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Biomedical subjects

R Cardinal

Publications and source records attributed to R Cardinal.

At least 55 records · Page 3Linked to original sources
PubMed1991

Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction. Is the origin of the tachycardia always subendocardially localized?

BACKGROUND: Left ventricular endocardial reentry is the conventional concept underlying surgery for ventricular tachycardia (VT). We assessed the incidences of patterns showing complete reentry circuits at either the subendocardial or subepicardial level and of patterns in which left ventricular endocardial mapping could only in part account for a reentrant mechanism. METHODS AND RESULTS: We retrospectively analyzed epicardial and left ventricular endocardial isochronal maps of 47 VTs induced in 28 patients with chronic myocardial infarction (inferior, 14 patients; anteroseptal, 14 patients). Electrograms were recorded intraoperatively from 128 sites with epicardial sock and transatrial left ventricular endocardial balloon electrode arrays. Given the methodology used in this study, the mapping characteristics of the tachycardias suggested five types of activation patterns: 1) complete (90% or more of VT cycle length) subendocardial reentry circuits in seven VTs (15%) and seven patients (25%), 2) complete subepicardial reentry circuits in four VTs (9%) and four patients (14%), 3) incompletely mapped circuits with a left ventricular endocardial breakthrough preceding the epicardial breakthrough in 25 VTs (53%) and 21 patients (75%), 4) incompletely mapped circuits with a left ventricular epicardial breakthrough preceding the endocardial breakthrough in three VTs (6%) and three patients (11%), and 5) a right ventricular epicardial breakthrough preceding the left ventricular endocardial breakthrough in eight VTs (17%) and seven patients (25%). After surgery, one type 3 VT and three type 5 VTs were reinducible. Thus, left ventricular endocardial reentry substrates (types 1 and 3) accounted for 68% of VTs, but substrates involving subepicardial (types 2 and 4) and deep septal layers (type 5) accounted for 32% of VTs. CONCLUSIONS: In a substantial number of VTs, a substrate localization that is at variance with the conventional concept can be detected by simultaneous epicardial and endocardial mapping and may require modification of the surgical approach conventionally aimed at endocardial layers.

Cardiac Pacing, Artificial↗
PubMed1990

Comparative accuracy of the vectorcardiogram and electrocardiogram in the localization of the accessory pathway in patients with Wolff-Parkinson-White syndrome: validation of a new vectorcardiographic algorithm by intraoperative epicardial mapping and electrophysiologic studies.

The scalar electrocardiograms (ECGs) and vectorcardiograms (VCGs) of 41 patients with Wolff-Parkinson-White (WPW) syndrome were used to compare the accuracy of these techniques in the identification of the site of preexcitation. The location of the accessory pathway (AP) was determined by endocavitary electrophysiologic studies in all patients and the location was confirmed during intraoperative epicardial mapping in 28 of them. The ECGs were classified according to Gallagher's criteria and with Milstein's algorithm, whereas the VCGs were classified according to a new two-step algorithm. The presence of multiple accessory pathways and coexisting myocardial infarctions were major limitations in both the VCG and ECG classification procedures. In patients with a single accessory pathway, three AP localizations (right free ventricular wall, posterior, or left free ventricular wall) were identified with the first step of the VCG algorithm, with an overall sensitivity (96.5%), specificity (90.7%), and positive predictive values (80%) that were greater than those obtained with the ECG Milstein algorithm (77.1%, 91.5%, and 75%, respectively). The second step of the VCG algorithm made it possible to identify an AP location in one of the following sites: anterior right, lateral right, posterior right, posterior left, lateral left, or anterior left ventricle. The overall sensitivity, specificity, and positive predictive values were greater for the second step of the VCG algorithm than for the ECG criteria proposed by Gallagher (43.6% versus 39.3%, 92.1% versus 87.4%, and 51.5% versus 33.3%, respectively). It was concluded that the VCG seems to be more specific and sensitive than the ECG in the identification of the preexcitation site and should be given preference in the initial evaluation of the WPW syndrome.

Adult↗
PubMed1990

Chronic doxorubicin induced cardiomyopathy in rabbits: mechanical, intracellular action potential, and beta adrenergic characteristics of the failing myocardium.

