Cessation Of Tachycardia Research Articles

Tachybradycardia in the isolated canine right atrium induced by chronic sympathetic stimulation and pacemaker current inhibition

The mechanisms of sinoatrial node (SAN) dysfunction in patients with chronically elevated sympathetic tone and reduced pacemaker current (I(f); such as heart failure) are poorly understood. We simultaneously mapped membrane potential and intracellular Ca(2+) in the Langendorff-perfused canine right atrium (RA). Blockade of either I(f) (ZD-7288) or sarcoplasmic reticulum Ca(2+) release (ryanodine) alone decreased heart rate by 8% (n = 3) and 16% (n = 3), respectively. Combined treatment of ZD-7288 and ryanodine consistently resulted in prolonged (> or =3 s) sinus pauses (PSPs) (n = 4). However, the middle SAN remained as the leading pacemaking site after these treatments. Prolonged exposure with isoproterenol (0.01 micromol/l) followed by ZD-7288 completely suppressed SAN but triggered recurrent ectopic atrial tachycardia. Cessation of tachycardia was followed by PSPs in five of eight RAs. Isoproterenol initially increased heart rate by 75% from baseline with late diastolic intracellular Ca(2+) elevation (LDCAE) from the superior SAN. However, after a prolonged isoproterenol infusion, LDCAE disappeared in the superior SAN, the leading pacemaker shifted to the inferior SAN, and the rate reduced to 52% above baseline. Caffeine (2 ml, 20 mmol/l) injection after a prolonged isoproterenol infusion produced LDCAE in the SAN and accelerated the SAN rate, ruling out sarcoplasmic reticulum Ca(2+) depletion as a cause of Ca(2+) clock malfunction. We conclude that in an isolated canine RA preparation, chronically elevated sympathetic tone results in abnormal pacemaking hierarchy in the RA, including suppression of the superior SAN and enhanced pacemaking from ectopic sites. Combined malfunction of both membrane and Ca(2+) clocks underlies the mechanisms of PSPs.

Flecainide single oral dose for management of paroxysmal supraventricular tachycardia in children and young adults

The efficacy of a single oral dose of flecainide to terminate paroxysmal supraventricular tachycardia (PSVT) was evaluated in 25 children and young adults. The subjects were selected from a group of 35 patients with recurrent attacks of PSVT evaluated by means of electrophysiologic study and intravenous electropharmacologic testing with flecainide. In all 25 patients the induced PSVT was stopped by intravenous flecainide and was then no longer inducible or nonsustained. All patients had normal hearts. At least 48 hours after acute intravenous testing, 25 patients underwent electrophysiologic study with a transesophageal catheter and PSVT was induced in all of them: atrioventricular reentrant tachycardia in 16 and atrioventricular nodal reentrant tachycardia in nine. During stable tachycardia, a single oral dose of flecainide (2.9 ± 0.3 mg/kg; 2.5 to 3.3 mg/kg) was administered. This approach was effective for termination of PSVT in 22 patients. The mean plasma level of flecainide at cessation of tachycardia was 277 ± 92 ng/ml (150 to 500 mg/ml). All 22 patients who responded were given a single oral dose of flecainide for recurrences of PSVT during follow-up. During a period of 12 ± 7 months (2 to 27 months) a total of 134 spontaneous episodes of PSVT were reported, and 127 of these episodes were terminated with periodic management. Thus oral periodic flecainide seems useful for management of PSVT in-selected patients.

Effects of atrial and ventricular tachycardia on the cardiovascular dynamics in reserpinized dogs

Hemodynamic effects of atrial and ventricular tachycardia in control dogs were compared with those in reserpinized dogs. In control dogs, at the onset of tachycardia, mean arterial pressure, cardiac output and myocardial contractile force decreased suddenly and then improved fairly soon toward control values. Myocardial contractile force generally increased above control. On the other hand, in reserpinized dogs, initial, abrupt decreases in mean arterial pressure, cardiac output and myocardial contractile force were followed by further decreases in these parameters before stabilizing at lower levels than those observed in control dogs. In addition, tachycardia was always accompanied by pulsus alternans with the alternation of the amplitude of myocardial contractile force. On cessation of tachycardia in control dogs, both mean arterial pressure and cardiac output increased suddenly and markedly before their recovery to controls, whereas in reserpinized dogs, both mean arterial pressure and cardiac output recovered very slowly without showing a phase of “reactive hyperemia.” The causative mechanisms responsible for the present observations are discussed.

Electrocardiographic Changes Associated with Induced Atrial Tachycardia

SummaryAtrial tachycardia, with retained 1:1 A– V conduction, and a duration of 24 hours, has been induced in 17 young pigs by means of a pace‐maker. The intracardiac electrode is advanced percutaneously through a neck vein. During induced tachycardia, an increase in the mean amplitude of the T wave is observed in the right chest lead. Immediately after the cessation of tachycardia, an increase in amplitude occurs in the animals with the highest ventricular rate during the experiment, whereas a decrease in amplitude of the T wave occurs in those with a lower rate. The changes in amplitude of the T wave observed in these experiments are in agreement with those seen in human subjects during and after physical work.The reasons why changes of the type seen on the ECGs recorded after paroxysmal tachycardia in the clinical series did not appear during these experiments are discussed. It is suggested that further experiments with tachycardia of more than 24 hours' duration should be made, to determine whether the post‐tachycardiac EGG changes can be reproduced experimentally. The method used in the present study is appropriate for this purpose.