IJC Metabolic & Endocrine 5 (2014) 3–6

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IJC Metabolic & Endocrine

journal homepage: http://www.journals.elsevier.com/ijc-metabolic-and-endocrine

Cardiac manifestations of myasthenia gravis: A systematic review

Poojita Shivamurthy a,⁎, Matthew W. Parker b,1
a
Department of Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-1235, USA
b
University of Connecticut Health Center, Hartford Hospital 80 Seymour Street, PO Box 5037, Hartford, CT 06102-5037, USA

a r t i c l e i n f o a b s t r a c t

Article history: Introduction: Myasthenia gravis is an autoimmune disorder targeting skeletal muscles. Striated cardiac muscle
Received 12 July 2014 can be a target for immune attack manifesting as heart failure, arrhythmia, and sudden death. We aimed to re-
Accepted 9 August 2014 view cardiac manifestations of myasthenia gravis, its underlying pathogenesis and clinical relevance.
Available online 15 August 2014 Method: We searched literature published from 2003 to 2013 on cardiac involvement in myasthenia gravis using
PubMed, Scopus and Ovid databases using the terms ‘heart failure’; ‘cardiomyopathy’; ‘myocarditis’; ‘arrhyth-
Keywords:
mia’; ‘coronary’; ‘heart’ and ‘myasthenia gravis’. Forty-one articles were chosen comprising of 29 case reports,
Myasthenia
Anti-striational
4 review articles and 8 retrospective/prospective studies.
Anti-Kv1.4 Result: Fifteen percent of myasthenia cases had thymoma. Most of them (97%) had antibodies against striated
Giant-cell muscle (anti-titin, anti-ryanodine and anti-Kv 1.4 antibodies). Older age, severe myasthenia and myocarditis
Anticholinesterase appeared to be associated with anti-striational antibodies. Takotsubo cardiomyopathy was the most commonly
Cardiomyopathy reported cardiomyopathy. Giant cell myocarditis was a rare but fatal manifestation associated with striational an-
tibodies however in-vitro study failed to produce their cytotoxic effects. T wave changes, QT prolongation, anti-
cholinesterase induced atrioventricular block and sudden death were less commonly reported. Abnormal
vasoconstrictive coronary response to acetylcholine, development of pericarditis and cardiac surgery leading to
myasthenia gravis has been reported.
Conclusion: Heart muscle is a target for autoimmune inflammation in myasthenia gravis. Advancing age,
thymoma, and anti-Kv1 antibodies appeared to be risk factors. Symptom overlap with myasthenia may result
in failure to recognize cardiac involvement. Prospective studies are needed to establish causal link with striational
antibodies and to make screening recommendations for cardiac involvement.
© 2014 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY-NC-SA
license (http://creativecommons.org/licenses/by-nc-sa/3.0/).

1. Introduction 2. Methods

Myasthenia gravis (MG) is a neuromuscular autoimmune disease.
Antibodies to nicotine acetylcholine receptors (AChR) at the neuromus-
cular junction cause defective neuromuscular transmission in skeletal
muscles that manifests as muscle weakness [1]. Myasthenia is known
to involve other body systems including the heart. MG patients have a
higher prevalence of cardiac manifestations in the presence of thymoma
(10–15%) [1]. The article reviews literature on cardiomyopathy, heart
failure, arrhythmias, coronary and valvular disease in MG.
We searched PubMed, Scopus and Ovid databases for articles in
English from 2003 to 2013. We found 94 articles for ‘myasthenia’ and
‘heart’, 47 for ‘cardiomyopathy’, 27 for ‘arrhythmias’, 17 for ‘heart fail-
ure’, 17 for ‘coronary disease’, 12 for ‘valve disease’, 30 for ‘myocarditis’
and 5 for ‘pericarditis’. We found 249 articles, 41 of which were selected
for review based on relevance to the topic. Among the 41 articles, 29
were case reports, 4 review articles, 5 case–control/retrospective stud-
ies, one in-vitro study and two were prospective studies.

3. Result and discussion

Abbreviations: MG, myasthenia gravis; AChR, acetylcholine receptor; MuSK, muscle

specific kinase; VGCC, voltage gated calcium channel; RyR, ryanodine receptor; ECG, elec-
trocardiogram; AV, atrioventricular; GCM, giant cell myocarditis; BP, blood pressure; TNF,
tumor necrosis factor.
⁎ Corresponding author. Tel.: +1 860 471 5712; fax: +1 860 679 4613.
E-mail addresses: poojita.shivamurthy@gmail.com (P. Shivamurthy),
Matthew.Parker@hhchealth.org (M.W. Parker).
1
Tel.: +1 860 972 4398; fax: +1 860 545 5631.
3.1. Anti-cardiac antibodies
AChR antibodies specific to skeletal muscles do not bind to heart
muscle [2]. Forty-eight percent of all MG cases and 97% of all thymoma
associated MG, have antibodies towards heart muscle [1,3]. Along with
AChR antibodies, thymoma patients exhibit abnormal humoral
response with anti-striational antibodies, anti-muscle specific tyrosine

