ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01249.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AH Shortening During ORT.Introduction:During extrastimulation or entrainment of orthodromic atrioventricular (AV) reciprocating tachycardia (ORT), the atriuni‐His (AH) interval as measured at the His‐bundle recording site is expected to lengthen due to extrastimu‐Lation‐dependent or pacing rate‐dependent slowing of AV nodal conduction by impulses that penetrate the tachycardia circuit. We report 6 patients in whom the AH interval “paradoxically” shortened during ORT in response to extrastimulation and rapid pacing from the proximal coronary sinus.Methods and Results:Accessory pathway location was right anterior (1 patient), right anteroseptal (1 patient), and left anterior (4 patients). Cycle length of ORT was stahle (variation ≤ 5 msec) and ranged from 325 to 410 msec. During ORT, extrastimulation and rapid pacing were performed from the proximal coronary sinus and the right atrium. Extrastimulation from the proximal coronary sinus late in diastole caused significant shortening of AH interval in all patients hy a mean of 18 ± 3 msec (range 15 to 20 msec). AH shortening was demonstrated without a change of either the timing or morphologic appearance of the low septal right atrium at the H is‐bundle recording site. This phenomenon was not ohserved during right atrial extrastimulation. Rapid pacing from the proximal coronary sinus at cycle lengths of 305 to 390 msec (i.e., 15 to 20 msec shorter than the cycle length of each ORT) again demonstrated shortening of AH interval in all patients by a mean of 15 ± 3 msec (range 10 to 20 msec). By contrast, rapid pacing from the right atrium demonstrated classical AH prolongation at any paced cycle length.Conclusion:AH shortening without a change of either the timing or morphologic appearance of the low septal right atrium at the His‐handle recording site confirms the existence of a distinct posterior atrial input to the AV node. In this setting low septal right atrial activation is not requisite for AV nodal conduction. Whether activation of the low septal right atrium is essential for. or contributes to, AV nodal conduction of atrial impulses from locations other than the proximal coronary sinus n

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01250.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Spontaneous Activity in Transgenic Mouse Heart and AT‐1 Myocytes.Introduction:We have generated transgenic animals that heritably develop atrial tumors composed of difTerentiated proliferating cardiomyocytes. Experiments were initiated to characterize (he electrical properties of these cells.Methods and Results:We show that the primary atrial tumors are composed of discrete foci that exhibit spontaneous automatic activity. A direct correlation was observed between tumor size and firing rate of these foci. In addition to the primary atrial tumors, we examined the propertie.s of cultured cardiomyocytes isolated from a transplantable transgenic tumor lineage (designated AT‐1 cells). Cultured AT‐1 cells arc al.so spontaneously automatic. The action potential eontiguration from these preparations is similar to that observed in nontransgenic atrial cardiomyocytes, albeit somewbat more depolarized and of longer duration. As would be expected for cardiomyocytes of atrial origin, the transgenic cardiornyocyte preparations hyperpolarize during muscarinic stimulation due to increased K+conductance mediated by a pertussis toxin sensitive G‐protein. Assessment of pbarmacologic blockage of the “if” pacemaker current suggests that the automaticity of both transgenic cardiomyocyte preparations may be of novel origin. In this context, the cultured AT‐1 cells sbowed spontaneous bebavior that was clearly of cellular origin; this activity was manifest as transient bursts of electrical activity followed by periods of electrical quiescence. this bursting pattern is unusual for normal adult cardiomyocytes, but has been observed in several other cell types. In the primary tumors, automatic behavior may arise from a similar cellular origin or alternatively from a microreentrant phenomena.Conclusion:Primary tumors and AT‐1 cells sbow essential atrial Electrophysiology with important

