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PubMed1993

Multiple modes of termination of re-entrant excitation around an anatomic barrier in the canine atrium during the action of d-sotalol.

In the chronically-instrumented animal and the isolated blood perfused heart, atrial re-entry via a fixed path around an anatomic obstacle has been described and is terminated by the class III antiarrhythmic agent d-sotalol. The precise mechanism by which d-sotalol terminates this arrhythmia is not known. In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart (n = 5) during episodes of sustained flutter and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. d-Sotalol was effective in terminating atrial re-entry in this model. In all episodes, block of the excitatory impulse in a specific region of the re-entrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described. The class III antiarrhythmic agent d-sotalol can terminate atrial re-entry in several ways. In one mode, complete conduction block of the re-entering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original re-entrant circuit occurs when there is failure of a lateral boundary. In both modes cycle length (CL) oscillations are observed.

Animals↗
PubMed1994

VDD pacing at short atrioventricular intervals does not improve cardiac output in patients with dilated heart failure.

Atrial synchronous pacing with short, nonphysiological atrioventricular (AV) intervals has been reported to increase cardiac output in selected patients with severe dilated heart failure. The aim of this study was to determine the acute effect of atrial synchronous pacing with short AV intervals in a consecutive series of patients with dilated heart failure. Twelve patients with a mean ejection fraction of 21% +/- standard error 2.5% were studied. Pacing catheters were placed in the high right atrium and right ventricular apex and a balloon flotation catheter in the pulmonary artery for measurement of cardiac output. Simultaneous transthoracic echocardiography was performed for measurement of left ventricular filling time and mitral regurgitation. In a randomized crossover design, measurements were made during VDD pacing at programmed AV intervals of 100 and 60 msec and during a control period in sinus rhythm. Left ventricular filling time increased at AV intervals of 100 and 60 msec (mean difference 37 +/- 9 and 34 +/- 11 msec, respectively, both P < 0.01 compared to control). Despite increases in ventricular filling time, stroke, and cardiac index declined with short atrioventricular intervals (at an AV interval of 60 msec, stroke index fell by 2.1 +/- 0.5 mL/m2, P < 0.05 and cardiac index by 125 +/- 45 mL/m2; P = NS). Heart rate was unchanged at both AV intervals (78 +/- 4.9 at control, 78 +/- 5.2 at 100 msec and 79 +/- 4.9 beats/min at 60 msec; P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

The effects of adenosine on isolated right atrial preparations from streptozotocin-diabetic rats.

1. The aim of the present study was to investigate the inhibitory effects of adenosine on the contractile force and chronotropic action of isolated right atrial preparations from streptozotocin (STZ)-diabetic rats. 2. The rats were anaesthetized with diethyl ether and STZ (65 mg kg(-1)) was injected intravenously via the tail vein. 3. Adenosine produced concentration-dependent decreases in the force of contraction and a negative chronotropic action of atria both in control and diabetic groups. The inhibition responses to adenosine were significantly higher in diabetic rat atria than control. 4. Dypiridamole incubation caused a significant potentiation of the inhibitory effect of adenosine on contractile force and chronotropic action of atria in the control group, but not in the diabetic group. In the presence of dipyridamole, the inhibitory effects of adenosine on measured parameters in diabetic rats were not significantly different from those in control rats. 5. These results suggested that atria from 6 weeks STZ-diabetic rats exhibited a supersensitivity to the negative inotropic and chronotropic effects of adenosine compared with atria from control rats because of an impairment in adenosine uptake mechanism. Altered sensitivity to effects of adenosine might reflect relatively early changes in the course of diabetes.

Adenosine↗
PubMed1993

Alterations in brain hexokinase activity associated with heart failure in rats.

