An intracardiac electrophysiological study was undertaken to examine 15 patients with paroxysmal supraventricular tachycardias. Allapinin intravenously given in a dose of 0.4 mg/kg, was tested for effects. The agent was demonstrated to cause a substantial inhibition of rapid retrograde pathway function in atrioventricular nodal tachycardia and abnormal antero- and retrograde pathway function. This is the major aspect of the drug's action that prevents the development of episodes of paroxysmal supraventricular tachycardias. The agent fails to virtually affect the function of the atrioventricular node in the anterograde direction in the two types of the tachycardia. Thus, allapinin has the mechanism of action that is typical of quinidine-like drugs used in supraventricular tachycardias.
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Article Synopsis
- The study aimed to determine if high levels of high-sensitivity troponin-T (hs-TnT) in patients with paroxysmal supraventricular tachycardia (PSVT) but no known cardiovascular disease increase the risk of death.
- Researchers reviewed data from 1,203 patients hospitalized from 2013 to 2020, finding that 65.8% had elevated hs-TnT levels.
- Results showed significantly higher short-term mortality (within 30 days) for patients with elevated hs-TnT, but long-term mortality (31-365 days) differences were not significant and may need further study.
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