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01251.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Rate Effects on Conduction and [K+]eDuring Ischemia.Introduction:The purpose nf our study was to determine if the slowing oflongitudinal intraventricular conduction in the in situ porcine heart during acute regional no‐flow ischemia was rate dependent. Further, we investigated whether any rate dependence could he correlated to a rate‐dependent component of the ischemiainduced rise in extracellular potassium concentration. [K+]e.Methods and Results:We studied in situ hearts in nine anesthetized open chest pigs in which acute no‐flow ischemia was induced by occlusion of the left anterior descending coronary artery. To determine the effects of steady‐state rate on the slowing of conduction and rise in [K+]eduring ischemia, we varied the rate of stimulation during sequential occlusions from 90 to 150 beats/min. Longitudinal conduction velocity was determined by unipolar electrodes embedded in a plaque that was sutured to the epicardial surface in the center of the ischemic zone. Myocardial [K+]ewas determined simultaneously by potassium‐sensitive electrodes placed at or within 1 to 2 mm of the epicardium in close proximity to the activation recording electrodes. Conduction vehxity decreased more rapidly at the more rapid rates of stimulation although the reduction in conduction velocity occurring prior to the onset of conduction block was similar at both rates. The potassium change was not rate dependent and rose at the same rate regardless of the rate of stimulation.Conclusion:Our study demonstrates that the steady‐state rate‐dependent component of the slowing of intraventricular conduction induced by acute ischemia in the in situ porcine heart occurs in the absence of a rate‐dependent component in the rise of [K+]e. Between rates of 90 and 150 beats/min, the rate dependence of the conduction slowing may be attributed to one or more potassium‐independent factors such as the rate‐dependent changes in resting membrane potential, in V̇maxof the action potential upstroke, and in cell‐to‐cell uncoupling, which have hcen observed in other

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01252.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Flecainide and Atrial Reentry.Introduction:Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y‐shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier.Methods and Results:To investigate the mechanism of flecainide‐induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 ± 24 msec) by 89% to 309 ± 77 msec (P<0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In flve episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (± 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long‐short cycle length oscillations led to return reexcitation by the impulse within the primary path and suhsequent termination.Conclusion:In summary, similar to our previous findings with the ClassIIIagent, d‐sotalol, two different modes of termination of atrial reentry were observed with

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01253.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Modification of Cardiac INaby α‐chymotrypsin.Introduction:Studies of tetrodotoxinsensitivc sodium current (INa) after modification of inactivation by intracellular enzymes in mammalian cells have demonstrated a markid increase in peak INaat test potentials near current threshold causing a large, negative shift of the peak INaconductance‐voltage relationship by approximately ‐20 mV. These findings support a kinetic model in which the unmodified Na channel has rapid and voltage‐independent inactivation from the open state. However, the kinetics of cardiac Na channels differ from those of mammalian nenronal Na channels. In particular, inactivation of cardiac Na channels has been proposed to be more voltage dependent than that of tetrodotoxin‐sensitive Na channels. To help understand the role of inactivation in cardiac Na channel kinetic hehavior, we studied Na currents before and after modification of inactivution by the proteolytic enzyme, α‐chymotrypsin.Methods and Results:Whole cell INawas measured in single canine cardiac Purkinje cells that were voltage clamped and internally perfused with a large‐bore suction pipette. The decay of INain response to step depolarizations was dramatically slowed after perfusion with intracellular α‐chyniotrypsin consistent with modification of inactivation. In contrast to mammalian tetrodotoxin‐sen‐sitive Na current, Boltzmann distribution fits to peak INaconductance‐voltage (GNa‐V) relationships after α‐chymotrypsin showed no change in either the potential at half maximum conductance (V1/2), after correction for the spontaneous background shift of INakinetics, or in the voltage‐dependence of conductance (i.e., slope factor of GNa‐V relationships). Maximal peak INaconductance increased by 18%. INatail‐current relaxations at potentials ≤−110 mV, after correction for spontaneous shifts in Na channel kinetics, were also similar before and after modification by α‐chymotrypsin.Conclusion:α‐chymotrypsin modified inactivation of cardiac INawith little or no change in activation, and cardiac Na channel inactivation was slow near threshold and played little role in determining V1/2

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01254.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Double Atrial Response. This case report describes a patient in whom a single ventricular depolarization resulted in a double atrial response and the initiation of atypical A V nodal reentrant tachycardia after successful radiofrequency ablation of typical AV nodal reentrant tachycardia using the slow pathway approach. (JCardiovasc Electrophysiol, Vol. 4, pp. 695–701, December 199