This study examined the activity of discrete regions of the brain as assessed with histological localization and photodensitometric quantification of the metabolic enzyme hexokinase in a group of rats with coronary occlusion (HF) and in sham-operated control rats. Three weeks after surgery, the mean left ventricular end diastolic pressure and right atrial pressure were elevated, and left ventricular peak systolic pressure was decreased in the HF group compared with the sham group; these findings are also observed during heart failure. In addition, histological data indicated that there was a 37.6 +/- 2.8% outer and 40.8 +/- 3.1% inner infarct of the myocardium in the group of rats with HF (n = 6). Rats in the control group had no observable damage to the myocardium (n = 6). Accompanying these symptoms of heart failure were significant increases in hexokinase activity in the parvocellular (pPVN, 16.3%) and magnocellular (mPVN, 17.6%) divisions of the paraventricular nucleus of the hypothalamus, and in the locus ceruleus (LC, 17.1%). No changes in hexokinase activity were observed in the median preoptic area, supraoptic nucleus (SON), subfornical organ, or posterior hypothalamus. These results reinforce the idea that heart failure (with coronary occlusion) is associated with changes in specific areas in the brain and that metabolic alterations in the pPVN, mPVN, and LC are likely related to alterations in vasopressin production, blood volume regulation, and sympathoexcitation observed in the heart failure state.

Animals↗
PubMed1996

Modulation of myocardial alpha 1- but not beta-adrenoceptors after 90-day tail-suspension.

We have previously demonstrated that prolonged simulated microgravity (tail-suspension) leads to cardiac alterations with increased resting heart rate, myocardial degradation changes and attenuated myocardial contractility. The present study investigated the potential role of adrenoceptor mechanisms underlying them. Changes of myocardial alpha 1-adrenoceptor (alpha 1-AR) and beta 1-adrenoceptor (beta-AR) in 90-day tail-suspended rats was investigated by the method of radioligand binding assay and application of Scatchard's method. The results showed significantly decreased quantity of specific binding of 125I-BE[2-beta-(4-hydroxy-3-[125I]indophenyl)-ethylaminomethyltetralone] to alpha 1-AR present in membrane derived from ventricular myocardium of the suspended animals, despite the affinity of the alpha 1-AR to 125I-Be was unchanged. But neither the quantity nor the affinity of beta-AR binding to 125I-Pindolol was significantly altered. In addition, the spontaneously beating rate of isolated right atria from tail-suspended animals showed little change in sensitivity and reactivity to the stimulations of graded phenylephrine (alpha-agonist, measured in the presence of beta-antagonist propranolol) and isoproterenol (beta-agonist), compared with the control rats. There were also no obvious differences of the effects of the isoproterenol on the contractility of isolated left ventricular papillary muscles between the two groups. Since myocardial alpha 1-AR mediated-effects include production of cardiac hypertrophy and enhancement of myocardial glucose uptake and glycolysis, the down-regulation of the alpha 1-AR may be a contributor to the cardiac cellular accumulation and the myocardial degradation changes as found in our tail-suspended rats. The data from this study also suggest that the myocardial beta-adrenoceptors are not affected by the prolonged tail-suspension.

Adrenergic alpha-Agonists↗
PubMed2004

Comparative effects of thiopental and propofol on atrial vulnerability: electrophysiological study in a porcine model including acute alcoholic intoxication.

BACKGROUND: Atrial tachyarrhythmias (AT) frequently complicate the perioperative period. Alcohol intoxication is a recognized causative factor for dysrrhythmias. We studied the effects of propofol and thiopental on atrial electrophysiology and vulnerability to AT in a closed-chest porcine model in which AT are facilitated by ethanol. METHODS: Thirty-eight pigs were randomly assigned to thiopental (T-group, n=19) or propofol (P-group n=19). All animals were assigned to undergo a right atrial electrical stimulation protocol (RASP) at baseline. Thirty pigs were assigned to undergo additional RASP during ethanol infusion, while the remaining eight were assigned to undergo additional RASP during saline infusion (control group). We analysed effective refractory period (ERP), and intra-atrial conduction interval (ICI) (between atrial sites 4 cm apart), at several cycle lengths (CL). RESULTS: There were no significant differences at baseline. During ethanol infusion, propofol produced a greater rate-dependent decrease in excitability, manifested by a longer minimum paced CL with 1:1 atrial capture: 145 (11) vs 164 (27) ms in the T- and P-group, respectively (P=0.01). Propofol was associated with a greater rate-related slowing in conduction: difference between ICI at CL of 300 ms and ICI at minimum CL: 30 ms in P-group and 22 ms in T-group (P<0.03). In the P-group we observed a longer duration of induced arrhythmias (145 (131) vs 74 (91) s, P<0.03) and a higher proportion with atrial flutter (AFl) (76 vs 19%, P<0.001). CONCLUSIONS: Propofol in this model was more arrhythmogenic than thiopental, as manifested by a longer duration of induced arrhythmias, particularly AFI.

