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Biomedical subjects

R Cardinal

Publications and source records attributed to R Cardinal.

At least 37 records · Page 2Linked to original sources
PubMed1995

Differential effects of lignocaine and hypercalcaemia on anisotropic conduction and reentry in the ischaemically damaged canine ventricle.

OBJECTIVE: Anisotropic conduction characteristics, which may be expressed as the ratio of conduction velocities in the longitudinal (Vlong) and transverse (Vtrans) fibre directions, have been shown to stabilise reentry and favour the induction of sustained, uniform ventricular tachycardia. The aim of this study was to investigate whether interventions affecting either excitability (lignocaine) or both excitability and cell coupling (hypercalcaemia) might produce differential effects on the Vlong/Vtrans ratio, and whether an intervention reducing this ratio might prevent the induction of sustained reentrant ventricular tachycardia. METHODS: The effects of hypercalcaemia [8.2(SD 3.8) mmol.litre-1] and lignocaine infusion [to 24.4(19) and 42.3(29) mumol.litre-1] on Vlong and Vtrans were determined from 127 electrograms recorded with a plaque electrode on the anterior left ventricular wall of healthy dogs or 3 d after occlusion of the left anterior descending coronary artery. Vlong and Vtrans were computed from isochronal maps displaying ellipsoid patterns with a long axis corresponding to longitudinal conduction and a short axis corresponding to transverse conduction, as determined during basic (S1) and premature (S2) stimulation from the centre of the plaque electrode. Infarcted heart preparations were subjected to programmed stimulation for induction of reentrant ventricular tachycardias. RESULTS: Hypercalcaemia reduced both Vlong and Vtrans (P < 0.05) but did not modify either the Vlong/Vtrans ratio or the induction and patterns of ventricular tachycardias. Lignocaine reduced Vlong and the Vlong/Vtrans ratio during premature stimulation (S2) of infarcted heart preparations (P < 0.05) and stabilised reentrant ventricular tachycardias in preparations in which only nonsustained, multiform ventricular tachycardias were induced under control conditions. CONCLUSIONS: Conduction velocities in the longitudinal and transverse directions can be differentially affected by selected pharmacological interventions, but the Vlong/Vtrans ratio is not a representative index of the facilitating influence of tissue anisotropy on reentry. Therefore, the role of anisotropy in this model of reentry is not confined to establishing disparity of a functional character between conduction velocities in the longitudinal and transverse directions.

Animals↗
PubMed1995

Clinical applications of BSM.

Body surface mapping (BSM) has now become a feasible clinical technique, providing useful information applicable to the diagnosis of cardiac arrhythmias and their treatment by surgical and endocardial catheter ablation. In WPW patients, validation of preexcitation patterns has been obtained by computer simulation and by direct epicardial mapping at surgery. BSM pacemapping has subsequently been developed to be used during radiofrequency catheter ablation. This method has been evaluated prospectively and its predictive accuracy assessed. The recognition of two distinct BSM patterns in idiopathic ventricular tachycardia, has led to the application of successful pacemapping for radiofrequency catheter ablation. The use of a realistic tri-dimensional heart-torso computer model has shown that specific sites of endocardial stimulation are related to distinct thoracic map patterns.

Body Surface Potential Mapping↗
PubMed1995

Regional distribution of atrial electrical changes induced by stimulation of extracardiac and intracardiac neural elements.

UNLABELLED: Autonomic nerves and intrinsic cardiac neural elements are known to influence the electrophysiologic and dynamic properties of the heart. This study describes the regional distribution in the canine atria of electrophysiologic effects induced by stimulation of the right and left cervical vagosympathetic complexes, the right atrial ganglionated plexus, and the right and left stellate ganglia. Local atrial effects were determined from changes in QRST area of unipolar electrograms recorded from multiple sites with plaque electrodes sewn onto the atria in 16 anesthetized dogs. RESULTS: (1) Although being very consistent in any given preparation, atrial changes varied between animals when similar neural structures were stimulated. (2) Among the common features identified between preparations, consistent effects were induced by neural stimulation in the region of the sinus node, indicating that this atrial region is the most richly innervated. (3) All other regions of the atria could be affected by stimulation of either right-sided or left-sided efferent nerves. (4) Responses to right atrial ganglionated plexus stimulation after atropine administration indicated that the corresponding fat pad contains both sympathetic and parasympathetic neural elements. CONCLUSION: This study demonstrates that there is considerable overlapping of atrial innervation affecting all regions of the atria, as well as the sinus node region.

