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PubMed2006

Unsupervised classification of ventricular extrasystoles using bounded clustering algorithms and morphology matching.

Ventricular extrasystoles (VE) are ectopic heartbeats involving irregularities in the heart rhythm. VEs arise in response to impulses generated in some part of the heart different from the sinoatrial node. These are caused by the premature discharge of a ventricular ectopic focus. VEs after myocardial infarction are associated with increased mortality. Screening of VEs is typically a manual and time consuming task that involves analysis of the heartbeat morphology, QRS duration, and variations of the RR intervals using long-term electrocardiograms. We describe a novel algorithm to perform automatic classification of VEs and report the results of our validation study. The proposed algorithm makes use of bounded clustering algorithms, morphology matching, and RR interval length to perform automatic VE classification without prior knowledge of the number of classes and heartbeat features. Additionally, the proposed algorithm does not need a training set.

Algorithms↗
PubMed1978

Post-extrasystolic potentiation of ischemic myocardium by atrial stimulation.

The response of acutely ischemic myocardium to post-extrasystolic potentiation (PESP) was evaluated in 11 mongrel dogs. Mercury-in-silastic length gauges were sutured to the epicardial surface of the left ventricle; left ventricular pressure was determined via an apical large-bore catheter-transducer system and controlled by volume manipulation. The anterior descending coronary artery was then ligated, and single premature atrial contractions were introduced via an external stimulator. Thirty minutes after occlusion, shortening during ejection had decreased an average of 81 +/- 8 per cent, from 1.30 +/- 0.29 to 0.32 +/- 0.05 mm. PESP initially induced a marked restoration toward normal segmental contraction as systolic shortening increased significantly to 1.14 +/- 0.23 mm. Additionally, paradoxic systolic expansion, when present, reverted to a normal pattern of contraction during PESP. Responsiveness to PESP deteriorated progressively with time over 3 hours following occlusion until the muscle became essentially totally unresponsive to this stimulus. It is concluded that a single premature atrial beat may be used to induce PESP and provides an effective stimulus for contractile reserve of acutely dysfunctional ischemic myocardium. Loss of responsiveness to PESP may represent the progression to nonviability following acute ischemia.

Animals↗
PubMed1983

Interactions among heart rate, autonomic activity, and arterial pressure upon the multiple repetitive extrasystole threshold in the dog.

The effects of heart rate, autonomic stimulation, and arterial blood pressure upon the multiple repetitive extrasystole threshold (MRET) were studied after coronary occlusion in anesthetized dogs. The MRET was unaffected by changes in heart rate. Sympathetic stimulation alone reduced the MRET from 52.4 +/- 3.7 (mean +/- SEM) to 41.3 +/- 2.7 mA. Vagal stimulation alone was without effect. During simultaneous sympathetic and vagal stimulation the threshold was 48.7 +/- 3.0 mA. This supports the contention that vagal activity serves mainly to oppose the tendency for sympathetic activity to lower the MRET. Reduction of blood pressure significantly decreased the average MRET from 38.6 +/- 2.5 to 34.4 +/- 1.8 mA. The presence of a post junctional site for the observed sympathetic-vagal interaction was investigated using isoproterenol infusion and vagal stimulation. Infusion of isoproterenol lowered the MRET. Vagal stimulation in this situation raised the MRET; the effect varied directly with the rate of isoproterenol infusion. This suggests that part of the vagal effect is exerted postjunctionally; that is, directly upon the myocardial cell and not merely by inhibition of adrenergic transmitter release at sympathetic nerve endings.

Adrenergic Fibers↗
PubMed1984

Prevention by a carbacyclin analogue (ZK 36 374) of digoxin-induced ventricular extrasystoles in guinea-pig myocardium.

Intravenous infusion of ZK 36 374 to the anesthetized guinea-pig or addition of the compound to the perfusion medium of the isolated perfused guinea-pig heart prevented digoxin-induced ventricular premature beats without altering the prolongation of the P-R interval by the glycoside. The prevention by ZK 36 374 of the ventricular extrasystoles induced by digoxin was obtained at lower concentrations while higher doses of the compound produced a dysrhythmic effect which terminated within a few min after the cessation of drug application.

Anesthesia↗
PubMed1990

Post-extrasystolic potentiation and the force-frequency relationship: differential augmentation of myocardial contractility in working myocardium from patients with end-stage heart failure.

