Rapid recovery of poststroke cardiac autonomic dysfunction: Causes to be considered

Author:

Wang Ruihao1ORCID,Moeller Sebastian2,Akhundova Aynur3,Marthol Harald4,Kollmar Rainer5,Köhrmann Martin6,Hilz Max J.17ORCID

Affiliation:

1. Department of Neurology University of Erlangen‐Nuremberg Erlangen Germany

2. Faculty of Health/School of Medicine Witten/Herdecke University Witten Germany

3. Department of Neurology Zentralklinik Bad Berka Bad Berka Germany

4. Department of Psychiatry, Addiction, Psychotherapy, and Psychosomatics Klinikum am Europakanal Erlangen Germany

5. Department of Neurology General Hospital Darmstadt Darmstadt Germany

6. Department of Neurology University Hospital Essen Essen Germany

7. Department of Neurology Icahn School of Medicine at Mount Sinai New York New York USA

Abstract

AbstractBackground and purposeAcute stroke frequently causes cardiovascular–autonomic dysfunction (CAD). Studies of CAD recovery are inconclusive, whereas poststroke arrhythmias may wane within 72 h. We evaluated whether poststroke CAD recovers within 72 h upon stroke onset in association with neurological improvement or increased use of cardiovascular medication.MethodsIn 50 ischemic stroke patients (68 ± 13 years old) who—prior to hospital‐admission—had no known diseases nor took medication affecting autonomic modulation, we assessed National Institutes of Health Stroke Scale (NIHSS) scores, RR intervals (RRIs), systolic and diastolic blood pressure (BP), respiration rate, parameters reflecting total autonomic modulation (RRI SD, RRI total powers), sympathetic modulation (RRI low‐frequency powers, systolic BP low‐frequency powers), and parasympathetic modulation (square root of mean squared differences of successive RRIs [RMSSD], RRI high‐frequency powers), and baroreflex sensitivity within 24 h (Assessment 1) and 72 h after stroke onset (Assessment 2) and compared data to those of 31 healthy controls (64 ± 10 years). We correlated delta NIHSS values (Assessment 1 – Assessment 2) with delta values of autonomic parameters (Spearman rank correlation tests; significance:p < 0.05).ResultsAt Assessment 1, patients were not yet on vasoactive medication and had higher systolic BP, respiration rate, and heart rate, that is, lower RRIs, but lower RRI SD, RRI coefficient of variance, RRI low‐frequency powers, RRI high‐frequency powers, RRI total powers, RMSSDs, and baroreflex sensitivity. At Assessment 2, patients were on antihypertensives, had higher RRI SD, RRI coefficient of variance, RRI low‐frequency powers, RRI high‐frequency powers, RRI total powers, RMSSDs, and baroreflex sensitivity but lower systolic blood pressure and NIHSS values than at Assessment 1; values no longer differed between patients and controls except for lower RRIs and higher respiration rate in patients. Delta NIHSS scores correlated inversely with delta values of RRI SD, RRI coefficient of variance, RMSSDs, RRI low‐frequency powers, RRI high‐frequency powers, RRI total powers, and baroreflex sensitivity.ConclusionsIn our patients, CAD recovery was almost complete within 72 h after stroke onset and correlated with neurological improvement. Most likely, early initiation of cardiovascular medication and probably attenuating stress supported rapid CAD recovery.

Publisher

Wiley

Subject

Neurology (clinical),Neurology

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