STUDY OBJECTIVE: The aim was to assess myocardial, electrophysiological, and adrenergic changes caused by chronic administration of doxorubicin. DESIGN: Doxorubicin induced cardiotoxicity was produced in three groups of rabbits by injecting doxorubicin 0.75 mg.kg-1 three times a week for 7, 9 and 11 weeks. There were 36 controls. All studies were conducted within 16 to 36 h after the last injection. Histological, mechanical, and action potential changes produced by doxorubicin were examined in vitro. The effects of doxorubicin on beta adrenergic receptors and cyclic adenosine monophosphate (AMP) generation in myocardial membrane preparations were also evaluated. EXPERIMENTAL MATERIAL: 145 New Zealand white rabbits, 2.4-2.7 kg, were used. After excision of the heart, a papillary muscle was used for mechanical studies, a portion of the septum for intracellular action potential studies, and the rest of the heart for histological or biochemical studies. MEASUREMENTS AND RESULTS: Histological studies showed widespread myocardial damage that became more severe as the cumulative doses increased. Right ventricular papillary muscles of doxorubicin treated rabbits had lower total tension (1.5 v 3.3 g.mm-2 for controls, p less than 0.05) and dT/dt, shorter contraction duration, and lower velocity of shortening than the control muscles under all loading conditions. The changes progressed as the cumulative doxorubicin dose increased. Action potential duration was shorter in the doxorubicin treated groups (APD50 = 76 v 62 ms for controls, p less than 0.01), although resting action potential amplitude was normal. Tension-frequency response (6-36 stimuli.min-1) and response to increasing calcium concentrations (2.54-6.32 mM) were attenuated in the doxorubicin group. Percent change in tension and dT/dt in response to noradrenaline (50 microM), isoprenaline (20 microM), or dibutyryl cyclic AMP (40 mM), was increased in the doxorubicin group v controls (300-600% v 100-200% respectively), despite chronic increase in circulating catecholamines, depletion of myocardial catecholamines, and no change in beta adrenergic receptor number or affinity. The apparent increase in beta adrenergic responsiveness in the doxorubicin group may have been partly due to decreased basal cyclic AMP production (13 v 31 pMol.mg-1 protein.min-1, p less than 0.01), although maximum catecholamine stimulated cyclic AMP production was only mildly decreased (251 v 315 pMol.mg-1 protein.min-1, p less than 0.05). CONCLUSIONS - The subacute effects of chronic doxorubicin become progressively more marked as the cumulative dose increases, and there are significant differences in the myocardial characteristics between this chronic model and other models of heart failure. These differences may be related to the cytotoxic effects of doxorubicin on membranes and membrane bound enzymes.

Action Potentials↗
PubMed1990

Cardiac responses to electrical stimulation of discrete loci in canine atrial and ventricular ganglionated plexi.

The purpose of the present study was to examine cardiac effects induced by electrical stimulation (1-4 V, 1 ms, 200 Hz) of discrete loci within the ganglionated plexi located on canine atria and ventricles. When 20 loci in the right atrial ventral ganglionated plexi of 11 anesthetized open-chest dogs were stimulated, bradycardia and/or right and left atrial force suppression occurred when, on average, 15% of these loci were stimulated. Bradycardia and atrial force suppression were elicited when, on average, 8% of 15 loci in the left atrial ventral ganglionated plexi of eight dogs was stimulated. When these loci were restimulated after acute decentralization, cardiac responses were attenuated or occasionally eliminated. After atropine (1 mg/kg iv) administration, repeat stimulation of loci in the right but not left atrial ganglionated plexus induced tachycardia. Stimulation of loci in the right ventricular ganglionated plexus after the subsequent administration of desipramine (1 mg/kg iv) in six dogs resulted in an increase in right ventricular conus intramyocardial pressure. After hexamethonium administration (10 mg/kg iv, followed by a continuous infusion of 1 mg.kg-1.min-1), sympathetic responses were no longer elicited from one of the five dogs in which loci in the right atrial ganglionated plexi and from two of the six dogs in which loci of the right ventricular ganglionated plexus had elicited responses. We conclude that atrial and ventricular ganglionated plexi contain efferent parasympathetic, efferent sympathetic, and afferent neurons.

Animals↗
PubMed1990

Spatial domain analysis of late ventricular potentials. Intraoperative and thoracic correlations.