Animals↗
PubMed1995

Electrode polarity does not alter the initial ventricular activation sequence during pacing with extracardiac electrodes.

Ventricular epicardial mapping was performed in six closed-chest anesthetized dogs to investigate the cardiac electrical response to external pacing. A right thoracotomy was performed, complete AV block was produced by formaldehyde injected into the AV node and a sock electrode array, comprised of 127 unipolar electrodes, was placed over the ventricles. Isopotential and isochronal epicardial maps were generated by computer from the unipolar electrograms. Unipolar stimulation pulses were applied between pairs of different types of cutaneous (metal, carbon) and esophageal (metal) electrodes, and recordings were performed at maximum lung inflation. Isopotential maps recorded during the stimulation artifacts showed that the epicardial electrical field was little affected by the type of electrode but depended mostly on electrode position. A reproducible and relatively uniform apex-to-base potential gradient was regularly produced with anteroposterior and anteroesophageal electrode configurations. This uniform potential gradient induced ventricular activation sequences that showed interindividual differences. Thus, for each dog, the areas of initial activation observed on the isochronal maps during pacing tended to remain the same (i.e., apical, lateral, and anterior) despite changes in the stimulation protocol. Inverting the polarity of the electrodes did not appreciably change the site of origin of activation (81% remained the same) and activation never originated from the area showing the most negative potential during the stimulation artifact. In conclusion, since electrode polarity does not seem to alter the ventricular activation sequence during cardiac pacing with extracardiac electrodes, the standard nomenclature for cutaneous patches, which defines the negative electrode as the "active" electrode, may have to be revised.

Animals↗
PubMed1995

Hypoxia-induced release of prostaglandins: mechanisms and sources of production in coronary resistance vessels of the isolated rabbit heart.

The mechanism of hypoxia-induced prostacyclin (PGI2) release was studied in isolated, modified Krebs-Henseleit buffer perfused rabbit hearts under constant-flow conditions. The contribution of vascular endothelium and the role of catecholamines and calcium influx through L-type calcium (Ca2+) channels in hypoxic release of PGI2 were investigated. Reduction in the perfusion solution PO2 (from 476 +/- 13 to 127 +/- 24 mmHg; 1 mmHg = 133.3 Pa) in the presence of glucose (5 mM) and pyruvate (2 mM) caused a significant release of 6-keto-PGF1 alpha, the stable metabolite of PGI2 (from 3.0 +/- 0.4 to 7.3 +/- 2.0 pmol.min-1.g-1, p < 0.05, n = 12), whereas no variation in washout of catecholamines in the perfusate was observed. Electrolysis of the perfusion buffer solution was used to destroy the endothelium. Endothelium impairment by electrolysis almost completely abolished the vasodilation induced by serotonin (5HT) and acetylcholine (ACh), without affecting that caused by papaverine. The basal release of 6-keto-PGF1 alpha was significantly enhanced after electrolysis. However, its release during hypoxia was completely abolished. In a separate group of normal hearts, verapamil (10(-7) M) completely blocked the release of 6-keto-PGF1 alpha during hypoxia. Similar results were obtained in 15 mM KCl arrested hearts challenged with hypoxia. Under normoxic conditions, isoproterenol (10(-7) M) induced a significant release of 6-keto-PGF1 alpha (from 2.9 +/- 0.5 to 5.3 +/- 0.8 pmol.min-1.g-1, p < 0.05, n = 9). To stimulate endogenous catecholamine release, hearts perfused with glucose-free buffer (pyruvate 14.8 mM) were submitted to hypoxia. Under these conditions, hypoxia was accompanied by an enhanced release of noradrenaline (from 1.3 +/- 0.5 to 19.7 +/- 7.8 pmol.min-1.g-1). Despite the increased noradrenaline washout in effluent, the hypoxia-induced release of 6-keto-PGF1 alpha in glucose-free perfused hearts was not enhanced. Our results suggest that endothelial cells are the major site of PGI2 synthesis during hypoxia and that myocardial contractility is a prime factor involved in this process. Verapamil reduction of PGI2 release is most probably through its negative inotropic effect. Although exogenous beta-adrenergic stimulation can induce PGI2 release, endogenous catecholamines do not appear to contribute to the hypoxia-induced release of PGI2.