http://dx.doi.org/10.1016/j.ijcme.2014.08.003
2214-7624/© 2014 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY-NC-SA license (http://creativecommons.org/licenses/by-nc-sa/3.0/).
4 P. Shivamurthy, M.W. Parker / IJC Metabolic & Endocrine 5 (2014) 3–6
kinase (anti-MuSK), anti-voltage gated calcium channel (anti-VGCC) an-
tibodies, antibodies against beta-adrenergic receptors and abnormal T
cell mediated immunity [3]. Anti-titin, anti-ryanodine receptor antibod-
ies (anti-RyR) and anti-Kv 1.4 antibodies (KCNA4 antibodies) [4], collec-
tively called anti-striational antibodies are commonly reported in MG
cases having cardiac involvement [1,5]. Titin is a giant protein in the skel-
etal and cardiac sarcomere. The immunogenic region of titin called MG
titin-30 is situated near the A/I-band junction [6]. RyR is a calcium release
channel located in the sarcoplasmic reticulum with important role in
regulating the excitation contraction coupling through calcium release
[1]. Kv 1.4 is a voltage gated potassium channel. Anti-titin antibody is de-
tected in 20–40%, anti-RyR in 13–38% and anti-Kv 1.4 in 12–15% of MG
cases [6]. Complement activation by striational antibodies and T cell
proliferative response have been reported [3,6] without proven clinical
significance. In non-MG patients, autoantibody to beta 1 adrenergic re-
ceptor has been associated with dilated cardiomyopathy [7].
Myocarditis developed in 37.5% MG patients with anti-striational
antibodies [5]. On immunological evaluation (n = 8), anti-titin, anti-
RyR and anti-Kv1.4 antibodies were present in 63%, 75% and 75% cases
respectively. Immunomodulatory treatment benefitted all. Among
those with myocarditis, heart failure and arrhythmias developed from
13 to 211 months after the onset of MG. Histological evaluation showed
widespread inflammatory infiltrates containing multi-nucleated giant
cells and myocardial degeneration with varying severities [5]. However,
an in-vitro study failed to show morphological changes or cytotoxic ef-
fects in human derived heart muscle cells by MG sera when compared
to healthy human sera [1].
Anti-Kv 1.4 antibody may be a potential marker for the development
of lethal autoimmune myocarditis [5,6]. A large study involving 650 MG
patients showed an incidence of 10.8% for anti-Kv 1.4 antibodies. Sixty
percent of them had abnormal electrocardiogram (ECG) [2]. Ultrasound
echocardiography of ex-vivo chick embryos exposed to these antibodies
showed significant suppression of heart muscle function. Anti-Kv 1.4
antibody has also been associated with QTc prolongation, lethal
arrhythmias including ventricular tachycardia, sick sinus syndrome,
complete atrial ventricular (AV) block, severe myocarditis, and sudden
death [2,6,8].
Currently, data that strongly supports pathogenic role of these
antibodies is lacking, however, they may influence cardiac function by
complement activation and T cell proliferation.
3.2. Heart failure and cardiomyopathy in MG
Giant cell myocarditis (GCM) and Takotsubo cardiomyopathy have
been associated with MG. GCM is often fatal while Takotsubo cardiomy-
opathy is reversible. Interestingly, both have very different pathogenesis.
2A: GCM is a severe form of myocarditis with myonecrosis and ser-
piginous infiltrate of chronic inflammatory cells including giant cells.
Twenty-two cases of GCM with thymoma and 12 autopsy cases of MG
with thymoma, polymyositis and myocarditis have been reported
[9,10]. Giant cells were found in 50% cases in both myocardium and
skeletal muscles [10].
CD3, CD68, CD20 and CD8 positive giant lymphocytes were found in
myocardium and skeletal muscles of a 68 year old with MG after she de-
veloped myocarditis [11]. GCM occurred in a 72 year old patient with
MG on azathioprine with no specific correlation between areas of
inflammation and IgG deposits on immunohistochemistry [9]. Both
cases had thymoma. There are two cases of GCM reported shortly
(7 to 10 days) following thymoma resection with one showing CD3
lymphocytes, CD68 histiocytes and giant cells [12]. Autopsy proven
myocarditis occurred in a case of stage IVa thymoma with positive
AChR antibody titers but without clinical MG following chemotherapy
[10]. Two cases of invasive thymoma developing GCM and myositis
were also reported [13,14]. All cases were fatal. Asymptomatic GCM in
a patient with MG with strongly positive striational antibodies was
eventually fatal [15].
Pathogenesis of GCM: Inflammation during muscle degeneration ac-
tivates myogenesis. Mononucleated myoblasts are induced, that fuse to
form multinucleated myocytes [11]. The etiology of inflammation is un-
clear and GCM is not specific to MG. Inflammatory chemotactic factors
may attract macrophages that fuse with each other during endocytosis
and form giant cells [11]. GCM has been reported in other autoimmune
disorders including Crohn's disease, rheumatoid arthritis, systemic
