Multiple sclerosis electrocardiogram

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D. Julinka Auta Fernandes

Overview

An electrocardiogram (ECG) is not used to diagnose multiple sclerosis (MS), and there are no ECG findings that are specific or diagnostic for MS.[1]

The principal roles of ECG in a person with MS are evaluation of suspected cardiovascular disease or arrhythmia, assessment of selected cardiovascular autonomic abnormalities, and cardiac safety monitoring when initiating certain disease-modifying therapies, particularly sphingosine-1-phosphate receptor modulators.

Electrocardiogram

ECG and the diagnosis of multiple sclerosis

An ECG does not establish or exclude a diagnosis of MS. The 2024 McDonald criteria do not include ECG findings as a diagnostic criterion.[1]

Therefore, ECG abnormalities such as atrial fibrillation, ventricular arrhythmias, PR-interval abnormalities, U waves, Q waves, bundle branch block, or other nonspecific ECG abnormalities should not be described as findings suggestive or diagnostic of MS. Such findings require evaluation according to standard cardiovascular practice and the clinical context.

Cardiovascular autonomic dysfunction

MS may be associated with abnormalities of cardiovascular autonomic regulation. A systematic review and meta-analysis of 43 studies involving 1,518 people with MS and 1,062 healthy controls found differences in several measures of heart rate variability (HRV), including reduced RMSSD, pNN50, high-frequency power, and low-frequency power in people with MS compared with healthy controls.[2]

Other systematic reviews have similarly reported abnormalities of cardiac autonomic regulation in MS, particularly involving measures of heart-rate variability, although studies have used heterogeneous methods.[3]

ECG-derived HRV assessment may provide information about autonomic cardiovascular regulation in selected patients or research settings. However, HRV abnormalities are not specific for MS and are not diagnostic criteria for MS.[2][3]

ECG-based HRV assessment should be selected according to the clinical question and is not routinely required in every patient with MS.

ECG and sphingosine-1-phosphate receptor modulators

ECG has an important role in the cardiac safety assessment of selected sphingosine-1-phosphate receptor modulators used for MS. These medications can cause reductions in heart rate and slowing of atrioventricular conduction, particularly during treatment initiation. ECG requirements differ among individual agents because of differences in dose-titration regimens and cardiac safety profiles.[4][5][6][7]

Fingolimod

Before initiating fingolimod, an ECG should be obtained as part of first-dose cardiac assessment. Initiation of fingolimod can cause bradycardia and atrioventricular conduction abnormalities.[4]

ECG should be obtained before the first dose of fingolimod and at the end of the 6-hour observation period.[4]

Additional monitoring should be provided if clinically important bradycardia or conduction abnormalities occur. Overnight continuous ECG monitoring is required in specified higher-risk circumstances, including certain pre-existing cardiovascular or cerebrovascular conditions, prolonged QTc or increased risk of QT prolongation, and concomitant treatment with drugs that slow heart rate or atrioventricular conduction.[4]

First-dose ECG monitoring may also be required when fingolimod is restarted after specified treatment interruptions.[4]

Siponimod

Before initiating siponimod, an ECG should be obtained in all patients to identify pre-existing conduction abnormalities. Siponimod can cause bradycardia and atrioventricular conduction delays, particularly during treatment initiation.[5]

Patients with certain pre-existing cardiac conditions, including sinus bradycardia with a heart rate below 55 beats per minute, first- or second-degree Mobitz type I atrioventricular block, or a history of myocardial infarction or heart failure, should undergo 6-hour first-dose monitoring. In these patients, ECG should be obtained before dosing and at the end of the observation period.[5]

If clinically significant bradyarrhythmia or conduction abnormalities occur, additional ECG monitoring should be performed according to the prescribing information.[5]

Ozanimod

Ozanimod is initiated using a dose-titration regimen that attenuates the magnitude of the initial heart-rate reduction.[6]

Before starting ozanimod, an ECG should be obtained to assess for pre-existing cardiac conduction abnormalities. Ozanimod can cause a transient decrease in heart rate and atrioventricular conduction delays, particularly during treatment initiation.[6]

The utility of routine first-dose ECG monitoring with the recommended ozanimod titration regimen is unclear. Cardiology consultation should be considered in patients with relevant conduction abnormalities or concomitant use of drugs that decrease heart rate or atrioventricular conduction.[6]

Ponesimod

Before initiating ponesimod, an ECG should be obtained to identify pre-existing conduction abnormalities. Ponesimod is initiated using a dose-titration regimen to reduce cardiac effects during treatment initiation.[7]

First-dose 4-hour monitoring is recommended for patients with sinus bradycardia with a heart rate below 55 beats per minute, first- or second-degree Mobitz type I atrioventricular block, or a history of myocardial infarction or heart failure occurring more than 6 months before treatment initiation and in stable condition.[7]

For patients requiring first-dose monitoring, ECG should be obtained before dosing and at the end of the 4-hour observation period.[7]

Additional ECG monitoring is required if clinically significant bradycardia or conduction abnormalities occur, according to the prescribing information.[7]

ECG abnormalities in patients with multiple sclerosis

ECG abnormalities in a patient with MS should not be considered characteristic ECG manifestations of MS.

