PubMed Health⌕ Search

Biomedical subjects

J Hilaire

Publications and source records attributed to J Hilaire.

10 recordsLinked to original sources
PubMed1989

Effects of falipamil (AQ-A 39) on heart rate and blood pressure in resting and exercising healthy volunteers.

Falipamil (AQ-A 39) is a new verapamil derivative which exerts antitachycardic effects by a direct action on the sinus node. Its effects on heart rate (HR), blood pressure (BP) and ECG intervals were studied in 12 healthy volunteers, at rest and during bicycle exercise tests. In a double-blind, cross-over, single-dose study, the effects of falipamil (100 and 200 mg) during 8-h post-dosing were compared with those of placebo. Falipamil did not modify resting HR, BP, and electrocardiogram (ECG) intervals significantly. Maximal exercise HR significantly decreased by 5.3 +/- 2.9 (SD)% and 11.2 +/- 3.6% 2 h after the 100- and 200-mg dose respectively, whereas placebo had no effect. Exercise BP was not significantly modified by falipamil. The slopes of HR-workload relationships significantly decreased with falipamil. Peak plasma concentrations of falipamil occurred 1-1.5 h after absorption, and the falipamil-induced decrease in exercise HR over 8 h postdosing was proportional to falipamil plasma concentrations. These results suggest that falipamil decreases HR at exercise in normal subjects and may exert antianginal effects in patients with myocardial ischemia.

Adult↗
PubMed1987

Electrophysiologic properties of falipamil (AQA-39)--a new bradycardiac agent.

Falipamil hydrochloride (AQA 39) is a new antiarrhythmic agent structurally related to verapamil. We evaluated the electrophysiologic properties of intravenous falipamil (1.5 mg kg-1 within 20 minutes) in 12 patients. The spontaneous cycle length was significantly (P less than 0.001) prolonged (+79 +/- 59 ms). Atrioventricular conduction was significantly (P less than 0.001) shorter due to AH interval shortening (-17 +/- 14 ms), most probably related to an anticholinergic effect. Similarly, the anterograde Wenckebach point occurred at a significantly (P less than 0.06) higher rate after falipamil (+10 +/- 7 beats min-1). No statistically significant effect was noted on the refractory periods of the AV node, although there was a trend to shortening. The refractoriness of the right atrium and ventricle was significantly prolonged. It is concluded that falipamil is a bradycardiac agent with electrophysiologic properties quite different from those of verapamil and similar to those of class IA antiarrhythmic agents.

Aged↗
PubMed1987

[Hemodynamic effects of a new alpha-1 antagonist, AR-C 239 administrated in intravenous bolus, in patients with cardiac insufficiency].

A new specific alpha-1 antagonist was studied in 16 patients with left ventricular failure. In Group I (8 patients) the drug was given as a 40 micrograms/kg intravenous bolus, and in Group II (8 patients) at the dose of 80 micrograms/kg. A thermodilution Swan-Ganz catheter, a Millar microtransducer introduced via the femoral artery were relayed to a SYSCOMORAM system to record the systemic artery pressures (SAP), pulmonary artery pressures (PAP), left ventricular pressures, and to calculate cardiac output and systemic and pulmonary arterial resistances (SAR, PAR) over a 30 minute period. In Group I (40 micrograms/kg), administration of AR-C 239 led to a significant decrease in PAP and SAP (-24 +/- 17 p. 100, p less than 0.02) with a fall in time-tension index (-20 +/- 19 p. 100, p less than 0.05) and a significant increase in LV stroke volume (+23 +/- 12 p. 100, p less than 0.01). At 80 micrograms/kg there was also a fall in LV filling pressures (-29 +/- 25 p. 100, p less than 0.05) and PAP (-38 +/- 28 p. 100, p less than 0.02) and an improvement in LV compliance (Gaaschisk -43 +/- 19 p. 100, p less than 0.01). These results show that AR-C 239 is a powerful vasodilator without secondary beta mimetic effects or influence on LV contractility; it may provide an effective means of treating cardiac failure.

Adult↗
PubMed1986

A new method for evaluating the effect of antiarrhythmic drugs on atrioventricular nodal conduction.

Electrophysiological variables were studied in 19 patients before and after one of three commonly used antiarrhythmic agents. The pacing rate at which alternating Wenckebach periods appeared in eight patients was significantly reduced by intravenous digoxin (0.01 mg/kg body weight). The atrioventricular nodal conduction time (A-H interval) and Wenckebach point were not significantly altered by digoxin. Intravenous propranolol (0.1 mg/kg body weight) in four patients did not affect the A-H interval, but it reduced the pacing rates at which the Wenckebach point and alternating Wenckebach periods occurred. Intravenous disopyramide (2 mg/kg body weight) significantly increased the pacing rate required to produce alternating Wenckebach periods but did not significantly alter the other indicators of atrioventricular conduction in seven patients. It is concluded that the pacing rate required to produce alternating Wenckebach periodicity may be a useful and sensitive variable in the evaluation of the effect of antiarrhythmic agents on atrioventricular nodal conduction.

Adult↗
PubMed1983

Cardiovascular effects of AQ-A 39 in healthy volunteers.

Ten healthy male volunteers performed maximal exercise tests on a bicycle ergometer. A control reading was obtained; at a second session propranolol 80 mg was given, and then placebo, 100 mg or 200 mg AQ-A 39 were administered in a randomised double-blind manner. At peak exercise, the heart rate averaged 191.6 beats/min during the control test, 185.8 beats/min after placebo, 172.4 beats/min with 100 mg of AQ-A 39 (-10%), 166.0 (beats/min) with 200 mg of AQ-A 39 (-13.4%); with 80 mg of propranolol, the heart rate averaged 132.8 beats/min and the workload accomplished was substantially lower than that accomplished with AQ-A 39 and placebo which remained the same as in the control test. No effect on blood pressure was observed. The rate pressure product was significantly reduced with AQ-A 39.

Adult↗
PubMed1982

Bidirectional tachycardia. Mechanism derived from intracardiac recordings and programmed electrical stimulation.

His bundle recordings and programmed electrical stimulation were performed in a 70-year-old woman with bidirectional tachycardia; the recordings demonstrated the infra-Hissian origin of the tachycardia. Occurrence of the His deflection slightly after the onset of ventricular depOlarization suggested that the origin of the tachycardia was located near the His bundle bifurcation. Recording of three atrial sites during tachycardia allowed the study of retrograde atrial activation. Two sets of fairly constant and alternating VA intervals were recorded. This fact is consistent with two ventricular circuits used alternatively. The tachycardia could also be interrupted with a single atrial or ventricular premature beat. It is postulated that the tachycardia is due to macroreentry involving the two fascicles of the left branch. This study suggests that reentry may be a possible mechanism in some cases of bidirectional tachycardia.

Aged↗