We studied post-extrasystolic potentiation (PESP) and frequency potentiation (FP) of human working myocardium isolated from the ventricles of 10 patients with end-stage heart failure (CHF) and 17 non-failing controls (CTL). The contractility index was peak isometric tension developed in vitro by trabeculae carneae (CTL n = 34, CHF n = 31); programmed electrical stimulation was used to initiate as well as alter the timing relationship of the contractile events. While holding constant the total number of contractions per unit of time, we compared the augmentation of contractile performance that occurred upon doubling the stimulation frequency (FP) to that of changing the stimulation pattern (PESP). In the CTL group we found that FP and PESP differed in their ability to augment cardiac contractile performance, PESP being more effective; 105 +/- 13% for PESP vs. 34 +/- 11% (mean +/- S.E.M.) for FP. In the CHF group, the inotropic response to PESP was similar to CTL; in contrast, the relative efficacy of FP (3 +/- 3%) compared to PESP (81 +/- 14%) was markedly diminished. Studies with positive inotropic agents revealed that the percent change in contractility induced by FP and PESP depends upon the relative inotropic state of the heart; however, the contractile response to PESP always equaled or exceeded those produced by clinically relevant concentrations of inotropic agents, particularly in CHF muscles. Agents that increase intracellular levels of adenosine 3',5'-cyclic monophosphate reversed the FP abnormalities seen in the CHF group, suggesting that deficient production of this second messenger in heart failure may cause the abnormal force-frequency relationship in failing myocardium. We conclude that the differential responses of myopathic muscle to PESP and FP may be caused by abnormal restitution processes during diastole. Our results suggest that PESP may be an effective therapeutic modality for patients with severe heart failure who have failed to adequately respond to inotropic drugs, and may serve as a useful indicator of cardiac contractile reserve in these patients.

Assisted Circulation↗
PubMed1994

Intracellular calcium transients in potentiated contractions induced by multiple extrasystolic beats in isolated perfused rat hearts.

Mechanisms underlying contractile potentiation induced by multiple extrasystolic contractions (ESC) were evaluated with surface fluorometry in isolated perfused rat hearts loaded with Indo-1/AM. After baseline pacing with a 400 ms interval, 1-25 ESC were interposed with a regular 160 ms interval followed by the postextrasystolic beat with a 400 ms interval. With an increase in the ESC number, left ventricular developed pressure and peak positive dP/dt increased in an exponential manner, reaching a plateau, that was the same for 3 extracellular Ca2+ ([Ca2+]o; 0.55 (n = 9), 1.25 (n = 11) and 2.75 mM (n = 7). Increased [Ca2+]o shifted this relationship left and upward, and with 2.75 mM [Ca2+]o developed pressure and dP/dt decreased after the maximum potentiation was obtained. The relationship between the ESC number and the amplitude of the Indo-1 fluorescence (F400/F510; an index of intracellular Ca2+ ([Ca2+]i)) was also exponential and was shifted left and upward by high [Ca2+]o; however, it lacked the declining phase. Thus, the relationship between the amplitude of F400/F510 and developed pressure or dP/dt consisted of a positively linear part until the maximum potentiation was obtained and a negatively linear part with a further increase in the amplitude of F400/F510. This observation suggests that although contractile potentiation is mediated by increased [Ca2+]i transients, the maximum response might be determined by the responsiveness of the sarcomere.

Animals↗
PubMed1995

Contractile and intracellular Ca2+ decay in potentiated contractions following multiple extrasystolic beats.

Developed pressure and intracellular Ca2+ ([Ca2+i) decay in postextrasystolic beats following multiple extrasystolic contractions (ESCs) was evaluated with surface fluorometry in atrioventricular-blocked perfused rat hearts loaded with Indo-1. After priming pacing at 400 ms intervals, 1-25 ESCs were interposed with a 160 ms interval, followed by 30 postextrasystolic beats with a 400 ms interval. Both left ventricular developed pressure and the amplitude of the Indo-1 fluorescence ratio (F400/F510: an index of [Ca2+]i) increased in a monoexponential manner with an increase in the number of ESCs. Both potentiated left ventricular developed pressure and the amplitude of F400/F510 transients returned to control in a monoexponential fashion. Consistent with this exponential decay, the relationship between developed pressure or the amplitude of F400/F510 transients in a postextrasystolic beat and that in the preceding beat was linear and the slope of a fitted line (recirculation fraction; RF) was evaluated as an index of rapidity of decay. The number of ESCs did not affect RF of developed pressure and the amplitude of F400/F510 transients. Reducing extracellular Ca2+ concentration (1.25 --> 0.55 mM), and perfusion with an acidic solution (pH = 6.8) significantly decreased RF of both developed pressure (0.85 +/- 0.06 --> 0.78 +/- P < 0.05 and 0.85 +/- 0.07 --> 0.78 +/- 0.06, n=8, P < 0.05, respectively) and the amplitude of F400/F510 (0.87 +/- 0.06 --> 0.78 +/- 0.05, P < 0.05, and 0.89 +/- 0.08 --> 0.78 +/- 0.07, P < 0.05, respectively). This study confirmed that, in all conditions evaluated, contractile decay was determined by [Ca2+]i decay and RF of contractile decay was an accurate estimate of [Ca2+]i decay in physiologically paced isolated perfused rat hearts.

