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Original Article
Cardiac autonomic function in patients with
myasthenia gravis: analysis of the heart‑rate
variability in the time‑domain
Sherifa Ahmed Hamed , Khaled Osama Mohamad , Mohamad Adam 2
1
1
1 Department of Neurology and Psychiatry, Assiut University Hospital, 71516 Assiut, Egypt.
2 Department of Cardiology, Assiut University Hospital, 71516 Assiut, Egypt.
ABSTRA CT
Aim: Myasthenia gravis (MG) is a neuromuscular transmission disorder caused by acetylcholine receptor autoantibodies. Cardiac
autonomic dysfunctions were rarely reported in patients with MG. Functional cardiac abnormalities were variable and reported in
patients at severe stages of the disease and with thymoma. We investigated cardiac functions in patients with MG using Ambulatory
24‑h electrocardiographic Holter‑Monitoring. Methods: This study included 20 patients with MG with a mean age of 28.45 ± 8.89 years
and duration of illness of 3.52 ± 1.15 years. The standard Holter reports include data for heart‑rate, ventricular ectopies (VEs),
supraventricular ectopies (SVEs), heart‑rate variability (HRV), ST, QT, atrial fibrillation and T‑wave alternans. Results: VEs, SVEs
and ST‑T changes were reported in 55%, 40% and 20% of patients respectively. Compared with healthy subjects (n = 20), HRV
components including SDNN, SDANN, SDNN Index, RMS‑SD and pNN50 (P = 0.001 for all) were reduced in patients indicating
sympathetic and parasympathetic autonomic dysfunctions. HRV abnormalities were reported in 30‑60% of patients. No significant
correlations were identified between SDNN, RMS‑SD, pNN50, and duration of illness. Conclusion: Depressed HRV may be an
early manifestation of autonomic neuropathy in patients with MG even in milder stages of the disease. This information is useful in
rating disease progression and the efficacy of therapeutic interventions.
Key words: Cardiac autonomic function, heart‑rate variability, myasthenia gravis
INTRODUCTION ventilation (myasthenic crisis). The diagnosis of
[3]
MG was based on the association between the following
Myasthenia gravis (MG) is a humoral immune parameters: clinical manifestations, presence of serum
[4]
attack to the skeletal muscle nicotinic acetylcholine anti-AChR antibody, definite clinical improvement on
receptors (nAChRs) at the neuromuscular junction injection of anticholinesterase, and a decremental
[1]
by autoantibodies. The cardinal symptoms of pattern of repetitive nerve stimulation. The thymus
[3]
MG is fatigue or fluctuating weakness in voluntary gland is abnormal in up to 90% of adults with MG, of
muscles with repeated or sustained exertion in the which 70% have enlarged thymic hyperplasia, whereas
course of the day, but improved by rest. MG has a 10-20% have benign thymic tumors or thymoma.
[1]
[5]
prevalence of 25-125/10 , with female to male ratio The current treatment for MG includes acetylcholine
6
of 3-2. About 2/3 of the patients has mild weakness, esterase inhibitors (AChE-Is) (as pyridostigmine),
[2]
[6]
which initially involve the ocular muscles, but may immunopharmacologic drugs, [7-12] and thymectomy. [13]
progress to generalized weakness in approximately
85% of patients. Respiratory muscle weakness occurs A few studies were carried out to investigate cardiac
in severe stages, which may require mechanical involvement in patients with MG. Some reported
nonspecific electrocardiographic (ECG) changes,
Access this article online Doppler imaging and conventional echocardiography,
[14]
Quick Response Code: while others reported variable results, which varied
Website: from asymptomatic specific ECG changes (as
www.nnjournal.net
abnormalities of the STI, [15] dispersion of QT and T
DOI: wave alternans [16] ), giant diffuse T waves, to clinically
10.4103/2347-8659.149419 manifest abnormalities (as conduction disturbances,
atrioventricular dissociation, wide QRS, [17] syncopal
Corresponding Author: Dr. Sherifa Ahmed Hamed, Department of Neurology and Psychiatry, Floor #7, Room #4, Assiut
University Hospital, 71516 Assiut, Egypt. E‑mail: hamed_sherifa@yahoo.com
Neuroimmunol Neuroinflammation | Volume 2 | Issue 1 | January 15, 2015 21