Alcoholic Intoxication↗
PubMed1994

Does endogenous adenosine have a role in the cardiac responses to isoprenaline and in the rapid fade of the inotropic response of perfused heart?

The role of endogenous adenosine during the beta-adrenoceptor responses to isoprenaline of guinea-pig isolated cardiac preparations was examined. Insignificant effects of adenosine deaminase (0.3 U.mL-1) on cumulative concentration--response curves for isoprenaline on isolated left and right atria and papillary muscles indicated a negligible depressant effect of endogenous adenosine during these responses. The increase in force of contraction to an infusion of isoprenaline (14 nM) in perfused spontaneously beating hearts rapidly waned while the infusion continued, whereas the increase in rate of contraction remained constant throughout the infusion. The degree of fade was less in paced preparations (5 Hz), indicating that it was only in part due to the rate increase exerting some mechanical constraint on the force of contraction. The P1-purinoceptor antagonist 8-phenyltheophylline (12 microM) and adenosine deaminase (0.3 U.mL-1) did not enhance the peak responses to the isoprenaline infusion. The fade of the inotropic response in both spontaneous and paced hearts was also not attenuated by the presence of 8-phenyltheophylline or adenosine deaminase. The fade was not, therefore, due to release of endogenous adenosine exerting a depressant effect. Whether this declining inotropic response represents a form of rapid desensitization remains to be determined.

Adenosine↗
PubMed1992

5-Hydroxytryptamine increases contractile force in porcine right atrium but not in left ventricle.

Positive chronotropic as well as inotropic effects of 5-hydroxytryptamine (5-HT) have been observed in pig atrial tissue, but no data are available about the direct effects of 5-HT on ventricular tissue. In the present study we investigated inotropic effects of 5-HT on atrial and ventricular trabeculae obtained from hearts of 3 months old pigs. The baseline isometric contractile force was significantly higher in ventricular (4.14 +/- 1.25 mN) than in atrial tissue (0.47 +/- 0.11 mN). A noradrenaline concentration-response curve (0.01 to 10 mumol/l) was used to check contractile responsiveness of the tissue and all responses were expressed as percentage of the response to 10 mumol/l noradrenaline. Noradrenaline caused a concentration-dependent increase in contractile force in both atrial and ventricular trabeculae. In contrast, though 5-HT (0.01 to 100 mumol/l) did increase force of contraction in atrial tissue (maximum: 72 +/- 20% of the response to noradrenaline 10 mumol/l), the contractility of ventricular trabeculae was not significantly affected (maximum: 12 +/- 6%). The present data show that, in contrast to atrial tissue, contractile force of ventricular tissue could not be significantly affected by 5-HT. To our knowledge, this is the first study to show that an agent which increased force of contraction in the atrium, did not have a corresponding effect on the ventricle. These findings may have important implications for a better understanding of the physiology and pharmacology of cardiac contractility.

Animals↗
PubMed2001

Right atrial pressure as measure of ventricular constraint in newborn lambs.

