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Tilt-table testing has become an important part of the evaluation of patients with unexplained syncope, although not every patient with vasovagal syncope requires it. Studies have attested to the effectiveness of the technique for providing direct diagnostic evidence of a patient's susceptibility to vasovagal syncope. This article reviews the need for tilt-table testing and the recommended methods for performing a test. In addition, a detailed classification of the hemodynamic patterns of collapse displayed over the course of a tilt-table study is provided. These distinctive collapse patterns document the evolution of a syncopal event and are particularly important to identify because they can influence the selection of therapy. [ABSTRACT FROM AUTHOR]

Mode switching for atrial tachyarrhythmias is a concept that originated from use of DDI mode and was introduced in the early 1990s to prevent dual-chamber pacemakers from ventricular tracking of rapid atrial rates. This article describes the currently available systems and discusses the advantages and disadvantages of the technique. The results of a preliminary randomized controlled trial of 1 algorithm and plans for a second study are presented. [ABSTRACT FROM AUTHOR]

The consensus process that culminated in this symposium established an algorithm to guide the diagnosis and treatment of patients with vasovagal syncope and related disorders. In some patients, the hemodynamic response to standing may identify an abnormality-postural orthostatic tachycardia syndrome or orthostatic hypotension-that can often be treated without further testing. When the response to standing is normal, tilt-table testing may be useful in making the diagnosis of vasovagal syncope and guiding treatment. In some patients, however, the diagnosis is clear from the history, and tilt-table testing may not be necessary. Not all patients with vasovagal syncope need to be treated, and many can be treated effectively with education, reassurance, and a simple increase in dietary salt. In evaluating the results of tilt-table testing, an important consideration is the distinction between vasovagal syncope and the dysautonomic response to tilt characterized by a gradual and progressive decrease in blood pressure that leads to syncope. Current practice patterns suggest that beta blockers, fludrocortisone, and midodrine, are commonly used to treat patients with vasovagal syncope, and patients with the dysautonomic response are generally treated with fludrocortisone and midodrine. Permanent pacing with specialized pacing algorithms should be considered for patients with frequent vasovagal syncope that is refractory to medical therapy. The guidelines proposed here are an amalgam of clinical experience, expert opinion, and research evidence; however, they do not suggest a standard of care for all patients. [ABSTRACT FROM AUTHOR]

This study assesses the vasovagal collapse pattern changes, i.e, heart rate (HR) and arterial blood pressure (BP) with a 2-stage tilt-test protocol using glyceryl trinitrate (GTN) provocation. With use of the 45-minute 60 degrees head-up Westminster protocol, 102 consecutive patients were studied. Sublingual GTN 300 microg was given to those with a negative passive tilt. Heart rate and BP patterns were classified according to the Vasovagal International Study classification (VASIS) and then compared between those with a positive passive tilt and those with a positive tilt after having been given GTN. Twelve patients did not tolerate tilt testing, and 16 had a negative response despite taking GTN. Thirty-five patients (20 women and 15 men, mean age 45 +/- 21 years [mean +/- SD]) did not take GTN and 38 (26 women and 12 men, mean age 53 +/- 22 years) had positive passive test results. When comparing the VASIS classification between the 2 groups, results showed: type 1, mixed BP and HR decreased without severe bradycardia (31% [passive] vs 54% [with GTN], p = NS); type 2A, BP decreased before HR decreased (20% vs 22%, p = NS); type 2B, HR decreased before or coincident with BP (34% vs 8%, p = 0.003); type 3, BP decreased without HR decrease (9% vs 0%, p = NS); exception 1, chronotropic incompetence (0% vs 13%, p = 0.026); and exception 2, excessive HR increase (6% vs 3%, p = NS). Thus, GTN use increases frequency of positive results from 34% to 73%. Older people with chronotropic incompetence, who may benefit from pacing, were identified. In younger people there was an increase in those with cardioinhibition. [ABSTRACT FROM AUTHOR]

The reproducibility of electrocardiographic (ECG) recordings in syncopal recurrences and the diagnostic role of nonsyncopal arrhythmias are not well known. The objective of this study was to analyse the reproducibility of the ECG findings recorded with implantable loop recorders in 41 patients with suspected neurally-mediated syncope who were included in the International Study on Syncope of Uncertain Origin-2 study and that had > or =2 events recorded by implantable loop recorders. In these patients, the electrocardiogram obtained with the first documented syncope (index syncope) was compared with other recorded events. Twenty-two patients had > or =2 syncopes, and their electrocardiograms were reproducible in 21 (95%): 15 with sinus rhythm, 5 with asystole, and 1 with ventricular tachycardia; 1 had asystole at first syncope and sinus rhythm at recurrent syncope. In 32 patients with nonsyncopal episodes, an arrhythmia was documented in 9, and all of them had the same arrhythmia during the index syncope (100% reproducibility); conversely, when sinus rhythm was documented (23 patients) during nonsyncopal episodes, an arrhythmia was still documented in 6 during the index syncope (70% reproducibility; p = 0.0004). In conclusion, the ECG findings during the first syncope are highly reproducible in subsequent syncopes. The presence of an arrhythmia during nonsyncopal episodes is also highly predictive of the mechanism of syncope, but the presence of sinus rhythm does not rule out the possibility of arrhythmia during syncope. Therefore the finding of an arrhythmia during a nonsyncopal episode allows the etiologic diagnosis of syncope, and eventually to anticipate treatment, without waiting for syncope.

The mechanisms underlying cardiac resynchronization therapy have consistently been studied at rest and remain ill defined. Peak stress total isovolumic time (t-IVT) is a major determinant of cardiac output (CO) in chronic heart failure. In this study, pharmacologic stress was used to assess the effects of atrioventricular (AV) delay shortening and ventricular resynchronization elements of cardiac resynchronization therapy. Thirty patients undergoing cardiac resynchronization therapy were studied <6 months after implantation. t-IVT and CO were measured during native activation (left bundle branch block), AV delay shortening (right ventricular dual-chamber pacing), and full resynchronization (atrio-biventricular pacing). Full resynchronization shortened peak stress t-IVT by 9.4 +/- 6.2 s/min (p <0.001) and increased peak stress CO by 0.9 +/- 0.4 L/min (p <0.001), with the effects in individual patients showing a large correlation (r = -0.64, p <0.001). In contrast, simple AV delay shortening did not shorten peak stress t-IVT nor increase peak stress CO, nor was CO at rest affected by full resynchronization or AV delay shortening. Of all measurements during native activation, the best predictor of gain in peak stress CO from full resynchronization was peak stress t-IVT (r = 0.75, p <0.001), with every 5 s/min increment in peak stress t-IVT during native activation predicting a 6% gain in peak stress CO. No conventional measures during native activation at rest or during stress (including QRS duration, the Tei index, tissue Doppler intraventricular delay, and t-IVT at rest) added significant additional information. In conclusion, only during stress does resynchronization consistently increase CO. Second, little of this increment in CO is achieved by AV delay shortening alone. Third, under native activation, long t-IVT during peak stress is the single best predictor of resynchronization-mediated increment in peak stress CO.