Syncope Diagnosis at Referral to a Tertiary Syncope Unit: An in-Depth Analysis of the FAST II.

OBJECTIVE: A substantial number of patients with a transient loss of consciousness (T-LOC) are referred to a tertiary syncope unit without a diagnosis. This study investigates the final diagnoses reached in patients who, on referral, were undiagnosed or inaccurately diagnosed in secondary care. METHODS: This study is an in-depth analysis of the recently published Fainting Assessment Study II, a prospective cohort study in a tertiary syncope unit. The diagnosis at the tertiary syncope unit was established after history taking (phase 1), following autonomic function tests (phase 2), and confirming after critical follow-up of 1.5-2 years, with the adjudicated diagnosis (phase 3) by a multidisciplinary committee. Diagnoses suggested by the referring physician were considered the phase 0 diagnosis. We determined the accuracy of the phase 0 diagnosis by comparing this with the phase 3 diagnosis. RESULTS: 51% (134/264) of patients had no diagnosis upon referral (phase 0), the remaining 49% (130/264) carried a diagnosis, but 80% (104/130) considered their condition unexplained. Of the patients undiagnosed at referral, three major causes of T-LOC were revealed: reflex syncope (69%), initial orthostatic hypotension (20%) and psychogenic pseudosyncope (13%) (sum > 100% due to cases with multiple causes). Referral diagnoses were either inaccurate or incomplete in 65% of the patients and were mainly altered at tertiary care assessment to reflex syncope, initial orthostatic hypotension or psychogenic pseudosyncope. A diagnosis of cardiac syncope at referral proved wrong in 17/18 patients. CONCLUSIONS: Syncope patients diagnosed or undiagnosed in primary and secondary care and referred to a syncope unit mostly suffer from reflex syncope, initial orthostatic hypotension or psychogenic pseudosyncope. These causes of T-LOC do not necessarily require ancillary tests, but can be diagnosed by careful history-taking. Besides access to a network of specialized syncope units, simple interventions, such as guideline-based structured evaluation, proper risk-stratification and critical follow-up may reduce diagnostic delay and improve diagnostic accuracy for syncope.

A cross-sectional nationwide survey of guideline based syncope units in the Netherlands: the SU-19 score-a novel validation for best practices.

AIMS: We aimed to identify all syncope units (SUs) in the Netherlands and assess the extent to which these SUs fulfil the essential requirements outlined by the consensus statements of the European Heart Rhythm Association and the European Society of Cardiology syncope guidelines. For this, we developed the SU-19 score, a novel guideline based validation tool for best practice. METHODS AND RESULTS: All outpatient clinics of cardiology, neurology, and internal medicine in the Netherlands were screened for presence of any form of structured specialized syncope care. If present, these were included as SUs and requested to complete a questionnaire regarding syncope care. We assessed all SUs using the SU-19 score regarding structure (3 points), available tests (12 points), and initial evaluation (4 points). Twenty SUs were identified in the Netherlands, both academic (5/20) and non-academic hospitals (15/20), 17/20 reported multidisciplinary involvement during initial evaluation. In 19/20, neurology, cardiology, or both were responsible for the syncope management. Non-physicians were involved performing the head-up tilt test (44%) and initial evaluation (40%). The mean SU-19 score was 18.0 ± 1.1, 45% achieved the maximum score of 19 points. Variations were observed in protocols for active standing test, carotid sinus massage, and head-up tilt test. CONCLUSION: There is a network of 20 SUs in the Netherlands. Forty-five per cent fully met the SU-19 score (mean 18.0 ± 1.1). Slight variety existed in protocols for autonomic function tests. Neurology and cardiology were mostly involved in syncope management. Non-physicians play an important role in syncope care.

Diagnostic yield and accuracy in a tertiary referral syncope unit validating the ESC guideline on syncope: a prospective cohort study.

AIMS: To assess in patients with transient loss of consciousness the diagnostic yield, accuracy, and safety of the structured approach as described in the ESC guidelines in a tertiary referral syncope unit. METHODS AND RESULTS: Prospective cohort study including 264 consecutive patients (≥18 years) referred with at least one self-reported episode of transient loss of consciousness and presenting to the syncope unit between October 2012 and February 2015. The study consisted of three phases: history taking (Phase 1), autonomic function tests (AFTs) (Phase 2), and after 1.5-year follow-up with assessment by a multidisciplinary committee (Phase 3). Diagnostic yield was assessed after Phases 1 and 2. Empirical diagnostic accuracy was measured for diagnoses according to the ESC guidelines after Phase 3. The diagnostic yield after Phase 1 (history taking) was 94.7% (95% CI: 91.1-97.0%, 250/264 patients) and increased to 97.0% (93.9-98.6%, 256/264 patients) after Phase 2. The overall diagnostic accuracy (as established in Phase 3) of the Phases 1 and 2 diagnoses was 90.6% (95% CI: 86.2-93.8%, 232/256 patients). No life-threatening conditions were missed. Three patients died, two unrelated to the cause of transient loss of consciousness, and one whom remained undiagnosed. CONCLUSION: A clinical work-up at a tertiary syncope unit using the ESC guidelines has a high diagnostic yield, accuracy, and safety. History taking (Phase 1) is the most important diagnostic tool. Autonomic function tests never changed the Phase 1 diagnosis but helped to increase the certainty of the Phase 1 diagnosis in many patients and yield additional diagnoses in patients who remained undiagnosed after Phase 1. Diagnoses were inaccurate in 9.4%, but no serious conditions were missed. This is adequate for clinical practice.

Pacing in vasovagal syncope: Physiology, pacemaker sensors, and recent clinical trials-Precise patient selection and measurable benefit.

The role of pacing in vasovagal syncope (VVS) is considered from a physiological basis. Most VVS patients lose consciousness due to hypotension before severe bradycardia/asystole occurs. Patients who benefit from dual-chamber pacing typically are older with highly symptomatic, late-onset, frequent and severe syncope with short/no prodrome and documented severe cardioinhibition. Tilt testing is of value in patients with recurrent unexplained syncope to identify important hypotensive susceptibility stemming from reduced venous return and stroke volume (SV). A negative tilt test in vasovagal patients with spontaneous asystole documented by an implantable/insertable loop recorder is associated with lower syncope recurrence rates after pacemaker implantation. Pacing may be more effective if triggered by sensor detection of a parameter changing earlier in the reflex than bradycardia when SV may still be relatively preserved. In this regard, detection of right ventricular impedance offers promise. Conservatism is recommended, limiting pacing in VVS to a small subset of symptomatic older patients with clearly documented cardioinhibition and paying particular attention to the timing of loss of consciousness in relation to asystole/bradycardia. Understanding VVS physiology permits application of well-timed, appropriate pacing that yields benefit for highly symptomatic patients.

Pacing in vasovagal syncope: A physiological paradox?

The physiological principles underlying pacemaker treatment in patients with vasovagal syncope have never been reviewed. Current knowledge suggests that pacing the right heart is unlikely to correct blood pressure during a vasovagal reaction. In adults, the reason for this is that stroke volume is dictated by central blood volume contained in the cardiopulmonary vessels within the chest (ie, left ventricular preload). Preceding posture-triggered vasovagal syncope, there is a significant fall in central blood volume and therefore in stroke volume and cardiac output long before the onset of bradycardia. This explains why high rate cardiac pacing does not improve cardiac output or blood pressure during presyncope. Contradictory results between physiological theory and trial evidence underlying pacemaker treatment at present cannot be explained. Placebo effects during pacing for vasovagal syncope should be considered. More work is needed to solve the dilemma.