[Restoration of sinus rhythm by lidocaine in a case of atrial fibrillation with high ventricular response in a patient with Wolf-Parkinson-White syndrome].
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Biomedical subjects
Publications and source records attributed to F Maddalena.
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A 22 years old man with ventricular preexcitation syndrome due to a left accessory pathway, was admitted because of orthodromic reciprocating tachycardia, 205 bpm in frequency. The patient was invited to perform a Valsalva Maneuvre, and at its ending, the tachycardia degenerated into atrial fibrillation (AF) associated with high ventricular rate, reverted to sinus rhythm by D.C. shock. The electrophysiologic study documented a left lateral by pass tract, with an anterograde refractory period of 230 msec. AF was inducible and had a minimal RR interval of 220 msec. Vagal stimulation, induced at the end of Valsalva maneuvre, probably caused dispersion of atrial refractorines and intraatrial reentry, converting the orthodromic tachycardia into atrial fibrillation.
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We analyzed by high amplification vectorcardiography the morphology of the QRS ending loop and the ST segment of patients with previously recorded Lown 4A, 4B ventricular arrhythmias and the healthy subject. Eight patients were affected by ischemic heart disease and 7 by arrhythmogenic right ventricular dysplasia. All had some irregularities at the end of the QRS or in the ST segment, on the standard ECG. The VCG showed one or more of these three morphologies: complete or incomplete ring, rapidly inscripted isodi-triphasic potentials, sinusoidal irregularities. In the 20 healthy subjects, the loop corresponding to the last 30 msec of the QRS, till the end of the afferent portion of T, was regular, without any particular morphology. We think that these aspects could be related to delayed fragmentation of the ventricular depolarization.
Heart rupture was found in 25 (4.4%) of 560 patients with myocardial infarction admitted to the Coronary Care Unit of the Department of Cardiology, Padua Medical School. Ten (40%) of them had a breaking of the free wall, 10 the interventricular septum, 4 (16%) a papillary muscle and 1 (4%) the ventricular wall with formation of a pseudoaneurysm. Thirteen patients died suddenly, the other 12 (48%) had cardiac catheterisation and later surgery. Four patients with interventricular defect died immediately after surgery, the other patients were discharged. Mortality was 68%; 30% on the patients with VSD as well as those with papillary muscle rupture and pseudo aneurysm survived.
After D.C. countershock to terminate cardiac arrhythmias, in 3 out of 8 patients studied, an increase in both plasma myoglobin (Mb) and CK-MB (assessed by radioimmunoassay) was found. In 2 patients there was an increase of only plasma Mb and in 1 an increase of only CK-MB. In 2 cases no increase of either parameters was found. It is suggested that the radioimmunoassay technique for measuring Mb and CK-MB might have a greater reliability than other techniques for the detection of myocardial damage.
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Creatinephosphokinase (CPK) and myoglobin (Mb) were measured in 15 patients admitted to the Coronary Care Unit for acute myocardial infarction (AMI). Blood samples were collected from the right atrium every six hours for 48 hours starting from the time of arrival in the Unit and were tested for CPK by a spectrophotometric technique and for Mb by an RIA method. Mb usually started to increase earlier than CPK and reached the peak plasma level more quickly. In five cases Mb but not CPK subsequently showed further increases during the course of the study. The suggestion is made that Mb measurements might be more reliable than CPK for the early detection and the initial followup of AMI.
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