A low-noise P-wave discriminating electrocardiogram in the diagnosis of complex cardiac arrhythmias.
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Arrhythmias, Cardiac↗
Biomedical subjects
R Mehra
Publications and source records attributed to R Mehra.
Late potentials and arrhythmogenesis.
There are three current prognostic indicators of ventricular electrical instability: categorization and stratification of spontaneous ventricular arrhythmias from standard ECG recordings; programmed electrical stimulation; direct recording of delayed depolarization potentials, usually referred to as late potentials. Of the three, the latter offers a new and promising approach. Late potentials represent delayed activation potentials of diseased myocardial zones and may prove to be a strong independent marker of the propensity to develop reentrant ventricular arrhythmias and sudden cardiac electrical death. The problem in identifying late potentials on the body surface is that the signal is smaller than the electrical noise produced by various sources. Two different techniques have been utilized to improve the signal-to-noise ratio: first, signal averaging, which is applicable to regular repetitive electrocardiographic signals but cannot detect moment-to-moment dynamic changes in the signal; second, low-noise or high-resolution electrocardiography that utilizes spatial averaging techniques as well as other noise-reducing measures to record the late potentials on a beat-to-beat basis. This technique has the potential of directly identifying malignant "reentrant" versus benign "focal" ventricular rhythms. The present report discusses the electrophysiologic basis of late potentials and the clinical results of both signal-averaged and low-noise recordings for evaluation of ventricular electrical instability, particularly in patients with ischemic heart disease.
Aged↗
Quantitative analysis of the high-frequency components of the signal-averaged QRS complex in patients with acute myocardial infarction: a prospective study.
We performed a prospective study of the high-frequency components of the terminal portion of the QRS complex in 50 patients with acute myocardial infarction (AMI) (mean age 63 +/- 10 years) within 3.25 +/- 2.45 days of the acute event. Signal averaging (400 beats) at a filter setting of 80 to 300 Hz was performed and the duration of the low-amplitude signals of less than 40 microV in the terminal portion of the QRS, the root-mean-square (RMS) voltage of the terminal 40 msec of the QRS complex, and the total duration of the signal-averaged QRS vector complex were measured. The low-amplitude signals were abnormally prolonged in 22 of 50 patients (44%); the RMS-V was abnormal (less than 20 microV) in 21 of 50 patients (58%), and the signal-averaged vector complex was abnormal (greater than 120 msec) in 15 of 46 patients (33%) without bundle branch block. There was no significant correlation between any of the signal-averaged parameters and site of AMI or total creatine kinase (CK) and CK-MB values. On the basis of the occurrence of spontaneous ventricular tachycardia in the acute and postcoronary care phase of AMI, the patients were divided into two groups. Group I consisted of 31 patients (62%) who had no documented ventricular tachycardia and group II consisted of 19 patients (38%) who had one or more runs of ventricular tachycardia. Fourteen of the 19 patients in group II (73.6%) had nonsustained ventricular tachycardia and five patients (26.3%) suffered sustained ventricular tachycardia/ventricular fibrillation or sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Reentrant ventricular arrhythmias in the late myocardial infarction period in the dog. 13. Correlation of activation and refractory maps.
Isochronal maps of ventricular activation were analyzed in dogs 3-5 days after ligation of the left anterior descending coronary artery utilizing a 64-channel multiplexer. Isochronal maps of the effective refractory period were determined from 62 epicardial sites and correlated with the activation maps. The ischemia occurring in the surviving epicardial layer prolonged refractoriness in a spatially nonuniform manner. The resulting pattern of refractoriness on the epicardial surface resembled concentric rings of isorefractoriness which increased in duration from the normal zone to the center of the ischemic zone. The formation of an arc of functional unidirectional conduction block occurred along the gradient of refractoriness and the exact location of the arc depended on the S1-S2 interval. When a short S1-S2 failed to induce reentry, fewer adjacent sites with sufficiently disparate refractoriness formed a smaller arc of block. A subsequent S3 encountered further nonuniformly shortened refractoriness (normal areas had shortened refractoriness greater than ischemic areas) and the arc of block was lengthened. This required a longer time for the wavefront to circulate around the arc. When it then reached the distal side of the arc, refractoriness had expired proximal to the arc and reentry occurred. Similarly, nonuniform shortening of refractoriness explained why one reentrant beat may or may not produce successive reentrant beats. Therefore, the spatial pattern of refractoriness forms the substrate for the arc of unidirectional conduction block that is fundamental to the development of ventricular reentry in this experimental model.
