Giornale italiano di cardiologia
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Electrophysiologic studies were performed in 10 patients (8 M, 2 F, mean age: 60.2 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. The cardiac arrest had always been sudden and unexpected. ⋯ The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of the follow-up. It is also noteworthy that amiodarone, alone or in combination, was given chronically to 6 of our patients (60%). These results 1) indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest, and 2) suggest that amiodarone may be effective in preventing sudden death in these patients.
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The prognostic value of the presence and degree of pulmonary arterial hypertension in chronic obstructive pulmonary diseases has been well established, but the natural history of the course of pulmonary artery mean pressure was relatively obscure until recent years. The first studies showed a modest increase in pulmonary artery mean pressure after an average delay of 3-5 years. ⋯ When putting together the data of Boushy and North, Schrijen et al. and Weitzenblum et al. which concern a relatively homogeneous group of 163 patients with severe chronic obstructive pulmonary diseases, it appears that changes in pulmonary artery mean pressure, after an average follow-up period of 4 years, were rather small, from 21.4 to 23.6 mmHg (0.5-0.6 mmHg/year). These results have been confirmed by a very recent study of our group concerning 93 chronic obstructive pulmonary diseases with patients followed-up for 5-12 years (mean = 90 months).
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Clinical Trial
Effects of oxygen therapy on pulmonary arterial hypertension in chronic obstructive lung disease.
In patients suffering from chronic obstructive lung disease pulmonary arterial hypertension is mainly due to anatomical lesions. For this reason it does not regress following acute administration of oxygen, unlike functional pulmonary arterial hypertension due to vasoconstriction, which superimposes itself on the anatomical lesions during exacerbations of respiratory insufficiency. At present there is convincing proof that protracted treatment with oxygen is able to reduce pulmonary arterial hypertension sustained by anatomical alterations. ⋯ S. (duration of follow-up: 6 months), the other in Great Britain (duration of follow-up: 5 years), have reached this conclusion. The effects of oxygen on pulmonary arterial hypertension are directly proportional to the number of hours in which oxygen is administered daily; in any case this number should not be below 15 hours/day. The reasons for which treatment with oxygen is not able to arrest the evolution of pulmonary arterial hypertension in some patients and the role of the reduction in blood viscosity due to oxygen therapy remain to be clarified.
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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.