Frequent ventricular ectopic activity without underlying cardiac disease: analysis of 45 subjects

Forty-five subjects, aged 2 weeks to 62 years, who presented with frequent (greater than 100/day) ventricular ectopic beats (VEBs) and without evidence of underlying cardiac disease were studied. The spectrum of ventricular dysrhythmia was assessed by 24-hour ambulatory electrocardiography and exercise tolerance test. Sinus rhythm was the prevailing rhythm in all subjects. VEB frequency averaged 444 +/- 454 per hour (range 0 to 1,863) over the 24-hour monitoring period and was not significantly different during waking or sleeping periods. There was no simple correlation of VEB frequency with prevailing sinus rate (r = -0.0006; p = not significant [NS]). The prevalence of complex VEBs (multiform, R-on-T and repetitive) was relatively high (18 of 45 patients), and was equally distributed about the median VEB frequency of 314 VEBs/hour (7 of 18 versus 11 of 18; NS). Of the 43 subjects who had exercise tests, 37 had VEBs during the preexercise rest phase, compared with only 11 at peak exercise (p less than 0.0001). To assess the short-term natural history of the VEBs, 27 subjects had repeat clinical examinations and 24-hour electrocardiograms at a mean interval of 8 months. All remained well. Although there was considerable individual temporal variability of VEB frequency in this subgroup, there was no significant change in group mean values (415 +/- 409 VEBs/hour initially versus 401 +/- 383 VEBs/hour at follow-up study; NS). The relative temporal constancy of VEB frequency in the group as a whole was also reflected in a high linear correlation of VEB frequency at initial and follow-up studies (r = 0.816; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of posture and respiration on body surface electrocardiogram

To define more fully the effects of posture and respiration on electrocardiographic (ECG) patterns, 120-lead body surface potential maps (BSPM) were recorded in 36 normal subjects (aged 21 to 48 years) during cyclic respiration in both supine and upright positions; and at static end-tidal inspiration, functional residual capacity (FRC), total lung capacity (TLC) and residual volume (RV). In addition, BSPMs were recorded at TLC and RV during the Valsalva and Müller maneuvers, respectively. P-wave, QRS and ST-segment time integrals were evaluated. From supine to upright position, there was an inferior torso shift of P-wave and QRS distributions, but no change in amplitude of their maximal or minimal values; ST-segment distributions were spatially unaltered, but there was a significant (p < 0.01) decrease in the maximal value. Relative to maps during cyclic respiration in the upright position, maps at end-tidal respiration were similar; maps at TLC, however, displayed an inferior displacement of P-wave and QRS distributions and a decrease of QRS maximal and minimal values (p < 0.01). Valsalva and Müller maneuvers were not associated with marked changes in the appearances of BSPMs. The magnitude of variability, as assessed by a root-mean-square index, was greatest between maps recorded at TLC and RV; the least variability occurred between maps recorded at end-tidal inspiration and FRC. The variability between maps recorded in the supine and upright positions was intermediate. When root-mean-square variability data of all interventions were normalized by dividing by the respective mean data range (maximum minus minimum) of each time integral, the variability of P wave > ST segment > QRS (p < 0.01).Thus, resting tidal volume respiration has little effect on body surface ECG patterns in normal adults. However, large volume respiration and posture change may substantially alter ECG body surface distributions and should be considered in states involving either factor.     

Cardiac rhythm,rate and ventricular repolarization properties in infants at risk for sudden infant death syndrome: Comparison with age- and sex-matched control infants

