(1/3178) Differential effects of a segment of slow conduction on reentrant ventricular tachycardia in the rabbit heart.
BACKGROUND: The purpose of this study was to compare differential effects of a segment of slow conduction during ventricular tachycardia (VT) due to depression of the action potential and electrical uncoupling. METHODS AND RESULTS: In 33 Langendorff-perfused rabbit hearts, a ring of anisotropic left ventricular subepicardium was created by a cryoprocedure. Reentrant VT was produced by incremental pacing. Slow conduction in a segment of the ring was created by selective perfusion of the LAD with 10 mmol/L potassium or 0.75 mmol/L heptanol. As a result, VT cycle length increased from 193+/-34 to 235+/-37 ms (potassium) and 227+/-42 ms (heptanol). Reset curves were made by applying premature stimuli proximal to the area of depressed conduction. In a ring of uniform anisotropic tissue, the reset curve was almost completely flat. Electrical uncoupling of part of the ring (nonuniform anisotropy) resulted in a mixed reset curve. In both substrates, early premature beats failed to terminate VT. Depression of part of the ring by increasing K+ resulted in a completely sloped reset curve, indicating a gap of partial excitability. Under these conditions, in 19 of 24 hearts, premature beats terminated VT by conduction block in the high K+ area. CONCLUSIONS: The nature of the area of slow conduction determines the type of reset response and the ability to terminate VT. (+info)
(2/3178) Junctional ectopic tachycardia evolving into complete heart block.
Transition from congenital junctional ectopic tachycardia to complete AV block was observed in an 8 month old girl, over a 36 hour period, during initial hospital admission. Two years later she had evidence of a rapidly increasing left ventricular end diastolic diameter, associated with lowest heart rates during sleep of < 30 beats/min. A transvenous permanent pacemaker was therefore implanted. This finding supports the idea that a pathological process in the area of the AV junction, initially presenting as junctional ectopic tachycardia may later extend to sudden complete atrioventricular block. (+info)
(3/3178) Regulation of sympathetic nerve activity in heart failure: a role for nitric oxide and angiotensin II.
The mechanisms by which sympathetic function is augmented in chronic heart failure (CHF) are not well understood. A previous study from this laboratory (Circ Res. 1998;82:496-502) indicated that blockade of nitric oxide (NO) synthesis resulted in only an increase in renal sympathetic nerve activity (RSNA) when plasma angiotensin II (Ang II) levels were elevated. The present study was undertaken to determine if NO reduces RSNA in rabbits with CHF when Ang II receptors are blocked. Twenty-four New Zealand White rabbits were instrumented with cardiac dimension crystals, a left ventricular pacing lead, and a pacemaker. After pacing at 360 to 380 bpm for approximately 3 weeks, a renal sympathetic nerve electrode and arterial and venous catheters were implanted. Studies were carried out in the conscious state 3 to 7 days after electrode implantation. The effects of a 1-hour infusion of sodium nitroprusside (SNP; 3 microgram . kg-1. min-1) on RSNA and mean arterial pressure (MAP) were determined before and after Ang II blockade with losartan (5 mg/kg) in normal and CHF rabbits. Changes in MAP were readjusted to normal with phenylephrine. Before losartan, SNP evoked a decrease in MAP and an increase in RSNA in both groups that was baroreflex-mediated, because both MAP and RSNA returned to control when phenylephrine was administered. In the normal group, losartan plus SNP caused a reduction in MAP and an increase in RSNA that was 152.6+/-9.8% of control. Phenylephrine returned both MAP and RSNA back to the control levels. However, in the CHF group, losartan plus SNP evoked a smaller change in RSNA for equivalent changes in MAP (117.1+/-4.1% of control). On returning MAP to the control level with phenylephrine, RSNA was reduced to 65.2+/-2.9% of control (P<0. 0001). These data suggest that endogenous Ang II contributes to the sympathoexcitation in the CHF state and that blockade of Ang II receptors plus providing an exogenous source of NO reduces RSNA below the elevated baseline levels. We conclude that both a loss of NO and an increase in Ang II are necessary for sustained increases in sympathetic nerve activity in the CHF state. (+info)
(4/3178) Regional differences in the recovery course of tachycardia-induced changes of atrial electrophysiological properties.
BACKGROUND: Regional differences in recovery of tachycardia-induced changes of atrial electrophysiological properties have not been well studied. METHODS AND RESULTS: In the control group (5 dogs), atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) were assessed before and every 4 hours for 48 hours after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. In experimental group 1 (15 dogs), AERP and inducibility of AF were assessed before and after complete AVJ ablation with 8-week rapid right atrial (RA) pacing (780 bpm) and VVI pacing. In experimental group 2 (7 dogs), AERP and inducibility of AF were assessed before and after 8-week rapid left atrial (LA) pacing and VVI pacing. AERP and inducibility and duration of AF were obtained from 7 epicardial sites. In the control group, atrial electrophysiological properties obtained immediately and during 48-hour measurements after pacing did not show any change. In the 2 experimental groups, recovery of atrial electrophysiological properties included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease of duration and episodes of reinduced AF. However, recovery of shortening and maladaptation of AERP and inducibility of AF was slower at the LA than at the RA and Bachmann's bundle. CONCLUSIONS: The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF. (+info)
(5/3178) Mapping propagation of mechanical activation in the paced heart with MRI tagging.