Animals↗
PubMed1995

[Identification of deep septal ventricular tachycardia substrates from epicardial breakthrough characteristics].

This study aimed to elucidate the relationship between the epicardial activation pattern and the site of origin of the ventricular tachycardia (VT) occurring from the interventricular septum, and to find epicardial breakthrough characteristics identifying VT substrates. Seven patients undergoing intraoperative mapping including right ventricular endocardial mapping were studied. Thirteen septal VTs, which were defined as VTs in which both right and left ventricular endocardial breakthroughs were on the septal aspect, were induced. The VT site of origin was identified from the site and timing of right and left septal endocardial breakthroughs. All VTs were classified into three groups according to the site of epicardial breakthrough: type A, epicardial breakthrough in the anterior interventricular area; type F, epicardial breakthrough in the right ventricular free wall; type P, epicardial breakthrough in the posterior interventricular area. All type F VTs had a right ventricular endocardial breakthrough in the anterior septum and preceded the left ventricular endocardial breakthrough, thereby indicating right anterior septal origin. In the types A and P, both the right and left endocardial breakthroughs were localized in consistent (anterior and posterior, respectively) halves of the septum, but their relative timing was inconstant. This result suggests that epicardial mapping, and even noninvasive methods like body surface mapping, can identify the site of origin of the septal VTs, especially when the epicardial breakthrough occurs in the right ventricular free wall.

Aged↗
PubMed1995

[Comparison of the infusion of acetylcholine into the artery of the sinoatrial node with the electric stimulation of cardiac parasympathetic nerves].

Atrial fibrillation occurring after open heart surgery largely depends on heterogeneous dispersion of refractoriness. To investigate the contribution of the autonomic nervous system in this phenomenon, we studied the regional distribution of neurally induced atrial electrophysiological events. Electrical stimulation of the right atrial fat pad, acetylcholine injection into the sinus node artery, and stimulation of the right and left vagosympathetic trunks were compared with respect to detailed atrial mapping. Unipolar electrograms were recorded from 127 atrial sites before and after neural stimulation or acetylcholine injection (10(-7) mol) in 8 anesthetized dogs. Regional changes in atrial repolarization were estimated by epicardial isointegral maps generated from computed values of the area under each electrogram and plotted on an atrial grid. The anatomical distribution of the sinus node artery was assessed by intra-arterial injection of microspheres. The effects of right and left vagal and right atrial fat pad stimulation extended contralaterally. Acetylcholine injected into the sinus node artery affected the lower left atrium whereas no microspheres could be found in this region upon microscopic examination. Therefore, this effect was possibly related to cholinergic activation of neuronal cell bodies located in the right atrial wall and projecting to the lower left atrium, supporting the hypothesis that local circuit neurons were involved in the activation of the intrinsic nervous system of the heart.

Acetylcholine↗
PubMed1994

Markedly different effects on ventricular remodeling result in a decrease in inducibility of ventricular arrhythmias.

OBJECTIVES: The purpose of this study was to determine whether the type and extent of ventricular remodeling after infarction influence inducibility of ventricular arrhythmias after infarction. BACKGROUND: Although serious ventricular arrhythmias after infarction are related to ventricular dysfunction, the relation between inducibility of ventricular arrhythmias and ventricular remodeling remains incompletely understood. METHODS: Rats that survived ligation of the left anterior descending coronary artery (n = 218) were randomized to receive placebo (saline solution) or captopril or propranolol therapy and were followed up for 5 weeks. Hemodynamic and neurohumoral blood measurements were obtained, and therapy was stopped. Two days later, susceptibility to ventricular arrhythmias was assessed by programmed electrical stimulation, and hearts were prepared for pathologic studies. RESULTS: Placebo-treated rats with a large myocardial infarction had ventricular dysfunction, marked neurohumoral activation, ventricular enlargement (endocardial circumference 16 +/- 3 [mean +/- SD] to 20 +/- 4 mm, p < 0.05) and increased cardiac fibrosis (volume density of collagen 2.3 +/- 0.8% to 5.6 +/- 2.4%, p < 0.05). In many rats this resulted in easily inducible ventricular arrhythmias (inducibility quotient 4.9 +/- 2.2). Captopril attenuated the development of ventricular dysfunction, neurohumoral activation, ventricular hypertrophy and dilation (endocardial circumference 18 +/- 3 mm) and cardiac fibrosis (3.1 +/- 0.8%, p < 0.05). These modifications were accompanied by decreased inducibility of ventricular arrhythmias (inducibility quotient 1.1 +/- 2.0, p < 0.05). Propranolol did not prevent ventricular dysfunction, had variable effects on neurohumoral activation and led to increased ventricular dilation (endocardial circumference 25 +/- 4 mm, p < 0.05) and cardiac fibrosis (7.7 +/- 1.2%, p < 0.05). Nevertheless, these morphologic changes led to decreased inducibility of ventricular arrhythmias (inducibility quotient 2.2 +/- 2.5%, p < 0.05). CONCLUSIONS: This study indicates that the inducibility of ventricular arrhythmias can be reduced as a result of markedly different effects on ventricular remodeling, indicating that the relation between ventricular remodeling, arrhythmias and survival is more complex than previously thought.

Animals↗
PubMed1994

Prolongation by captopril of action potential duration in the normal and hypertrophied rat ventricle: direct action or inhibition of the local angiotensin converting enzyme?

OBJECTIVE: The aims were: (1) to study the acute effects of captopril on the action potential characteristics of ventricular fibres from the normal rat, (2) to compare the effects of captopril with those of perindoprilat, a non-thiol angiotensin I converting enzyme (ACE) inhibitor, (3) to determine the electrophysiological properties of the peptide substrates of converting enzyme, bradykinin and angiotensin I, and (4) to investigate whether the effects of captopril occurring in the healthy heart also occur in two models of ventricular hypertrophy. METHODS: Action potentials were recorded with the standard glass microelectrode technique in right ventricular preparations excised from rat hearts and superfused under baseline conditions and with drug containing or peptide containing Tyrode solution. Ventricular hypertrophy was induced in response to hypertension (unilaterally nephrectomised, DOCA-salt model) or 4 week old left ventricular infarction. RESULTS: In preparations from normal rat hearts, captopril increased action potential duration in a concentration dependent fashion [EC50 = 3.5 x 10(-8) M; maximum effect = 44(SEM 5.1)% prolongation at 10(-5) M for action potential duration at 90% repolarisation, APD90]. Perindoprilat similarly caused a dose dependent increase in action potential duration, but with 100 times greater potency [EC50 = 3.1 x 10(-10) M; maximum effect = 71(11)% prolongation at 10(-5) M for APD90]. SQ 14,534, a stereoisomer of captopril with one hundredth the ACE inhibitor potency, had no significant effect on action potential duration at 10(-5) M. Angiotensin I and bradykinin caused concentration dependent prolongation of action potential, but angiotensin II (10(-6) M) had no effect. Captopril (10(-5) M) had no significant effect in the hypertrophied right ventricle from DOCA-salt hypertensive rats, but significantly increased APD90 [39(4.9)%] in right ventricular preparations from rats with 4 week old anterior left ventricular infarction. CONCLUSIONS: In the rat, captopril prolongs action potential duration, an effect possibly due to local accumulation of bradykinin and angiotensin I.

Action Potentials↗
PubMed1994

Minimal modification of canine ventricular myocyte cell surface beta adrenoceptors despite desensitisation of ventricular function during exogenous beta adrenoceptor challenge.

OBJECTIVE: The aim was to determine whether a 120 min exposure of ventricular myocytes to beta agonist challenge alters ventricular cell surface beta adrenergic receptors concomitant with desensitisation of ventricular function. METHODS: Supramaximal doses of isoprenaline (1 microgram.kg-1.min-1 intravenously) were given continuously to anaesthetised dogs for 15 (n = 6), 60 (n = 2), and 120 (n = 6) min. Changes induced during beta adrenoceptor challenge in right and left ventricular systolic pressures were correlated with right and left ventricular myocyte beta adrenoceptor number and affinity. RESULTS: Isoprenaline initiated early augmentation in right [23(SEM 3)-78(10) mm Hg] and left [82(6)-186(11) mm Hg] ventricular intramyocardial systolic pressures. After 5 min of continuous exogenous beta agonist challenge these pressures were reduced to 42(4) mm Hg and 104(16) mm Hg, respectively, even though the agonist challenge persisted. Throughout the subsequent 115 min exposure period these pressures remained relatively similar. Despite these inotropic effects the number (Bmax) and affinity (Kd) of ventricular myocyte beta adrenergic cell surface receptors, as determined by the tissue slice technique, were similar before and after 15, 60, and 120 min exposure to isoprenaline. CONCLUSIONS: (1) After the desensitisation of the initial enhancement of ventricular inotropism that occurs during the first 5 min of a beta agonist challenge, inotropism remains relatively constant for the next 115 min exposure. (2) Desensitisation of ventricular inotropism elicited during 2 h exposure of the in situ heart to a beta agonist challenge is not primarily due to altered myocyte cell surface beta adrenergic receptor number or affinity.

Animals↗
PubMed1992

Effect of congestive heart failure on clentiazem pharmacokinetics in a dog model.

Clentiazem, 8-chloro diltiazem, is a calcium channel blocker currently undergoing evaluation for the treatment of stable angina and hypertension. As patients with ischaemic disorders often present some degree of heart failure, the aim of this study was to investigate the effect of congestive heart failure on clentiazem (200 micrograms kg-1, i.v. bolus) pharmacokinetics in a canine model. Congestive heart failure was induced in six dogs by rapid ventricular pacing (240 beats min-1) for 3-5 weeks. Clentiazem pharmacokinetics was studied in each dog under the control condition and after the development of clinical signs of heart failure (ascites, dyspnea, fatigue). Blood samples were collected up to 480 min post-dose. Clentiazem plasma concentrations were determined by high performance liquid chromatography. The area under the plasma concentration versus time curves (AUC0-infinity) was significantly increased in congestive heart failure dogs (8.8 +/- 1.6 vs 21.8 +/- 1.4 micrograms min ml-1) (mean +/- SEM). These changes were related to a reduction of the volume of distribution of the central compartment (0.9 +/- 0.1 vs 0.2 +/- 0.11 kg-1) and total body clearance (1.9 +/- 0.4 vs 0.7 +/- 0.21 h-1 kg-1). It is concluded that, in our model, congestive heart failure significantly modifies clentiazem disposition. These results suggest that caution should be exercised when clentiazem is given to patients with a low ejection fraction and a compromised cardiac function. Reduced loading and maintenance doses might be recommended in patients with severe congestive heart failure.

Animals↗
PubMed1992

Interpretation of epicardial mapping by means of computer simulations: applications to calcium, lidocaine and to BRL 34915.

