[Tissue-type plasminogen activator]. / Attivatore tessutale del plasminogeno.

Tissue-type plasminogen activator (t-PA) is a serine protease that converts a zymogen plasminogen into an active serine protease, namely, plasmin. Plasmin is the proteolytic enzyme that degrades fibrin. In the absence of fibrin, e.g., in circulating plasma, t-PA activates plasminogen at a very slow rate. However, when fibrin is present, this activity is enhanced two to three orders of magnitude. As a consequence of these kinetic characteristics, plasmin is predominantly generated on the fibrin surface. This in turn results in a relative sparing of circulating fibrinogen and other plasma proteins to plasmin--mediated degradation. Following the demonstration of the potential of natural t-PA as a thrombolytic agent, an intensive effort was launched to enhance its production by recombinant DNA technology. The pharmacological action and the clinical efficacy of t-PA has been tested by several Authors in the treatment of acute myocardial infarction (AMI), and more recently, of pulmonary embolism, a condition for which this drug seems to be very promising: from this point of view this short article provides evidence that the various thrombolytic agents are of equal ability in mediating the rapid lysis of a coronary thrombus after i.v. administration when given appropriately and at the proper time; clinical experience provides little support for the contention of the superiority of t-PA over other thrombolytic agents, particularly for coronary thrombolysis. We are waiting for the results that will come from the GISSI-2 study, that is comparing streptokinase (SK) vs. t-PA in AMI's patients.

[Amiodarone prophylaxis of ventricular tachycardia in ischemic cardiopathy]. / Profilassi con amiodarone della tachicardia ventricolare nella cardiopatia ischemica.

Sustained ventricular tachycardia (VT) in coronary heart disease (CHD) represents a major risk factor for sudden death. The Authors evaluated the prophylactic efficacy of the chronic administration of amiodarone (A) on this arrhythmia and simultaneously the trend of ventricular extrasystole during the antiarrhythmic treatment. Twenty-three patients were examined, 17 with post-infarction cardiopathy and 6 with mixed angina. They showed either 1 or more episodes (2 patients) of sustained VT involving hemodynamic difficulties. The ejection fraction (EF) ranged between 20 and 45% average (35.2 +/- 9). All patients underwent a basal 24 hour ECG 3 days after the VT cardioversion, and every 6 months. All subjects took A orally for a period ranging from 7 to 67 months (average 23.04 +/- 14) at the dose of 800 mg/day 7 for days, and then 200 or 400 mg/day according to the presence or absence of ventricular extrasystoles (VE) greater than or equal to 30/hr and/or Lown's class (L) greater than or equal to 3. No patients died suddenly during the follow-up; 6 of them died for causes other than arrhythmia. Four of them showed only 1 sustained VT relapse after a period of 6 to 11 months. Two of these 4 patients showed a persistent increase of the number of VE and L-class while, in the remaining 2 patients, the number of VE remained substantially unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

[External post-infarction rupture of the heart. Retrospective anatomo-clinical analysis of 70 cases]. / Rottura di cuore, esterna, post-infartuale. Analisi anatomo-clinica retrospettiva di 70 casi.

A retrospective comparison was made between the clinical and pathological findings pertaining to: a) 70 cases of rupture of the ventricular free wall following myocardial infarction (RC group), b) 70 cases of acute myocardial infarction (AMI) where death intervened in the absence of cardiac rupture (NR group) and c) 70 cases (clinical findings only) of patients with AMI admitted to the hospital (IM group). The history of the RC group disclosed a considerably lower percentage of previous myocardial infarctions (p less than 0,005) as compared to the control groups. In the same group systemic hypertension after myocardial infarction was more frequent (p less than 0,025) than in the others. Shock, heart failure, bundle branch blocks were significantly less common in the RC group than in the NR group, and severe arrhythmias were found in a significantly lower percentage than in both the control groups. An electrocardiographic pattern of anterior AMI was more frequent in the RC group than in the IM group (p less than 0,05). Death was preceded by sudden loss of consciousness in 83% of the RC cases and in 51% of the NR cases (p less than 0,005), by severe chest pain respectively in 19% and 9% of the two groups (p less than 0,05). More than 25% of the patients of both RC and NR groups died within the first 24 hours, almost half within the third day after the onset of AMI. On autopsy the AMI was anterior and/or lateral in 77% of the cases in the RC group and in 44% of the NR group (p less than 0,005). In all the cases except one rupture had occurred in the area of the infarction. The site of rupture was anterior in 64% of the cases, posterior in 16%, lateral in 11%, and apical in 9%. Scars larger than 5 mm were noted in 17% of the cases in the RC group as compared to 37% in the NR group (p less than 0,01). Left ventricular hypertrophy was present in 16% of the RC cases and in 31% of the NR group (p less than 0,05). Finally the characteristics of patients at risk of cardiac rupture following myocardial infarction seem to be: absence of previous infarctions, anterior localization of AMI, sustained hypertension after myocardial infarction, absence of serious hemodynamic and arrhythmic complications.