Thrombolytic therapy in cardiogenic shock: Effect of increased aortic pressure and rapid tPA administration
Autor: | R M Prewitt, P J Garber, A L Mathieson, J S Geddes, John Ducas, J N Patton |
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Rok vydání: | 1995 |
Předmět: |
medicine.medical_specialty
business.industry medicine.medical_treatment Cardiogenic shock Hemodynamics Thrombolysis Emergency Nursing medicine.disease Tissue plasminogen activator Blood pressure Internal medicine Heart failure Emergency Medicine medicine Cardiology Aortic pressure Myocardial infarction Cardiology and Cardiovascular Medicine business medicine.drug |
Zdroj: | Scopus-Elsevier |
ISSN: | 0300-9572 |
DOI: | 10.1016/0300-9572(95)99856-6 |
Popis: | Objectives To investigate the effect of an increase in aortic pressure combined with rapid tissue plasminogen activator infusion on hemodynamic stability and patency of the infarct-related artery in patients with acute myocardial infarction complicated by profound hypotension or cardiogenic shock. Background Thrombolytic therapy improves mortality in relatively stable patients with acute myocardial infarction but not in patients with cardiogenic shock. Recent canine studies have demonstrated that a moderate increase in low aortic pressure improves thrombolysis. Conceivably, then, decreased thrombolytic efficacy in cardiogenic shock is due, at least in part, to a low aortic pressure impairing delivery of the thrombolytic agent. Patients and methods For patients presenting within 6 h of an acute myocardial infarction complicated by profound hypotension or cardiogenic shock, an inotropic agent was rapidly administered to increase the systolic aortic pressure to approximately 110 mmHg, and 100 mg of tissue plasminogen activator was administered intravenously over 45 to 60 mins. Results Eight consecutive patients meeting the study criteria were treated over 18 months. In six of eight patients, the inotropic agent increased systolic blood pressure over 10 mins, from a mean of 64 +/- 12 mmHg to 102 +/- 12 mmHg. In the two patients whose blood pressure did not increase, early angiography in one demonstrated occlusion of the infarct-related artery, and both of the patients died. In the other six patients there was clinical and hemodynamic evidence of early reperfusion, and infarct-related arteries were patent on angiography. These six patients survived at least 30 days, with four having a favourable clinical outcome and two having a functional limitation due to heart failure. Conclusions These results are consistent with experimental data indicating that an increase in aortic pressure combined with rapid tissue plasminogen activator infusion may increase thrombolytic efficacy when an acute myocardial infarction is complicated by profound hypotension or cardiogenic shock. |
Databáze: | OpenAIRE |
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