Using 24-hour ambulatory electrocardiographic recordings and 120-lead body surface potential maps, prevailing cardiac rate and rhythm, incidence and frequency of dysrhythm and rate and pattern of ventricular repolarization at the body surface were compared in 17 infants at risk for sudden infant death syndrome (SIDS) and 17 age- and sex-matched control subjects. Sinus rhythm was the prevailing rhythm in both study groups and there were no intergroup differences in average overall awake or asleep sinus rates, nor in temporal variability of sinus rate. Atrial and ventricular ectopic activity were equally uncommon in both study groups. Although there were smooth and bipolar body surface distributions of ST-T and QRST time integrals in both study groups, the average rate of ventricular repolarization (QTc), measured from the 12-lead electrocardiogram, 120-lead body surface potential maps and 24-hour electrocardiography, was consistently shorter in the at-risk group than in the control group. However, temporal variability of QTc was not different between the 2 groups. Thus, significant cardiac dysrhythm and QT prolongation are not found in infants at increased risk for SIDS. Rather, there is an abbreviated ventricular repolarization interval in at-risk infants. In combination with the findings of intergroup similarity of average sinus rate and temporal variability of sinus rate and ventricular repolarization rate, the data suggest a subtle, constant difference in cardiac autonomic activity, most likely an Increase in sympathetic tone, in at-risk subjects. The role of this altered cardiac autonomic activity in the causation of SIDS remains undetermined.     

QT interval variability on the body surface

To assess the effects of measurement methodology on QT determinations and to define the spectrum of QT values, including interlead variability, on the body surface, we measured QT in each of 120 simultaneously-recorded, signal-averaged ECG leads in 10 normal subjects and 14 patients with QT prolongation (lead II QTc greater than 440). Two separate, but related, methods of QT measurement were utilized. Method A was a relatively conventional technique in which ST-T offset was defined as the time instant of return of the T wave to a P-P baseline, or as the point of U-on-T intersection. Method B was a more rigorous method, which defined ST-T offset in a similar manner, and in addition discarded from analysis all QT values from leads with monophasic ST-T waveform in which the QT values were greater than the longest QT from leads with definite U waves. Method B was utilized to minimize factitious prolongation of QT by inapparent U-on-T. By both methods the mean body surface QTc values were significantly greater (p less than 0.001) in the patient group (482 +/- 65 [S.D.] msec, method A; 447 +/- 43 msec, method B), than in the normal subject group (399 +/- 14 msec, method A; 396 +/- 12, method B). Interlead QTc variability (difference between the longest and shortest QT) was considerable with both methods and in both study groups. Expressed as percent of average body surface values, the mean interlead QTc variability in normal subjects averaged 22 percent with method A and 19 percent with method B; in the patient group, however, it averaged 32 percent with method A and only 18 percent with method B. In absolute terms, the mean variability in the patient group with method A (155 +/- 62 msec) was significantly greater (p less than 0.001) than that of the normal group (89 +/- 33 msec); with method B, interlead variability was the same (p = NS) in the normal (76 +/0 27 msec) and patient groups (80 +/- 44 msec). This latter finding suggests the possibility that the repolarization abnormality in patients with QT prolongation may occur relatively uniformly throughout the ventricular myocardium. Thus, measurement techniques are important in multiple-lead QT determinations. Although reduced by techniques designed to minimize factitious QT prolongation, interlead QT variation is considerable over the torso surface, in both normal subjects and patients with repolarization abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)     

Temporal evolution of body surface map patterns following acute inferior myocardial infarction

We studied the evolution of body-surface potential map (BSPM) patterns in 32 patients following first acute inferior myocardial infarction. Initial BSPMs were obtained at a mean of 79 hours post-infarction; follow-up BSPMs, a mean of eight months post-infarction. Temporal area-of-difference maps, constructed by subtracting initial from follow-up group-mean BSPMs, revealed reciprocal changes over the superior and inferior torso for both Q-zone and ST-segment time-integral distributions. The temporal changes in Q-zone patterns were small but definite: over the inferior torso there was a relative gain in Q-zone values and, over the superior torso, a relative decrease. In contrast, there were marked spatial and quantitative changes of ST-segment distributions during the follow-up period. Over the superior torso, particularly anteriorly, there was a gain in ST-segment values; over the inferior torso, a decrease. With the small temporal changes in Q-zone time-integral distributions, individual Q-zone maps continued to reflect a pattern of inferior myocardial infarction at follow-up. In contrast, the marked temporal changes in ST-segment time-integral distributions resulted in individual map patterns at follow-up that were nearly indistinguishable from normal ST-segment maps. The relatively small changes in depolarization time-integral patterns during the early post-infarction period suggest that the Q-zone patterns of the acute phase of myocardial infarction reflect near-irreversible or completed myocardial damage. The marked normalization of repolarization time-integral patterns during the recovery phase suggests, however, that there are also considerable areas of myocardium-at-risk during the early phase of the infarction process which stabilize with time.     