Although the lungs and pericardium constrain the heart and limit cardiac output, no method exists to assess this constraint in sick newborns. We hypothesize that a useful estimate of ventricular constraint may be obtained by measuring right atrial pressure (P(RA)) in the newborn. To test this hypothesis, we measured P(RA), thoracic inferior vena caval pressure (P(IVC); saline-filled catheters), and ventricular constraint (pericardial pressure, P(PER); liquid-containing balloon) in 4-wk-old (neonatal, n = 12) and 3-day-old (newborn, n = 6) anesthetized lambs. The measurements were made while LV filling pressure was altered (0-20 mmHg) and while positive end-expiratory pressure (PEEP) was maintained at 2.5 or 15 cmH2O. In all of the lambs, a strong linear relationship (r) existed between P(RA) and P(PER) (P(RA) = 1.19 P(PER) + 0.0, r = 0.99) and between P(IVC) and P(PER) (P(IVC) = 1.24 P(PER) + 0.1, r = 0.99; PEEP of 2.5 cmH2O). Similar relationships were also observed with increased PEEP (P(RA) = 1.29 P(PER)-1.2, r = 0.98 and P(IVC) = 1.32 P(PER)-1.2, r = 0.97). Because P(RA) provides an accurate measure of ventricular constraint in the normal lamb, it may be a useful measure of ventricular constraint in the sick newborn.

Animals↗
PubMed1993

Estrogen-induced left ventricular chamber enlargement in ewes.

We studied the chronic effect of administration of a single large intramuscular dose of 17 beta-estradiol on left ventricular chamber size and output in the ewe. Fourteen oophorectomized ewes were successfully instrumented and studied, with measurements made of left ventricular, aortic, right and left atrial pressures, left ventricular stroke volume, and left ventricular minor axis dimension. Unanesthetized ewes were studied before and 1, 2, and 3 wk after intramuscular administration of 0.6 mg/kg 17 beta-estradiol (7 ewes) or 1.5 ml sesame oil placebo (7 ewes). Left ventricular end-diastolic pressure-end-diastolic dimension (LVEDP-EDD) and left ventricular end-diastolic pressure-stroke volume (LVEDP-SV) relationships were quantified during graded inferior vena caval occlusion and volume infusion. Left ventricular end-diastolic diameter was larger after estrogen but not after placebo administration. The LVEDP-EDD relationship shifted progressively rightward, indicating left ventricular chamber enlargement in the estrogen group but was unchanged in the placebo group. The plateau limb of the LVEDP-SV relationship in the estrogen group shifted up from a mean stroke volume of 77.1-89.5 ml/beat and did not change in the placebo group. We conclude that administration of a single large intramuscular dose of 17 beta-estradiol resulted in left ventricular chamber enlargement and increased stroke volume in the ewe.

Animals↗
PubMed1996

Incomplete reentry and epicardial breakthrough patterns during atrial fibrillation in the sheep heart.

BACKGROUND: The mechanisms underlying atrial fibrillation and its initiation are not fully understood. Our hypothesis is that atrial fibrillation results from complex activation involving the subendocardial muscle network. METHODS AND RESULTS: We have used video imaging to study the sequence of activation on the surface of the right atrium of the Langendorff-perfused sheep heart during pacing, atrial fibrillation, and its initiation. We recorded transmembrane potentials simultaneously from over 20,000 sites. We observed two types of patterns of wave propagation during the initiation of atrial fibrillation. The first type resulted from heterogeneties of refractoriness and transmural propagation near the stimulating electrode. The second type involved heterogeneity in conduction away from the pacing site. During atrial fibrillation, the average period of activation was 138 +/- 25 ms (n = 6), and complete reentrant pathways were never observed. Propagation patterns were characterized by a combination of incomplete reentry, breakthrough patterns, and wave collisions. Incomplete reentry occurred when waves propagated around thin lines of block and then terminated. Breakthrough patterns were frequent and occurred every 215 ms on average. The location of these breakthrough sites and the lines of block during incomplete reentry were not randomly distributed but appeared to be related to preferential propagation in the underlying subendocardial muscle structures. A computer model of atrial free wall connected to a pectinate muscle suggested that subendocardial muscles lead to epicardial breakthrough patterns that act to destabilize reentry. CONCLUSIONS: These results suggest that the complex three-dimensional structure of the atria plays a major role in the activation sequences during atrial fibrillation and its initiation.

