The heart in myasthenia gravis.
The cardiac changes associated with myasthenia gravis have been reviewed and specific areas explored. There is no doubt concerning the involvement of the myocardium in this disease as indicated by clinical, ECG, vectorcardiographic, and autopsy data. The doubt lies in the precipitating factor for the pathology found. On the one hand the whole picture could be a direct result of the pathologic process of myasthenia gravis. On the other hand the patient with myasthenia gravis, during the natural history of the disease, encounters many iatrogenic and coincidental variables which could influence the nature of the clinical findings and autopsy data. One fact seems reasonably clear: The association of myocardial pathology with thymoma, especially malignant thymoma, is well established for the more severe form of the myocardial disease. Furthermore, the hypothesis that cardiac muscle antibodies give rise to such reactions is attractive, although not fully resolved. If such cases are excluded then there remain others where cardiac pathology could be due to other disease, primarily coronary heart disease, in the older group. In addition, the mode of death of some patients indicates that intercurrent respiratory problems could play a part. Most patients in this group do not seem to have cardiac abnormalities due to the pathologic process of myasthenia. There is in addition a small group where very striking cardiovascular findings suggestive of myocarditis are found. There is not necessarily a thymoma and no other specific etiologic factors can be found. These are rare cases and might still be related to disorders of immune mechanisms. In conclusion it can be stated that, although there is now a considerable body of evidence concerning the heart in myasthenia gravis, the implication of specific pathology for this neuromuscular disorder affecting the heart must be considered, in the traditional Scottish legal sense, as "not proven."
D001145:Arrhythmias, Cardiac / Q000209:etiology; D002800:Cholinesterase Inhibitors / Q000009:adverse effects; D004357:Drug Synergism; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008012:Lidocaine / Q000009:adverse effects / Q000627:therapeutic use; D008614:Meperidine / Q000627:therapeutic use; D008691:Methadone / Q000627:therapeutic use; D009020:Morphine / Q000009:adverse effects / Q000627:therapeutic use; D009157:Myasthenia Gravis / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D009205:Myocarditis / Q000188:drug therapy / Q000209:etiology; D009206:Myocardium / Q000473:pathology*; D009469:Neuromuscular Junction / Q000187:drug effects; D010672:Phenytoin / Q000009:adverse effects / Q000627:therapeutic use; D011343:Procaine / Q000009:adverse effects / Q000627:therapeutic use; D011802:Quinidine / Q000627:therapeutic use; D014672:Vectorcardiography
D002800:Cholinesterase Inhibitors; D011343:Procaine; D010672:Phenytoin; D009020:Morphine; D008012:Lidocaine; D008614:Meperidine; D011802:Quinidine; D008691:Methadone