The temporal evolution of three-dimensional (3-D) strain maps derived from magnetic resonance imaging (MRI) tagging were used to noninvasively evaluate mechanical activation in the left ventricle (LV) while seven canine hearts were paced in situ from three different sites: the base of the LV free wall (LVb), the right ventricular apex (RVa), and the right atrium (RA). Strain maps plotted against time showed the evolution of shortening over the entire LV midwall and were used to generate mechanical activation maps showing the onset of circumferential shortening. RA pacing showed rapid synchronous shortening; LVb pacing showed a wave front of mechanical activation propagating slowly and steadily from the pacing site, whereas RVa pacing showed regions of rapid and slower propagation. The mechanical (M) activation times correlated linearly with the electrical (E) activation (M = 1.06E + 8.4 ms, R = 0.95). The time for 90% activation of the LV was 63.1 +/- 24.3 ms for RA pacing, 130.2 +/- 9.8 ms for LVb pacing, and 121.3 +/- 17.9 ms for RVa pacing. The velocity of mechanical activation was calculated for LVb and RVa pacing and was similar to values reported for electrical conduction in myocardium. The propagation of mechanical activation for RVa pacing showed regional variations, whereas LVb pacing did not. (+info)
(6/3178) Mechanism linking T-wave alternans to the genesis of cardiac fibrillation.
BACKGROUND: Although T-wave alternans has been closely associated with vulnerability to ventricular arrhythmias, the cellular processes underlying T-wave alternans and their role, if any, in the mechanism of reentry remain unclear. METHODS AND RESULTS: -T-wave alternans on the surface ECG was elicited in 8 Langendorff-perfused guinea pig hearts during fixed-rate pacing while action potentials were recorded simultaneously from 128 epicardial sites with voltage-sensitive dyes. Alternans of the repolarization phase of the action potential was observed above a critical threshold heart rate (HR) (209+/-46 bpm) that was significantly lower (by 57+/-36 bpm) than the HR threshold for alternation of action potential depolarization. The magnitude (range, 2.7 to 47.0 mV) and HR threshold (range, 171 to 272 bpm) of repolarization alternans varied substantially between cells across the epicardial surface. T-wave alternans on the surface ECG was explained primarily by beat-to-beat alternation in the time course of cellular repolarization. Above a critical HR, membrane repolarization alternated with the opposite phase between neighboring cells (ie, discordant alternans), creating large spatial gradients of repolarization. In the presence of discordant alternans, a small acceleration of pacing cycle length produced a characteristic sequence of events: (1) unidirectional block of an impulse propagating against steep gradients of repolarization, (2) reentrant propagation, and (3) the initiation of ventricular fibrillation. CONCLUSIONS: Repolarization alternans at the level of the single cell accounts for T-wave alternans on the surface ECG. Discordant alternans produces spatial gradients of repolarization of sufficient magnitude to cause unidirectional block and reentrant ventricular fibrillation. These data establish a mechanism linking T-wave alternans of the ECG to the pathogenesis of sudden cardiac death. (+info)
(7/3178) Atrioventricular nodal ablation and implantation of mode switching dual chamber pacemakers: effective treatment for drug refractory paroxysmal atrial fibrillation.
OBJECTIVE: To assess the effect of atrioventricular node ablation and implantation of a dual chamber, mode switching pacemaker on quality of life, exercise capacity, and left ventricular systolic function in patients with drug refractory paroxysmal atrial fibrillation. PATIENTS: 18 consecutive patients with drug refractory paroxysmal atrial fibrillation. METHODS: Quality of life was assessed before and after the procedure using the psychological general wellbeing index (PGWB), the McMaster health index (MHI), and a visual analogue scale for cardiac symptoms. Nine of the patients also underwent symptom limited exercise tests and echocardiography to assess left ventricular systolic function. RESULTS: The procedure allowed a reduction in antiarrhythmic drug treatment (p < 0.01). PGWB and symptom scores improved (p < 0.01) but the MHI score did not change. Left ventricular systolic function and exercise capacity were unchanged. CONCLUSIONS: Atrioventricular node ablation and implantation of a DDDR/MS pacemaker is effective treatment for refractory paroxysmal atrial fibrillation, producing improved quality of life while allowing a reduction in drug burden. The popularity of the treatment is justified, but further studies are needed to determine optimum timing of intervention. (+info)
(8/3178) Predictors of atrial rhythm after atrioventricular node ablation for the treatment of paroxysmal atrial arrhythmias.
OBJECTIVE: To assess the natural history of the atrial rhythm of patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation. DESIGN AND SETTING: A retrospective cohort study of consecutive patients identified from the pacemaker database and electrophysiology records of a tertiary referral hospital. PATIENTS: 62 consecutive patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation between 1988 and July 1996. MAIN OUTCOME MEASURES: (1) Atrial rhythm on final follow up ECG, classified as either ordered (sinus rhythm or atrial pacing) or disordered (atrial fibrillation, atrial flutter or atrial tachycardia). (2) Chronic atrial fibrillation, defined as a disordered rhythm on two consecutive ECGs (or throughout a 24 hour Holter recording) with no ordered rhythm subsequently documented. RESULTS: Survival analysis showed that 75% of patients progressed to chronic atrial fibrillation by 2584 days (86 months). On multiple logistic regression analysis a history of electrical cardioversion, increasing patient age, and VVI pacing were associated with the development of chronic atrial fibrillation. A history of electrical cardioversion and increasing patient age were associated with a disordered atrial rhythm on the final follow up ECG. CONCLUSIONS: Patients with paroxysmal atrial arrhythmias are at high risk of developing chronic atrial fibrillation. A history of direct current cardioversion. (+info)