The aim of this work was to compare experimental investigations on effects of lidocaine, calcium and, BRL 34915 on reentries to simulated data obtained by use of a model of propagation based on the Huygens' construction method already described in previous works. Calcium and lidocaine effects are investigated on anisotropic conduction conditions. In both cases, reduction in conduction velocities are observed. In lidocaine case, a refractory area is located along the longitudinal axis. In agreement with experimental electrical mapping, the simulations show that the stabilization of reentrant excitation is mainly due to the existence of this refractory area around which the reentrant circuit can develop. The experimental study shows that BRL 34915 has both arrhythmogenic and antiarrhythmic effects. A detailed electrophysiological analysis has shown that drug infusion act on normal cardiac cells by decreasing the relative and absolute refractory period. BRL 34915 action is simulated by a decrease in the refractory period showing that the time frequency of the reentrant activity is increased and that the spatial size where the reentry is developing is becoming smaller. These two effects are arrhythmogenic, the simulated data being so in good agreement with the experimental ones.

Animals↗
PubMed1992

Distinct activation patterns of idioventricular rhythms and sympathetically-induced ventricular tachycardias in dogs with atrioventricular block.

To investigate mechanisms of ventricular impulse formation in response to sympathetic stimulation in the healthy canine heart in situ, we compared the patterns of ventricular activation during the idioventricular rhythms arising after complete atrioventricular (AV) block and ventricular tachycardias induced by RSG or LSG stimulation. Isochronal maps were generated by computer from 116-127 unipolar electrograms recorded from the entire ventricular epicardium in 15 open chest, anesthetized dogs. In eight of these, bipolar electrograms were recorded with plunge electrodes from 11 selected endocardial sites located below epicardial breakthrough areas. Intracardiac recordings from the His-Purkinje system were made with electrode catheters. After electrograms were recorded during sinus rhythm, complete AV block was induced by injecting formaldehyde into the AV node and idioventricular rhythms occurred spontaneously at a rate of 37 +/- 12 beats/min (mean +/- SD, n = 25). During idioventricular rhythms, endocardial activation preceded the earliest epicardial breakthrough, which occurred in either the right anterior paraseptal region, antero-apical left ventricle, or postero-apical left ventricle. These sites were consistent with a focal origin in the subendocardial His-Purkinje system. Total epicardial activation times lasted for 47 +/- 13 msec (n = 40). Idioventricular rhythms were suppressed by overdrive pacing (intermittent trains of ten beats with decremental cycle length from 500 to 200 msec) or by intravenous calcium infusion (to plasma levels of 10.1-15.2 mM). Right or left stellate ganglion stimulation increased idioventricular rhythm rates (to 52 +/- 13 beats/min, n = 28) and also induced, in all preparations, ventricular tachycardias that had significantly faster rates (189 +/- 55 beats/min, n = 27, P less than 0.005). Ventricular fibrillation was induced after brief runs of ventricular tachycardia in five of the preparations. During ventricular tachycardias, epicardial activation occurred on the right ventricular outflow tract or the postero-lateral wall of the left ventricle, and preceded endocardial activation in 50% of cases. Total epicardial activation times (103 +/- 29 beats/min) were significantly longer than during idioventricular rhythms (P less than 0.005). Ventricular tachycardias displayed overdrive excitation at critical pacing cycle lengths (360-280 msec) and were not suppressed by calcium infusion. Thus, differential mechanisms of impulse formation with distinct localizations can be elicited from healthy ventricular myocardium.

Animals↗
PubMed1992

Prolonged supramaximal stimulation of canine efferent sympathetic neurons induces desensitization of inotropic responses without a change in myocardial beta-adrenergic receptors.

OBJECTIVE: To investigate whether desensitization of inotropic responses elicited during prolonged efferent sympathetic neural stimulation is due to decreased responsiveness of myocardial beta-adrenergic receptors or to alterations in the efferent sympathetic neurons innervating the heart. DESIGN: Increasing doses of noradrenaline and isoproterenol were administered intravenously before and during prolonged (20 mins) stimulation of the intrathoracic efferent sympathetic nervous system of eight dogs. Cardiac augmentor responses were correlated with liberation of catecholamines by the heart. In a second group of experiments (nine dogs), right and left ventricular beta-adrenergic receptor number and affinity were determined before and during such stimulations. MAIN RESULTS: Similar ventricular augmentations were induced when isoproterenol or noradrenaline was administered before and after 20 mins of efferent sympathetic neural stimulation. During the early peak stimulation response, no further augmentations were induced by isoproterenol or noradrenaline. Liberation of noradrenaline by the heart followed a similar course after an initial peak, while noradrenaline values fell to levels which were 6% of those attained during peak response after 20 mins of continuous stimulation. The Bmax and Kd of ventricular beta-adrenergic receptors were similar before and after 20 mins of efferent sympathetic neural stimulation. CONCLUSIONS: Desensitization of ventricular inotropism that occurs during prolonged cardiac efferent sympathetic nervous system stimulation is not primarily due to alteration of myocyte cell surface beta-adrenergic receptors or to a change in myocyte responsiveness to beta-adrenergic agonists, but rather to a reduction in noradrenaline release by sympathetic efferent post ganglionic neurons presumably reflecting a reduction in the activity of these neurons despite continued stimulation.