Potential abnormalities may include:

  • Sinus bradycardia or other heart-rate abnormalities, particularly during initiation of S1P receptor modulator therapy.
  • Atrioventricular block or PR-interval prolongation, particularly during initiation of S1P receptor modulator therapy.
  • QTc prolongation, particularly in the presence of pre-existing QT prolongation, electrolyte abnormalities, concomitant QT-prolonging medications, or specific drug-related risks.

These findings are nonspecific and should be evaluated according to standard cardiovascular practice. Their presence does not establish a diagnosis of MS.[4][5][6][7]

Ambulatory ECG monitoring

Ambulatory ECG monitoring, including Holter monitoring or longer-duration rhythm monitoring, is not routinely indicated solely because a patient has MS.

Ambulatory ECG monitoring may be appropriate when symptoms or clinical findings suggest intermittent arrhythmia, including unexplained palpitations, syncope, presyncope, episodic bradycardia, unexplained tachycardia, or other suspected intermittent rhythm disturbances.

The choice and duration of ambulatory monitoring should be based on symptom frequency and standard cardiovascular practice.

ECG in patients with cardiovascular symptoms

Patients with MS should undergo cardiovascular evaluation according to their symptoms and individual cardiovascular risk factors. A 12-lead ECG is appropriate when clinically indicated, including evaluation of chest pain, suspected ischemia, palpitations, syncope or presyncope, unexplained dyspnea, suspected arrhythmia, or suspected medication-related cardiac effects.

These cardiovascular indications should be distinguished from MS diagnosis: ECG is not a routine diagnostic investigation for MS.

Interpretation of an abnormal ECG

An abnormal ECG in a patient with MS should not automatically be attributed to MS. The differential diagnosis should include primary cardiac disease, myocardial ischemia, electrolyte abnormalities, medication effects, autonomic dysfunction, structural heart disease, conduction-system disease, and primary cardiac arrhythmias.

ECG findings should be interpreted together with the patient's symptoms, cardiovascular history, medication list, and physical examination.

References

  1. 1.0 1.1 Montalban, Xavier; Lebrun-Frénay, Christine; Oh, Jiwon; Arrambide, Georgina; Moccia, Marcello; Amato, Maria Pia; Amezcua, Lilyana; Banwell, Brenda; Bar-Or, Amit; Barkhof, Frederik; Butzkueven, Helmut; Ciccarelli, Olga; Chataway, Jeremy; Cohen, Jeffrey A.; Comi, Giancarlo; Correale, Jorge; Deisenhammer, Florian; Filippi, Massimo; Fiol, Julie; Freedman, Mark S.; Fujihara, Kazuo; Granziera, Cristina; Green, Ari J.; Hartung, Hans-Peter; Hellwig, Kerstin; Kappos, Ludwig; Kimbrough, Dorlan; Killestein, Joep; Lublin, Fred; Marignier, Romain; Marrie, Ruth Ann; Miller, Aaron; Otero-Romero, Susana; Ontaneda, Daniel; Ramanathan, Sudarshini; Reich, Daniel; Rocca, Maria A.; Rovira, Àlex; Saidha, Shiv; Salter, Amber; Sastre-Garriga, Jaume; Saylor, Deanna; Solomon, Andrew J.; Sormani, Maria Pia; Stankoff, Bruno; Tintoré, Mar; Tremlett, Helen; Van der Walt, Anneke; Viswanathan, Shanthi; Wiendl, Heinz; Wildemann, Brigitte; Yamout, Bassem; Zaratin, Paola; Calabresi, Peter A.; Coetzee, Timothy; Thompson, Alan J. (2025). "Diagnosis of multiple sclerosis: 2024 revisions of the McDonald criteria". The Lancet Neurology. 24 (10): 850–865. doi:10.1016/S1474-4422(25)00270-4. PMID 40975101 Check |pmid= value (help).
  2. 2.0 2.1 Mirmosayyeb, Omid; Yazdan Panah, Mohammad; Alinejadfard, Mohammadreza; Oraee, Soroush; Vaheb, Saeed; Shaygannejad, Vahid (2026). "Heart rate variability in people with multiple sclerosis: A systematic review and meta-analysis". Acta Neurologica Belgica. 126 (1): 67–83. doi:10.1007/s13760-025-02829-5. PMID 40587005 Check |pmid= value (help).
  3. 3.0 3.1 Findling, Oliver; Hauer, Lisa; Pezawas, Thomas; Rommer, Patrick S.; Struhal, Wolfgang; Sellner, Johannes (2020). "Cardiac Autonomic Dysfunction in Multiple Sclerosis: A Systematic Review of Current Knowledge and Impact of Immunotherapies". Journal of Clinical Medicine. 9 (2): 335. doi:10.3390/jcm9020335. PMID 31991711.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 "GILENYA (fingolimod) prescribing information" (PDF). U.S. Food and Drug Administration. 2025.
  5. 5.0 5.1 5.2 5.3 5.4 "MAYZENT (siponimod) prescribing information" (PDF). U.S. Food and Drug Administration. 2026.
  6. 6.0 6.1 6.2 6.3 6.4 "ZEPOSIA (ozanimod) prescribing information". DailyMed, U.S. National Library of Medicine.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 "PONVORY (ponesimod) prescribing information". DailyMed, U.S. National Library of Medicine.

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