Randomized comparison of intravenous versus intracoronary streptokinase for myocardial infarction.

The efficacy of intravenous (i.v.) thrombolytic therapy has not been firmly established in comparison with the intracoronary (i.c.) route of administration. In a randomized trial of 28 patients who underwent angiography before and during i.v. and i.c. administration of streptokinase (STK), recanalization was achieved in 73% of patients who received the drug by the i.c. route, compared with 62% of patients who received the drug by the i.v. route (difference not significant). Reopening took 28 minutes for i.c. STK and 39 minutes for i.v. STK. Patients in whom recanalization was successful using either route of administration had shorter euglobulin lysis times and lower fibrinogen levels than did patients in whom it was not successful (p less than 0.05). Bleeding complications were closely correlated with heparinization after thrombolysis rather than with STK itself. These results in a limited patient series suggest that early administration of i.v. STK in the emergency department may yield recanalization rates similar to those for the i.c. route and may benefit myocardial preservation by restoring flow much earlier.

Prolongation of the human cardiac monophasic action potential by sotalol.

Sotalol and propranolol are nonselective beta-adrenergic blocking agents. Sotalol at low concentration, unlike propranolol, prolongs the duration of the transmembrane action potential. In a double-blind study, the electrophysiologic effects of intravenous sotalol (0.30 or 0.60 mg/kg; n = 9) were compared with intravenous propranolol (0.15 or 0.20 mg/kg; n = 8) in 17 patients with use of bipolar suction electrodes in the right atrium and right ventricle to determine whether sotalol prolongs the monophasic action potential duration in man. After administration of sotalol, there were significant increases (paired t test) in the Q-T interval (p less than 0.001), right atrial effective refractory period (p less than 0.05), right ventricular effective refractory period (p less than 0.005), right atrial monophasic action potential duration at 90% repolarization (p less than 0.01), and right ventricular monophasic action potential duration at 90% repolarization (p less than 0.005). Prolongation of the monophasic action potential duration was dependent on plasma sotalol concentration. There were no significant changes in these variables after propranolol. The spontaneous cycle length and Wenckebach cycle length increased significantly in both groups, and the mean blood pressure decreased in both, although not significantly after propranolol. In summary, sotalol but not propranolol prolonged atrial and ventricular effective refractory periods and lengthened the monophasic action potential and the Q-T interval of human myocardium after intravenous infusion. The ability to acutely prolong repolarization at therapeutic plasma concentration is unique among known competitive beta-adrenergic receptor antagonists.

Lower-esophageal sphincter function does not determine resting upper-esophageal sphincter pressure.

Records of 269 esophageal motility studies were reviewed to determine the relationship between lower-esophageal sphincter (LES) function and upper-esophageal sphincter (UES) pressure. Average and greatest UES pressures were similar in patients with LES pressures less than 10 mm Hg or greater than 20 mm Hg, and in patients with and without gastroesophageal reflux as determined by an intraesophageal pH electrode test. Although teliologically appealing, the belief that patients with weak lower-esophageal sphincters and gastroesophageal reflux have stronger upper-esophageal sphincters to guard against pharyngeal reflux and aspiration cannot be confirmed by current manometric techniques.