SYNCOPE –a complex syndrome of several causes

Abstract

Keywords: nordsync, syncope, syncope-ethiology, syncope-mechanism.A patient presenting with a transient loss of con-sciousness (TLOC) can be a real challenge for theclinician with short- and long-term outcomes rang-ing from an isolated and benign event to a poten-tially lethal arrhythmia and sudden cardiacdeath.[1] The problem is not uncommon: between1% and 2% of all admissions at the EmergencyDepartments are related to TLOC, and one of threepatients will finally be hospitalized [2–4]. In theprimary care, we may expect two TLOC incidencesper 1000 person-years[5] but this number is prob-ably underestimated as other sources report 4–5times higher occurrence[6, 7]. Syncope, a tempo-rary impairment of circulation leading to suddenbrain hypoperfusion, is the absolutely dominantcause of TLOC.[8, 9] The main etiology of syncopeconsists of neurocardiogenic reflexes, autonomicdisorders (such as orthostatic hypotension), pri-mary cardiovascular disease (arrhythmic and/orstructural heart disease), or combination of these[1]. Accordingly, syncope excludes by definitionneurological diseases such as epilepsy, and syn-cope mimics such as psychogenic pseudo syncopalattacks. Today, handling of patients with syncopalattacks often results in long term rotation withinthe health care system between various specialists,general practitioners, cardiologists, neurologists,internists, geriatricians, otolaryngologists, paedia-tricians, and even psychiatrists without receivingthe proper diagnosis and treatment. A solutionproposed by various consensus groups would be tofollow specially designed diagnostic algorithms, orto create dedicated ‘syncope units’.[1, 10, 11]However, patients with syncope constitute not onlya clinical problem but an economical one as well. InSouthern Sweden, in Region Skane, 3 312 patients(2 760 per million inhabitants) were diagnosedwith syncope (ICD-10 code R55.9) during the year2009 according to the official statistic reports. Thetotal annual costs for the health care system werelarge: 1,9 million € directly at the ED; 8,3 million €in patients with fractures; 10,7 million € in patientswith arrhythmias; and 17,0 million € in patientswith valve disease. Consequently, there is adistinct need to improve the management of syn-cope, when we consider both clinical and economicaspects.As mentioned above, syncope can be regarded asan aggregation of different etiological factors undera common umbrella of the cardinal symptom, atime-limited circulatory disorder resulting in a lossof consciousness and a spontaneous recovery. In aseries of review articles published in this issue ofJournal of Internal Medicine, three main syncopaltriggers, neurocardiogenic reflexes, syndromes oforthostatic intolerance, and a primary cardiacdisease are discussed. All authors participated inthe First Nordic Symposium on Syncope ‘Nord-Sync2011’, which was held 20–21st of October,2011 in Malm€o, Sweden. First, Wieling and col-leagues revisit carotid sinus hypersensitivity (CSH)as an example of classical reflex syncope.[12] Theysuggest that CSH should be thought of as being acontinuum on a spectrum between cardioinhibi-tion and vasodilation. Based on new experimentaland epidemiological data, they also propose amodified and stricter set of criteria for diagnosinga symptomatic CSH, traditionally named as carotidsinus syndrome. Further, Fedorowski and Meland-er explore the history, pathophysiology, epidemiol-ogy and clinical consequences of orthostaticintolerance syndromes, a heterogonous groupcharacterised by impaired hemodynamic responseon standing. [13] They focus on orthostatic intol-erance as a ‘hidden danger’, which leads to synco-pal attacks per se or, alternatively, evokes a reflexsyncope, increases the mortality and cardiovascu-lar disease risk, and complicates treatment ofconcomitant diseases such as hypertension andheart failure. Finally, a review by Arnar [14] takesus on a brief and concise trip across the structuralchanges in the heart and primary arrhythmias, allof which can result in a syncopal attack. Thisauthor underlines a well-known fact, that thepresence of structural heart disease and/or afamily history of sudden unexplained death areassociated with a worse prognosis and warrant amore comprehensive cardiac investigation includ-ing genetic testing if indicated.