[Reentry circuits in paroxysmal supraventricular tachyarrhythmia during sick sinus syndrome].
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Biomedical subjects
Publications and source records attributed to A Lotto.
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246 cases of acute myocardial infarction in subjects aged 70 or less, with clinical symptoms beginning no more than 8 hours before, altered enzymes, abnormal Q wave, ST segment and T wave, were studied. 99 of them received, on hospital admission, an intramuscular injection of 250 mg of lidocaine, 147 an injection of saline. In the following 3 weeks, significant differences were observed in the appearance of severe arrhythmias (no cases in the treated group and 18 cases in the placebo group, p less than 0,001) and of heart failure (39 cases in the treated group and 79 in the placebo group, p less than 0,05) and in mortality (3 cases in the treated group and 18 in the placebo group, p less than 0,05).
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The aim of this study was to determine the oxigen affinity actually present in vivo in blood from patients with acute myocardial infarction. Patients with uncomplicated acute myocardial infarction had normal value of P50 in vivo (partial pressure of oxygen at which 50 percent of the hemoglobin is saturated with oxygen at fixed levels of pHand PC02 present in vivo). Also the values of P50 in vivo of blood from patients with low cardiac output with mild or severe heart failured did not differ from the normal mean. This was the consequence of an increase of 2, 3-diphosphoglycerate levels (which reduces the oxygen affinity of hemoglobin) and of the immediate effect of alkalosis (Bohr effect). By contrast, the values of P50 in vivo were significantly increased in patients with cardiogenic shock. This could be ascribed to the state of acute acidiosis present in these patients. In these conditions the changes in the values of P50 in vivo play an important role in the oxygen delivery to the tissues. However, high values of P50 do not enhance oxygen delivery when a severe arterial hypoxemia (P02 smaller than 40-45 mm Hg) is also present.
186 out of 391 patients with acute myocardial infarction were treated with C-3 and 205 with placebo in a multicenter, double-blind clinical trial. Ensuing complications were treated in the same way in both groups. C-3 was injected i.v. slowly at the dose of 2 g statim plus 6 g by continuous drip infusion over 24 hrs for 5 days. During treatment, clinical progress was influenced only in regard to cardiac failure since in the C-3 group the improvement was more significant than in the placebo one (P less than 0.0025). Mortality rates were 8.1% and 11.2% for the C-3 and placebo groups, respectively. The difference in mortality was significant (P less than 0.05) for patients treated with C-3 for more than 24 hours. Mortality in male patients treated with C-3 for more than 12 hours was significantly lower (P less than 0.025). In patients less than 60 years old mortality rate was significantly lower (P less than 0.05) and was more so in patients receiving C-3 for more than 12 hours (P less than 0.025). Mortality due to complications was lower in the C-3 group, with arrhythmias (9.8% vs 14.2%), cardiogenic shock (69.2% vs 75%), and cardiac failure (9% vs 19.4%). Results agree with the hypothesis that C-3 may be effective in acute myocardial infarction by improving the action of traditional antiarrhythmic drugs, and augmenting myocardial contraction energy.
48 His bundle recordings were performed on 30 patients with acute mycardial infarction and various degrees of atrioventricular block. Studies were undertaken at the time of transvenous pacemaker insertion and/or removal from the right ventricle, without pharmacological or electrical stimulation tests. The connections between site of the infarcted area and localization of the a-v block were investigated, to identify uncommon relations. Several atypical cases were observed: among 12 cases of patients with anterior infarction, 6 had prolonged P-H interval, with prolonged H-V interval in 4 cases, and normal H-V interval in the remaining 2 cases. Among the 18 cases of inferior infarction, 5 had prolonged H-V interval, 2 of which had a normal P-H interval and 3 with prolonged P-H interval. In the latter cases, the identification of a two-step a-v block by His bundle recordings was shown to be important from the clinical and prognostic viewpoint. Nevertheless, it is evident that the His bundle recording is insufficient by itself to provide any evidence of the inner pathogenetical mechanism of these phenomena, and only various hypotheses can be advanced.
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