Action Potentials↗
PubMed2003

Global repolarization sequence of the right atrium: monphasic action potential mapping in health pigs.

The aim of the study was to explore the global sequence of atrial repolarization and its correlation to that of activation. Endocardial monophasic action potentials (MAPs) were sequentially recorded from 51 +/- 14 sites in the right atrium of ten healthy pigs using the CARTO electroanatomic mapping system. Local activation time (AT), MAP duration, and 90% repolarization time (RT) were obtained, and from these data, color coded three-dimensional maps of AT and RT sequences and spatial distribution of MAP duration were reconstructed. The results of the study were: (1) An activation sequence was recognizable in all maps, starting from the posterosuperior wall and ending in the posteroinferior wall near the tricuspid annulus. (2) The repolarization sequence was also recognizable in all maps, and mainly followed the sequence of activation. (3) A significant positive correlation between the RT and AT was observed in all maps with an average r value being 0.571 +/- 0.159 (P < 0.01 - 0.0001), suggesting that progressively later AT associates with progressively longer RT. (4) No consistent correlation between the MAP duration and AT was found. In conclusion, repolarization gradients exist over the atrial endocardium in healthy pigs. The repolarization sequence follows the same sequence as the activation, suggesting that the spatiotemporal pattern of activation is an important determinant of the characteristics of the repolarization sequence.

Action Potentials↗
PubMed2000

False-negative and false-positive ECG diagnoses of Q wave myocardial infarction in the presence of right bundle-branch block.

Right bundle-branch block (RBBB) has not traditionally been seen as an obstacle to ECG diagnosis of Q wave myocardial infarction (MI)--in clinical electrocardiography and vectorcardiography--because this conduction disturbance is not believed to cause significant alterations in the spatial orientation of initial excitation wavefronts. In the era of large-scale clinical trials, however, where serial ECG analysis is among the major diagnostic tools in MI classification, both false-positive and false-negative diagnoses of MI in the presence of RBBB have become increasingly evident. Because of the limited detectability of Q wave MI by ECG in the presence of RBBB, the electrocardiographic finding of Q wave MI should not be regarded as an independent diagnostic tool. It is best to utilize independent corroboration to establish the diagnosis of transmural infarction when RBBB is present. Further investigations are warranted to better delineate sensitivity, specificity, and predictive value of Q wave MI in the presence of RBBB.

Atrial Function, Right↗
PubMed1993

Evaluation of the right atrial venous oxygen saturation as a physiologic monitor in a neonatal model.

Pulmonary artery (PA) mixed venous saturation (SvO2) has become a crucial monitor in the adult intensive care unit, but is not used in neonates because of the difficulty in PA catheterization. We evaluated the possibility of utilizing the right atrial venous oxygen saturation (RAvO2), which is easily accessed in the neonate, as a monitor of the effects of mechanical ventilation and intravascular volume in an animal model selected to be the size of the human neonate. A continuous RAvO2 monitoring catheter was placed into the right atrium of 16 normal rabbits (2.2 to 4.1 kg). Oxygen delivery was manipulated by alterations in peak inspiratory pressure (PIP) (n = 6), positive end-expiratory pressure (PEEP) (n = 6), or by progressive hypovolemia (n = 4). RAvO2 decreased with onset of mechanical ventilation alone from 69% +/- 6% to 61% +/- 5% (P < .01). As the PIP was increased from 12 to 21 cm H2O, the RAvO2 progressively decreased from 59% +/- 4% to 49% +/- 6% (P < .05). As the PEEP was increased from 3 to 9 cm H2O, the RAvO2 progressively decreased from 64% +/- 5% to 33% +/- 16% (P < .01). RAvO2 approached baseline after return to continuous positive airway pressure (CPAP) of 3 cm H2O. Progressive phlebotomy to a total of 10 mL/kg resulted in a decrease in RAvO2 from 70% +/- 6% to 27% +/- 5% (P < .001). Volume resuscitation resulted in an increase in RAvO2 to near baseline. Peripheral arterial oxygen saturation remained at a constant 100% throughout each protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Synergistic effects of vasopressin plus epinephrine during cardiopulmonary resuscitation.