lupus erythematosus etc. [11]. Risk factors for GCM include increased
age and thymoma.
2B: Stress induced cardiomyopathy i.e. Takotsubo cardiomyopathy
is a transient reversible form of left ventricular dysfunction often
presenting as acute coronary syndrome in the absence of significant
coronary stenosis. It is precipitated by emotional or physical form of
stress which causes a catecholamine surge [16] resulting in suppressed
myocardial function. Animal models have demonstrated transient
hypocontraction of cardiac muscle upon exposure to high levels of cat-
echolamines [17].
MG can precipitate severe stress particularly during a crisis episode
[17–22]. Takotsubo cardiomyopathy developed in patients on plasma-
pheresis and intravenous immunoglobulin during myasthenia crisis
[17,18,20–22]. A case of heart failure with difficulty weaning the patient
off the ventilator despite aggressive therapy was retrospectively diag-
nosed to have myasthenia crisis [19]. Recurrent Takotsubo cardiomyop-
athy occurred with every episode of myasthenia crisis in an elderly
female [23]. MG and cardiomyopathy developed concurrently in a
68 year-old 4 weeks after mitral valve replacement. There was no asso-
ciation with thymoma and all cases were related to myasthenia crisis.
In conclusion, older patients with severe MG appear to be at a higher
risk for developing stress-induced cardiomyopathy. GCM was seen
more often in elderly cases with thymoma and was often fatal. Routine
testing of striational antibodies is not currently indicated as no large
prospective study has proved its association with MG.
A case–control study analyzed left ventricular long-axis function in
MG [7]. Tissue Doppler imaging was used in 22 MG patients along
with 22 matched controls before and after pyridostigmine. Tissue veloc-
ities were analyzed at systole (S′), early (E′) and late (A′) diastole. Peak
systolic strain was analyzed at the time of aortic valve closure. MG
patients had a significantly higher systolic and diastolic blood pressure
(BP) than controls (p = 0.007 and 0.017 respectively). Systolic BP
remained high after pyridostigmine (p = 0.009). Mean early diastolic
AV-plane velocity detects changes in left ventricular diastolic function,
which is undetectable by measurement of ejection fraction. It was
significantly lower in patients than controls (7.7 cm/s versus 9 cm/s,
p = 0.0036) before pyridostigmine. This effect disappeared after
pyridostigmine. Before pyridostigmine, S′ and E′ were lower in MG
patients but without statistical significance. Patients had a lower peak
systolic strain than controls (−18.8% versus −21.6%, p = 0.011). This
study suggested a pyridostigmine responsive decreased left ventricular
function. Systolic BP was a significant determinant for difference in the
two groups as these effects disappeared after adjusting for same [7].
3.3. Myasthenia gravis and pericarditis
Two cases of constrictive pericarditis post-irradiation for invasive
thymoma were reported [24]. A case of transudative pericardial effusion
and atrial flutter with AV block that resolved with plasmapheresis and
immunosuppressive therapy was reported [25]. Radiation treatment
for thymoma may increase risk for pericarditis.
3.4. Myasthenia gravis and arrhythmias
Available literature is based on analysis of electrocardiograms (ECG)
of MG patients. Sudden cardiac deaths have been reported but no defi-
nite association has been discovered. Fluctuations in heart rate is mostly
due to autonomic dysfunction and less so due to pathology of conduc-
tion system itself. Hence, we will review autonomic function in MG.
 P. Shivamurthy, M.W. Parker / IJC Metabolic & Endocrine 5 (2014) 3–6
MG patients experience wide fluctuation in heart rate and BP [23].
Two studies found different answers. A prospective study of 64 MG
patients with age and gender matched controls showed that rate and
duration of increase in heart rate and BP with stress was significantly
higher than controls. Orthostasis tests and isometric handgrip test
showed increased sympathetic activity. There was no significant differ-
ence in parasympathetic function; however, pyridostigmine treatment
in MG patients compared to controls could have obscured the pic-
ture [23]. Comparing MG group for heart rate and BP variation with
and without anticholinesterases is not studied. In another study, 21 pa-
tients with MG and thymoma had Ewing and baroreflex sensitivity test
at rest. Sympathetic activity of heart rate variability did not differ signif-
icantly between patients and controls; however, significant decrease in
measures of short-term vagal variations in heart rate variability was
noted indicating parasympathetic impairment [26]. Impaired baroreflex
can cause conduction abnormalities including atrial fibrillation and sud-
den death. This study showed increased incidence of atrial fibrillation,
