Novel Methods for Quantification of Vasodepression and Cardioinhibition During Tilt-Induced Vasovagal Syncope

Author:

van Dijk J. Gert1ORCID,Ghariq Maryam1,Kerkhof Fabian I.1,Reijntjes Robert1,van Houwelingen Marc J.2,van Rossum Ineke A.1,Saal Dirk P.13,van Zwet Erik W.4,van Lieshout Johannes J.56,Thijs Roland D.17,Benditt David G.8

Affiliation:

1. From the Department of Neurology (J.G.v.D., M.G., F.I.K., R.R., I.A.v.R., D.P.S., R.D.T.), Leiden University Medical Centre, the Netherlands

2. Department of Experimental Cardiology, Erasmus Medical Centre, Rotterdam, the Netherlands (M.J.v.H.)

3. Franciscus Gasthuis en Vlietland, Rotterdam/Schiedam, the Netherlands (D.P.S.)

4. Department of Medical Statistics (E.W.v.Z.), Leiden University Medical Centre, the Netherlands

5. Department of Internal medicine, University Medical Centre, Amsterdam, the Netherlands (J.J.v.L.)

6. MRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, Queen’s Medical Centre, School of Life Sciences, University of Nottingham Medical School, United Kingdom (J.J.v.L.)

7. Stichting Epilepsie Instellingen Nederland, Heemstede, the Netherlands (R.D.T.)

8. Cardiovascular Division, Arrhythmia Center, Department of Medicine, University of Minnesota, Minneapolis (D.G.B.).

Abstract

Rationale: Assessing the relative contributions of cardioinhibition and vasodepression to the blood pressure (BP) decrease in tilt-induced vasovagal syncope requires methods that reflect BP physiology accurately. Objective: To assess the relative contributions of cardioinhibition and vasodepression to tilt-induced vasovagal syncope using novel methods. Methods and Results: We studied the parameters determining BP, that is, stroke volume (SV), heart rate (HR), and total peripheral resistance (TPR), in 163 patients with tilt-induced vasovagal syncope documented by continuous ECG and video EEG monitoring. We defined the beginning of cardioinhibition as the start of an HR decrease (HR) before syncope and used logarithms of SV, HR, and TPR ratios to quantify the multiplicative relation BP=SV·HR·TPR. We defined 3 stages before syncope and 2 after it based on direction changes of these parameters. The earliest BP decrease occurred 9 minutes before syncope. Cardioinhibition was observed in 91% of patients at a median time of 58 seconds before syncope. At that time, SV had a strong negative effect on BP, TPR a lesser negative effect, while HR had increased (all P <0.001). At the onset of cardioinhibition, the median HR was at 98 bpm higher than baseline. Cardioinhibition thus initially only represented a reduction of the corrective HR increase but was nonetheless accompanied by an immediate acceleration of the ongoing BP decrease. At syncope, SV and HR contributed similarly to the BP decrease ( P <0.001), while TPR did not affect BP. Conclusions: The novel methods allowed the relative effects of SV, HR, and TPR on BP to be assessed separately, although all act together. The 2 major factors lowering BP in tilt-induced vasovagal syncope were reduced SV and cardioinhibition. We suggest that the term vasodepression in reflex syncope should not be limited to reduced arterial vasoconstriction, reflected in TPR, but should also encompass venous pooling, reflected in SV.

Funder

Dr Earl E Bakken family

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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