For investigation of late potentials seen on the signal-averaged electrocardiogram, intracardiac and thoracic distributions of terminal activity were analyzed in 16 patients undergoing cryosurgery for ventricular tachycardia after remote myocardial infarction. The body surface potentials measured with 63 time-averaged unipolar leads were compared with epicardial and endocardial potential maps in six patients without and 10 patients with bundle-branch block. Intracardiac post-QRS activity, defined as extending beyond the thoracic QRS offset, was found in five of six patients without bundle-branch block (83%) and in five of 10 patients with bundle-branch block (50%), corresponding to 4 +/- 5% of the total number of electrograms in each patient. Fragmentation, double deflections, and single deflections were observed in 27%, 34%, and 39%, respectively, of these post-QRS electrograms. Post-QRS activation patterns that were stable from beat to beat showed slow propagation around or within areas of conduction block. Post-QRS activity was most often observed on both epicardial and endocardial surfaces (five of 10 patients). In the six patients without post-QRS activity, an area of late activity displaying low-amplitude deflections that were masked by the terminal activation of the normal myocardium was identified. Isopotential maps of the high-pass-filtered (55-Hz) thoracic and intracardiac signals demonstrated a close spatial correlation between the location, amplitude, and orientation of the potential extrema observed over the thoracic, epicardial, or endocardial surfaces during post-QRS activity. The thoracic patterns were generally dipolar with close extrema for anteroseptal or apical sites of post-QRS activity and more distant extrema for other sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[The origin of late potentials in patients with ventricular tachycardia after myocardial infarction].

In order to study the origin of late potentials, their distribution was analyzed in 16 patients who had undergone surgery for arrhythmia due to ventricular tachycardia following myocardial infarction. The potentials were measured in sinus rhythm using 63 unipolar leads placed on the chest before the operation, then on the epicardium and endocardium during the operation. Epicardial and/or endocardial activity extending beyond the QRS complex measured from unfiltered chest signals and characterized by slowed propagation at the edge or inside of necrotic regions, stable from one beat to the next, and showing simple (39 per cent), double (34 per cent) or fragmented (27 per cent) deflections on the electrocardiograms were observed in 5/6 patients without bundle-branch block and in 5/10 patients with block. Similar activity but which did not extend after the QRS was detected in the 6 other patients. For signals filtered at 55 Hz, a close correlation between the distribution of chest, epicardial and endocardial potentials was observed, thus allowing approximate location of the origin of late potentials from the chest. Anterior or apical sites corresponded to close extrema in the precordial region, whereas the other sites were associated with more distant extrema. An analysis of potential distribution thus gives a better understanding of the electrogenesis of late potentials as well as their detection on the chest.

Aged↗
PubMed1989

Differential effects of abrupt cycle length changes on the refractoriness of accessory pathway, His-Purkinje system, atrial and ventricular myocardium in Wolff-Parkinson-White syndrome.

We compared the response of the accessory pathway (AP), the atrial myocardium, the His-Purkinje system (HPS) and the ventricular myocardium during steady state (constant cycle length) and following an abrupt alteration in cycle length in 23 patients with Wolff-Parkinson-White syndrome. The durations of the anterograde and retrograde refractory periods were measured during constant drive cycle lengths of 600 and 400 ms (Method I) and during an abrupt change in cycle length of either short-to-long (400 to 600 ms) (Method II) or long-to-short (600 to 400 ms) (Method III) just before the extra stimulus. The mean durations of the anterograde effective refractory periods of the APs were 295 +/- 43, 243 +/- 39 and 273 +/- 37 ms at 600, 400 and 400 to 600 ms cycle lengths, respectively. For the atrial effective refractory periods at the three cycles, they were 238 +/- 18, 217 +/- 11 and 241 +/- 17 ms, respectively. During ventricular stimulation, the mean durations of the retrograde effective refractory periods of the APs were 263 +/- 25, 245 +/- 19 and 253 +/- 21 ms at cycle lengths of 600, 400 and 400 to 600 ms, respectively. For the relative refractory periods of the HPS, they were 335 +/- 29, 239 +/- 23 and 367 +/- 38 ms, respectively and, for the effective refractory periods of the ventricular myocardium, they were 227 +/- 17, 206 +/- 15 and 215 +/- 18 ms, respectively. The retrograde effective refractory period of the HPS could be measured in only five patients at the three cycles (600, 400 and 400 to 600 ms) and the mean values were 265 +/- 57, 225 +/- 14 and 305 +/- 27 ms, respectively. With Method III, AP and ventricular myocardium responded in a cumulative manner while HPS demonstrated paradoxical effect. Compared to Method I, changes with Methods II and III were statistically significant for all variables measured. During all three cycles, the retrograde effective refractory period of the HPS exceeded the effective refractory period of the AP; and the HPS demonstrated progressive conduction delay while the AP responded to no or minimal delays when the V1V2 intervals were similar. An abrupt cycle length change of the short-to-long type facilitated the induction of orthodromic tachycardia during ventricular pacing.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Opposite effects of lidocaine and diltiazem on electrophysiologic alterations in acutely ischemic porcine myocardium.

