BACKGROUND: Bolus thrombolytic therapy is a simplified means of administering thrombolysis that facilitates rapid time to treatment. TNK-tissue plasminogen activator (TNK-tPA) is a highly fibrin-specific single-bolus thrombolytic agent. METHODS AND RESULTS: In TIMI 10B, 886 patients with acute ST-elevation myocardial infarction presenting within 12 hours were randomized to receive either a single bolus of 30 or 50 mg TNK-tPA or front-loaded tPA and underwent immediate coronary angiography. The 50-mg dose was discontinued early because of increased intracranial hemorrhage and was replaced by a 40-mg dose, and heparin doses were decreased. TNK-tPA 40 mg and tPA produced similar rates of TIMI grade 3 flow at 90 minutes (62.8% versus 62.7%, respectively, P=NS); the rate for the 30-mg dose was significantly lower (54.3%, P=0.035) and was 65. 8% for the 50-mg dose (P=NS). A prespecified analysis of weight-based TNK-tPA dosing using median TIMI frame count demonstrated a dose response (P=0.001). Similar dose responses were observed for serious bleeding and intracranial hemorrhage, but significantly lower rates were observed for both TNK-tPA and tPA after the heparin doses were lowered and titration of the heparin was started at 6 hours. CONCLUSIONS: TNK-tPA, given as a single 40-mg bolus, achieved rates of TIMI grade 3 flow similar to those of the 90-minute bolus and infusion of tPA. Weight-adjusting TNK-tPA appears to be important in achieving optimal reperfusion; reduced heparin dosing appears to improve safety for both agents. Together with the safety results from the parallel Assessment of the Safety of a New Thrombolytic: TNK-tPA (ASSENT I) trial, an appropriate dose of this single-bolus thrombolytic agent has been identified for phase III testing.

Aged↗

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Standards and concepts in valve surgery. Report of the task force: European Heart Institute (EHI) of the European Academy of Sciences and Arts and the International Society of Cardiothoracic Surgeons (ISCTS).

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Aortic Valve Insufficiency↗

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Selection bias in the use of thrombolytic therapy in acute myocardial infarction. The SAVE Investigators.

OBJECTIVE: To determine whether clinical selection for thrombolytic therapy for acute myocardial infarction results in a skewed population for subsequent adverse cardiovascular events. DESIGN: A comparison of the clinical features of the patients in the Survival and Ventricular Enlargement Study who either had or had not received thrombolytic therapy was conducted in both univariate and multiple logistic regression analyses. SETTING: Hospitalized patients experiencing acute myocardial infarction from 112 broadly representative, private, academic, and government hospitals in the United States and Canada. PATIENTS: All patients in the Survival and Ventricular Enlargement Study had had a recent myocardial infarction (less than 16 days) and had a left ventricular ejection fraction of 40% or less. INTERVENTION: Thrombolytic therapy was administered to 733 patients and was not given to 1498. MAIN OUTCOME MEASURES: The comparisons with respect to use of thrombolytic therapy were formulated after the completion of enrollment and indicated that the majority of patients did not receive thrombolytic therapy. RESULTS: The 1498 (67.1%) patients who did not receive thrombolytic therapy were at higher risk (older age, lower functional capacity, greater likelihood of a history of prior myocardial infarction, angina, diabetes, and hypertension) for subsequent cardiovascular events and, as anticipated, were more likely to have concomitant gastrointestinal and neurological diseases. A multiple logistic regression analysis indicated that older age, prior myocardial infarction, impaired functional status, employment status, diabetes, and neurological diseases were predictors of use of thrombolytic therapy. CONCLUSION: Although the Survival and Ventricular Enlargement Study population was selected for left ventricular dysfunction, the majority of patients who currently are judged clinically as unsuitable for thrombolytic therapy have a higher risk for adverse cardiovascular events.

Captopril↗

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