Both epinephrine (Epi) and vasopressin (VP) increase coronary perfusion pressure (CPP) when administered during cardiac arrest. Given their different mechanisms of action we tested the hypothesis that during cardiopulmonary resuscitation (CPR) a combination of VP plus Epi would be superior to either agent alone. Epi(40 microg/kg), VP(0.3 U/kg) and the combination of both agents were assessed in a porcine model of ventricular fibrillation (VF). Maximum CPP (diastolic aortic-right atrial pressures) during CPR was similar among the groups but the time course of action was different in each group: with Epi + VP the increase in CPP was significantly more rapid than with VP alone whereas the CPP remained significantly higher for a longer periods of time with VP or VP + Epi versus Epi alone. Left ventricular blood flow (ml/min per g) determined during CPR two min after drug administration was similar between groups: Epi 1.06 +/- 0.16; VP 0.82 +/- 0.26; Epi + VP 0.83 +/- 0.14 (P = N.S.). Post drug administration. 2 min, cerebral blood flow (ml/min per g) in the VP group (0.76 +/- 0.15) was more than two times higher compared with Epi alone (Epi:0.30 +/- 0.08, P < 0.01 versus VP) and Epi plus VP (Epi + VP:0.23 +/- 0.03, P < 0.01 versus VP). We conclude that combination of VP + Epi during cardiac arrest results in a more rapid rise in CPP when compared with VP alone and a more sustained elevation in CPP than observed with Epi alone. Thus, the synergistic effects of these two potent vasopressor agents may be of benefit during CPR.

Adrenergic Agonists↗
PubMed2004

Transmembrane action potential heterogeneity in the canine isolated arterially perfused right atrium: effect of IKr and IKur/Ito block.

The role of electrical heterogeneity in development of cardiac arrhythmias is well recognized. The extent to which transmembrane action potential (TAP) heterogeneity contributes to the normal electrophysiology of well-oxygenated atria is not well defined. The principal objective of the present study was to define regional and transmural differences in characteristics of the TAP in isolated superfused and arterially perfused canine right atrial (RA) preparations under baseline, rapidly activating delayed rectifier K(+) current (I(Kr)) block, and combined block of ultrarapid delayed rectifier and transient outward K(+) current (I(Kur)/I(to) block). Superfused preparations that survived generally displayed a triangle-shaped TAP. Exceptions included cells from the crista terminalis, where TAPs with a normal plateau could be recorded. In contrast, most TAPs recorded from throughout the perfused RA displayed a spike-and-dome and/or plateau morphology. The perfused RA displayed a heterogeneous distribution of repolarization, V(max), and spike-and-dome morphology along the epicardial and endocardial surfaces as well as transmurally, in the region of the upper crista terminalis. I(Kr) block with E-4031 prolonged repolarization homogeneously in the perfused RA, whereas I(Kur)/I(to) block using low concentrations of 4-aminopyridine abbreviated action potential duration at 90% repolarization heterogeneously, leading to a reduction in dispersion of repolarization. Our data indicate that the electrical heterogeneities, previously described for the canine ventricle, also exist within the atria and that I(Kr) block does not accentuate and I(Kur)/I(to) block reduces RA dispersion of repolarization. Our study also points to major differences in the transmembrane activity recorded using superfused vs. arterially perfused atrial preparations.

Action Potentials↗
PubMed1996

Single lead DDD system: a comparative evaluation of unipolar, bipolar, and overlapping biphasic stimulation and the effects of right atrial floating electrode location on atrial pacing and sensing thresholds.