Acidosis↗
PubMed1986

Can the site of origin of ventricular extrasystoles enhance the localisation of exercise-induced ischaemia?

Previous work from the Departments of Cardiology and Nuclear Medicine, Guy's Hospital, London, has enabled an atlas of the electrocardiographic appearances of ectopics from individual ventricular sites to be compiled. This has been used to investigate the relationship between regions of myocardial ischaemia and the site of origin of exercise-induced ventricular arrhythmias. Two hundred and ten patients underwent maximal exercise testing on a bicycle ergometer, prior to thallium scintigraphy. All 12 leads of the electrocardiogram were recorded simultaneously at rest, immediately post-exercise and then for several minutes afterwards. Thallium scintigraphy was performed immediately and 4 hours post-exercise. Twenty-nine patients of the 210 had ventricular arrhythmias on exercise. Two had dilated (congestive) cardiomyopathy, 1 had hypertrophic cardiomyopathy and 26 were subsequently proven to have ischaemic heart disease. Fifteen of those patients with coronary artery disease and ventricular arrhythmias had otherwise negative exercise tests. Patients with reversible posterior (circumflex) defects had right bundle branch block extrasystoles with a limb lead QRS axis of -60 degrees to -150 degrees. Reversible inferior defects demonstrated ectopic activity with left bundle branch block and a superior axis. Ectopics of septal origin could present with either right or left bundle branch block and an inferior axis from the upper septum, or superior axis from the lower septum. In patients with ischaemic heart disease the 12-lead electrocardiographic appearance of ventricular arrhythmias enables their site of origin to be localised thus suggesting ischaemia in a particular coronary artery territory.

Aged↗
PubMed2004

Prognostic significance of right ventricular extrasystoles.

UNLABELLED: Extrasystoles (RVES) from the right ventricular outflow tract (RVOT) are a common arrhythmia in routine ECGs. METHODS: In this prospective study 56 consecutive patients with RVES (22 males, 34 females) were examined for morphological and/or functional right ventricular (RV) abnormalities by 12-lead, Holter, exercise ECGs, transthoracic echocardiography and signal averaging. The follow-up time was 3.1-15.8 years (arithmetic mean +/- SD = 7.2 +/- 1.6 years; median, 6.9 years). Patients with hyperthyroidism, structural cardiovascular and/or lung diseases were excluded. RESULTS: A total of 57.1% of the patients with RVES presented with echomorphologic abnormalities of the right ventricle (RV). In 26.8% the echomorphologic right ventricular abnormalities progressed in 33.3% of patients with normal RVs at baseline (group I) and in 21.9% of those with abnormal RVs at baseline (group II). No significant differences were found between the 2 patient groups in terms of age at onset, family history, ECG changes, late potentials and malignant right ventricular outflow tract arrhythmias on 24-h and exercise ECGs. While females predominated in group I, males were numerous in group II (p = 0.006). Sustained ventricular tachycardia, syncope or sudden death were absent throughout the follow-up. CONCLUSION: Patients with RVES carry a good prognosis in terms of morbidity and mortality no matter whether echomorphologic abnormalities are present or not.

Adult↗
PubMed1977

Intermittent parasystole with concealed extrasystolic bigeminy during myocardial infarction.

A 72-year-old man demonstrated persistent intermittent ventricular parasystole for 6 days during an acute inferior wall myocardial infarction. Entrance block failure occurred at a critical interval of 1.24 sec. after parasystolic beats with resetting of the parasystolic cycle length. The first ectopic beat in each parasystolic series showed coupling to its second preceding conducted beat, and successive cycle lengths in each series usually showed gradual shortening. Concealed extrasystolic bigeminy was also demonstrated between parasystolic series with the number of intervening conducted beats conforming to the formula 2n + 2. After interpolated parasystolic beats, this formula became 2n + 3.

Aged↗
PubMed1984

The use of cross-correlation function for the alignment of ECG waveforms and rejection of extrasystoles.