Animals↗
Implications of nutrition education versus food supplementation in pre-school children.
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Adult↗
Reentrant ventricular arrhythmias in the late myocardial infarction period. II. Burst pacing versus multiple premature stimulation in the induction of reentry.
Isochronal maps of ventricular activation were analyzed in dogs 1 to 5 days after infarction utilizing a 64 channel multiplexer. Only dogs in which circus movement reentry could not be induced by a single premature stimulus were analyzed. Reentrant rhythms could be successfully induced equally by multiple (double or triple) premature stimuli and by burst pacing. Successive premature stimuli as well as successive beats during burst pacing resulted in progressively longer arcs of functional conduction block or slower circulating wave fronts, or both, that succeeded in reexciting myocardial zones on the proximal side of the arc of block to initiate reentry. However, for manifest reentry to be induced by burst pacing, the paced run had to be terminated after the beat that resulted in a critical degree of conduction delay. Otherwise, reentrant activation could be confined (concealed) by the subsequent paced wave front, which could also arrive earlier to the reentrant circuit zone of slow conduction resulting in block and interruption of reentry. Termination of a paced run after this beat would not result in reentry. If the paced run was extended past this beat, a new sequence of ventricular activation patterns characterized by progressively longer arcs of block or slower conduction, or both, developed again. The number of beats in a paced run that could initiate reentry varied with the cycle length of pacing, as well as in different experiments, and was difficult to standardize. It is therefore concluded that random burst pacing as a technique for induction of reentrant rhythms should probably be abandoned in favor of multiple premature stimulation.
Animals↗
Appraisal of a Low Noise Electrocardiogram.
Two low noise electrocardiographic systems were designed to record low amplitude His-Purkinje potentials in the PR segment and delayed depolarization potentials in the ST-T segment from the body surface on a beat to beat basis. In one system, a bipolar electrode was utilized and the noise level was optimally reduced to 2 to 2.5 microV by a combination of noise reduction techniques. In the second system, better noise reduction (1 to 1.5 microV) was achieved by utilizing spatial averaging from 16 pairs of electrodes and a specially designed volume conductor electrode. The low noise electrocardiogram using the volume conductor electrode identified the His-Purkinje potential (up to 6 microV in amplitude) in 43% of patients compared with 71% recorded in the signal-averaged electrograms from the same patients. However, in contrast to the signal-averaged electrogram, only the low noise electrocardiogram could identify the His-Purkinje potential when moment to moment dynamic changes of the temporal relation of the P wave and QRS complex occurred. On the other hand, the low noise electrocardiogram recorded low amplitude, late diastolic potentials in the ST-T segment of postinfarction patients who showed a propensity to develop ventricular tachyarrhythmias. The diastolic potentials either: 1) remained constant in successive sinus beats, 2) varied in configuration, amplitude and timing in successive sinus beats, or 3) were only recorded in the diastolic interval preceding possible "reentrant" ventricular beats. The present study proves the feasibility of recording low amplitude His-Purkinje potentials and late diastolic potentials on the body surface on a beat to beat basis utilizing low noise electrocardiographic systems. Recording of late diastolic potentials on a beat to beat basis has the exciting potential of directly identifying malignant "reentrant" versus benign "focal" ventricular rhythms. However, the clinical relevance of these potentials remains to be established.
Adult↗
Reentrant ventricular arrhythmias in the late myocardial infarction period. 9. Electrophysiologic-anatomic correlation of reentrant circuits.
