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188 C. Călin et al. 10 The particular characteristics of the first case may be summarized as follows: The symptomatic conduction disturbances with frequent episodes of syncope in a patient with myasthenia gravis who necessitated permanent pacing. The difficulties we encountered in the establishment of conduction disturbances etiology (due to the disease or to the treatment with acetylcholinesterase inhibitors). The second case shows a different kind of cardiac involvement in myasthenia gravis – the ECG changes (giant diffuse T waves in a patient with cardiovascular risk factors) which needed further investigation and long term surveillance. Miastenia gravis este o boală musculară autoimună caracterizată prin slăbiciune şi oboseală musculară. Prevalenţa bolii este de aproximativ 1:7500 cu maxim în decadele 2 şi trei la femei şi cinci şi şase la bărbaţi, deşi poate apare la orice vârstă. Boala are o uşoară predominanţă feminină cu un sex ratio de 3:2. Afectarea cardiacă în miastenia gravis poate lua câteva forme, mergând de la modificări EKG asimptomatice la tahicardie ventriculară, miocardită, tulburări de conducere, insuficienţă cardiacă şi moarte subită (3, 4, 5). Vă prezentăm în continuare două cazuri de miastenia gravis care au dezvoltat semen şi simptome de afectare cardiovasculară care au necesitat internare într-un serviciu de cardiologie pentru evaluare şi tratament. Astfel, primul caz este particular prin prezenţa tulburărilor de conducere simptomatice, cu frecvente sincope care au necesitat cardiostimulare permanentă precum şi prin dificultatea stabilirii etiologiei tulburării de conducere (datorată bolii în sine sau tratamentului cu inhibitori de acetilcolinesterază). Cel de-al doilea caz prezintă afectarea cardiacă manifestată prin modificări de ischemie difuze, care a necesitat investigaţii suplimentare şi urmărire. Corresponding author: Carmen Ginghină, MD, PhD, FESC, FACC 100, V. Lascăr Str. 020506 Bucharest, Romania E-mail: carmenginghina2001@yahoo.com REFERENCES 1. AASHIT K. SHAH, MD, Myasthenia Gravis, Emedicine, 10, 2006. 2. FAUCI A., BRAUNWALD E., KASPER D., Harrison’s Principles of Internal Medicine, Ed. 16, McGraw-Hill. 3. GUGLIN M., CAMPELLONE J., HEINTZ K., PARILLO J., Cardiac disease in myasthenia gravis: a literature review. J. Clin. Neuromusc. Dis., 2003; 4:199–203. 4. HEMENDER S., MD, RICHARDSON, STEVEN K., Pericarditis in Myasthenia Gravis, Cardiology in Review, 2004, 12(3):134–137. 5. BRAUNWALD E., LIBBY P., BONOW R., MANN D., ZIPES D., Braunwald’s Heart Disease – A Textbook of Cardiovascular Medicine, Ed. 8, Saunders, 2007: 2149. 6. BRIGNOLE M., ALBONI P., BERGFELDT L., BLANC J., Guidelines on Management (Diagnosis and Treatment) of Syncope- Update 2004, Europace (2004), 6, 467–537. 7. THYGESEN K., ALPERT J., WHITE D. on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the redefinition of Myocardial Infarction. Universal definition of myocardial infarction. EHJ 2007; 28(20):2525–2538. 8. WALDER L.A., SPODICK D.H., Global T wave inversion. J. Am. Coll. Cardiol., 1991; 17:1479. 9. FRANK J.H., COOPER G.W., BLACK W.C., PHILLIPS L.H., 2 nd , Iodinated contrast agents in myasthenia gravis. Neurology, 1987 Aug., 37(8):1400–1402. 10. APETREI E., RUGINA M., STOIAN I., ALEXANDRU D., COMAN I., GINGHINA C., Should electrocardiographic changes precede the appearance of echocardiographic hypertrophy in familial hypertrophic cardiomyopathy (Study of 51 families). Congresul ESC 2007, 1–5 September 2007, Vienna. 11. CHANDRASEKARAN B., KURBAAN A.S., Myocardial infarction with angiographically normal coronary arteries. J. R. Soc. Med., 2002; 95(8):398–400. 12. COHLE S., LIE J.T., Myasthenia Gravis-Associated Systemic Vasculitis and Myocarditis with Involvement of the Cardiac Conduction Tissue. Cardiovasc. Pathol., 1996; 5:159–162.
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