CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 9/10, October/November 2013
AFRICA
e3
valve, to reduce the risk of rupture of the left ventricular
posterior wall after mitral valve replacement, the posterior mitral
leaflet with attached chordae is preserved.
An MG patient is often the subject of cardiac disease, as was
the case with our patient. According to Hofstad
et al.
,
10
16% of
patients with MG have signs of cardiac disease, which is a much
higher frequency than that found in the general population.
This strongly indicates that these otherwise unexplained signs
of heart disease are related to or caused by MG. Such findings
are more frequent among thymoma patients (50%) than among
non-thymoma patients (12%).
The histological changes in the striated muscle found in MG
are muscle fibre atrophy and varying degrees of inflammation.
10
The inflammatory lesions range from discrete accumulations
of lymphocytes without tissue destruction to extensive
myonecrosis with heavy inflammatory cell infiltration and signs
of regeneration. Hearts microscopically examined by Hofstad
et
al.
had inflammatory infiltrates in the myocardium, with varying
degrees of muscle fibre degeneration or necrosis.
10
The cardiac findings may be caused by mechanisms specific
to MG or they may represent non-specific myocardial damage.
The focal, spotty localisation of the myocardial changes
indicates that the heart pathology has a causal relationship with
MG. Moreover, clinical evaluation usually represents the first
diagnostic step for a patient with suspected MG. The evaluation
of MG-related symptoms could be difficult as the cardiac disease
may mask them.
In our case, the pre-operative clinical status was not correctly
addressed as the cardiac symptoms were predominant. Hence,
the diagnosis of myocarditis in this patient was guided by the
intra-operative and histological findings, which led to revaluation
of the pre-operative clinical conditions.
Conclusion
A dynamic hypothesis concerning the correlation between
myocarditis due to myasthenia gravis and left ventricular rupture
after mitral valve replacement is presented. Additionally, we
believe that endomyocardial biopsy should be considered in this
group of patients.
References
1.
Drachman DB. Myasthenia gravis.
N Engl J Med
1994;
330
(25):
1797–1810.
2.
Vincent A, Palace J, Hilton-Jones D: Myasthenia gravis.
Lancet
2001;
357
: 2122–2128.
3.
Xu BY, Pirskanen R, Lefvert AK. Antibodies against beta1 and beta2
adrenergic receptors in myasthenia gravis.
J Neuroimmunol
1998;
91
:
82–88.
4.
Zamecnik J, Vesely D, Jakubicka B,
et al
. Muscle lymphocytic
infiltrates in thymoma associated myasthenia gravis are phenotypi-
cally different from those in polymyositis.
Neuromuscul Disord
2007;
17
(11–12): 935–942.
5.
Treasure RL, Rainer WG, Strevey TE, Sadler TR. Intraoperative left
ventricular rupture associated with mitral valve replacement.
Chest
1974;
66
: 511–514.
6.
Sersar SI, Jamjoom AA. Left ventricular rupture post mitral valve
replacement.
Clin Med Cardiol
2009;
3
: 101–113.
7.
Karlson KJ, Ashraf MM, Berger RL. Rupture of left ventricle following
mitral valve replacement.
Ann Thorac Surg
1988;
46
: 590–597.
8.
Otaki M, Kitamura N. Left ventricular rupture following mitral valve
replacement.
Chest
1993;
104
: 1431–1435.
9.
Reardon MJ, Letsou GV, Reardon PR, Baldwin JC. Left ventricular
rupture following mitral valve replacement.
J Heart Valve Dis
1996;
5
: 10–15.
10. Hofstad H, Ohm OJ, Mørk SJ, Aarli JA. Heart disease in myasthenia
gravis.
Acta Neurol Scand
1984:
70
: 176–184.
