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Symptoms and Signs Associated with Syncope in Young People

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Symptoms and Signs Associated with Syncope in Young People ARTICLE Original Article ORIGINAL Symptoms and Signs Associated with Syncope in Young People with Primary Cardiac Arrhythmias a,b,c a,b Judith M. MacCormick, MBChB , Jackie R. Crawford, NZCS , d b,e b,e Seo-Kyung Chung, PhD , Andrew N. Shelling, PhD , Cary-Anne Evans, MSc (Med) , b,d a,b b,f Mark I. Rees, PhD , Warren M. Smith, MBChB , Ian G. Crozier, MBChB , b,g a,b,∗ Hugh McAlister and Jon R. Skinner, MD a Green Lane Paediatric and Congenital Cardiac Service, Auckland City/Starship Children’s Hospital, Auckland, New Zealand b Cardiac Inherited Diseases Group (CIDG), Auckland City/Starship Children’s Hospital, Auckland, New Zealand c Children’s Hospital Boston, Boston, MA, United States d Institute of Life Science, School of Medicine, Swansea University, Swansea, United Kingdom e Department of Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand f Department of Cardiology, Christchurch Hospital, New Zealand g Department of Cardiology, Waikato Hospital, New Zealand Background: It is often reported that clinical symptoms are useful in differentiating cardiac from non-cardiac syncope. Studies in the young are rare. This study was designed to capture the symptoms and signs reported by patients with cardiac syncope before the patients or their attending clinicians knew the final diagnosis. Methods: Retrospective case-note review of 35 consecutive unrelated gene-positive probands with a proven cardiac channelopathy. Results: The presentation leading to diagnosis of cardiac channelopathy was resuscitated sudden cardiac death in 7 patients; syncope in 20; collapse with retained consciousness in 2; palpitations in 1 and an incidental finding in 5. For the 20 patients with syncope (LQTS 18, Brugada syndrome 2), median age at presentation was 13.9 years (1.8 day to 40.8 years). Of the 17 patients able to describe the onset of syncope, 11 (65%) had at least one symptom prior to collapse, though none reported nausea. Dizziness or lightheadedness was the most frequent symptom, being experienced by 8 (47%). Nine (of 20) patients (45%) had witnessed seizure-like activity and 8 (40%) had urinary incontinence. Nineteen patients were capable of describing the post-syncopal period, of whom 15 (79%) reported symptoms, the most common (12; 65%) being drowsiness or exhaustion. Conclusions: Cardiac syncope in the young frequently presents with symptoms and signs that are typically associated with other causes of transient loss of consciousness, including vasovagal syncope and seizure disorders. The presence of symptoms may not be as helpful in differentiating arrhythmic from non-arrhythmic events as is often supposed. A thorough history, appropriate investigations and a high index of suspicion remain essential in the assessment of syncope. (Heart, Lung and Circulation (2011);20:593–598) © 2011 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Long QT syndrome; Brugada syndrome; Syncope; Symptoms; Arrhythmia; Seizure Introduction hilst reflex syncope, orthostatic hypotension and Received 8 March 2011; received in revised form 21 April W primary seizure disorders are relatively common 2011; accepted 27 April 2011; available online 26 May 2011 in the general population, cardiac syncope is rare. Stud- ies examining symptomatic presentation of syncope have Abbreviations: LQTS, long QT syndrome; RSCD, resuscitated sudden cardiac death; KCNQ1, official symbol of the potassium mostly included older patients and/or have been dom- voltage-gated channel, KQTlike subfamily member 1 gene; HERG, inated by orthostatic or neurocardiogenic syncope [1,2]. human ether a go-go related gene (also know as KCNH2); SCN5A, Although syncope is common in the young [3], events official symbol of the “sodium channel, voltage gated, typeV, due to cardiac arrhythmias have important prognos- alpha sub-unit” gene. ∗ tic implications, and are often the first evidence of Corresponding author at: Greenlane Paediatric and Congen- ital Cardiac Services, Starship Childrens Hospital, Park Road, a life threatening arrhythmic condition [4–10]. Prompt Grafton, Auckland, New Zealand. Tel.: +64 9 3074949; recognition of cardiac events is important, as appropri- fax: +64 9 6310785. ate intervention can significantly reduce mortality and E-mail address: [email protected] (J.R. Skinner). © 2011 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of 1443-9506/04/$36.00 Australia and New Zealand. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.hlc.2011.04.036 Downloaded for Anonymous User (n/a) at Auckland District Health Board - HQ 1810 from ClinicalKey.com.au by Elsevier on October 05, 2018. For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved. ORIGINAL 594 MacCormick et al. Heart, Lung and Circulation Symptoms and signs of syncope in the young (2011);20:593–598 ARTICLE 8 morbidity [11–15]. We have previously reported that Event triggers by genotype misdiagnosis as seizure disorder is common in LQTS, 7 resulting in inappropriate treatments and potentially pre- ventable deaths of family members in some cases [16]. It 6 Exertion is often reported that symptoms are useful in differentiat- Stress ing cardiac from non-cardiac syncope. Our observations 5 Rest from clinical practice suggested that this may not be 4 Other correct. We aimed to describe the symptoms and signs associated with syncopal episodes in a series of patients 3 Number of patients with subsequently diagnosed cardiac channelopathies. In particular, we wanted to capture these aspects of the 2 history as they were originally reported before the final 1 diagnosis was known to the patients or their attending clinicians. 0 KCNQ1 HERG SCN5A Methods Fig. 1. Triggers for cardiac events (syncope or cardiac arrest) by Patients were identified from the New Zealand Cardiac genotype amongst 27 patients with cardiac channelopathies in whom Inherited Disease Registry. This registry enables confi- the trigger could be obtained from the history (see text). KCNQ1, linked to long QT type 1; HERG linked to long QT type 2, SCN5A dential storage of clinical and genetic information for the linked to long QT type 3 and Brugada syndrome. purposes of clinical management and research into inher- ited cardiac disease. Ethical approval for the registry has been obtained from the regional ethics committee. as European in 25 (71%), Maori in 4 (11.5%), Pacific in 4 Between 2000 and 2005, 84 families underwent molec- (11.5%) and Chinese in 2 (6%). ular diagnostic screening through the Cardiac Inherited Disease Registry. A member of each family underwent Mode of Presentation genetic screening of five long QT (LQT) syndrome genes: Resuscitated sudden cardiac death requiring DC car- KCNQ1, HERG, SCN5A, KCNE1, and KCNE2, and the dioversion (RCSD) was the presenting event leading to spectrum of mutations have been previously described diagnosis of a cardiac channelopathy in seven patients, [17,18]. The current review is limited to living probands four of whom had mutations in the SCN5A gene. Twenty with a genetically confirmed cardiac channelopathy, who patients presented with syncope or transient loss of con- consented for the storage of detailed clinical informa- sciousness. Other symptomatic presentations included tion. There were 35 consecutive unrelated New Zealand collapse with retained consciousness in two patients patients who fulfilled these criteria. and palpitations in one. In the remaining probands, the A retrospective review of patient medical records was diagnosis of channelopathy was entertained following undertaken. Use of national unique patient identifica- incidental findings: electrocardiographic QTc prolonga- tion codes allowed inclusion of cases from nine different tion in three, prenatal bradycardia in one, and ventricular centres. The notes from the initial presentation, either to tachycardia on Holter monitoring in one. the emergency department or specialist outpatient clinic, Of the 20 patients with transient loss of consciousness, were reviewed by the first author. Routine demographic 15 presented acutely to a hospital emergency department, data was collected. Detailed information regarding the whilst five were initially seen in an outpatient clinic. presenting event was extracted from the patient records. This included the patient’s description of symptoms Triggers for Cardiac Events before and after the event, as well as any witness observa- tions. Triggers for the 27 events involving either RSCD or syn- cope were identified (Fig. 1). Tw o of the exercise-associated Results are expressed as median values with ranges for syncopal events occurred following, rather than during, nonparametric data and frequency (percent) for categori- exertion. An additional two patients had post-exertion cal variables. symptoms without syncope. One collapsed with retained consciousness following jogging. The other experienced Results a headache after playing soccer, with corresponding ven- tricular tachycardia on Holter monitoring (and subsequent Thirty-five consecutive unrelated probands were identi- detection of an SCN5A mutation). fied as gene-positive cases (Fig. 1). Diagnoses were LQT1 in 18 (with mutations in KCNQ1) and LQT2 in 10 (with mutations in HERG). Seven had mutations in the cardiac Symptoms Prior to Syncope sodium channel gene (SCN5A); presenting as LQT3 in 3, Excluding the patients with RSCD, there were 20 patients Brugada Syndrome
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