogenic syncope is both a common and complex clinical disorder. Although recent research has clarified some of the pathophysiological mechanisms involved, much still remains either unknown or incompletely understood. Further investigation into this condition will not only enhance our knowledge of this and other related disorders, but will shed greater light on the influences of the brain and autonomic system on heart rate and blood pressure regulation and aid in our understanding of the complex interrelationships of neurocardiology.

Cerebral syncope : loss of consciousness associated with cerebral vasoconstriction in the absence of systemic hypotension

Transcranial Doppler (TCD) ultrasonography done during headupright tilt induced neurocardiogenic syncope has demonstrated that cerebral Vasoconstriction occurs concomitant with (or precedes) loss of consciousness. This article demonstrates evidence that cerebral blood flow changes alone (vasoconstriction), in the absence of systemic hypotension, may result in syncope. Five patients (4 men, 1 woman; mean age 41 ± 17 years) with recurrent unexplained syncope were evaluated by use of an upright tilt table test for 45 minutes with or without an infusion of low dose isoproterenol. TCDoppler ultrasonography was used to assess middle cerebral artery systolic velocity (Vs); diastolic velocity (Vd); mean velocity (Vm); and pulsatility index (PI = Vs = Vd/Vmean). Syncope occurred in five patients during the baseline tilt and in one patient during isoproterenol infusion. During tilt induced syncope, at an average mean arterial pressure of 89 ± 16 mmHg, TCD sonography showed a 2%± 10% increase in systolic velocity; a 51%± 27% decrease in diastolic velocity; and a 131 %± 87% increase in pulsatility index. One patient underwent continuous electroencephalographic recording during tilt, which demonstrated diffuse slow wave activity (indicating cerebral hypoxia) at the time of syncope concomitant with the aforementioned TCD changes in the absence of systemic hypotension. These fndings reflect an increase in cerebrovascular resistance secondary to arteriolar vasoconstriction distal to the insonation point of the middle cerebral artery, that occurred concomitant with loss of consciousness and in the absence of systemic hypotension. We conclude that in some individuals abnormal baroreceptor responses triggered during orthostatic stress may result in a derangement of cerebral autoregulation leading to cerebral vasoconstriction with resultant cerebral hypoxia in the absence of systemic hypotension.

Fluoxetine hydrochloride for the treatment of severe refractory orthostatic hypotension

OBJECTIVE To evaluate the usefulness of fluoxetine hydrochloride in the treatment of patients with severe refractory orthostatic hypotension. DESIGN Prospective, nonrandomized study. PATIENTS Five patients (3 men, 2 women with a mean age of 67 +/- 7 years with chronic symptomatic orthostatic hypotension resistant to or intolerant of other therapies. METHODS Symptoms and orthostatic responses were recorded in the baseline state. Fluoxetine hydrochloride 20 mg orally once daily was started and patients were reevaluated after 6 to 8 weeks of therapy. RESULTS All patients demonstrated orthostatic hypotension (20 mm Hg or greater decline in systolic blood pressure) associated with symptoms (eg, dizziness, vertigo, near syncope) in the baseline state. After 6 to 8 weeks of fluoxetine therapy, 2 patients reported resolution of all symptoms, 2 had a marked reduction in symptoms, and 1 patient experienced no effect. Orthostatic responses were attenuated in 4 of the 5 patients (80%). CONCLUSION Fluoxetine hydrochloride may be an effective therapy for some patients with recurrent severe orthostatic hypotension refractory to other forms of therapy.

The use of methylphenidate in the treatment of refractory neurocardiogenic syncope.

Recurrent neurocardiogenically mediated episodes of hypotension and bradycardia are a common cause of recurrent syncope that can be identified by head upright tilt table testing. While the use of β‐blockers, theophylline, fludrocortisone, disopyramide, and serotonin re‐uptake inhibitors can be helpful in preventing further episodes, some patients are unresponsive to or poorly tolerant of these agents. We investigated the use of the central nervous system stimulant and peripheral vasoconstrictor methylphenidate in preventing both tilt induced and spontaneous neurocardiogenic syncope. Seven patients (all women, mean age 31 ± 15 years) with recurrent syncope and positive head upright tilt induced hypotension/bradycardia (refractory to normal therapy) were placed on methylphenidate 10 mg orally three times per day. Six of the seven patients became both tilt negative and clinically asymptomatic over a 7‐month follow‐up period. We conclude that methylphenidate may be an effective therapy in patients with recurrent neurocardiogenic syncope refractory to other forms of therapy.

Current trends in etiology, diagnosis, and management of neurocardiogenic syncope.

Recurrent episodes of unexplained syncope are among the most frequent of complaints referred to physicians for evaluation. Traditional methods of evaluation were both time consuming and expensive and left many patients without a diagnosis. Although neurocardiogenically mediated episodes of hypotension and bradycardia were felt to be a common cause of syncope, this was traditionally a diagnosis of exclusion. The emergence of head-upright tilt-table testing has provide a valuable method for identifying individuals predisposed to neurocardiogenic syncope and has also allowed for a better understanding of this phenomena. This article reviews the pathophysiology of neurocardiogenic syncope, the use of head-upright tilt-table testing in its diagnosis, and the potential therapies used to prevent recurrences.

Two-Vessel Coronary Artery Dissection in the Peripartum Period Case Report and Literature Review

The authors report a case of early peripartum myocardial infarction resulting from spontaneous dissection of the left anterior descending coronary artery and right coronary artery in a twenty-four-year-old woman. This is the first report of double-vessel coronary dissection involving both the left and right coronary arteries diagnosed antemortem and successfully treated.

Neurally mediated syncope with an update on indications and usefulness of head-upright tilt table testing and pharmacologic therapy.

Neurally mediated episodes of hypotension and bradycardia (neurocardiogenic syncope) are a common cause of recurrent syncope. Clinically, these episodes may present as an isolated event with an identifiable stimulus, or manifest as a syndrome of recurrent idiopathic syncopal events. The technique of head-upright tilt table testing has emerged as a safe and effective modality to identify individuals with this disorder. The use of isoproterenol as an adjunct to tilt table testing is widely employed although controversial. Whereas the mechanism of neurally mediated syncope is incompletely understood, effective therapies are available. Multiple pharmacologic agents, either alone or in combination, have proven effective in preventing recurrent episodes. The role of cardiac pacing as therapy for a subgroup of patients who manifest severe bradycardia or asystole remains controversial as well. Additional study is necessary to further define the mechanism of neurally mediated syncope, provide new therapeutic strategies, and perhaps provide alternative diagnostic techniques.