A cellular model for the simulation of activation in the ventricular myocardium.

A digital computer model of cardiac activation was used to investigate the relationship between cellular orientation and conduction and propagation of the ventricular activation wave front. The results of the simulation for a single cycle initiated in fully recovered tissue under normal and simplified pathological conditions (ischemia and infaraction) indicate (a) that the conduction velocity of the cellular action potential in ventricular cardiac tissue may be several (3-5) times greater than is normally considered to be the case, (b) that the ventricular activation wave front propagates transmurally from endocardium to epicardium despite fiber orientation parallel to these surfaces, without the need for assuming the existence of either lateral contacts between adjacent cells or fibers with a transmural orientation, (c) the wave front of activation propagates through ventricular cardiac tissue with an anisotropic phase velocity, (d) the presence of ischemia and infarction gives rise to tangential spread of activation, and (e) small subendocardial infarcts should not be considered to be electrically silent.     

The conversion of phenylalanine to tyrosine in man. Direct measurement by continuous intravenous tracer infusions of L-[ring-2H5]phenylalanine and L-[1-13C]tyrosine in the postabsorptive state

Steady state phenylalanine and tyrosine turnover and the rate of conversion of phenylalanine to tyrosine in vivo were determined in 6 healthy postabsorptive adult volunteers. Continuous infusions of tracer amounts of L-[ring-²H₅]phenylalanine were administered intravenously for 13–14 hr. After 9–10 hr, a priming dose followed by a continuous infusion of L-[1-¹³C]tyrosine was added and maintained, along with the [²H₅]phenylalanine infusion, for 4 hr. Venous plasma samples were obtained before the initiation of each infusion and every 30 min during the course of the combined [²H₅]phenylalanine and [¹³C]tyrosine infusion for determination of isotopic enrichments of [²H₅]phenylalanine, [¹³C]tyrosine, and [²H₄[tyrosine by gas chromatograph-mass spectrometric analysis of the N-trifluoroacetyl-, methyl ester derivatives of the amino acids. Calculated from the observed enrichments, free phenylalanine and tyrosine turnover rates were 36.1 ± 5.1 μmole · kg^?1 · h^?1 and 39.8 ± 3.5 μmole · kg^?1 · h^?1, respectively. Phenylalanine was converted to tyrosine at the rate of 5.83 ± 0.59 μmole · kg^?1 · h^?1, accounting for approximately 16% of either the phenylalanine or the tyrosine flux. The results indicate that the normal basal steady state phenylalanine hydroxylase activity in vivo in man is lower than that obtained from phenylalanine loading studies. This supports the existence of some type of substrate activation of the enzyme as reflected in the previously reported exponential relationship between phenylalanine concentration and phenylalanine hydroxylase activity in vitro. The use of continuous simultaneous infusions of tracer amounts of stable isotope-labeled phenylalanine and tyrosine provides a direct means for studying physiological regulation of phenylalanine hydroxylase activity in vivo.     

The effect of acetylsalicylic acid on plasma glucose and the response of glucose regulatory hormones to intravenous glucose and arginine in insulin treated diabetics and normal subjects