We studied isochronal maps of ventricular activation during ventricular arrhythmias induced by programmed premature stimulation in dogs 3-5 days after ligation of the left anterior descending coronary artery. The entire epicardial surface and selective intramural sites were recorded using a computerized multiplexing technique. The electrophysiologic data were correlated with the anatomic characteristics of the infarction. In nine of 17 dogs (55%), the induced ventricular rhythm was due to reentrant activation in the surviving epicardial layer overlying the infarction. The irregular epicardial layer (up to 4 mm thick) had grossly intact myocardial fibers on microscopic examination but showed abnormal electrophysiologic characteristics. The stimulated premature beat that initiated reentry produced a continuous arc of functional conduction block within the surviving epicardial layer. The activation wave front circulated slowly around both ends of the arc of block, rejoined on the distal side of the arc before breaking through the arc to reactivate an area proximal to the block. This resulted in splitting of the initial single arc of block into two arcs. Reentrant activation continued as two synchronous circuits that traveled clockwise around one arc and counterwise around the other. Reentry spontaneously terminated when the leading edge of both reentrant circuits encountered refractory tissue, resulting in the coalescence of the two arcs of block into one. The present study may increase the understanding of the electrophysiologic mechanism of some ventricular repetitive responses and tachyarrhythmias induced by programmed premature stimulation in the clinical laboratory.
Animals↗
Reentrant ventricular arrhythmias in the late myocardial infarction period. Interruption of reentrant circuits by cryothermal techniques.
Both sustained and nonsustained ventricular tachycardias were reproducibly induced in dogs 3 to 5 days after ligation of the left anterior descending coronary artery. Isochronal maps of ventricular activation were constructed from close bipolar electrograms recorded from the entire epicardial surface and selected intramural sites by a computerized multiplexing technique. The electrophysiologic data were correlated with the anatomic characteristics of the infarction. The induced tachycardias were due to reentrant activation in the surviving epicardial layer overlying the infarction. Cooling or cryoablation was applied to localized epicardial sites along the reentrant circuit to reversibly or permanently interrupt reentrant activation. The reentrant circuit could be consistently interrupted when cooling or cryoablation was applied to the distal part of the common reentrant wave front proximal to the site of earliest reactivation. Localized cooling of the site of earliest reactivation usually failed to interrupt reentry because the common reentrant wave front reactivated other sites close to the original reactivation site. Before interruption of reentry, cooling resulted in characteristic changes in conduction of the reentrant wave front. The study (1) fulfills Mines' criteria that circus movement reentry is the mechanism of the induced rhythms in this canine experimental model and (2) identifies the critical site along the reentrant circuit at which cryothermal ablation (or surgical interruption) of reentrant activation could be successfully accomplished.
Animals↗
Triggered ventricular rhythms in 1-day-old myocardial infarction in the dog.
Triggered activity developed in depolarized Purkinje fibers (maximum diastolic potential -59.3 +/- 9.9 mV) during superfusion with normal Tyrode's solution in 84% of subendocardial preparations from 1-day-old canine infarct. Triggered activity occurred when a delayed afterdepolarization attained threshold potential and spontaneously terminated after a subthreshold delayed afterdepolarization. Triggered activity was initiated either by stimulated beats or by the background slow Purkinje automaticity. When multiple stimulated beats were required, the amplitude of the afterdepolarization increased and the coupling interval decreased when the stimulation frequency and/or the number of stimulated beats increased. Varying degrees of entrance and exit block around sites of triggered activity were common, and some triggered activity manifested as a parasystolic rhythm. In preparations showing subthreshold delayed afterdepolarizations, both epinephrine (2.5 x 10(-6) M) and increasing [Ca++]o, (from 2.7 to 8.1 mM) increased the amplitude of afterdepolarizations and resulted in triggered activity. On the other hand, verapamil (2.2 x 10(-6) M) resulted in exit block around sites of triggered activity and/or completely suppressed afterdepolarizations and triggered activity. Isochronal mapping of endocardial activation during the initiation and perpetuation of triggered activity elucidated a focal site of origin from Purkinje fibers overlying the infarct and showed no evidence of a circus movement of excitation. The in vitro triggered activity may explain the spontaneous multiform ventricular rhythms seen in the intact heart.
Action Potentials↗
Noninvasive His Bundle electrogram: value of three vector lead recordings.
Studies were conducted in 45 patients to determine whether the reliability of the measurement of the His bundle potential from the body surface was increased by signal averaging of three simultaneously recorded electrocardiographic potentials from horizontal (X), frontal (Y) and sagittial (Z) axes as opposed to recording of any of these. Potentials from the X, Y and Z leads were amplified by 250,000, filtered between 80 hertz (12 dB/octave) and 200 hertz (24 dB/octave) and signal averaging of 1,000 beats was performed. The His bundle potential could be clearly defined in 25 of the 45 patients in the X, Y, or Z lead. His bundle potentials were evident in the X lead in 17 (68 percent) of these 25 patients, in the Y lead in 19 (77 percent) and in the Z lead in 11 (44 percent). No single lead gave satisfactory His bundle electrographic potentials in all patients. In 20 patients the His bundle electrogram could not be recorded because terminal atrial activity overlapped activity of the His bundle potential. The three lead system defined the His bundle potential in a significantly greater number of patients than did the best single lead because it (1) displayed the vectorial lead with the largest His bundle potential, (2) permitted validation of the His bundle potential in more than one lead, and (3) displayed the vectorial lead with the most isoelectric terminal P wave. It is concluded that reliable His bundle potential measurements are obtained in a significantly greater number of patients with use of the simultaneous three lead system than with use of any single lead.
Bundle of His↗
Ventricular activation patterns of spontaneous and induced ventricular rhythms in canine one-day-old myocardial infarction. Evidence for focal and reentrant mechanisms.
We studied isochronal maps of ventricular activation during spontaneous multiform ventricular rhythms (rates 120-190/min) and pacing-induced ventricular tachyarrhythmias (rate 230-450/min) in dogs 1 day after myocardial infarction. Recordings were obtained from the entire epicardial surface and from selected endocardial and intramural sites utilizing a computerized multiplexing technique. Spontaneous ventricular rhythms had a focal origin from the surviving subendocardial Purkinje network underlying the infarction and showed frequent shift of the pacemaker site. On the other hand, fast ventricular tachyarrhythmias were consistently induced in the same dogs by bursts of rapid ventricular pacing or programmed premature stimulation and had a tendency to degenerate into ventricular fibrillation. Pacing-induced rhythms were due to reentrant activation that developed mainly in the surviving, electrophysiologically abnormal, epicardial layer overlying the infarction. The last stimulated heat that initiated reentry resulted in a continuous arc of functional conduction block and two slowly circulating activation fronts around both ends of the arc of block. The activation fronts rejoined on the distal side of the arc of block before breaking through the arc to reactivate an area proximal to the block. This resulted in splitting of the initial single arc of block into two separate arcs. Reentrant activation subsequently continued as two synchronous circuits which conducted in clockwise and counterclockwise directions, respectively. Reentry spontaneously terminated when the leading edge of both reentrant circuits encountered refractory tissue and failed to advance. The presence of two synchronous circuits was the hallmark of a stable reentrant activation. The development of three or more asynchronous circuits resulted in an activation pattern that was "prefibrillatory." This pattern was seen to develop during pleomorphic ventricular rhythms and ventricular tachycardias of the torsades de pointes type that degenerated into ventricular fibrillation. Ventricular fibrillation was maintained by continuously changing multiple asynchronous circuits. The transition from a stable reentrant activation pattern to that of ventricular fibrillation was probably related to nonhomogeneous shortening of refractoriness in different parts of the myocardium.
Animals↗
Signal averaging of electrocardiographic potentials: a review.
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Action Potentials↗
Time dependence of unipolar cathodal and anodal strength-interval curves.
Following pacemaker electrode attachment, greater ventricular vulnerability to arrhythmias exists in an acutely ischemic ventricle with a unipolar anodal than cathodal stimulus falling on the T wave, due to the shorter refractory period exhibited by an anodal stimulus. In order to determine the relationship between anodal and cathodal refractory period at various times following endocardial electrode insertion, ventricular strength-interval curves were determined in nine dogs. With stable electrode position, serial measurements were made for a mean duration of 44 days. It was observed that during the first five days, the anodal refractory period was significantly shorter than cathodal, but within 15-20 days this relationship was reversed in all dogs. The longer anodal refractory period was observed up to the end of each study. These results suggest that due to shorter anodal refractory period, greater vulnerability to arrhythmias may occur with an anodal than cathodal stimulus in the initial 15-20 days following electrode insertion.