Single lead DDD pacing using unipolar or bipolar stimulation is limited by high atrial threshold. Overlapping biphasic (OLBI) waveform stimulation via atrial floating ring electrodes may preferentially enhance atrial pacing and avoid diaphragmatic pacing. Single lead DDD pacing with OLBI atrial pacing was studied in 12 patients (6 men and 6 women; mean age 74 +/- 7 years) with complete heart block. At implantation, atrial bipolar rings (area 27 mm2, separation 10 mm) were positioned at radiological defined high, mid, and low right atrial (RA) levels, and P wave amplitude and atrial and diaphragmatic pacing thresholds were determined in each position using unipolar, bipolar, and OLBI stimulation in random order. Although statistically insignificant, both the maximum and minimum sensed P wave amplitudes tended to be lower in the low RA position. Independent of the stimulation modes, minimum atrial pacing threshold occurred in the mid-RA. At mid-RA, the atrial pacing threshold was significantly lower with OLBI pacing compared with either unipolar or bipolar mode (3.9 +/- 2.2 V vs 6.7 +/- 3.5 V and 6.9 +/- 3.5 V, P < 0.05). Although the diaphragmatic thresholds were similar, OLBI pacing modes in the mid-RA and final location significantly improved the safety margin for avoidance of diaphragmatic pacing compared with unipolar mode. There was no correlation between atrial pacing and sensing threshold. At predischarge testing, all but one patient who developed atrial fibrillation had satisfactory atrial capture and a stable atrial pacing threshold (day 0: 2.6 +/- 1.1V vs day 2:3.2 +/- 1.3V, P = NS). However, diaphragmatic pacing occurred in four of 11 (36%) patients, especially in the upright position (sitting and standing). Our preliminary clinical results suggest that OLBI pacing via atrial floating ring electrodes can reduce the atrial pacing threshold. To optimize atrial pacing and sensing, the bipolar electrodes should be located at the mid-RA level first, although the high RA is an alternative. Despite significant improvements in the safety margin for diaphragmatic pacing with OLBI pacing, diaphragmatic stimulation remains a clinical problem.

Aged↗
PubMed2000

Failure of coronary sinus pacing in reducing local atrial conduction delay in patients with atrial fibrillation after successful internal cardioversion.

Recent studies suggested that distal coronary sinus (CS) pacing may prevent atrial fibrillation (AF) by reducing site dependent intraatrial conduction delay. The aim of this study was to investigate the effect of high right atrial (HRA) and distal CS pacing on local conduction delay in patients with AF. The study population consisted of 10 patients with persistent AF after transvenous atrial defibrillation and 10 control subjects. The local conduction delays along the anterolateral right atrium (RA), in the CS, and at the right atrial septum (RAS), and the incidence of AF in response to an atrial extrastimulus during HRA and distal CS pacing at a drive cycle length of 400, 500, and 600 ms were evaluated. In patients with AF, distal CS and HRA pacing are associated with more prominent and similar extent of conduction delay within the atria, without any significant difference in the dispersion of conduction delay and susceptibility to AF induction (70% vs 60%, P = 0.9). In normal controls, distal CS pacing reduces the conduction delay at the RAS and CS ostium and decreases the dispersion of conduction delay and the propensity for AF induction (0% vs 50%, P = 0.03) compared to HRA pacing. The pacing drive cycle length has no significant effect on conduction delay in patients with AF and normal controls (P > 0.05). Compared to normal controls, patients with AF have significantly longer conduction delay at the RAS and along the anterolateral RA during HRA and distal CS pacing. The result of this study demonstrates that the effect of HRA and distal CS pacing on the local atrial conduction delay in patients with and without AF differ significantly. These patients with AF may have more diffuse atrial anisotropy causing the changes in conduction, and pacing from distal CS in these patients dose not reduce the propensity for AF.

Atrial Fibrillation↗