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Central Autonomic Dysfunction Delays Recovery of Fingolimod Induced Heart Rate Slowing.

Hilz MJ, Intravooth T, Moeller S, Wang R, Lee DH, Koehn J, Linker RA - PLoS ONE (2015)

Bottom Line: They did not reduce parasympathetic HR-parameters upon standing-up.After Valsalva-strain-release, their parasympathetic HR-slowing in response to BP-overshoot was four times higher than in the other participants (p<0.05).The autonomic cardiovascular dysfunction in MS-patients with delayed HR-re-acceleration upon Fingolimod-initiation suggests that MS-related central autonomic lesions compromise HR-re-acceleration upon Fingolimod.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany.

ABSTRACT

Background: In multiple sclerosis (MS) patients, Fingolimod may induce prolonged heart-rate slowing which might be caused by MS-related central autonomic lesions.

Objectives: To evaluate whether MS-patients with prolonged heart-rate slowing (> six hours) upon Fingolimod show cardiovascular-autonomic dysfunction before Fingolimod-initiation.

Methods: Before Fingolimod-initiation, we recorded electrocardiographic RR-intervals (RRIs) and blood-pressure (BP) at rest, upon standing-up, during metronomic deep-breathing, Valsalva-maneuver, and "sustained-handgrip-exercise" in 21 patients with relapsing-remitting MS, and 20 healthy persons. We calculated sympathetic and parasympathetic cardiovascular parameters, including low- (LF) and high-frequency (HF) powers of RRI- and BP-oscillations, RRI-RMSSDs, RRI- and BP-changes during handgrip-exercise, parasympathetic heart-rate-slowing in relation to BP-overshoot after Valsalva-strain-release. We compared values of healthy persons and patients with and without prolonged heart-rate slowing after Fingolimod-initiation (ANOVA; significance: p<0.05).

Results: Upon Fingolimod-initiation, 7/21 patients had prolonged HR-slowing. Before Fingolimod, these patients had higher resting BP and higher BP increase during handgrip-exercise than had the other participants (p<0.05). They did not reduce parasympathetic HR-parameters upon standing-up. After Valsalva-strain-release, their parasympathetic HR-slowing in response to BP-overshoot was four times higher than in the other participants (p<0.05).

Conclusions: The autonomic cardiovascular dysfunction in MS-patients with delayed HR-re-acceleration upon Fingolimod-initiation suggests that MS-related central autonomic lesions compromise HR-re-acceleration upon Fingolimod.

Trial registration: German Clinical Trial Register DRKS00004548 http://drks-neu.uniklinik-freiburg.de/drks_web/setLocale_EN.do.

No MeSH data available.


Related in: MedlinePlus

Mean heart rate immediately before Fingolimod-initiation and during 8 hours of monitoring after Fingolimod-initiation in MS patients with (n = 7) and without (n = 14) prolonged HR slowing.
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pone.0132139.g002: Mean heart rate immediately before Fingolimod-initiation and during 8 hours of monitoring after Fingolimod-initiation in MS patients with (n = 7) and without (n = 14) prolonged HR slowing.

Mentions: Upon Fingolimod-initiation, all 21 MS patients showed HR-slowing (Fig 2), but no patient suffered from arrhythmia or atrioventricular blockage. None of the patients developed any ECG changes during or at the end of the first Fingolimod dosing, and all patients remained clinically asymptomatic. In 14 patients, HR re-increased within 6 hours, while seven patients had HR-slowing for more than 6 hours, and only re-increased HR within 8 hours. Patients with prolonged HR-slowing had lowest HRs (52.5 ± 5.1 beats/min) after 6 hours while patients without prolonged HR-slowing had lowest HRs (56.5 ± 6.7 beats/min) after 5 hours. HRs at rest, before Fingolimod intake, and the lowest HRs after Fingolimod intake did not differ between both patient groups (p > 0.05).


