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To evaluate efficacy and tolerability of the systemic infusion of 1,500,000 streptokinase units in 30', we treated 26 consecutive patients with acute myocardial infarction within 3 hours of the onset of chest pain. They were 23 men and 3 women, mean age was 59 +/- 8 years. None of them had a history of previous myocardial infarction. From clinical and electrocardiographic data, as well as from creatine kinase curves, we assumed myocardial reperfusion in 19 patients (73%). Within 30' after infusion, thrombin time increased to more than 300" in 25/26 patients (96%). Streptokinase induced hypotension (which we defined as a decrease in systolic blood pressure of more than 30 mmHg) in 13 patients (50%), and in 5 of them (19%) systolic blood pressure fell below 90 mmHg. Hypotension was counteracted by adopting the Trendelenburg position in 7 patients, and by an intravenous infusion of atropine in 5. In the remaining patient, streptokinase infusion was slowed down. Due to these interventions, a non-significant decrease in systolic blood pressure was observed from 129 +/- 26 to 112 +/- 20 mmHg at the end of the infusion. Streptokinase-induced hypotension was not predicted either by clinical, or electrocardiographic, or chest X-ray film data, or laboratory findings. No other side-effects occurred. Hence, the infusion of 1,500,000 streptokinase units in 30' in the acute phase of myocardial infarction is active, and well tolerated. It must be emphasized, however, that during the infusion, hypotension occurs frequently and unpredictably, sometimes reaching alarm levels. This makes the monitoring of systolic blood pressure imperative during streptokinase infusion.

In the article the authors illustrate: a) a community detection program designed to identify subjects with high blood pressure for treatment; b) the degree of participation; c) the cost of realization; d) the prevalence of arterial hypertension. A total of 4.149 subjects, or 65% of the examined population over age 8, were screened. The opportunity to have their blood pressure checked were offered with a letter of invitation to a centralized ambulatory. The cost of realization was L. 360 for every screened subject. The prevalence of hypertension was 20.4%.

In an oligosymptomatic patient with recent acute anterior myocardial infarction, two-dimensional and Doppler echocardiography allowed us to detect, unmistakably, the presence of an apical pseudoaneurysm. Prompt and successful repair was made without performing left ventriculography. To our knowledge, this is the first case of pseudoaneurysm referred for surgery on the basis of echocardiographic findings.

The aim of this study was to assess the correspondence between two-dimensional echocardiographic (2D-Echo) and anatomic features of left ventricular thrombi (LVT), with particular reference to LVT shape and dimensions. The study population was composed of 23 patients who were admitted to our intensive cardiac care unit with an anterior acute myocardial infarction and who died during the hospitalization. Every patient underwent serial echocardiographic examinations, the last one performed within the 24 hours preceding death. The diagnosis of LVT required the agreement of three independent observers. Doubtful cases were considered as negative. With regard to shape, the LVT were defined as mural or protruding. Two measures of the LVT were obtained in each case: the longest dimension and the greatest one perpendicular to the initial dimension. At post-mortem examination we obtained sections of the heart comparable with an echocardiographic four chamber view. LVT were detected by 2D-Echo in 12/23 cases. Post-mortem examination confirmed the presence of LVT in these 12 patients. A thin apical thrombotic layer, whose presence had been defined previously as doubtful, was observed in another patient. The sensitivity of 2D-Echo was 92% and the specificity 100%. At 2D-Echo, shape was mural in 2 patients and protruding in 10. Complete agreement was found between 2D-Echo and anatomic findings as far as the morphology of LVT is concerned. The 2D-Echo measurements of LVT showed a high correlation with autopsy (r = 0.95; r = 0.86); we conclude that 2D-Echo provides accurate evaluations of the shape and the dimensions of LVT.

Gallium-67-citrate imaging has been recently proposed, in addition to endocardial biopsy, to detect myocardial inflammation in idiopathic dilated cardiomyopathy (IDCM). In order to evaluate the clinical usefulness of this method, 33 patients (pts) suffering from IDCM, 24 pts with various other cardiac diseases (inflammatory etiology in 7), and 11 controls underwent Gallium-67 scintigraphy (anterior and 30 degrees left anterior oblique projections; acquisition at 48 and 72 hrs). In 31 pts repeated scintigraphic examinations (at least two) were obtained. Scans were interpreted by two independent observers. Positivity of scintigrams was based on three different criteria: 1) myocardial activity greater than that of the sternum; 2) presence of focal myocardial activity; 3) semiquantitative index (index = activity of sternum/myocardial activity). Significant differences, either in the percentage of positive scans or in the values of the semiquantitative index, were found between controls and all pts with cardiac diseases. However, no difference was observed when comparing pts with IDCM to pts with other cardiac diseases. Finally, among the pts with cardiac disorders other than IDCM, the qualitative and semiquantitative results of the 7 pts with inflammatory etiology of the disease were similar to those obtained in the remaining 17. Of those pts who underwent longitudinal study, about a third showed modified scintigraphic results later on. No significant difference in behaviour was observed between IDCM and other cardiac disorders. Therefore, we conclude that Gallium 67-citrate imaging does not appear to be a suitable method for the identification of pts. with IDCM. The usefulness of this technique should be tested in samples of pts should previously selected with other more specific methods.

We describe a family with a high frequency of supravalvular aortic stenosis. The family includes 5 generations and 80 subjects (prospective study in 66, on whom physical examination, ECG, M-mode and two-dimensional echocardiogram were performed, and retrospective analysis of available data in 14). This is the largest family group with this disease studied so far. Thirty-six subjects (45%) were found to be affected. On the basis of the echocardiographic image and of the haemodynamic gradient (when available), three different degrees of supravalvular aortic stenosis were identified. The disease was found to be severe in 8 subjects (22%), moderate in 6 (17%), mild in 13 (36%) and undefined in 8 (22%). In 4 cases multiple pulmonary stenoses were associated with supravalvular aortic stenosis, while in one subject multiple pulmonary stenoses were noted in the absence of aortic abnormalities. In the family we studied, the supravalvular aortic stenosis gene is transmitted with a pattern of inheritance consistent with an autosomal dominant trait with variable expressivity and penetrance (penetrance coefficient = 0.86). A high mortality rate in early childhood was observed, while symptoms and ECG abnormalities were not related to the degree of the stenosis. Furthermore, we found a high rate of mitral valve echocardiographic abnormalities, such as mitral prolapse and systolic anterior motion. The absence of Williams dysmorphic somatic features in the many generations as well as in the large number of patients we studied, appears to exclude the coexistence of Williams and Eisenberg's syndromes in the same family group.