Atrial strain is the main determinant of release of atrial natriuretic peptide.

We studied the response of atrial natriuretic peptide to the hemodynamic and renin-aldosterone variations occurring in four patients who developed cardiac tamponade, either occurring in idiopathic fashion in one or secondary to metastatic involvement of the pericardium in three. Right atrial pressure, heart rate and arterial blood pressure were monitored and serial blood samples were taken before and over three hours after pericardiocentesis. During cardiac tamponade, normal levels of atrial natriuretic peptide (mean +/- SEM: 54 +/- 7.4 pg/ml) were observed in the plasma despite increased right atrial pressure (23 +/- 3.8 cm H2O) and heart rates (98 +/- 4.4). Removal of pericardial fluid (540 to 1160 ml) was associated at first with a 200% increase in plasma concentrations of atrial natriuretic peptide (108 +/- 8.8 pg/ml; P less than 0.001), then with a gradual decline toward normal levels, simultaneous with the normalization of right atrial pressure and heart rate. Activity of renin and concentrations of aldosterone in the plasma were increased during tamponade and returned gradually to normal after pericardiocentesis (3.8 +/- 0.9 to 1.2 +/- 0.3 ng/ml/h and 20 +/- 4.2 to 9 +/- 3.2 ng/dl, respectively; P less than 0.01). These data confirm that atrial strain, not intracavitary pressure in itself nor heart rate, is the main determinant of the acute release of atrial natriuretic peptide, which is associated with a suppressing effect on the renin-aldosterone system. In addition, our data indicate that secretion of atrial natriuretic peptide during cardiac tamponade is not stimulated by secondary hyperaldosteronism.

2:1 and phase 4 peri-infarction block.

A patient with acute inferior and anteroseptal myocardial infarction initially developed a 2 : 1 AV block with alternate conducted ventricular complexes showing aberrancy, and later Wenckebach-type, 2nd-degree AV block with aberrancy of the beats following a long diastolic pause. Intracavitary recording suggested that aberrancy was related to an intraventricular block. ECG and VCG recordings excluded the site of block as being in the main bundles or in the fascicles of the left bundle. The patient therefore showed evidence for a 2 : 1 and later a phase 4 peripheral block, defined also as a peri-infarction block because of the underlying etiology of the block. The block could be localized in the posterior wall of the right ventricle, by the marked rightward and posterior orientation of the middle and terminal electrical forces evident in the vectorcardiogram.

[Evolution of ventricular depolarization in the acute phase of inferior and posteroinferior myocardial infarction (author's transl)]. / Evoluzione della depolarizzazione ventricolare nella fase acuta dell'infarto inferiore e postero-inferiore

Twenty-five patients, hospitalized within 24 hours from the beginning of the precordiaglia due to acute diaphragmatic infarction, with or without a posterior extension, underwent the ECG and VCG recordings for the first consecutive twenty days and on the fortieth day, in order to study the development of ventricular depolarization. To diagnose an infarction of the diaphragmatic and posterior walls the usual ECG and VCG paramaters were used; the ECG was found to be less useful above all for the difficulty of measuring the variations, in the loss of the electrical forces. The electrodes were always placed in the same points suitably signed. Several evolutive modalities of the diaphragmatic infarction were observed; in 52% of the cases the loss of the inferior electrical forces reaches its maximum expression quickly, then it remains almost constant. In 12% of the cases the necrosis increases very clearly, tardily, between the ninth and fourteenth day. In 24% a precocious reduction of the electrical extension of the infarction on the eighth-twelfth day is observed. In 12% of the cases there are irregular oscillations during the whole acute phase. In all cases more or less stressed daily or cyclic oscillations were present. In nine cases an extension of the infarction to the posterior wall was evident; among these in five, two peaks are present; in two an initial increase, in the other two an initial decrease of the electrical extension of the necrosis; then, more or less stressed daily or cyclic oscillations. In another nine cases a single reading of the tracings do not let us diagnose a posterior extension; this is possible only through an "in series" reading. The clinical course and the humoral data do not give any contribution to the interpretation of the founded evolutive variabilities. The necrosis, therefore, must not be considered a zone of homogeneous and global stuffing, but composed of cellular groups in several and variable anatomo-metabolic situations conditioning the observed electrical instabilities.

Does intravenous streptokinase therapy facilitate the formation of anti-heart antibodies in acute myocardial infarction?

Streptokinase (SK), a nonenzymatic protein produced by group C beta haemolytic streptococci, is a potent antigen. It is used worldwide as a thrombolytic agent in the treatment of acute myocardial infarction (AMI). Specific antiheart antibodies (AHA) have been found with a significantly high incidence in patients with AMI, and after streptococcal infection as a result of stimulation by constituents of the group A streptococci antigenically cross-reactive with sarcolemmal portion of the muscle fiber of the heart. Since there may be partial antigenic identity of group C streptococcal membranes with membranes isolated from group A streptococci, we have designed a prospective study to evaluate the incidence of serum AHA (and of other organ-specific and non-organ-specific antibodies) in 36 patients with AMI, 14 of whom treated with SK. AHA, of IgG class, were of the sarcolemmal-subsarcolemmal type, and did not fix complement. They were found in 4/36 patients already on admission; of the 32 patients negative, none developed AHA later, on days 7, 15 and 21 of hospitalization, also after treatment with SK (in 14 cases). There was no significant difference either within or between the two SK-treated and non-SK-treated groups also with regard to the incidence of organ-specific and non-organ-specific autoantibodies. These findings do suggest that the intravenous SK therapy does not facilitate the formation of AHA in AMI.