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Diffusion bonding of metallic glasses and crystalline metals utilizing excellent superplasticity of monolithic bulk metallic glasses (BMGs) within supercooled liquid region has been found to be an efficient method to improve the room temperature plasticity and fracture toughness of metallic glass. A Zr-based BMG/copper laminated composite was fabricated by copressing method, and the interface bonding status was characterized by scanning electron microscopy (SEM) and high-resolution transmission electron microscopy. No void or crack is detected, and the interface is a metallurgical bonding of atomistic level. Although the BMG retains amorphous state after copressing at 390 °C, the region of the amorphous-crystalline mixture structure with the width of 30-40 nm occurred within the diffusion zone. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In 22 patients with atrioventricular reentrant tachycardia incorporating a retrogradely conducting accessory pathway, electrophysiologic studies were done before and after oral digoxin, 1.25 mg, and propranolol, 160 to 240 mg, each given in 4 divided doses at 6-hour intervals. Before digoxin and propranolol, all 22 patients had induction of sustained tachycardia. After the medication six patients lost the ability to induce atrial echo and one lost the ability to sustain tachycardia due to an increased retrograde accessory pathway or atrial refractoriness or both. Six patients lost the ability to induce or sustain tachycardia due to increased atrioventricular nodal refractoriness. In the remaining nine patients with inducible sustained tachycardia, cycle lengths of tachycardia were prolonged. These findings suggest that combined use of oral digoxin and propranolol is useful in selected patients with atrioventricular reentrant tachycardia.

Electrophysiologic studies were performed before and 2 hours after the oral administration of 270 mg of diltiazem in 3 divided doses at 8-hour intervals in 36 patients with paroxysmal supraventricular tachycardia (SVT). Before diltiazem, all 36 patients had induction of sustained SVT: 24 with atrioventricular (AV) reentrance incorporating an accessory pathway (Group 1) and 12 with AV nodal reentrance (Group 2). After diltiazem, 20 patients in Group 1 lost the ability to induce or sustain SVT because of increased anterograde normal pathway refractoriness in 19 patients and increased retrograde accessory pathway refractoriness in 1. Eight patients in Group 2 could no longer induce or sustain SVT because of increased anterograde slow pathway refractoriness in 2 patients and increased retrograde fast pathway refractoriness in 6. Diltiazem concentration in the blood, measured in 29 patients, was 156 +/- 75 ng/ml (mean +/- standard deviation). Fifteen patients, 2 with and 13 without induction of sustained SVT after diltiazem, were discharged on the same dosage of diltiazem and followed up 5 +/- 3 months. The former 2 patients had attacks of sustained SVT, whereas the latter 13 have been free of sustained SVT. In conclusion, oral diltiazem prevents induction and sustenance of paroxysmal SVT in most patients and may be used as an alternative agent for the prophylaxis of SVT.

Electrophysiologic study, isoproterenol infusion, and serial treadmill exercise tests before and after administration of propranolol, verapamil, lidocaine, and procainamide were done in three patients with exercise-triggered ventricular tachycardia. In all three patients, organic heart diseases were absent. Ventricular tachycardia was reproducibly provoked with exercise and with isoproterenol infusion. Propranolol (tested in three patients) and lidocaine (tested in two patients) effectively prevented exercise provocation of tachycardia. Verapamil terminated tachycardia in all three patient and successfully prevented exercise provocation of tachycardia in only two patients. Procainamide was ineffective in one patient and was partially effective in two patients. In the latter two patients, ventricular ectopies, couplets, and short salvos remained provocable with exercise. Electrical stimulations with incremental ventricular pacing and ventricular extrastimulus testing failed to induce tachycardia in all three patients. These findings strongly suggest that repetitive rhythmic activities related to the catecholamine-sensitive afterdepolarizations are probably responsible for the exercise-triggered ventricular tachycardia.

Factors determining tachycardia induction using ventricular stimulation in atrioventricular (AV) nodal reentrant tachycardia utilizing the slow pathway for anterograde and the fast pathway for retrograde conduction were analyzed in 53 patients. Sixteen patients had tachycardia induced by ventricular stimulation. In 15, tachycardia was inducible with incremental ventricular pacing. In 4 of these 15 patients, the tachycardia was also induced with V1V2 testing, while in 11 patients, the tachycardia was not induced with V1V2 testing. In 9 of the latter 11 patients, tachycardia could be induced with V1V2V3 testing, suggesting that the retrograde effective refractory period (ERP) of the right bundle (RB) or the relative refractory period of the His-Purkinje system (HPS) was the limiting factor for tachycardia induction during V1V2 testing. In the remaining one patient, tachycardia was induced with V1V2V3 testing, which provoked a premature ventricular beat, leading to tachycardia induction. Tachycardia was not induced by ventricular stimulation in 37 patients. Factors deterring tachycardia induction in these patients may be related to the retrograde ERP or functional refractory period (FRP) of the HPS, the retrograde ERP of the fast pathway, and an insufficient conduction delay of the circuit (retrograde fast and anterograde slow pathway) to allow anterograde conduction of the slow pathway. In conclusion, AV nodal reentrant tachycardia can be induced by ventricular stimulation in approximately 30% of patients with incremental ventricular pacing and/or ventricular extrastimulus testing. Induction of tachycardia with ventricular stimulation, nevertheless, is frequently limited by the retrograde FRP or ERP of the HPS, the retrograde ERP of the fast pathway, and possibly by an insufficient conduction delay of the circuit.

Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.