The effects of oral acetylsalicylic acid (ASA) 3.2 g a day for 5 days on glucose and glucose regulatory hormones were examined in 4 normal subjects, and in 14 insulin requiring diabetic subjects, 9 of whom had significant residual Beta cell function as assessed by C-peptide secretion and 5 of whom did not. In all subjects plasma samples were assayed for glucose, C-peptide, glucagon, growth hormone, and cortisol during sequential intravenous glucose and arginine infusions while the subject was receiving ASA or placebo. The plasma samples from the normal subjects were assayed for insulin.ASA significantly increased early insulin release (p < 0.02) and decreased plasma glucose (p < 0.02) in response to intravenous glucose in the normal subjects. ASA had no effect on glucose or hormone responses to intravenous arginine.The C-peptide positive diabetics had a significantly lower basal plasma glucose while receiving ASA, and this difference persisted throughout the test (p < 0.02). C-peptide levels were similar to control during ASA ingestion. ASA had no significant effect on plasma glucose in the C-peptide negative diabetics.ASA significantly increased fasting plasma glucagon in the normal subjects (p < 0.05) and C-peptide negative diabetics (p < 0.05). There was a significant positive correlation between the changes in plasma glucose and plasma glucagon both basally and 10 min after the commencement of the glucose infusion for the C-peptide negative diabetics but not for the C-peptide positive diabetics or the normal subjects. ASA had no effect on plasma growth hormone or cortisol levels.The reduction of plasma glucose by ASA in man is dependent on continuing β cell function. In the absence of β cell function the stimulatory effect of ASA on glucagon production becomes the major determinant of ASA's effect on plasma glucose. The effects of ASA on pancreatic islet function appears to be the major determinant of its effect on glucose handling.     

Changing electrocardiographic recording technology and diagnostic accuracy of myocardial infarction criteria. Improved standards for evaluation of ECG measurement precision

An analytical study was performed to estimate the magnitude of the visual Q wave duration bias produced by pressurized ink round stylus electrocardiographic (ECG) recorders. With a paper speed of 25 mm/sec and the ECG tracing width of 0.25 mm, the visually measured Q waves are on the average 8 msec too short. The corresponding error with the older type flat stylus recorder is less than 2 msec. Considerable differences can thus be anticipated in the frequency of observed ECG abnormalities in studies which use different types of electrocardiographs. The effect of the visual Q wave duration measurement bias on the diagnostic ECG classification was investigated in a group of 237 patients with old myocardial infarction and 299 subjects with no clinical evidence of infarction. An 8 msec measurement bias toward too short Q wave duration was observed to result in a potential loss of diagnostic accuracy of about 25% in some ECG coding categories. As a corrective procedure, it is recommended that the baseline width produced by a round recording stylus of uniform thickness irrespective of the vertical deflection velocity should be less.     

Stroke masking electrocardiographic abnormalities

Strokes may mimic or mask electrocardiographic abnormalities. An example of the little known masking phenomenon is described.     

The performance of three visual coding procedures and three computer programs in classification of electrocardiograms according to the minnesota code

A test library composed of the ECG's of 228 patients with clinically proven myocardial infarction and 294 subjects without clinical evidence of infarction was used to assess the performance of three visual coding procedures and three computer programs designed to classify ECGs according to the Minnesota Code. The results showed that visual coding performed by one experienced senior coder tended to be more consistent than visual coding relying on two less experienced coders and arbitration of disagreements by a supervisor. There was no significant difference in coding results when only one preprocessed complex was coded in comparison with the more elaborate coding of the whole source ECG using majority rule. The coding performance of the three computer programs was similar to that of the visual coding procedures. It is concluded that computer coding of ECGs according to the Minnesota Code is feasible. Combined optimal use of automated coding and visual verification of selected items may still further improve coding precision. However, when judged against an ECG independent standard, the accuracy of all coding procedures in discriminating infarcts from non-infarcts according to the Minnesota code criteria is rather limited. 'Soft' criteria give a reasonable sensitivity with low specificity whereas the use of 'hard' criteria with adequate specificity results in a substantial drop in sensitivity.     

A simple procedure for positioning precordial ECG and VCG electrodes using an electrode locator.

Methodological differences in the placement of precordial ECG electrodes are a major problem in multicenter clinical trials and epidemiological studies. Trend analysis and realization of the full potential of computer programs for serial comparison demands reduction of technical sources of variation in the electrocardiogram (ECG) and vectorcardiogram (VCG) and particularly errors in locating ECG electrodes. The ECG electrodes locator described here reduces a major precordial uncertainty in the identification of the midclavicular and the anterior axillary lines. It simplifies positioning and provides a numeric record of the key precordial electrode positions, facilitating control of electrode placement errors in serial recordings.