[ST segment alternams in myocardial infarct: apropos of a case]. / L'alternanza del tratto ST nell'infarto miocardico: a proposito di un caso.

Alternans of the ST segment is frequent in Prinzmetal's angina and is referred to a dyshomogeneity of myocardial refractoriness during ischemia. Reports of this phenomenon in myocardial infarction are, on the contrary, extremely rare. A case of alternans of the ST segment in a man with myocardial infarction is described. Based on the previous experimental reports, the hypothesis is advanced that delayed and blocked electrical activity of the ischemic area may be responsible for the event observed. This phenomenon is probably not infrequent in myocardial infarction.

[Neurological complications of the acute myocardial infarction (author's transl)]. / Le complicanze neurologiche nella fase acuta dell'infarto miocardico.

In a consecutive series of 750 patients with acute myocardial infarction, 11 (1.46%) suffered neurological complications. The pathogenesis of these neurological incidents (embolia or hypotension) remained uncertain in all the cases presented here. Neurological incidents (3 TIA, 8 strokes) were more frequent in elderly patients, in which they represented a very serious complication with high fatality. No clear relationship could be established with infarct size nor with the anticoagulant therapy.

Alternans of the ST segment and T wave in acute myocardial infarction.

A case of isolated alternans of the ST segment and T wave in a man with myocardial infarction is reported. Based on the previous experimental reports, the hypothesis is advanced that delayed and blocked (2:I) activity of the ischemic area may be responsible for the phenomenon observed.

Atrial repolarization: its role in ST elevation.

In four patients, ectopic supraventricular rhythm (or beats) with cephalad anomalous atrial activation and, generally, a short PR, were always associated with an ST elevation in the leads with a negative P wave. An inverted Ta wave appears to be responsible for the ST elevation.

[The causes of death after acute myocardial infarction (author's transl)]. / Le cause di morte nell'infarto miocardico acuto.

Following a brief outline on problems concerning methodology, the cause of death is analysed in 110 patients dying from acute myocardial infarction during hospitalization. Autopsy studied were carried out in 78 cases. Of the various causes, the most frequent were forms of contractile insufficiency (EPA, shock, shock + EPA, biventricular congestive heart failure) which were responsible for 50.90% of cases; followed by cardiac rupture (considered in a single group with electromechanic dissociations of the patients not submitted to autopsy studies since in the experience of the Authors cardiac rupture almost always presents with this pattern) with a frequency of 29%. The frequency of arrhythmias, on the other hand, is very low, particularly in the coronary care unit where it is practically a negligible causa mortis 2.72%): even if sudden death, in patients who were not monitored, is included amongst the arrhythmias, the percentage is still only about 10%. Embolism (usually pulmonary, but systemic in one case) was the cause of death in 5 patients (4.54%). Three patients over 80 years of age died from ischemic cerebral episodes. Age, sex, and site of infarction, do not appear, in the present series, to have a determinant effect in the cause of death; a higher frequency of rupture in the female sex was not, for example, confirmed. On the basis of the observations in the present series, any relationship between cardiac rupture and anticoagulating therapy, steroid treatment, application of endocavitary stimulators, or early ambulation is excluded. It is also excluded that reanimation, as hypothesized by some Authors, may be responsible for rupture.

The effects of manganese on aconitine-induced ventricular tachycardia.

Isolated rabbit heart with independent perfusion of a small left ventricular area was used to study the effect of manganese ions on aconitine-induced ventricular tachycardia. Manganese chloride 4 mM in Locke solution exhibited a constant preventive or suppressive effect versus aconitum-induced rhythm disorders. It is concluded that the interpretation of aconitine cardiotoxic effects on the sole basis of phase 3 modifications require further evidence, and that an increased diastolic depolarization rate may well explain, at least in this experimental model, the genesis of arrhythmias induced by this drug.