The cross-correlation function for alignment of ECG waveforms and rejection of artifacts was studied. ECG waveforms were recorded and digitized (10-bit resolution) at 1.28 KHz and were processed with a CDC 6600 computer. The cross-correlation function was calculated using the cross spectrum and the fast Fourier transform algorithm. The maximum value of the cross-correlation function and the time location of that value were searched for (a) the similarity between the waveforms (for elimination of extrasystoles), and (b) measuring the relative time delay (for the waveform's alignment in the averaging process) between the ECG waveforms. Prior to the correlation procedure each of the ECG waveforms was filtered through a nonrecursive digital bandpass filter. Experiments with various filters indicated that when low-frequency cutoff at 30 Hz and high-frequency cutoff at 250 Hz were used the maximum value of the cross-correlation function was higher than 0.9 for most of our recorded waveforms and more accurate results were obtained.

Arrhythmias, Cardiac↗
PubMed2000

Sinus escape-capture bigeminy and sinus extrasystolic bigeminy.

Blocking conduction between the sinus node and the atria (SA block) can be responsible for symptomatic rhythm problems. However, in atrial escape-capture bigeminy with SA block, when atrial escape P waves originate in a site within or close to the sinus node, the diagnosis of SA block is not easy. Electrocardiograms were selected from 7 people with atrial bigeminy because (1) all atrial deflections (P waves) were almost the same in shape and in length of PR intervals, (2) comparatively long PP intervals alternated with comparatively short PP intervals, and (3) occasionally the atrial bigeminy changed to normal regular sinus rhythm in which 2 or more sinus P waves were found in succession. An attempt is made to clarify the mechanism for these cases. When regular sinus rhythm changed to bigeminal rhythm, the long PP interval introduced the bigeminy in 3 cases, indicating the presence of "sinus" escape-capture bigeminy; whereas the short PP interval introduced the bigeminy in the other 4 cases, indicating the presence of "sinus" extrasystolic bigeminy. In cases of sinus escape-capture bigeminy associated with SA block, the cases may occasionally be diagnosed wrongly as ordinary sinus arrhythmia not associated with SA block. Therefore, it seems that sinus escape-capture bigeminy is not so rare as is generally believed. Patients with SA block often require implantation of the artificial pacemaker. Thus, the authors believe that differentiation of sinus escape-capture bigeminy from other forms of "sinus" bigeminy is clinically important.

Adult↗
PubMed1976

Vectorial characteristics of ventricular extrasystoles stimulated during cardiac catheterization.

Ventricular extrasystoles (VES) from different areas of the ventricular muscle mass were obtained by mechanical stimulation of inflow and outflow regions of the right ventricle (RV) and apical and basal portions of the left ventricle (LV) during cardiac catheterization. Cube system vectorcardiogram (VCG) patterns of VES from each location were analyzed to determine the specificity of vector orientation from each site. Transverse plane VCG distinguished between nonseptal LVES and RVES, while a combination of transverse and either sagittal or frontal planes permitted further localization of septal VES to inflow or outflow regions of the RV and apical and basal areas of the LV.

Adult↗
PubMed1977

Spontaneous gap phenomenon in atrioventricular conduction produced by His bundle extrasystoles.

A gap in atrioventricular conduction is a zone within the cardiac cycle during which premature impulses are blocked in the conduction system, while impulses of greater or lesser prematurity are conducted. This has previously been produced only by atrial or ventricular stimulation techniques. This report demonstrates a spontaneous gap produced by His extrasystoles.

Atrioventricular Node↗
PubMed1980

Effect of amitriptyline antidotes on repetitive extrasystole threshold.

The effect of amitriptyline that leads to ventricular tachycardia was evaluated by the repetitive extrasystole threshold (RET) technique in 18 dogs. The RET was 28.8 +/- 7.9 mamp before and 8.2 +/- 5.3 mamp after amitriptyline, p less than 0.001. Physostigmine, propranolol, sodium bicarbonate, and left stellate ganglionectomy reversed the effect of amitriptyline on RET. We conclude that amitriptyline overdose predisposes to sudden death by lowering the ventricular fibrillation threshold. This cardiotoxic effect is mediated partly through the central nervous system and can be inhibited by increased plasma binding (bicarbonate), cholinergic stimulation (physostigmine), beta adrenergic blockade (propranolol), and sympathetic denervation (left stellate ganglionectomy).

Amitriptyline↗
PubMed1999

Effects of [Na+]o, [Ca2+]o and cyclopiazonic acid on decline of post-extrasystolic potentiation and twitch kinetics in guinea-pig and human myocardial preparations.