To investigate the actions of lidocaine and diltiazem on the ischemic alterations associated with the onset of acute ischemic arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine (2.4-3.8 micrograms/mL of plasma) or diltiazem (390-510 ng/mL) in open-chest anesthetized pigs. Sixty-one unipolar electrograms were continuously recorded in the ischemic zone. Isochronal maps and isopotential maps were determined by computer analysis. The magnitude of beat-to-beat alternation of unipolar waveforms was described by the difference between the time integrals subtended by electrograms of consecutive beats. Activation times were prolonged by ischemia and the ST segment became elevated. Delay and ST elevation developed at a faster rate in the presence of lidocaine than under control conditions, but were reduced by diltiazem. ST-T alternation was not significantly different between control and lidocaine occlusions, but the incidence of negative T waves and that of ventricular tachycardia degenerating to fibrillation were higher in lidocaine occlusions than in control occlusions. In contrast, unipolar waveform alternation and negative T waves were virtually abolished by diltiazem, even at fast pacing rates (180-210 beats/min) at which diltiazem did not reduce ST elevation. Ventricular arrhythmias also were abolished by diltiazem. Thus, lidocaine and diltiazem produce opposite effects on the ischemic alterations most closely associated with the initiating mechanism of tachycardia. This could be related to differences between these drugs with regard to their actions on transmembrane currents during repolarization.

Animals↗
PubMed1989

Surgical treatment of ventricular tachycardia. Regional cryoablation guided by computerized epicardial and endocardial mapping.

Extended cryoablation as a single method of myocardial ablation was used for surgical treatment of 33 patients with ventricular tachycardia associated with coronary artery disease. Surgery was guided by roving-probe mapping in 14 patients and by computerized epicardial and computerized, left ventricular, endocardial, multielectrode mapping in 19 patients. In the latter group, the anatomic correlation between sites of the earliest epicardial activation (EA-EPI) and those of the earliest endocardial activation (EA-ENDO) was found to be consistent in the apical region. In contrast, the EA-ENDO corresponding to the EA-EPI localized in the left anterolateral and posterobasal free-wall regions could be localized either in an underlying area or on the septum. All tachycardias with EA-EPI in anterior and posterior right ventricular regions had their corresponding EA-ENDOs in the interventricular septum. EA-ENDO preceded EA-EPI in 33 of 41 tachycardias studied. The converse was observed in the remaining eight tachycardias. Cryoablation was applied regionally in areas corresponding to EA-ENDO, along with standard aneurysmectomy and coronary artery bypass grafting when indicated. Among the entire group of 33 patients, there were two (6%) operative deaths. Ventricular tachycardias recurred spontaneously in two (6%) patients and remained inducible in four (13%), of whom one (3%) died suddenly. After hospital deaths were taken into account, actuarial survival was 74 +/- 9% (mean +/- SD) at 48 months after operation. Among the 10 patients who had an EA-EPI on the right ventricle and an EA-ENDO on the interventricular septum, deep septal involvement was suspected, and arrhythmic failure occurred in five patients; in contrast, complete surgical success was obtained in all nine patients who did not display this pattern during intraoperative investigation. We conclude that regional cryoablation alone in areas of the earliest left ventricular activation is highly effective for treatment of ventricular tachycardia, except in a subset of patients with specific markers of deep septal involvement, which can be detected by computerized epicardial and endocardial mapping.

Action Potentials↗
PubMed1988

Sinus rhythm mapping in a canine model of ventricular tachycardia.

