Orthostatic instability is an important co-factor and trigger of reflex syncope

Transcription

1 Orthostatic instability is an important co-factor and trigger of reflex syncope Artur Fedorowski 1,2, Philippe Burri 2, Steen Juul-Möller 2, and Olle Melander 1,2 1 Lund University, Sweden 2 Skåne University Hospital, Malmö, Sweden ESC Congress Munich, August 25-29, 2012

2 Clinical Research Center Lund University Skåne University Hospital, Malmö Nothing to disclose

3 The Syncope Study of Unselected Population in Malmö (SYSTEMA) The rationale and aim of the study The overview of methodology How common is coincidence of orthostatic intolerance and reflex syncope? What predicts overlap? Conclusions Lund University / Faculty of Medicine 2012

4 Why do we faint? Syncope is a T-LOC due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery. Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

5 Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

6 Prevalence of the causes of syncope in the EGSYS-2 study.5 The EGSYS study was aimed at assessing the management of syncope as recently defined by ESC guidelines.1,2 The results of this study probably represent the current standard for the management of syncope. Brignole M Heart 2007;93: Copyright BMJ Publishing Group Ltd & British Cardiovascular Society. All rights reserved.

7 ESC Guidelines > overlap? Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

8 Aim of the present study To assess relationship of orthostatic intolerance with two common syncope diagnoses: vasovagal reflex and carotid sinus hypersensitivity; To identify predictors of overlap between orthostatic intolerance and reflex syncope.

9 Flowchart of SYSTEMA Study Patients with suspected pre- or syncope referred to Syncope Unit Evidence of cardiac (ECG, ECHO, Holter etc.), neurological (CT/MR, EEG), toxic, and other definite causes -> exclusion Syncope of unknown or suspected dysautonomic/reflectory origin -> inclusion Expanded HUT Information & education Intervention if needed Further tests if needed (ILR?) Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

10 Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

11 HUT protocol Continuous BP and ECG monitoring Supine, cannulation, blood sample nr 1 after 15 min, Carotid sinus massage (CSM) in supine position (pos/neg) Head-up tilt and CSM if needed Tilt back, 5 min rest and head-up tilt nr 2 Blood sample nr 2 after 3 min Observation for 20±5 min (orthostatic response?/ vasovagal reflex?) GTN (glyceryl trinitrate) challenge if needed and observation for 15 min Valsalva; specific provocation tests; Initial (rapid) orthostatic response (under active rising) if needed Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

12 Characteristics of SYSTEMA population (n=478) Characteristics Percentage or Mean (±SD) Age (yrs) 58±21 Gender (men, %) 44.1 Current smoker (%) 15.5 Time from first syncope (yrs) 8±12 [0-65] Number of syncopal attacks (n) 9±21 [0-250] History of hypertension (%) 40.4 History of coronary event (%) 8.4 History of angina pectoris (%) 9.4 History of stroke (%) 7.9 Diabetes (%) 7.7 Atrial fibrillation (%) 6.7 Systolic BP supine (mmhg) 136±23 Diastolic BP supine (mmhg) 72±10 Heart rate supine (bpm) 69±11 Department of Clinical Sciences, Clinical Research Center, Skåne University Hospital, Malmö, Sweden

13 Etiology of syncope in SYSTEMA (n=478)

14 Classical OH and VVS

15 Lund University / Faculty of Medicine 2012 Delayed OH and VVS

16 Lund University / Faculty of Medicine 2012 POTS and VVS

17 Overlap within VVS (n=271) VVS alone VVS & OH VVS & POTS

18 CSM during the early tilt phase

19 CSM during the late tilt phase

20 Overlap with CSH (n=81) CSH alone CSH & OH

21 OH + CSH + VVS

22 How did we identify the common correlates of overlap? Logistic regression among VVS or CSH patients Adjusted for age and gender Presence of OH or POTS as a dependent variable Tested covariates: anamnestic data, clinical characteristics, medications, if appropriate, plasma adrenaline, noradrenaline, and renin.

23 Predictors of OH in VVS (n=271)

24 Predictors of POTS in VVS (n=271)

25 Predictors of OH in CSH (n=81)

26 Conclusions 25% of vasovagal patients and 50% of patients with CSH may have OH as a trigger and co-factor of syncopal attack. Advancing age, increasing number of attacks, history of major CE or cancer, negative Valsalva, treatment with loop diuretics and/or ACEI; all of these are predictors of overlap between VVS and OH Younger age and treatment with ACEI seem to favor overlap between CSH and OH.

27 Thank you for your attention!