The decline of post-extrasystolic potentiation was investigated in atrial and ventricular muscle of guinea-pigs and in human atrial muscle. This decline is described in terms of the recirculation fraction (RF) for calcium in myocardial cells. Under control conditions, the mean values for RF were as follows: 0.61 +/- 0.03 in the guinea-pig atrium, 0.32 +/- 0.05 in the guinea-pig ventricle and 0.51 +/- 0.10 in the human atrium. Upon increasing calcium concentrations within the range of 0.5-10 mM or decreasing the sodium to 70%, the steady-state force and recirculation fraction increased concomitantly in all three types of muscles. Cyclopiazonic acid (CPA), in a 5-20 microM concentration, decreased force in the guinea-pig preparations and decreased RF. The effects of CPA were great in atrial muscle, 20 microM CPA decreasing RF from 0.61 to 0. 39. In ventricular muscle, this effect was small and not statistically significant. When changing calcium or sodium concentrations, increased force was accompanied by slower relaxation in atrial muscle, but an unchanged or slightly faster relaxation in ventricular muscle. In guinea-pig myocardium, CPA (5-20 microM) prolonged the time to peak force (TPF), but it slowed relaxation only in the ventricle. Reducing the calcium outflow by Na/Ca exchange increased RF as expected, and reducing the SR calcium re-uptake decreased RF. These interventions were also expected to reduce the rate of decline of intracellular calcium, but relaxation was not consistently prolonged. This indicates that factors other than the SR calcium pump and sarcolemmal Na/Ca exchange determine, or at least influence, the rate of relaxation.

Action Potentials↗
PubMed2000

[Ca2+]i following extrasystoles in guinea-pig trabeculae microinjected with fluo-3 - a comparison with frog skeletal muscle fibres.

Force production of cardiac muscle is highly dependent on the interval between the excitations. The aim was to investigate relations between intracellular calcium ([Ca2+]i) and force when a stimulus protocol, with three extrasystoles (ESs) at various intervals, was used. The relation between [Ca2+]i and force was compared with that in frog skeletal muscle fibre. Fluo-3 was microinjected into thin cardiac trabeculae to monitor [Ca2+]i. During steady-state [Ca2+]i consisted of a rapid rise (phase 1) that lasted until peak dF/dt (rate of force development) and was followed by a slower rise (phase 2) that coincided with the action potential and had a peak after peak force. The decline in [Ca2+]i outlasted the duration of the contraction. As the ES intervals were prolonged, there was a gradual restitution of force and of the amplitude and rate of rise of phase 1 [Ca2+]i. Peak dF/dt was linearly related to the amplitude of phase 1 [Ca2+]i during restitution and potentiation of force. Skeletal muscle fibres were loaded with fluo-3-AM. From [Ca2+]i the amount of calcium bound to troponin ([Ca-T]) as a function of time was estimated. Force production of the skeletal muscle fibre could be predicted from [Ca-T] when the signal was delayed (time constant 36 ms). This finding indicates that the recorded [Ca2+]i in skeletal muscle represents activator calcium. In cardiac muscle probably only phase 1 [Ca2+]i represents activator calcium. Phase 2 [Ca2+]i probably represents calcium entry during the action potential and does not activate the contractile system to any significant extent.

Action Potentials↗
PubMed2003

Spontaneous recovery of myocardial asynergic segments following acute myocardial infarction. The role of post-extrasystolic potentiation echocardiography in the predischarge evaluation.

AIMS: Predischarge identification of viable myocardium with a spontaneous recovery over time can be helpful in decision-making process following acute myocardial infarction (AMI). An intriguing hypothesis is that identification of viability in myocardial asynergic segments with or without spontaneous recovery over time may require an inotropic stimulus of a different intensity. To test this we used post-extrasystolic potentiation (PESP), which represents an inotropic stimulation of a different intensity as a function of coupling interval. METHODS AND RESULTS: Myocardial viability was assessed by PESP echocardiography in 86 patients with a first uncomplicated AMI. Spontenous changes in contractile function of viable but asynergic segments at predischarge were evaluated by a follow-up resting echocardiogram 1 month later. Viable myocardium of left ventricular asxynergic segments with spontaneous recovery or persistence of dysfunction showed its first significant improvement for different values of coupling interval during PESP (409+/-18 vs 336+/-23ms (milliseconds), P<0.0001). An arbitrary cut-off value for RR interval >or=380ms, correctly identified 91% of myocardial segments undergoing spontaneous recovery, while 99% of asynergic myocardial segments with spontaneous recovery had a threshold coupling interval >or=380ms. CONCLUSION: At predischarge following AMI, asynergic but viable myocardial segments by PESP with spontaneous recovery of contraction over time require an inotropic stimulus of lesser intensity to acutely improve contraction pattern than viable and asynergic segments without this favourable outcome.

Adult↗