The relationship between electrograms recorded during sinus rhythm and the activation sequence during ventricular tachycardia induced by programmed stimulation was investigated in a canine model of myocardial infarction. Thirteen dogs were studied 3 days (n = 10) or 14 days (n = 3) after coronary occlusion. Sixty-three unipolar electrograms were simultaneously recorded with a sock electrode array connected to a digital recording system, and analyzed by computer. Bipolar electrograms were recorded sequentially from the same sites with an analog recorder. Categories of unipolar electrograms were defined with reference to the QRS complex during sinus rhythm as follows: Class A included electrograms with an intrinsic deflection inscribed within the QRS complex, class B included those which did not exhibit any intrinsic rs deflection, and class C included those with an intrinsic deflection inscribed later than QRS. The epicardial distribution of each class of electrograms was significantly different between the preparations with, and those without inducible tachycardia (72% versus 63% of electrograms being in class A, 20% versus 35% in class B, and 8% versus 2% in class C; p less than 0.005). When tachycardia was inducible, class C epicardial electrograms were located in an area extending across the region of infarction, which corresponded to the common reentrant pathway of figure-of-eight patterns mapped during tachycardia. When ventricular tachycardia was not inducible, class B electrograms were recorded all over this region. The morphology of bipolar electrograms had no predictive value in identifying the common reentrant pathway. These results support the view that the inducibility of reentrant tachycardia is dependent upon critically located delayed activity detected during sinus rhythm by unipolar recordings.

Animals↗
PubMed1988

Catheter recording of left atrial activation from left pulmonary artery in the Wolff-Parkinson-White syndrome: validation of the technique with intraoperative mapping results.

Accurate localization of accessory pathways (AP) in the Wolff-Parkinson-White (WPW) syndrome requires detailed atrial mapping. Coronary sinus catheterization is so far the most accurate method of left atrial mapping, but it can be technically difficult in some patients. We evaluated the feasibility of left atrial mapping from the left pulmonary artery in 24 patients with WPW syndrome. All patients except one underwent surgical cryoablation of their AP and the results of intraoperative mapping are available for comparison. Mapping in sinus rhythm showed recording of atrial activity in the distal left pulmonary artery occurred 56 +/- 20 ms after activation of high right atrium and 24 +/- 4 ms after activation in the His bundle area, but coincident with left atrial activation in the distal coronary sinus (56 +/- 20 and 53 +/- 13, respectively). Mapping during ventricular pacing or orthodromic tachycardia could differentiate patients as having a right sided, left sided or paraseptal first site of activation. Eleven patients had a left lateral AP, four had a left posterior AP, five had left posteroseptal AP and one had a left anterior AP. The remaining three patients had a right sided AP. Intraoperative results correlated with pre-operative findings in 22 out of 23 (95%) patients who underwent surgical ablation of AP. Thus, recordings form the left pulmonary artery reflect left atrial activity and may be of aid in localizing an AP, especially when coronary sinus recordings cannot be obtained. This technique, however, should not replace the more accurate method of coronary sinus mapping.

Adult↗
PubMed1988

Coronary sinus norepinephrine concentrations during ventricular tachycardia induced by left stellate ganglion stimulation in dogs.

Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and alpha-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p less than 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.

Animals↗
PubMed1988

Demonstration of hysteresis in refractoriness of canine ventricular myocardium.

The properties and determinants of hysteresis during ventricular effective refractory period (VERP) measurements by an extrastimulus technique were determined in 15 anesthetized open-chest dogs as well as in isolated ventricular muscle (n = 6). VERP was determined both by decreasing the S1-S2 interval and also by increasing S1S2. Hysteresis was then calculated by subtracting the VERP obtained with the decreasing S1S2 from the VERP obtained with the increasing S1S2. The effects of basic cycle length, pulse width, stimulation intensity, and the number of basic drives on VERP and hysteresis were evaluated. VERP was shorter for long pulse width, high stimulation intensities, and shorter basic cycle lengths. These modifications were not associated with significant changes of hysteresis. VERP was shorter during decreasing S1S2 than during increasing S1S2. Hysteresis was greater with 6 basic drive cycles than with 12 (P less than 0.001) in both in vivo and in vitro preparations. The data suggest that 1) hysteresis occurs during VERP measurements; 2) hysteresis is independent of stimulation modality; and 3) hysteresis decreases with the number of basic drive cycles.

Animals↗
PubMed1988

Epinephrine release from the heart during left stellate ganglion stimulation in dogs.