Animals↗
PubMed1991

Epicardial distribution of ST segment and T wave changes produced by stimulation of intrathoracic ganglia or cardiopulmonary nerves in dogs.

Sixty-three ventricular epicardial electrograms were recorded simultaneously in 8 atropinized dogs during stimulation of acutely decentralized intrathoracic autonomic ganglia or cardiopulmonary nerves. Three variables were measured: (1) isochronal maps representing the epicardial activation sequence, (2) maps depicting changes in areas under the QRS complex and T wave (regional inhomogeneity of repolarization), and (3) local and total QT intervals. Neural stimulations did not alter the activation sequence but induced changes in the magnitude and polarity of the ST segments and T waves as well as in QRST areas. Stimulation of the same neural structure in different dogs induced electrical changes with different amplitudes and in different regions of the ventricles, except for the ventral lateral cardiopulmonary nerve which usually affected the dorsal wall of the left ventricle. Greatest changes occurred when the right recurrent, left intermediate medial, left caudal pole, left ventral lateral cardiopulmonary nerves and stellate ganglia were stimulated. Local QT durations either decreased or did not change, whereas total QT duration as measured using a root-mean-square signal did not change, indicating the regional nature of repolarization changes. Taken together, these data indicate that intrathoracic efferent sympathetic neurons can induce regional inhomogeneity of repolarization without prolonging the total QT interval.

Animals↗
PubMed1991

Body surface isopotential mapping of the entire QRST complex in the Wolff-Parkinson-White syndrome. Correlation with the location of the accessory pathway.

Body surface potential maps were recorded during sinus rhythm and during atrial pacing at the time of electrophysiologic studies in 42 patients with Wolff-Parkinson-White syndrome. The locations of the accessory pathways were determined by epicardial mapping during surgery in 34 patients and by multicatheter endocavitary electrophysiologic studies in eight additional patients. During delta wave inscription, the shape and extension of areas of the negative and positive potentials on the thorax correlated better with the preexcitation site (69% of patients) than with the localization of the minimum potential alone (45.2% of patients). Typical potential distributions were present from the beginning of the delta wave and remained stationary during the first half of the QRS complex. During marked preexcitation, the superposition of atrial activity on the delta wave produced a mixed pattern in the earliest maps. However, these alterations of early delta thoracic potential distribution did not persist longer than 30 msec. The spread of the negative potentials during the last half of the QRS complex also characterized each localization: right-sided preexcitation reproduced the depolarization sequence of left bundle branch block, left-sided preexcitation reproduced that of right bundle branch block, and posterior pathways resembled left anterior fascicular block. Anterior left ventricular and more anterior left lateral ventricular preexcitations mimicked a right bundle branch block-left posterior fascicular block pattern. There was good correlation between the body surface potential map obtained during the ST segment and the site of the right-sided preexcitation. However, in left-sided preexcitations, ST patterns concordant with delta wave patterns were found less frequently than in right-sided preexcitations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Transitions among atrial fibrillation, atrial flutter, and sinus rhythm during procainamide infusion and vagal stimulation in dogs with sterile pericarditis.

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (greater than 1 min duration, monomorphic; regular cycle length, 127 +/- 12 ms, mean +/- SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, less than 1 min; cycle length, 129 +/- 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 +/- 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6-25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.

Animals↗