ventricular and supra ventricular extra systoles and prolonged QTc in
MG with thymoma. Older studies cited in this study have shown low
plasma noradrenergic activity and compensatory high adrenergic activ-
ity suggesting sympathetic deficiency. One possible explanation for au-
tonomic dysfunction is that 20% of thymoma cases and about 3% of MG
without thymoma have antibodies to the ganglionic AChR. Ganglionic
AChR antibodies are seen in autoimmune autonomic gangliopathy but
only in about 50%. Overlap of muscular and ganglionic AChR antibodies
may be due to the alpha 1 subunit of muscle AChR and alpha 3 subunit
of ganglionic AChR which is immunogenic [26].
Non-specific T wave changes, QT prolongations increased frequency
of first-degree AV block have been reported with MG [27]. A retrospec-
tive observational study involving 117 patients showed nonspecific
ECG changes [28]. Sixty percent of those with anti-Kv 1.4 antibody
had ECG abnormalities, most common being T wave abnormality and
QT prolongation [2]. Anti-Kv1.4 antibody was also associated with
more severe form of MG, lethal arrhythmias including ventricular
tachycardia, sick sinus syndrome, complete AV block and sudden
death [2,5,6,29,30].
3.5. Myasthenia gravis and medication interactions
Anticholinesterases reduce action potential duration and slow down
sinus rate, which can be reversed with atropine. A novel selective ace-
tylcholinesterase inhibitor C-547, an alkylammonium derivative of
6-methyluracil, had no such cardiac effects [31]. Muscarinic effect of
pyridostigmine combined with central vagotonic effects of anesthetics
used during surgery can cause profound bradycardia, hypotension,
and bronchospasm [32]. Stokes-Adams attacks and AV blocks have
been reported with use of pyridostigmine and should be strongly con-
sidered in the differential for syncope, bradycardia, and weakness [33].
Disopyramide, quinidine and procainamide can block muscarinic ACh
receptor-mediated signaling and precipitate myasthenia crisis [34].
Calcium channels have a substantial role in muscle contraction.
Cardiogenic shock caused by a single dose of verapamil was reported
in an elderly patient with AChR and antistriational antibodies [35]. MG
muscle showed a 70% to 89% reduction in the number of AChR per neu-
romuscular junction with calcium channel blockers [35]. Verapamil
slows calcium ion influx, prolongs refractory period of nodal cells and
may depress contractility. Unlike diltiazem, it blocks both fast and late
cardiac sodium currents. In MG, calcium dependent depolarization is
compromised, conduction capacity strongly relies on the cardiac sodi-
um current (Ina) which is blocked by verapamil [35].
3.6. Myasthenia gravis and coronary disease
Normal coronary arteries dilate in response to acetylcholine while
vasoconstriction is noted in vessels with damaged endothelium. The
endothelium is prone to vasoconstriction by physostigmine [36].
5
Diffuse spasm of the left anterior descending artery due to anticholines-
terase therapy has occurred [37]. Coronary vasospasm causing non-
obstructive myocardial infarction shortly after starting pyridostigmine
was reported. It was successfully treated with verapamil [37,38]. A
myocardial infarction day after starting immunosuppressant has also
been observed [39]. Cytokine mediated vasoconstriction, plaque rup-
ture and anti-tumor necrosis factor (TNF) effect are potential explana-
tions. TNF, inhibited by immunosuppressant confers resistance against
heat shock proteins and decreases free radicals. Studies that control
for coronary disease risk factors are needed.
3.7. Myasthenia gravis and post-surgical cardiac complications
Cases of newly diagnosed MG weeks after coronary bypass
and pericardiotomy have been reported [40,41]. It can be purely co-
incidental but the thymus contains myoid cells that can express AChR
molecules, which can be released during surgery [40]. The release of
thymic AChR, could increase an existing subclinical antibody response,
or allow AchR to be presented to immune system that leads to MG [41].
No significant literature linking MG and valvular disease was found.
4. Conclusions
MG is a multi-system disorder and the heart is a potential target for
immune attack. Incidence of heart disease related to MG remains largely
unknown. Overlap of symptoms like fatigue, dyspnea and poor exercise
tolerance between MG and cardiac disease may lead to under recogni-
tion of cardiac manifestations. Most published data are case studies
or retrospective case–control studies; these suggest an association of
thymoma, anti-Kv 1.4 antibodies and advancing age with cardiac in-
volvement in MG. Prospective studies will be needed prior to making
recommendations for cardiac screening in MG. Antistriational antibodies
present an intriguing possible link between MG and cardiovascular
disease.
Conflict of Interests
None
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