Animals↗
Hepatotrophic effects of insulin on glucose, glycogen, and adenine nucleotides in hepatocytes isolated from fed adult rats.
In vivo observations have suggested that there is an hepatotrophic effect of insulin. By contrast, subsequent in vitro work, using the isolated perfused liver system, showed no effect or indeterminate effects of insulin on the transport of glucose into the hepatocyte. However because this system may not have endured long enough to show such an influence we explored the transport of glucose using a 48-h suspension culture of hepatocytes isolated from young adult fed rats, the suspension being infused continuously with insulin at a rate approximating the maximum entering portal blood in the fed state. (In a separate study phloridzin was added after 2 h of incubation.) DNA, intracellular glucose and its inward transport, glycogen, and the adenine nucleotides were measured at intervals. By comparison with control or untreated cells, insulin-treated cells showed significantly more DNA and intracellular glucose, and the differences were abolished by phloridzin. Glucose transport rates fell to low values in untreated controls and still lower with insulin plus phloridzin, but the initial rate was maintained to the end (48 h) by insulin alone. Results for glycogen were similar to those for intracellular glucose. There was a close correlation (r = 0.96) between these two. The total adenine nucleotide pool and the concentration of ATP were maintained for about 24 h and fell to half their initial values by 48 h. Insulin had increased these concentrations significantly by 6 h. Although concentrations of ADP and AMP decreased gradually in all groups of cells, insulin enhanced the level of ADP by 12 h but had no measurable effect on that of AMP. The energy charge increased slightly throughout incubation but more so (by 6 h) in the presence of insulin. In conclusion the data support the concept that in the longer term (greater than 12 h) insulin in the portal circulation maintains the characteristic free permeability of the hepatocyte to glucose and this permits a variety of effects related to glucose entry into the hepatocyte.
Adenine Nucleotides↗
Hepatotrophic effects of insulin on glucose, glycogen, and adenine nucleotides in hepatocytes isolated from fasted adult rats.
Previous evidence that portal blood insulin is an hepatotrophic factor led to this study of its effect on hepatocytes, isolated from fasted rats, in suspension culture. Control hepatocytes (C), noninsulin-treated, and those infused continuously at low (LI) and high (HI) levels of insulin were compared concurrently with regard to their survival, glucose transport, and intracellular concentrations of glucose, glycogen, and adenine nucleotides, over a 48-hr period of incubation. Low insulin was adjudged to be comparable to portal insulin concentrations in fasted animals and HI to those in fed animals. All hepatocytes had been depleted of glucose, glycogen, and adenine nucleotides at the start of the study by prior fasting of the rat. For the first 6 hr of culture, there was little difference between C, LI, and HI with reference to the above parameters. In contrast, after 48 hr of incubation, cell survival, as judged by the DNA content, was signficiantly lower in C compared with LI and HI. The transport of 3--0-[methyl-3H] D-glucose was also significantly lower in C compared with LI and HI. The higher uptakes in both LI and HI were reduced by phloridzin, which had little effect on C. Correspondingly, the intracellular glucose concentrations in C were significantly lower than the extracellular glucose concentrations in contrast to those in LI and HI, which were comparable. For intracellular concentrations of glycogen and adenine nucleotides, the results of LI and HI were amalgamated as they were not significantly different from each other at 48 hr. Upon analysis, glycogen values were significantly higher for insulin-treated cells. Similarly, the total adenine nucleotide p-ol (ATP + ADP + AMP) also was clearly higher in HI + LI than in C. These results indicate that contrary to findings in studies with the perfused liver that have been of a short-term nature, insulin is necessary in the longer term (greater than 12 hr) for maintaining the transport of glucose into hepatocytes; thereby insulin promotes the maintenance of intracellular glucose, glycogen, and adenine nucleotide concentrations, and also enhances cell survival.
Adenine Nucleotides↗
Comparison of cathodal, anodal, and bipolar strength-interval curves with temporary and permanent pacing electrodes.
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Arrhythmias, Cardiac↗
Termination of ventricular tachycardia with bursts of rapid ventricular pacing.
Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 5 12 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent tachycardia.
Adolescent↗