Accuracy of measurements derived from intracardiac unipolar electrograms: A simulation study.

The ventricular action potential duration (APD) is a fundamental determinant of cardiac electrical stability and can be estimated by measuring the activation recovery interval (ARI) from the unipolar electrogram (UEG), which represents the electrical activity of the heart at the tissue level. Under experimental conditions, automatic estimation of ARIs is challenging due to non-related interferences and low signal-to-noise ratios (SNRs). In this simulation study, we investigated how the reliability of ARI estimates is affected by noise and artefacts in the UEG. Real-like electrograms were generated using a 257-node whole heart model to synthesize 20 real-like UEGs exhibiting constant and dynamic ARI patterns. Controlled degrees of noise and contamination (ectopic beats) were added to obtain a range of signal qualities. The generated recordings were automatically analyzed using a proposed standard method to estimate the ARI. The performance was compared with two improvements of the standard method including a narrow search window and a correlation filter. The results show that the robustness of automatic ARI analysis was dramatically improved by using the proposed improvement methods. For typical recordings with a SNR of 10dB and filtered with often used cutoff frequency of 30Hz to measure repolarization, the average mean absolute error of the estimations was reduced from 16.2ms (range:12.2-29.0ms) for the standard method to 11.6ms (range:6.0-13.4ms) for the improved method. The standard deviation was reduced from 38.2ms (range:26.8- 58.5ms) to 14.6ms (range:7.6-16.9ms). Detection of cyclical variation of ARI was also improved by using the improvement strategy: for 0.2Hz ARI oscillations with an amplitude of 5ms, the highest average detection rate increased from 41% for the standard method to 100% using the improved method for recordings with a SNR of 10dB.

Unified rate-dependent atrioventricular nodal function: consistent recovery and fatigue properties revealed with S1S2S3 protocols and different recovery indexes.

BACKGROUND: Rate-dependent nodal properties are commonly assessed with premature protocols performed at different basic rates. Because characteristics of responses differ with recovery time index, the true nature of nodal rate-dependent properties is elusive. OBJECTIVES: The purpose of this study was to reveal consistent nodal rate-dependent properties regardless of selected recovery index. METHODS: With S(1)S(2)S(3) protocols, we independently varied basic and pretest cycle lengths and thereby distinguished cumulative from noncumulative effects of rate on nodal conduction time in rabbit heart preparations. Nodal responses to 30 basic and pretest cycle length combinations (five with identical basic and pretest cycles as in standard protocols) were analyzed using both atrial (AA) and His-atrial (HA) intervals as recovery index. RESULTS: AA and HA curves had an identical shape for any of 30 steady-state conditions. When assessed with constant pretest cycle lengths, cumulative effects (fatigue) of shortened basic cycle lengths were also independent of recovery index. Shortening of pretest cycle length at fixed basic rates led to apparent inhibitory and facilitatory effects when assessed with AA and HA curves, respectively. These effects vanished when a single long cycle was inserted after the pretest cycle. In all responses including those obtained with standard protocols, combined effects of basic and pretest cycle lengths set nodal conduction time. CONCLUSION: S(1)S(2)S(3) protocols reveal consistent nodal recovery and fatigue properties regardless of recovery index used. Changes in nodal function curves arising from the use of different recovery indexes mainly depend on pretest effects. This study provides a new approach to a unified interpretation of nodal recovery and fatigue properties.

Spontaneous onset of ventricular fibrillation in Brugada syndrome with J wave and ST-segment elevation in the inferior leads.

We report the case of a 52-year-old man with variant Brugada syndrome who was successfully resuscitated from ventricular fibrillation (VF). Resting ECG showed J wave and ST-segment elevation in the inferior leads but no coved or saddleback ST-segment elevation in the right precordial leads. Pilsicainide infusion provoked coved-type ST-segment elevation in the right precordial leads and mild ST-segment elevation 80 ms after the J point in the inferior leads. During an emergency, 12-lead ECG showed that spontaneous onset of VF was preceded by left bundle branch block and superior axis-type ventricular extrasystoles. The present case provides additional information on the site of origin of VF in patients with Brugada syndrome.

T-wave alternans phase following ventricular extrasystoles predicts arrhythmia-free survival.

OBJECTIVE: The purpose of this study was to assess the value of T-wave alternans (TWA) following ventricular extrasystoles in predicting arrhythmia-free survival. BACKGROUND: Stratifying risk for sudden death in patients with coronary disease and moderate left ventricular (LV) dysfunction remains a challenge. We hypothesized that, in such patients, a discontinuity in beat-to-beat T-wave alternation (TWA phase reversal) following single ventricular extrasystoles reflects transiently exaggerated repolarization dispersion, and predicts spontaneous ventricular arrhythmias. METHODS: We studied 59 patients with ischemic LV dysfunction (mean LV ejection fraction 38.7 +/- 5.3%) and nonsustained ventricular tachycardia undergoing programmed stimulation. TWA was computed spectrally from the ECG during ventricular pacing, and TWA phase reversal was reflected by a discontinuity in T-wave oscillation after single ventricular extrasystoles. RESULTS: Patients induced into ventricular arrhythmias (n = 36) had greater TWA magnitude (V(alt): 6.60 +/- 6.46 microV vs 2.61 +/- 1.97 microV; P = .001) and more frequent TWA phase reversal (62.1% vs 44.4%; P = .02) than those who were not (n = 23). During a mean follow-up of 36 +/- 12 months, positive TWA (V(alt) > or =1.9 microV) and TWA phase reversal both (P < .05) predicted events (all-cause mortality, ventricular tachycardia, ventricular fibrillation). Univariate predictors of arrhythmia-free survival were TWA phase reversal (P < .005), positive TWA (P < .05), age (P = .008), and LV mass index (P = .043). On multivariate analysis, only TWA phase reversal and age predicted events; if TWA phase was excluded, only positive TWA and age predicted events. CONCLUSION: Phase reversal in TWA following ventricular extrasystoles predicts spontaneous ventricular arrhythmias and all-cause mortality in patients with moderate ischemic LV dysfunction and was a better predictor than positive TWA or programmed ventricular stimulation.

Extrapotentials and allorhythmias as an expression of experimental parasystole.

UNLABELLED: The aim of the study was to investigate the dynamics of experimental parasystole taking into consideration the peculiarities of recurrent arrhythmias recorded in clinical settings. MATERIAL AND METHODS: The experiments were conducted on isolated right atria of seven chinchilla rabbits. Parasystolic arrhythmias using periodical one-site electrostimulation were provoked in one atrium, where the sinus node was not affected, and in two atria with the spontaneous low value activity of pacemakers. The parasystolic arrhythmias by the dual-site periodical pacing were provoked in four atria, in which the spontaneous activity had disappeared, while the membrane potential of cardiomyocytes remained at the level of 70 to 80 mV. RESULTS: The parasystolic arrhythmias of the shape of single extrapotentials were obtained in atria when the periods of excitation impulses were within the limits of 0.9-1.2 s, and the differences between these periods being relatively small (0.04-0.2 s). The increase of these differences resulted the various allorhythmias. In cases of single extrapotentials, the recurrence periods of arrhythmias reached 5.6-29 s; while in cases of allorhythmias they shortened to 2.4-4.8 s. CONCLUSION: The parasystoles in isolated atria of rabbits can be induced by two competitive excitation sources. They may manifest themselves through single extrapotentials or allorhythmias, whose form depends on the duration of the periods of excitation impulses, the difference between these durations, as well as on effective refractory periods of atrial cardiomyocytes. The determination and evaluation of the recurrence period of these arrhythmias can serve in any given clinical situation as a supplementary criterion.

Effects of class I antiarrhythmic drugs on the digitalis-induced triggered activity arrhythmia model: a rationale for the short-term use of class I drugs against triggered arrhythmias.

Delayed afterdepolarization (DAD)-induced triggered activity has been considered to be one of the generation mechanisms of ventricular arrhythmias in the presence of intracellular Ca2+ overload. In this study, we analyzed the antiarrhythmic effects of class I antiarrhythmic drugs, namely, disopyramide, procainamide, mexiletine, and flecainide, on a recently developed DAD-induced triggered arrhythmia model, which consists of a canine ventricular septum preparation cross-circulated with a blood-donor dog. After intravenous administration of ouabain to the donor dog, triggered arrhythmias were consistently induced in the cross-circulated preparation by train stimulation (cycle length: 300 ms; train number: 15). Intracoronary administration of disopyramide, procainamide, mexiletine, and flecainide as well as lidocaine suppressed the triggered arrhythmias at clinically relevant doses. Similar doses have been demonstrated to suppress intraventricular conduction in the same experimental model. These results suggest that the Na+ channel inhibition by class I drugs is an effective pharmacological intervention for suppressing Ca2+ overload, which may provide a rationale for the short-term use of class I drugs against the triggered arrhythmias in clinical practice.

Catheter ablation of paroxysmal atrial fibrillation initiated by non-pulmonary vein ectopy.

BACKGROUND: Most of the ectopic beats initiating paroxysmal atrial fibrillation (PAF) originate from the pulmonary vein (PV). However, only limited data are available on PAF originating from the non-PV areas. METHODS AND RESULTS: Two hundred forty patients with a total of 358 ectopic foci initiating PAF were included. Sixty-eight (28%) patients had AF initiated by ectopic beats (73 foci, 20%) from the non-PV areas, including the left atrial posterior free wall (28, 38.3%), superior vena cava (27, 37.0%), crista terminalis (10, 3.7%), ligament of Marshall (6, 8.2%), coronary sinus ostium (1, 1.4%), and interatrial septum (1, 1.4%). Catheter ablation eliminated AF with acute success rates of 63%, 96%, 100%, 50%, 100%, and 0% in left atrial posterior free wall, superior vena cava, crista terminalis, ligament of Marshall, coronary sinus ostium, and interatrial septum, respectively. During a follow-up period of 22+/-11 months, 43 patients (63.2%) were free of antiarrhythmic drugs without AF recurrence. CONCLUSIONS: Ectopic beats initiating PAF can originate from the non-PV areas, and catheter ablation of the non-PV ectopy has a moderate efficacy in treatment of PAF.

Electrophysiologic characteristics of the spontaneous onset and termination of atrial fibrillation.

Electrophysiologic characterization of the onset and termination of atrial fibrillation (AF) is poorly defined. Our study population consisted of 21 consecutive patients (mean age 58 +/- 9 years, 6 women) with intermittent (10 patients) or persistent (11 patients) AF. Mapping of the left atrium (LA) and the right atrium (RA) during initiation and termination of AF was performed with a 64-electrode basket catheter. A total of 92 spontaneous AF onsets (in 16 patients) and 63 spontaneous AF terminations were analyzed. Irrespective of the origin of the triggering atrial premature complex (APC), the onset of AF was preceded by an intermediary rhythm that consisted of repetitive firing from the focus that generated the initial APC, reentry around the mitral annulus, or typical atrial flutter. The earliest fibrillatory activity was constantly produced by circumvented regions (generators) localized most frequently in the posterior wall of the LA. Generators of fibrillatory activity were not observed in the RA for any of the patients. In the RA, AF is maintained by a mixture of macro-reentry and driving wave fronts of left atrial origin. Four modes of AF termination were observed: a multifocal rhythm (19 episodes, 30%), left atrial tachycardia (17 episodes, 27%), direct conversion to sinus rhythm (15 episodes, 24%), and conversion to typical atrial flutter (12 episodes, 19%). A repetitive rapid rhythm initiated most often by APCs plays a crucial role in the initiation of AF via activation of the generators of fibrillatory activity. The LA plays a central role in the initiation of AF by serving as a substrate for generators of fibrillatory activity. Termination of AF consists of a heterogenous group of unstable rhythms.

Clinical implications of fetal magnetocardiography.

OBJECTIVES: To test the usefulness and reliability of fetal magnetocardiography as a diagnostic or screening tool, both for fetuses with arrhythmias as well as for fetuses with a congenital heart defect. METHODS: We describe 21 women with either a fetal arrhythmia or a congenital heart defect discovered during prenatal evaluation by sonography. Four fetuses showed a complete atrioventricular block, two an atrial flutter, nine ventricular extrasystole, and one a complete irregular heart rate. Five fetuses were suspected to have a congenital heart defect. In all cases magnetocardiograms were recorded. RESULTS: Nine fetuses with extrasystole showed a range of premature atrial contractions, premature junctional beats or premature ventricular contractions. Two fetuses with atrial flutter showed typical flutter waves and four fetuses with complete atrioventricular block showed an uncoupling of P-wave and QRS complex. One fetus showed a pattern suggestive of a bundle branch block. In three of four fetuses with confirmed congenital heart defects the magnetocardiogram showed abnormalities. CONCLUSION: Fetal magnetocardiography allows an insight into the electrophysiological aspects of the fetal heart, is accurate in the classification of fetal arrhythmias, and shows potential as a tool in defining a population at risk for congenital heart defects.

[Ventricular pre-excitation: electrophysiopathology, criteria for interpretation and clinical diagnosis. References for geriatrics]. / La pre-eccitazione ventricolare: elettrofisiopatologia, criteri interpretativi e inquadramento clinico. Riferimenti di Geriatria.

The authors review the state-of-the-art on ventricular pre-excitation in medical and arrhythmological literature in order to facilitate the recognition of the various clinical forms, like classic and occult Wolff Parkinson withe syndrome and Lown Ganong Levine syndrome. A historical introduction reviews our electrophysiopathological knowledge of the electrical activation and conduction of ventricular pre-excitation compared to normal, starting from the anatomic discovery of conduction pathways to the possible use of transesophageal electrostimulation and endocavity mapping to study electric potentials. Avantgarde technologies have also been developed to eliminate anomalous pathways firstly by using a direct current dirscharge and secondly radiofrequency. Atrioventricular electric activation has been widely illustrated in normal subjects in order to create a model for comparison with pathological ventricular pre-excitation: the upper left portion of the septum is no longer the first zone to trigger the kinetic mechanism compared to the early fascicular fraying of the homonymous branch. Instead the upper right part of the septum is activated earlier owing to the anomalous fascia connected on this side to the right branch through their septal arborisations. As a result, this new conduction pathway activates the ventricular masses earlier through an anomalous route, given that there is no further contact with the atrioventricular nodes which act as a control. A similar situation is found in the left branch block where the ventriculogram is late with a normal PR, unlike pre-excitation when an early delta wave is present with a short PR. Electric conduction is also illustrated based on new knowledge of the circuit structures and the rings theory. Orthodromic tachycardia is distinguished from the antidromic form, double accessory pathway tachycardia, ectopic reciprocant atrial fibrillation tachycardia and occult bundle tachycardia which is studied using transesophageal stimulation with a time threshold of 70 ms for ventricular-atrial retrograde activation. The stimulation techniques using single or repeated extrastimulus are explained for this purpose, as well as those with serial extrastimulation and the physical characteristics of the circuit based on the ratio between voltage and resistance. The authors also report the practical aims of electrostimulation for determining the electric threshold of the anomalous circuit in terms of refractoriness, electric atrial stability, reciprocity and the occurrence of the macro re-entry. Lastly, the authors describe electric conduction by anomalous pathways based on the criterion of conduction and activation, both of which are analysed and compared on the basis of the intrinsicoid deflection morphology on the surface ECG: the aberrant qRs usually suggests an antidromic ventricular activation and retrograde conduction between atrium and ventricle, while normal intrinsicoid deflection demonstrates that the activation is orthodromic and the conduction anterograde, namely ventricle-atrial. Having been reproduced in a synoptic synthesis, these manifestations show a regular electrophysiological pattern because they are dissimilar from the behaviour of the monophasic bioelectric potential of the cardiac cells specialised in the conduction of the stimulus, whether they represent a normal or pathological electric pathway. The study is rounded off by the analysis of the reciprocant tachycardias and their re-entry varieties related to the type of the anomalous bundles. A number of types of re-entry can be identified: sinusal re-entry (micro re-entry), atrial re-entry, re-entry in the atrio-ventricular node, re-entry tachycardia and the so-called triggered type. The discussion of the electrophysiopathological aspects of pre-excitation is followed by the clinical forms of ventricular pre-excitation that can be divided into 3 main types. The different ECG clinical pictures are set out in the summary table, together with the type of shunt and activation and possible variants, following Rosenbaum s classic paint: the common type B, the rare type A and a last variant, the C type. This section also describes the positional peculiarities of the Kent-Paladino bundle, the left ventricular, septal (anterior and posterior) and the multiple-bundle ones. The authors also illustrate the criterion and meaning of endocavity mapping in the search for anomalous bioelectric potentials that identify the pathway or the location of the endocardiac bundle and/or foci to be eliminated. A new echocardiographic technique is described with a conventional M mode, digitalised 2D and tissular Doppler which has a comparable ability to identify the anomalous pathways of electric conduction using a non-invasive method. (ABSTRACT TRUNCATED)

Mechanism of spontaneous transition from typical atrial flutter to atrial fibrillation: role of ectopic atrial fibrillation foci.

Paroxysmal AF has been known to be initiated by ectopic beats, especially in the pulmonary veins (PVs), and radiofrequency catheter ablation could cure it. We considered that the spontaneous transition from typical atrial flutter to AF also could be initiated by ectopic beats. Twenty patients (18 men, mean age 66 +/- 14 years) with episodes of spontaneous transition from typical atrial flutter to AF were included in this study. They underwent detailed mapping of both atria. All the patients had spontaneous AF initiated by ectopic beats, and all of them had typical atrial flutter and spontaneous transition from typical atrial flutter (12 patients with counterclockwise atrial flutter and 8 patients with clockwise atrial flutter) to AF. The transition was initiated by ectopic beats from the PVs (17 foci, 85%), crista terminalis (2 foci, 10%), and superior vena cava (1 focus, 5%). After successful ablation of AF foci, typical atrial flutter was induced again, but no spontaneous transition was found after at least 10 minutes of observation. We concluded that paroxysmal AF and spontaneous transition from typical atrial flutter to AF were initiated by ectopic beats, and successful catheter ablation of the ectopic foci can eliminate paroxysmal AF and spontaneous transition from typical atrial flutter to AF.

[Determination of coronary-myocardial reserve by stress echocardiography in patients with programmed pacemaker]. / Opredelenie koronarno-miokardial'nogo rezerva metodom nagruzochnoi ékhokardiografii u bol'nykh s programiruemym élektrostimuliaorom.

AIM: To study coronary-myocardial reserve in patients with a programmed pacemaker. MATERIALS AND METHODS: Stress-echocardiography was performed in 64 patients with coronary heart disease (CHD). The stress was induced by a gradual increase in the frequency of electrostimulation (ES) by 10 imp/min from initial 90 imp/min to threshold value which was defined as the frequency threshold of myocardial ischemia induction (FT). RESULTS: Registration of defects in local left ventricular contractility and cardiodynamics in frequent heart ES identified patients with predominant coronary and myocardial failure. Low FT (100-110 imp/min) indicates poor coronary reserve while a considerable rise of the end diastolic pressure in the left ventricle indicates limited myocardial reserve. Positive results of the test in isolated ventricular ES were obtained in 90.9%, in atrial ES in 72.7% of patients. CONCLUSION: As a highly informative and reproducible method, stress echocardiography can be employed for optimization of antianginal therapy in CHD patients with a pacemaker.

Autologous blood donation before myocardial revascularization: a Holter-electrocardiographic analysis.

The influence of preoperative autologous blood donation on myocardial ischemia and arrhythmias was evaluated in 24 patients scheduled for coronary artery bypass grafting (CABG). All had a Holter recorder placed 24 hours before predonation (day 1), the cassette was changed prior to donation, and the recording continued for 24 hours thereafter (day 2). Each patient served as his or her own control, and observations made on day 2 were compared with those of day 1. Ischemia was quantitated by calculating the duration (C.Dur.) and the area (C. Area) of ischemic ST segment depressions, and ventricular premature beats (VPB) were classified according to the Lown grading system. Twenty-one men and 3 women were monitored. On day 1, 9 patients had 20 ischemic events, 3 being symptomatic. Nine patients demonstrated ischemia on day 2, representing a total of 3 symptomatic and 26 silent events. When comparing the two monitoring periods, 7 patients had longer or more severe ST segment depression whereas 6 other patients presented with more severe VPBs on day 2. Three patients had less ischemia on day 2, one remained stable, and 13 had no ischemia throughout the study. Silent ischemia was significantly more prolonged (C.Dur.Sil 316 v 152 sec, P < 0.05) and more intense (C. Area Sil 8 v 3.8 mm.min, P < 0.05) on day 2. Moreover, on top of a normal circadian distribution of ischemic events in the morning and in the evening, 40% of events were related to the donation or to a trip to the hospital. No preoperative characteristic helped to detect patients at risk.(ABSTRACT TRUNCATED AT 250 WORDS)

[The comparative efficacy of verapamil, nifedipine and propranolol in patients with IHD and an enhanced risk of a fatal outcome]. / Sravnitel'naia éffektivnost' verapamila, nifedipina i propranolola u bol'nykh IBS s povyshennym riskom letal'nogo iskhoda.

In a randomized controlled trial 329 postmyocardial infarction patients with high-grade ventricular extrasystoles were divided into 3 groups. Group 1 of 112 patients received calcium antagonists (verapamil, nifedipine, verapamil+nifedipine), group 2 of 100 patients received propranolol hydrochloride, group 3 consisted of 117 controls. The aim of the study was to elucidate the effect of the above drugs on sudden death and repeated nonfatal infarction risk. The mean follow-up duration made up 16 +/- 0.9, 16.8 +/- 1.1, 20.8 +/- 1.0 months for groups 1,2 and 3, respectively. 35 patients of the treatment groups turned out inappreciable because of early discontinuation of chemotherapy. Overall lethality for the groups 1, 2 and 3 reached 0.9%, 4% and 12% of patients, respectively. Most of lethal outcomes in the controls were sudden. Repeated nonfatal myocardial infarction arose less frequently in groups 1 and 2, but the difference was insignificant.

The effect of superoxide dismutase in the myocardium during reperfusion in the dog.

The aim of the study was to investigate the pathological role of free radicals during myocardial reperfusion. Low (0.5 mg/kg body weight) and high doses (5 mg/kg) of superoxide dismutase (SOD) were infused into the left atrium of mongrel dogs for 4 min starting 29 min after ligation and 1 min before reperfusion of the left anterior descending coronary artery (LAD). Arterial blood pressure, heart rate, electrocardiogram, and the regional contractile force of the left ventricle were monitored throughout the ligation (30 min) and reperfusion periods (20 min). Concentrations of creatine kinase (CK) and malondialdehyde (MDA) in the coronary sinus blood were determined before (0 min) and during ligation (15 and 25 min) and during reperfusion of the LAD (2, 7, and 20 min). In other groups of dogs, the effect of the two doses of SOD on epicardial blood flow was investigated during ligation and reperfusion by the measurement of epicardial temperature using a thermocardiograph. Experimental subjects were mongrel dogs of either sex (n = 25), weight 10-35 kg. Compared to controls (mean +/- SEM, 43.1 +/- 1.2; n = 7), the number of ventricular extrasystoles during the first 5 min of reperfusion was significantly (p < .001) decreased in dogs treated with the high dose (15.01 +/- 2.14; n = 5), but not in those receiving the low dose of the drug (34.6 +/- 5.66; n = 5). The concentrations of CK increased gradually until the end of reperfusion without differences among the different groups. Plasma MDA was the highest in control dogs 7 min after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Synergistic action of postextrasystolic potentiation and diperdipine on left ventricular wall motion abnormalities in coronary heart disease.

The effects on left ventricular function of postextrasystolic potentiation and the dihydropyridinic calcium antagonist diperdipine, alone or in combination, were studied in 14 patients with coronary heart disease by means of two consecutive left ventricular angiographies. To ensure the reproducibility of coupling intervals of the extrasystolic and postextrasystolic beats, the heart was paced during both angiographies. Results showed that postextrasystolic potentiation and diperdipine improved left ventricular ejection fraction to the same degree, but the mechanisms of such an improvement were different and consisted, respectively, of a positive inotropic effect associated with an increase in preload and a slight increase in preload coupled with a marked decrease in afterload. Diperdipine did not abolish the inotropic component of postextrasystolic potentiation, and a combination of the two interventions had additive effects on the improvements in left ventricular ejection fraction and regional wall motion analyzed by the centerline method. Ventricular segments that were normokinetic or hypokinetic during the control basal cycle responded equally to postextrasystolic potentiation and to diperdipine, whereas the former intervention alone had no significant effect on akinetic segments. Diperdipine restored the responsiveness of akinetic segments to postextrasystolic potentiation, a finding that, although it remains to be confirmed by independent techniques, may be interpreted as a possible consequence of improved calcium metabolism or coronary flow in ischemic but still viable myocardium. However, it is concluded that the calcium antagonist revealed a contractile reserve in most of the severely asynergic areas, which would have otherwise been judged to be irreversibly damaged on the basis of the unresponsiveness to postextrasystolic potentiation alone.

Real time recognition of complete atrioventricular blocks.

Common heart arrhythmia monitors are limited to the electrical activity of the ventricles. Severe cardiac malfunctions exhibit typical defects of atrioventricular conduction which often can be efficiently treated with medicine or electrotherapy. The method described here enables the detection of complete atrioventricular blocks and may be used for the improvement of arrhythmia monitoring.

[Ca2+]i transients in the cardiomyopathic hamster heart.

Intracellular [Ca2+] transients were studied in isolated hearts of healthy and cardiomyopathic hamsters in late failure perfused with glucose or pyruvate. Hearts of healthy hamsters developed similar pressures when perfused with either glucose or pyruvate, and [Ca2+]i transients were comparable in amplitude when perfused with either substrate. On the other hand, hearts of cardiomyopathic hamsters in late failure developed normal pressure when perfused with pyruvate but developed depressed pressure (50%) when perfused with glucose. The amplitude of [Ca2+]i transients fell severely and was associated with a high diastolic [Ca2+]i in cardiomyopathic hamster hearts when the perfusate was switched from pyruvate to glucose. The high phosphomonoester sugars as evidenced by 31P nuclear magnetic resonance studies and the depressed oxygen consumption in the cardiomyopathic hamster hearts perfused with glucose reflect an inhibition in glycolysis and a subsequent decrease in mitochondrial activity. Without an adequate delivery of substrate to the mitochondria in the cardiomyopathic hamster, the myocardium is no longer capable of maintaining its [Ca2+]i homeostasis.