Plasma epinephrine (E) and norepinephrine (NE) concentrations were measured (radioenzymatic assay) in blood samples simultaneously withdrawn from the aorta (Ao) and coronary sinus (CS) on 10 anesthetized dogs immediately before and during a 1-min period of electrical stimulation of the left stellate ganglion (4 V, 4 ms, 10 Hz). Heart rate and systolic blood pressure significantly increased in response to electrical stimulation (152 +/- 8 to 180 +/- 15 beats/min and 128 +/- 12 to 149 +/- 12 mmHg, mean +/- SE; P less than 0.05). Plasma NE concentrations were not significantly different in the Ao and the CS (432 +/- 110 and 319 +/- 67 pg/ml) before the stimulation, whereas a net removal of E was present across the myocardium (Ao, 172 +/- 61; CS, 71 +/- 22 pg/ml). A large NE spillover in the CS was observed during the stimulation (Ao, 1,555 +/- 513; CS, 10,583 +/- 3,753 pg/ml). A significant output of E from the myocardium was also present (Ao, 165 +/- 42; CS, 291 +/- 74 pg/ml) during the stimulation. Determination of NE and E concentrations by high-performance liquid chromatography in five of the dogs confirmed the observation made with the radioenzymatic assay, i.e., a significant uptake (66%) of blood-borne E was present across the myocardium in the control situation (Ao, 320 +/- 97; CS, 110 +/- 23 pg/ml), whereas plasma E concentrations in the CS (280 +/- 61 pg/ml) were 1.5 times the values found in Ao (184 +/- 56 pg/ml) under electrical stimulation. These observations give further support to the hypothesis that endogenous tissue E can act as a cotransmitter of sympathetic fibers.

Animals↗
PubMed1988

Anisotropic conduction and functional dissociation of ischemic tissue during reentrant ventricular tachycardia in canine myocardial infarction.

We measured the conduction characteristics at the epicardial surface of the left anterior ventricular wall in the in situ canine heart before and 3 to 5 days (n = 9 dogs) after permanent occlusion of the left anterior descending coronary artery (LAD). During ventricular stimulation generating wavefronts conducted along the longitudinal or the transverse fiber direction, 61 unipolar electrograms were recorded with a fine-meshed plaque electrode. Before occlusion, the fastest conduction velocity was consistently found in a direction perpendicular to the nearby LAD segment (longitudinal direction), and the slowest velocity in a direction parallel to the LAD segment (transverse fiber direction). In 3- to 5-day-old infarct preparations, a layer of subepicardial muscle with 1 to 3 mm thickness survived over necrotic tissue. The velocities and directions of fast and of slow conduction measured in ischemic subepicardial muscle were not significantly different from preocclusion values during stimulation at a basic rate, but excitability was found to be depressed in response to premature stimuli. Premature impulses initiated in nonischemic myocardium and conducted into ischemic tissue in the longitudinal or in the transverse directions induced sustained (greater than 100 beats) monomorphic tachycardias during which figure-eight activation patterns were mapped with sock-array electrodes. During these tachycardias, the direction of the common reentrant wavefront of the figure-eight pattern was preferentially oriented along the longitudinal fiber direction, independently of the direction of the initiating impulse. When polymorphic beats were induced, tachycardia terminated spontaneously within 20 beats, or changed to a monomorphic pattern, as described above. In conclusion, the anisotropic organization of surviving subepicardial muscle overlying an infarct provides a spatial constraint that determines a preferential direction of reentrant propagation and may contribute to sustaining monomorphic tachycardia.

Animals↗
PubMed1988

Termination of sustained ventricular tachycardia by ultrarapid subthreshold stimulation in humans.

Our purpose was to investigate the efficacy, safety, and electrophysiological mechanism of ultrarapid subthreshold electrical stimulation in terminating sustained ventricular tachycardia (VT) in humans. Fifteen patients with inducible sustained hemodynamically stable VT and whose VT cycle length ranged between 295 and 440 msec (337 +/- 60 msec) were included in this study. The stimulation threshold and ventricular myocardial effective refractory period were determined during VT, and the values ranged between 0.4 and 1.2 mA (mean, 0.7 +/- 0.3 mA) and between 185 and 245 msec (mean, 225 +/- 20 msec), respectively. Trains of ultrarapid subthreshold stimulation were delivered with cycle lengths of 100 to 10 msec in decremental steps of 10 msec. A 5-second pause was allowed between each step (decrement). A 2-msec pulse width was used in all patients, and a 4-msec pulse width was also tested in eight patients. Any apparent captured beat was disregarded. In eight (53%) patients, ultrarapid subthreshold stimulation terminated VT, and in the remaining seven (47%) patients, it did not. The lowest subthreshold stimulation that effectively terminated VT was 0.05 mA. In 10 patients, the site of early activity during VT was determined by endocardial catheter mapping, and subthreshold stimulation more effectively terminated VT in eight patients when it was applied close to the site of early activity. In seven patients who underwent mapping-guided arrhythmia surgery, subthreshold stimulation was applied close to the site of early activity and successfully terminated VT. In no patient did subthreshold stimulation produce acceleration of VT or induce ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