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01255.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Congenital Arrhythmias and Heart Block. Electrical instability of the heart has numerous congenital origins. This review approaches the problems from a morphological standpoint, utilizing selected examples from my own studies of the human cardiac conduction system performed during the last three decades. Subjects discussed include multifocal Purkinje cell tumors, benign congenital polycystic tumors of the AV node, several types of congenital heart hlock, postnatal morphogenesis of the AV node and His bundle (including considerations of persistent fetal dispersion and crib death), the Wolff‐Parkinson‐White syndrome, left superior vena cava, focal fibromuscular dysplasia of small coronary arteries, hereditary neuromus‐cular or musculoskeletal diseases, familial atrial fibrillation, long QT syndrome, and apoptosis of the heart. In many congenital disorders of cardiac electrical activity, both arrbythmias and conduction disturbances may occur. How the abnormal anatomy may relate to cardiac electrical instahility is discussed, including certain clinical matters to he consi

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01256.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Physiological Effects of ANP. hypotension caused by atrial natriuretic peptide (ANP) is often not accompanied by the anticipated increases in beart rate or sympathetic nerve activity. the sympathetic inhibitory action of ANP occurs in cardiac and noncardiac sympathetic nerves, and has been demonstrated in conscious or anesthetized animals as well as in humans. The sympathetic inhibition by ANP occurs after atropinization but is abolisbed after va‐gotomy. Thus, ANP alters sympathetic nerve activity by influencing cardiopulmonary barore‐ceptors, wbich in turn is mediated by vagal afferents. In addition to the effects of ANP on cardiopulmonary baroreceptors, ANP affects arterial baroreceptors. ANP dilates the ascending aorta where some of the arterial baroreceptors are located, causing resetting of these arterial baroreceptors. When ANP is microinjected into the cerebroventricle or nucleus tractus soli‐tarii, it causes inhibition of sympathetic nerve activity. It has been shown tbat ANP inhibits sympathetic ganglionic transmission and augments cardiac parasympathetic effects on heart rate. Thus., ANP may play important roles in cardiovascular regulation by influencing sympathetic nerve activity and beart rate in addition to the direct vasodilating and renal ef

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01257.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Spiral Waves. Several mechanisms have been proposed to explain the electrocardiographic patterns observed during various forms of polymorphic ventricular tachycardias, including torsades de pointes. Such mechanisms include the coexistence of either multiple foci or multiple exit pathways from single foci giving rise to various forms of aberrant ventricular activation sequences. For example, the simultaneous firing of two widely spaced foci at slightly different frequencies has heen used to explain the undulating electrocardiogram that is characteristic of torsades de pointes. However, in spite of some supporting experimentalevidence, such an idea remains conjectural from the clinical point of view. Here I discuss a mechanism that has heen proposed recently to explain both monomorpbic and polymorpbic patterns (including undulating patterns) of ventricular tachycardia. the hypothesis is derived from tbf theory of spiral wave activity in excitable media, and from recent experiments using bigh resolution optical mapping in isolated two‐dimensional ventricular muscle preparations tbat demonstrate tbat spiral wave activity may account for self‐sustaining reentrant activation. Sucb studies bave led to the observation that the behavior of the spiral center, the core, plays a key role in determining the electrocardiograpbic manifestation of the arrhythmia. Indeed, a stationary position of the core results in a monomorphic pattern of activation. On the other band, beat‐to‐beat changes in the core position (i.e., drifting) leads to irregular patterns of activation. In fact, when drifting occurs in one direction, it gives rise to a Doppler shift in the excitation period in such a way that two coexisting frequencies are manifest, one ahead of and one behind the drifting core. the activation frequency in the region ahead of the core is always higher than that behind the core. Under such conditions, electrocardiographic recordings of the activity demonstrate an undulating pattern, which resembles that of torsades de pointes. When the core drifts in various directions, a potymorpbic pattern is manifest. Thus, depending on spiral core dynamics, monomorphic. undulating, or completely irregular patterns maybe observed. Moreover, transitions between such patterns can also occur. For example, drifting spirals giving rise to polymorphic activation can become stationary and result in monomorphic activation as a result of anchoring of the core to a small discontinuity (e.g., an artery or small scar) in the tissue. Direct extrapolation of such results to clinical cases is not appropriate. However, the observations discussed in this article offer a new testable hypothesis in which a common mechanism is postulated for the electrocardiograpbic patterns associated with monomorphic and polymorphic tachy

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01258.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY