The incidence of cardiac arrhythmias during exercise stress testing: a focus on patients with severe obesity undergoing sleeve gastrectomy.

INTRODUCTION: Obesity is associated with a higher risk of cardiac arrhythmias. Sleeve gastrectomy (SG) is a common bariatric surgery with beneficial effects on weight loss and comorbidities. The study aimed to investigate the prevalence of arrhythmias during maximal exercise testing in patients with moderate-severe obesity and to evaluate the impact of SG on these arrhythmic events. METHODS: All patients with moderate or severe obesity who were considered suitable candidates for SG between June 2015 and September 2020 were recruited. Each patient underwent three incremental, maximal, ECG-monitored cardiopulmonary exercise test 1 month before and 6 and 12 months after SG; the frequency and complexity of ventricular premature beats (VPBs) and atrial premature beats (APBs) have been evaluated during rest, exercise and recovery phases. RESULTS: Fifty patients with severe obesity (BMI 46.39 ± 7.89 kg/m2) were included in the study. After SG, patients presented a decreased BMI (34.15 ± 6.25 kg/m2 at 6 months post-SG and 31.87 ± 5.99 kg/m2 at 12 months post-SG). At 6 months post-SG, an increase in VPBs, mainly during the recovery phase, was observed. At 12 months post-SG, a reduction in VPBs compared with the 6 months evaluation was showed. CONCLUSION: Although in the early post-surgical phase the risk of exercise-induced arrhythmias may be higher, SG does not seem to increase the occurrence of arrhythmias in the long-term. No life-threating arrhythmias were found during post-SG evaluations.

Cryptogenic Stroke In The Context of Pandemic-Related Stress: The Role of Arterial Hemodynamics.

BACKGROUND: Up to 45% of ischemic strokes are cryptogenic, which is an impediment to proposing preventative measures. In this investigation we aimed to study underlying heart arrhythmias in patients with cryptogenic stroke, taking into consideration the context of the COVID-19 pandemic and stressful lockdown conditions. SUBJECTS AND METHODS: In this cross-sectional study we observed 52 patients with cryptogenic stroke >1 month after acute presentation, and a control group consisting of 88 patients without stroke. All patients undewent the laboratory and instrumental investigation consisting of the following: lipid spectrum; hemostasiograms; hemoglobin A1c; transthoracic or/and transesophageal echocardiography; 24-hours monitoring of ECG; computer tomography or magnetic resonance imaging of the brain. We studied the hemodynamics of the common carotid arteries using Doppler ultrasound imaging and digital sphygmography (SG). RESULTS: The groups were indentical with respect to the preponderance of study parameters (sex, age, comorbidities, instrumental and laboratory data). The ischemic stroke group had a statistically significant difference in the prevalence of the first type of extrasystolic arrhythmia according to our gradation of extrasystoles, which are ventricular systoles of extrasystolic contraction appearing before the transmitral blood flow peak (peak E in echocardiography). We observed that earlier ventricular systoles of extrasystole in the cardiac cycle predicted for greater growth of hemodynamic and kinetic parameters. Calculating the indices of a four-field table established the significant relationship between the moment of appearance of extrasystolic ventricular contraction in the cardiac cycle and the risk for cryptogenic stroke (normalized value of the Pearson coefficient (C`) of the two paramaters was 0.318). CONCLUSIONS: Extrasystolic arrhythmia appeared as an additional risk factor of earlier stroke. The most dangerous type of arrhythmia was when the ventricular contraction of the extrasystole appeared before the transmitral blood flow peak in the cardiac cycle. This observation could present a risk-marker for brain-related cardiovascular complications such as stroke, which might be patients suffering from different internal diseases, especially in the context of environmental stress conditions of the current pandemic and its related lockdown measures.

Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2.

Extrasystoles lead to several consequences, ranging from uneventful palpitations to lethal ventricular arrhythmias, in the presence of pathologies, such as myocardial ischemia. The role of working versus conducting cardiomyocytes, as well as the tissue requirements (minimal cell number) for the generation of extrasystoles, and the properties leading ectopies to become arrhythmia triggers (topology), in the normal and diseased heart, have not been determined directly in vivo. Here, we used optogenetics in transgenic mice expressing ChannelRhodopsin-2 selectively in either cardiomyocytes or the conduction system to achieve cell type-specific, noninvasive control of heart activity with high spatial and temporal resolution. By combining measurement of optogenetic tissue activation in vivo and epicardial voltage mapping in Langendorff-perfused hearts, we demonstrated that focal ectopies require, in the normal mouse heart, the simultaneous depolarization of at least 1,300-1,800 working cardiomyocytes or 90-160 Purkinje fibers. The optogenetic assay identified specific areas in the heart that were highly susceptible to forming extrasystolic foci, and such properties were correlated to the local organization of the Purkinje fiber network, which was imaged in three dimensions using optical projection tomography. Interestingly, during the acute phase of myocardial ischemia, focal ectopies arising from this location, and including both Purkinje fibers and the surrounding working cardiomyocytes, have the highest propensity to trigger sustained arrhythmias. In conclusion, we used cell-specific optogenetics to determine with high spatial resolution and cell type specificity the requirements for the generation of extrasystoles and the factors causing ectopies to be arrhythmia triggers during myocardial ischemia.

Slow antegrade excitation and delayed retrograde activation through an "inexcitable zone": A basis for arrhythmia formation in infarcted myocardium ex vivo.

INTRODUCTION: The electrophysiologic mechanism for rate-dependent PVBs associated with double potentials (DPs) was investigated in infarcted canine hearts using bipolar and intracellular microelectrode recordings. METHODS AND RESULTS: Dogs exhibiting rate-related ventricular ectopic beats (coupling interval, 390 ± 54 milliseconds) during sinus rhythm or atrial pacing were studied 4-5 days (N = 63) or 25 days (N = 16) following anterior descending coronary artery ligation. Sites of DP and rate-dependent arrhythmia formation were identified in vivo using bipolar recordings for subsequent ex vivo studies. Rate-dependent conduction delays with increasing duration isoelectric intervals representing very slow conduction were observed at sites of DP formation, frequently provoking both manifest and concealed reentry (non-stimulated beats) over a narrow range of paced cycle lengths. Both slow antegrade and retrograde activation across an inexcitable gap (reflection) were integral components of extrasystole formation. Retrograde reflection to a region of very slow conduction (mid-potential) during antegrade activation was routinely observed at 4-5 days (42 of 63 preparations, 67%) and 25 days (22 of 26 preparations, 85%) postcoronary artery ligation. Reflection and premature re-activation of the proximal site was then observed in 6 of 63 (9%), and 3 of 26 preparations (12%). CONCLUSION: The present experiments demonstrate DP formation and rate-dependent constant-coupled late epicardial premature beats in infarcted dog hearts. Microelectrode recordings at DP sites demonstrating prolonged isoelectric intervals display very slow conduction preceding distal activation and "reentrant" re-activation of more proximal sites, representing reflection as an arrhythmia mechanism in ischemically injured epicardium during subacute myocardial infarction.

Different Impacts of Atrial Fibrillation and Cardiac Premature Contractions on the Health-Related Quality of Life in Elderly People: The Yilan Study.

Atrial fibrillation (AF) is currently recognized as one of the most common cardiac arrhythmias worldwide, with the increasing prevalence that has been estimated to be as high as 9% among the elderly. Health-related quality of life (HRQoL) has become an important patient-centered health outcome measurement, but the impacts created by AF and other arrhythmias with similar symptoms, such as frequent atrial and ventricular premature contractions (APCs and VPCs, defined as ≥ 3 beats/5 minutes), have not been extensively evaluated. The Yilan Study is a population-based community health survey, which in part aims to evaluate the prevalence and impacts of these arrhythmias on the HRQoL in a community dwelling elderly population. A total of 1,732 citizens from the Yilan, Taiwan, aged 65 years or older (45.8% male) were enrolled and visited at their homes, where HRQoL was measured utilizing the Short Form-12 Health Survey. Each participant's heart rhythm was recorded with an electrocardiographic monitor for 5 minutes. The results disclosed that the prevalence of AF of this aged population was 5.8%, similar to the mean global prevalence. Besides, the prevalence of frequent APCs and frequent VPCs in these elderly people were 7.1% and 5.5%, respectively. After multiple regression analysis, elderly people with AF had lower scores in the physical component of HRQoL, while those elderly people with frequent VPCs had lower scores in the mental component. Ultimately, these findings can provide additional useful and population-specific information about AF, and assist medical professionals in designing more effective strategies for cardiac arrhythmia treatments.

Dantrolene suppresses ventricular ectopy and arrhythmogenicity with acute myocardial infarction in a langendorff-perfused pacing-induced heart failure rabbit model.

INTRODUCTION: Dantrolene prevents arrhythmogenic Ca(2+) release during heart failure (HF). However, direct evidence to support its antiarrhythmic effects in failing hearts with acute myocardial infarction (AMI) is lacking. METHODS AND RESULTS: HF was induced by right ventricular pacing (312 beats/min, 4 weeks) in 19 rabbits. AMI was induced by coronary artery ligation in rabbits surviving chronic pacing (n = 17). The hearts were quickly excised and Langendorff-perfused for simultaneous membrane potential and intracellular Ca(2+) (Cai ) optical mapping when ventricular fibrillation (VF) occurred or 4 hours after AMI. The VF inducibility was defined as the ability to provoke sustained VF (>2 minutes) by pacing. Dantrolene (10 µM) was administered after baseline studies. Spontaneous VF occurred in 5 rabbits (SVF group). The ventricular premature beat (VPB) burden was significantly higher in the SVF group than the non-SVF group (P < 0.05). Dantrolene suppressed VPB burden (P = 0.03) and prolonged action potential duration (APD; P < 0.05) to reduce VF inducibility (P < 0.05). However, dantrolene shortened immediate postshock APD50 even if VF storm was suppressed. CONCLUSION: In failing hearts with AMI, VPB burden plays a pivotal role in SVF occurrence. Dantrolene suppresses VPBs and/or prolongs repolarization to inhibit spontaneous VF and reduce VF inducibility.

Alternating Early Afterdepolarizations Underlying Bradycardia-Dependent Macroscopic T Wave and Discordant Mechanical Alternans.

BACKGROUND: Macroscopic T wave alternans (macro-TWA) often heralds the onset of Torsades de Pointes in patients with QT prolongation. However, the mechanisms underlying macro-TWA remain unclear. We examined the cellular and ionic basis for macro-TWA in rabbits with left ventricular hypertrophy (LVH). METHODS: The renovascular hypertension model was used to induce LVH in rabbits. Action potentials were simultaneously recorded from epicardium and endocardium together with a transmural ECG and isometric contractility in arterially perfused left ventricular wedges. Late sodium current (INa-L) was recorded in single-isolated left ventricular myocytes with the whole cell patch-clamp technique. RESULTS: Macro-TWA and accompanied mechanical alternans occurred spontaneously in 8 of 33 LVH rabbits (P<0.05, versus 0/15 in controls) and were induced by an INa-L enhancer ATX-II at 1 to 3 nM in additional 7. Macro-TWA and mechanical alternans occurred discordantly, that is, that longer QT interval and larger T wave were associated with weaker isometric contvractility. Alternating early afterdepolarizations in the endocardium caused macro-TWA in 12 of 15 LVH rabbits and, therefore, early afterdepolarization-dependent R-from-T extrasystoles and Torsades de Pointes always originated from the beats with longer QT and larger T wave during macro-TWA. INa-L density was significantly larger in LVH myocytes than that of control myocytes. Macro-TWA, mechanical alternans, R-from-T extrasystoles, and Torsades de Pointes were all abolished by INa-L blocker ranolazine or mexiletine. CONCLUSIONS: LVH enhances INa-L density and promotes alternating early afterdepolarizations in the left ventricular endocardium that manifest as macro-TWA with discordant mechanical alternans. INa-L blockade abolishes macro-TWA, mechanical alternans, early afterdepolarization-dependent R-from-T extrasystoles, and Torsades de Pointes.

Successful catheter cryoablation of Hisian ectopy using 2 new diagnostic criteria based on unipolar and bipolar recordings of the His electrogram.

We describe the case of a 61-year-old woman who underwent successful catheter cryoablation of a symptomatic Hisian ectopy. Diagnosis was based on features of the HV interval assessed from a bipolar recording during mapping. The location of the arrhythmic focus was identified using simultaneous unipolar and bipolar recordings of the His electrogram. This case report highlights the use of 2 new criteria for the diagnosis and mapping of Hisian ectopy, and the successful use of cryothermia for the ablation of extrasystoles arising from the His bundle.

Inferior Vena Cava as a Trigger for Paroxysmal Atrial Fibrillation: Incidence, Characteristics, and Implications.

BACKGROUND: Identifying nonpulmonary vein triggers during atrial fibrillation (AF) ablation is of great importance. Currently, there are limited data on AF triggered by the inferior vena cava (IVC). OBJECTIVES: This study was performed to investigate the incidence, characteristics, and implications of IVC triggers for AF. METHODS: A total of 661 patients who underwent initial paroxysmal AF ablation were included. After pulmonary vein isolation, ectopic beats that triggered AF were further studied. Activation mapping and angiography were performed to confirm the location of ectopic origin. Electrocardiographic analysis of the ectopic P-wave (P'-wave) was performed. RESULTS: Six patients (0.91%) with AF triggered by the IVC were confirmed. The mean distance from the earliest activation site to the IVC ostium was 6.8 ± 2.5 mm (5.2 to 11.2 mm). Furthermore, the arrhythmogenic foci within the IVC were all located at the apical hemisphere of the IVC (3 at the septal side and 3 at the anterior side). A total of 2.3 ± 0.5 applications of radiofrequency energy were delivered to eliminate IVC triggers. The mean duration of the P' wave was 91.2 ± 11.2 milliseconds (81 to 108 milliseconds), which was narrower than that of the sinus P-wave (115.2 ± 19.3 milliseconds [87 to 139 milliseconds]; P = 0.002). Moreover, the configuration of all P' waves in the inferior leads was negative. During a mean follow-up period of 25.5 ± 7.3 months, all 6 patients remained arrhythmia free without antiarrhythmic drugs. CONCLUSIONS: IVC trigger, a rare but latent source of paroxysmal AF, could be identified and safely eliminated by focal radiofrequency ablation. Ectopic beats originating from the IVC presented with narrow P'-wave duration and negative P' waves in all inferior leads.

Circa(ultra)dians of single extrasystoles in chronic respiratory failure versus health at lowland.

BACKGROUND: The circa- and ultradians of the single extrasystoles' frequency in patients with chronic respiratory insufficiency (CRI) in lowlands (Kosice 210 m) were studied by the testing of following null hypotheses: their average frequency as well as rhythmicity is the same as at health. METHODS: In 54 elderly males with CRI, mean numbers of supraventricular (SV) and ventricular (VE) extrasystoles were calculated for each 24 hours. The Halberg cosinor regression was used to test the presence of the 24-hour rhythm and its 2nd to 10th harmonics, i.e. ultradians with the period lengths of 12 to 2.4 hours. The resulting approximating function for either extrasystole type included its point, 95% confidence for mean and 95% tolerance for one individual. The results were compared with those obtained at health at alpha = 0.05. RESULTS: The daily mesors in CRI were 20.9 for SV, for VE 17.6 extrasystoles per hour and subject. This was significantly (20.3 (SV) and 17.0 (VE)) higher than at health. Significant periodic harmonic components were 3 in CRI versus 6 at health for SV and 6 in CRI versus 1 at health for VE. The dominating CRI rhythm was the 8 hour ultradian for SV and circadian for VE while at health the circadian rhythm was leading for every type of extrasystoles. CONCLUSION: The most remarkable effect of CRI versus health at lowlands is a marked increase of the frequency of every type of extrasystoles. SV extrasystoles exert more rhythmicity at health while the VE in disease (Tab. 1, Fig. 1, Ref. 20).

Fetal extrasystole may predict poor neonatal outcome.

Extrasystoles particularly premature atrial contractions noted during labour on the fetal heart rate monitoring strip are usually thought to be benign. In pregnancies complicated by fetal infection and/or the fetal inflammatory response syndrome, there are some data that extrasystoles noted during the intrapartum period may be related to neonatal sepsis and eventual poor neonatal outcome including death or neonatal encephalopathy. Additional observations are needed to substantiate this hypothesis.

Predictive power of increased QT dispersion in ventricular extrasystoles and in sinus beats for risk stratification after myocardial infarction.

BACKGROUND: QT dispersion, commonly measured in sinus beats (QTd-S), can also be calculated in premature ventricular beats (QTd-V). To date, no studies have addressed the relation between these 2 variables. METHODS AND RESULTS: In 148 patients with remote myocardial infarction and premature ventricular beats on a routine ECG, QT dispersion, defined as the difference between the maximum and the minimum QT interval across the 12-lead ECG, was calculated separately for the ventricular extrasystole and the preceding sinus beat. In the total group of patients, QTd-V was greater than QTd-S (83+/-33 versus 74+/-34 ms, respectively; P=0.001). During a follow-up period of 35+/-17 months, arrhythmic events (sustained ventricular tachycardia, ventricular fibrillation, or sudden death) were noted in 30 patients. A QTd-V of >/=100 ms was a stronger univariate marker of arrhythmic events than was a QTd-S of >/=100 ms, and multivariate analysis selected only prolonged QTd-V (hazard ratio 3.81, 95% CI 2.2 to 11.2) and low ejection fraction (hazard ratio 3.05, 95% CI 1.6 to 7.6) as independent predictors of arrhythmic events. CONCLUSIONS: The magnitude of QTd-V was greater than that of QTd-S in the total group of patients. Prolonged QTd-V is associated with a significantly increased risk for arrhythmic events in postinfarction patients, and the prognostic significance of QTd-V exceeds that of QTd-S.

Pulmonary vein morphology in patients with paroxysmal atrial fibrillation initiated by ectopic beats originating from the pulmonary veins: implications for catheter ablation.

BACKGROUND: Successful ablation of ectopic beats originating from the pulmonary veins (PV) could eliminate paroxysmal atrial fibrillation (PAF). However, information about the structure of the PV in patients with PAF that is initiated by PV ectopic beats has not been reported. METHODS AND RESULTS: We studied the morphology of the PVs and measured their diameters in 3 groups of patients. Group I included 52 patients (aged 66+/-14 years; 44 men) with focal atrial fibrillation (AF) from the PVs. Group II included 8 patients (aged 50+/-10 years; 3 men) with focal AF from the superior vena cava or cristal terminalis. Group III included 23 control patients (aged 55+/-16 years; 17 men). Of the control patients, 11 had AV node and 12 had AV reentrant tachycardia. After an atrial transseptal procedure, selective PV angiography using a biplane system with a right anterior oblique view of 30 degrees, a left anterior oblique view of 60 degrees, and a cranial angle of 20 degrees was performed. The ostial and proximal portions of the right and left superior PVs (RSPV and LSPV) were significantly dilated in group I patients compared with those in groups II and III. Furthermore, the ostia of the RSPV and LSPV were significantly dilated in group II compared with group III patients. However, the mean diameters of the inferior PVs were similar between the 3 groups. Comparisons of the individual PV diameters among the 3 subgroups of group I (which was divided according to where the ectopic focus was located) showed nonselective dilatation of the PV. CONCLUSIONS: Nonspecific dilatation of the ostia and proximal portion of superior PVs were found in patients with PAF initiated by ectopic beats from the superior PVs.

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.

Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation.

BACKGROUND: The Brugada syndrome is characterized by marked ST-segment elevation in the right precordial ECG leads and is associated with a high incidence of sudden and unexpected arrhythmic death. Our study examines the cellular basis for this syndrome. METHODS AND RESULTS: Using arterially perfused wedges of canine right ventricle (RV), we simultaneously recorded transmembrane action potentials from 2 epicardial and 1 endocardial sites, together with unipolar electrograms and a transmural ECG. Loss of the action potential dome in epicardium but not endocardium after exposure to pinacidil (2 to 5 micromol/L), a K(+) channel opener, or the combination of a Na(+) channel blocker (flecainide, 7 micromol/L) and acetylcholine (ACh, 2 to 3 micromol/L) resulted in an abbreviation of epicardial response and a transmural dispersion of repolarization, which caused an ST-segment elevation in the ECG. ACh facilitated loss of the action potential dome, whereas isoproterenol (0.1 to 1 micromol/L) restored the epicardial dome, thus reducing or eliminating the ST-segment elevation. Heterogeneous loss of the dome caused a marked dispersion of repolarization within the epicardium and transmurally, thus giving rise to phase 2 reentrant extrasystole, which precipitated ventricular tachycardia (VT) and ventricular fibrillation (VF). Transient outward current (I(to)) block with 4-aminopyridine (1 to 2 mmol/L) or quinidine (5 micromol/L) restored the dome, normalized the ST segment, and prevented VT/VF. Conclusions-Depression or loss of the action potential dome in RV epicardium creates a transmural voltage gradient that may be responsible for the ST-segment elevation observed in the Brugada syndrome and other syndromes exhibiting similar ECG manifestations. Our results also demonstrate that extrasystolic activity due to phase 2 reentry can arise in the intact wall of the canine RV and serve as the trigger for VT/VF. Our data point to I(to) block (4-aminopyridine, quinidine) as an effective pharmacological treatment.

Relation between ventricular arrhythmia and sudden cardiac death in patients with acute myocardial infarction: the predictors of ventricular fibrillation.

Continuous electrocardiographic monitoring was recorded in 102 patients during the first 48 hours after the onset of myocardial infarction. One hundred forty-eight episodes of ventricular tachycardia having an ectopic rate of 180/min or more and without a background of treatment with antiarrhythmic drugs were analyzed; these included 125 cases of ventricular tachycardia that terminated spontaneously and 23 cases that deteriorated to ventricular fibrillation. Episodes of ventricular tachycardia with a polymorphic configuration were more frequent in the group with than in the group without ventricular fibrillation (30.4 and 8%, respectively). The incidence of ventricular tachycardia continuing for more than 100 QRS complexes was 20 times greater in the group with ventricular fibrillation, and ventricular tachycardia initiated by and R on T ventricular premature beat was recorded three times more often in this group. The 10 minute pretachycardia interval in both groups showed no significant difference in the incidence, complexity, intensity or dynamic pattern of ventricular premature contractions. The data provide reason to doubt the significance of ventricular premature beats as harbingers of sudden death from ventricular fibrillation. Rather, ventricular tachycardia with an ectopic rate of 180/min or more, a polymorphic configuration and persistence for more than 100 QRS complexes (or initiated by an R on T ventricular premature beat) is a more reliable predictor of the occurrence of ventricular fibrillation.

Effect of postextrasystolic potentiation on systolic bulging of ischemic myocardium.

Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined. By 5 min after the left anterior descending coronary artery was occluded, there was regional bulging. Postextrasystolic potentiation diminished the extent of bulging by increasing both isovolumic and ejection percent systolic shortening (isovolumic -9.1 +/- 2.0% to -5.9 +/- 1.7%, p less than 0.008; ejection 2.2 +/- 0.7% to 4.3 +/- 2.0%, p less than 0.008). The tension-length loops after coronary occlusion showed an exponential upstroke and almost superimposed downstroke consistent with passive movement. The loops were unchanged by postextrasystolic potentiation. Wall tension data showed that bulging was reduced because of a shift down the tension-length curve as end-systolic wall tension was reduced by augmented nonischemic contraction. Similar results were seen at 60 min of coronary occlusion. This study demonstrates that the decrease in bulging seen with postextrasystolic potentiation is due to changes in loading conditions and not to contractile reserve.

Spontaneous sustained ventricular tachycardia in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) Trial.

