Giornale italiano di cardiologia
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An 83-year-old woman was found unconscious several hours after she had fallen and fractured her lower limbs in a very cold cellar. On admission she was in shock and had metabolic acidosis, anemia and hypokalemia; her axillary and rectal temperature was 23 degrees C. ⋯ These changes reverted to normal when body temperature returned to 37 degrees C. Moreover a transient, hypothermia-associated increase of QRS voltage was noted.
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In order to investigate the natural history and to evaluate the long-term risk of progression of the intraventricular (IV) conduction disturbances (CD) that complicate acute myocardial infarction (AMI), we prospectively followed the electrophysiological evolution of the IVCD in 47 patients admitted to our CCU in the years 1978-81 (34 anterior wall AMI, 13 inferior wall AMI; LAFB in 7, RBBB in 12, RBBB + LAFB in 13, RBBB + LPFB in 7, and LBBB in 8 cases). Only patients who acquired the IVCD after AMI and who did not develop 2 or 3 or 3 degrees degree AV blocks during the acute phase were considered. A His bundle recording (HBR) was obtained in every patient at the time of IVCD appearance. ⋯ Two patients died suddenly during the follow-up period, both had had HV prolongation during AMI; all other deaths were due to reinfarction or to congestive heart failure. Our data indicate that patients who develop an IVCD, without advanced AV block, during AMI, do not exhibit late progressive deterioration of their infra His bundle conduction, whether it was normal or prolonged during AMI. The risk of late AV block seems to be negligible for patients with normal HV interval, while it cannot be overlooked in patients with prolonged HV interval during the acute phase of myocardial infarction.