Central Autonomic Dysfunction Delays Recovery of Fingolimod Induced Heart Rate Slowing.

Hilz MJ, Intravooth T, Moeller S, Wang R, Lee DH, Koehn J, Linker RA - PLoS ONE (2015)

Mean heart rate immediately before Fingolimod-initiation and during 8 hours of monitoring after Fingolimod-initiation in MS patients with (n = 7) and without (n = 14) prolonged HR slowing.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493029&req=5

pone.0132139.g002: Mean heart rate immediately before Fingolimod-initiation and during 8 hours of monitoring after Fingolimod-initiation in MS patients with (n = 7) and without (n = 14) prolonged HR slowing.
Mentions: Upon Fingolimod-initiation, all 21 MS patients showed HR-slowing (Fig 2), but no patient suffered from arrhythmia or atrioventricular blockage. None of the patients developed any ECG changes during or at the end of the first Fingolimod dosing, and all patients remained clinically asymptomatic. In 14 patients, HR re-increased within 6 hours, while seven patients had HR-slowing for more than 6 hours, and only re-increased HR within 8 hours. Patients with prolonged HR-slowing had lowest HRs (52.5 ± 5.1 beats/min) after 6 hours while patients without prolonged HR-slowing had lowest HRs (56.5 ± 6.7 beats/min) after 5 hours. HRs at rest, before Fingolimod intake, and the lowest HRs after Fingolimod intake did not differ between both patient groups (p > 0.05).

Bottom Line: They did not reduce parasympathetic HR-parameters upon standing-up.After Valsalva-strain-release, their parasympathetic HR-slowing in response to BP-overshoot was four times higher than in the other participants (p<0.05).The autonomic cardiovascular dysfunction in MS-patients with delayed HR-re-acceleration upon Fingolimod-initiation suggests that MS-related central autonomic lesions compromise HR-re-acceleration upon Fingolimod.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany.

ABSTRACT

Background: In multiple sclerosis (MS) patients, Fingolimod may induce prolonged heart-rate slowing which might be caused by MS-related central autonomic lesions.

Objectives: To evaluate whether MS-patients with prolonged heart-rate slowing (> six hours) upon Fingolimod show cardiovascular-autonomic dysfunction before Fingolimod-initiation.

Methods: Before Fingolimod-initiation, we recorded electrocardiographic RR-intervals (RRIs) and blood-pressure (BP) at rest, upon standing-up, during metronomic deep-breathing, Valsalva-maneuver, and "sustained-handgrip-exercise" in 21 patients with relapsing-remitting MS, and 20 healthy persons. We calculated sympathetic and parasympathetic cardiovascular parameters, including low- (LF) and high-frequency (HF) powers of RRI- and BP-oscillations, RRI-RMSSDs, RRI- and BP-changes during handgrip-exercise, parasympathetic heart-rate-slowing in relation to BP-overshoot after Valsalva-strain-release. We compared values of healthy persons and patients with and without prolonged heart-rate slowing after Fingolimod-initiation (ANOVA; significance: p<0.05).

Results: Upon Fingolimod-initiation, 7/21 patients had prolonged HR-slowing. Before Fingolimod, these patients had higher resting BP and higher BP increase during handgrip-exercise than had the other participants (p<0.05). They did not reduce parasympathetic HR-parameters upon standing-up. After Valsalva-strain-release, their parasympathetic HR-slowing in response to BP-overshoot was four times higher than in the other participants (p<0.05).

Conclusions: The autonomic cardiovascular dysfunction in MS-patients with delayed HR-re-acceleration upon Fingolimod-initiation suggests that MS-related central autonomic lesions compromise HR-re-acceleration upon Fingolimod.

Trial registration: German Clinical Trial Register DRKS00004548 http://drks-neu.uniklinik-freiburg.de/drks_web/setLocale_EN.do.

No MeSH data available.


Related in: MedlinePlus