OBJECTIVES: We compared the QRS waveforms of the initial and subsequent complexes of spontaneous sustained monomorphic ventricular tachycardia and the rhythm induced at electrophysiologic study to test the theory that premature ventricular complexes "trigger" spontaneous ventricular tachycardia and that a stable substrate exists such that the spontaneous arrhythmia can be reproduced at electrophysiologic study. BACKGROUND: Failure rates have been high in several recent studies in which prevention of ventricular tachyarrhythmias was guided by suppression of premature ventricular complexes or induced ventricular tachycardias. METHODS: Digital waveform analysis was used to distinguish events of ventricular tachycardia initiated by configurationally distinct, possibly triggering, complexes (type 1) from events in which the initial QRS waveforms were identical to subsequent complexes, suggesting no requirement for premature ventricular beats (type 2). RESULTS: Of 1,102 episodes of spontaneous ventricular tachycardia, 73 (6.6%) were type 1; 1,012 were type 2 (91.8%); and 17 (1.5%) were uncertain. Of 59 patients only 14 (24%) had only type 1 episodes (group 1), whereas 37 patients (63%) had predominantly type 2 events (group 2) (p < 0.0001). Sustained ventricular tachycardia was inducible in all group 1 patients, and in most (57%) the induced rhythm was similar to the spontaneous rhythm. Ventricular tachycardia could not be induced in 7 patients from group 2 (19%), and in 18 patients (49%) the induced and spontaneous rhythms were dissimilar. Recurrence of arrhythmia rates differed according to the guidance method in group 2. CONCLUSIONS: Discrepancies between observed and predicted modes of initiation of ventricular tachycardia and between spontaneous and induced rhythms could result in inappropriate guidance and subsequent failure of antiarrhythmic treatment.

Relation between myocardial injury and postextrasystolic potentiation of regional function measured by two-dimensional echocardiography.

An experimental study was designed to validate postextrasystolic potentiation assessment of myocardial viability or functional reserve of cardiac segments after acute coronary occlusion. Segmental systolic fractional area changes and wall thickening in pacing-induced postextrasystolic beats were mapped in 12 closed chest dogs by two-dimensional echocardiography during a control period and from 20 minutes to 3 hours after occlusion of the left anterior descending coronary artery. The extent of myocardial ischemic and necrotic zones was evaluated in left ventricular slices and subsegements corresponding to echographic cross sections. During two-dimensional echocardiography, left ventricular segments that were found to be neither ischemic nor necrotic always exhibited a significant augmentation of both fractional area change and wall thickening during the postextrasystolic beat that followed an induced premature contraction with a 42.4% coupling interval. In segments without necrosis but with varying degrees of ischemia, significant postextrasystolic potentiation was also demonstrated, even after 3 hours of occlusion. In contrast, segments that developed more than 80% necrosis failed to potentiate systolic fractional area change after 2 hours, and systolic wall thickening, even after 20 minutes of coronary occlusion. Statistical evaluation revealed a characteristic threshold at 41 to 60% necrosis, beyond which no potentiation of function could be elicited 3 hours after occlusion. Extrapolation from the experimental data suggests that when two-dimensional echographic studies in myocardial ischemia indicate postextrasystolic augmentation of segmental left ventricular function, the latter segments may be assumed to contain only small infarcts or to consist of reversibly ischemic and normal myocardium. Conversely, segments that fail to exhibit postextrasystolic potentiation can be assumed to be more than 60% necrotic.

Tachycardia- and bradycardia-dependent atrioventricular block: observations regarding the mechanism of block.

A case of paroxysmal bradycardia- and tachycardia-dependent atrioventricular (AV) block is described in a patient with right bundle branch block. The His bundle recordings demonstrated the site of the AV block to be distal to the His bundle recording site (probably in the left bundle branch). Whereas AV block distal to the His bundle occurred at an atrial paced cycle length of 700 ms, intact ventriculoatrial (VA) conduction was present up to a ventricular paced cycle length of 400 ms. Resumption of AV conduction was dependent on a critical HH or RH (in case of escapes) interval. These findings suggest that the bradycardia-dependent block is related to a time-dependent decrease in the amplitude of the current intensity of the proximal segment during late diastole. Spontaneous diastolic depolarization during late diastole resulted in impaired anterograde (AV) conduction but facilitated retrograde (VA) conduction. These findings are consistent with experimental "in vitro" observation in the sucrose gap model of AV block.