A. Borgeat of ti/. ; Pulmonary cdciiia and Becker’s inuscular dystrophy 129 always as benign as usually described (Mabry t’t I’ 1965; Zellweger et a/. , 1967), since despite medical ill.. rhtrdPy the clinical condition of this patient deteriorated Essively, calling for cardiac transplantation one year yr% Jfter the established diagnosis. References 61,,y~rBBc. Misra S. Somani PN, Chaterji AM: Congestive cardi- oniyopilthy in a fanuly of Becker X-linked nluscular dystrophy. post Grcid Mcd J 53. 12 (1977) Mabry CC, Roeckel IE, Munich RL, Robertson D: X-linked pseu- dohypertrophic muscular dystrophy with a late onset and slow progression. Nerc, Engl J Mcd 20, 1062 (1965) Markand ON, North RR, D’Agostino AN, Daly DD: Benign sex- linked muscular dystrophy. Neurology 19, 617 (1969) Perloff JK, de Leon AC, O’Doherty D: The cardiomyopathy of progressive muscular dystrophy. Circu1nr;im 33. 625 (1966) Vrints C, Mercelis R, Vazagt E. Snoneck J. Martin JJ: Cardiac manifcstations of Becker-type muscular dystrophy. Atra Curdiol 38, 479 (1983) Zellweger H, Hanson JW: Slowly progressive X-linked recessive muscular dystrophy (type I11 b). Arch Inrcm Mcd 120, 525 ( 1967) Myocardial Bridging of Coronary Arteries Associated with an Impending Acute Myocardial Infarction K. B. BESrE7TI. M.D . L. A. FINZI, M.D..* F. T. v. AMARAL, M.D.,* A. L. SECCHES. M.D..* J. s. M. OLIVEIRA, M.11.. Ph.D.t Clinical Staff of the University Hospital, Department of Internal Medicine, and Clinical Staff, Santa Lydia Hospital; *Clinical Staff. Sio Francisco Hospital; ?Department of Pathology, Faculty of Medicine of Ribeirrio Preto, Ribeirso Preto, Brazil Summary: A 57-year-old woman developed severe substernal chest pain rddiating to the left arm accompanied hy pallor and marked diaphoresis. These symptoms appeared at rest, lasted 45 minutes, and terminated spntaneously. The patient had been treated for mild hypertension during the last 6 months. An ECG tracing obtained at the beginning of treatment was unremarkable. However, an ECG tracing recorded shortly after the end of the symptoms showed T-wave inversion in all anterior leads. Coronary arteriography was then performed and showed no fixed obstructive coronary artery disease. Nonetheless, a lengthened and constricted myocardial bridging of both the left anterior descending coronary artery and its major diagonal branch was detected. Also, he left anterior descending coronary artery was observed very short. terminating before the cardiac apex. The kft ventricle was hypertrophied. The patient was treated with a beta-blocking agent which eliminated all symptoms. ECG tracing obtained about three months after the onset of the clinical picture was nornial. Our findings suggest that marked myocardial ischemia at rest does oc- cur in patients having myocardial bridges under special circumstances, such as lengthened and constricted my- ocardial bridging of a short coronary artery which sup- plies a hypertrophied ventricle. This anomaly should be taken into account as a possible cause of a threatened my- ocardial infarction, which may be successfully treated with a beta-blocking agent. Key words: coronary vessel anomalies, congenital heart defects Introduction The recognition of high-risk patients for acute myocardi- al infarction (AMI) constitutes a major goal for modem cardiology. It has recently been demonstrated that a characteristic ECG pattern may be associated with an im- pending AMI. In this situation, a critical stenosis is found high in the left anterior descending coronary artery (LAD) (Zwaan et al., 1982). On the other hand, myocardial bridging of the LAD is considered to be benign in the ah- sence of any other cardiac abnormality (Kramer et al., 1982). Although in most cases myocardial bridging causes atypical chest pain (Kramer et (I/. , 1982; Noble et d., 1976). it can be associated with angina pectoris (Noble ct a/. , 1976), AM1 (Faruqui et (I/., 1978) and sudden death after strenuous exercise (Morales et ul., 1980). However, myocardial bridging of coronary arteries has not been