Does thrombolysis produce cholesterol embolisation?
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Adult↗
Biomedical subjects
F M Turazza
Publications and source records attributed to F M Turazza.
[Tissue-type plasminogen activator].
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.
Arterial Occlusive Diseases↗
[Tissue-type plasminogen activator (t-PA): comments on results of the GISSI-2 study].
12,490 patients from the GISSI-2 trial were randomly allocated to alteplase (recombinant tissue-type plasminogen activator, t-PA) or streptokinase (SK) and beginning 12 hours after the start of thrombolytic therapy to subcutaneous heparin or no heparin. No significant differences in hospital mortality were found between the two thrombolytic treatments as well as between heparin and no heparin administration. The incidence of major cardiac complications was also very similar in the different groups. The incidence of major bleedings was significantly higher in SK and heparin treated patients, whereas the overall incidence of stroke was similar in all groups. SK and t-PA with or without post-thrombolytic heparin treatment appear equally effective and safe for use in routine conditions care, in all patients with acute myocardial infarction (AMI).
Heparin↗