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Biomedical subjects

A R Denniss

Publications and source records attributed to A R Denniss.

At least 19 recordsLinked to original sources
PubMed1992

Electrophysiologic studies in patients with unexplained syncope.

This study examined the role of electrophysiologic study in the evaluation of patients with unexplained syncope. The incidence of abnormalities (conduction disease, supraventricular tachycardia, ventricular tachycardia) was compared in patient groups with and without heart disease, and the effect of treatment of these abnormalities on recurrence of syncope was examined. Electrophysiologic study was performed in 111 consecutive patients with syncope, with antiarrhythmic medications being discontinued 1 week prior to study. There was no mortality associated with the procedure and only 9 patients (8%) had complications (groin haematoma, atrial fibrillation or brady-arrhythmias persisting after the procedure). Abnormalities were detected in 31 of 73 patients with heart disease (42%) but in only 6 of 38 patients with no heart disease (16%, P less than 0.01). During follow-up, syncope recurred in 2 of 37 patients (5%) treated because of abnormal findings, compared with a recurrence rate of 24% (18 of 74 patients) in the untreated group (P less than 0.05). Probability of remaining free from syncope at 2 years was 0.94 in the treated group and 0.72 in the untreated group (P less than 0.05). Mortality during follow-up was confined to the heart disease group with 5 of 30 treated patients in this group dying (17%) compared with 3 of 43 untreated patients (7%, P = not significant). Syncope patients with heart disease were thus more likely to have a diagnostically useful study than patients with normal hearts. Treatment directed at correction of abnormalities detected at electrophysiologic study reduced recurrence of syncope but did not significantly affect mortality. Syncope did not appear to be a prelude for sudden death in patients with normal hearts. Electrophysiologic study had no mortality and low morbidity.

Adolescent↗
PubMed1989

Distribution and function of human ventricular beta adrenergic receptors in congestive heart failure.

This study examined the characteristics and distribution of sarcolemmal and light vesicular beta-adrenergic receptors (BAR) in left ventricular myocardium from 15 adults (aged 17 to 58 years) without left ventricular dysfunction or coronary artery disease and 29 patients (aged 14 to 53 years) with end-stage congestive heart failure (CHF). Sarcolemmal and intracellular fractions were prepared by 40,000 x g and 108,000 x g centrifugation, respectively. Agonist and antagonist binding properties were assessed by nonlinear computer modelling of isoproterenol-125I-pindolol (IPIN) displacement curves. Adenylate cyclase activity was also examined. Distribution of intracellular and sarcolemmal BAR was similar in normal and failing left ventricular myocardium, with intracellular BAR comprising 4.5 +/- 2.2% of total BAR in normal human heart and 5.7 +/- 5.1% of total BAR in CHF patients. For sarcolemmal BAR, antagonist affinity was similar for normal and CHF patients (KD IPIN in normals, 21.7 +/- 2.6 pM; KD IPIN in CHF, 20 +/- 2.3 pM). Agonist affinity was somewhat higher in CHF patients (KD isoproterenol in normals, 33 +/- 4.9 nM; KD isoproterenol in CHF, 6.2 +/- 1.5 nM). Sarcolemmal BAR number was reduced in CHF from 21.4 +/- 2.9 to 16.4 +/- 1.3 fmol/mg protein (P less than 0.04). Cyclic AMP production (pmol/mg protein/min above basal) was less in CHF after Gpp(NH)p stimulation (normals, 82 +/- 20; CHF, 27 +/- 9; P less than 0.01) and after stimulation with Gpp(NH)p + isoproterenol (normals, 129 +/- 25; CHF, 56 +/- 13; P less than 0.02). Stimulation with manganese + forskolin resulted in similar levels of cyclic AMP production in normals and in CHF patients. We conclude that: (a) sarcolemmal BAR number is reduced in CHF, but BAR are not redistributed intracellularly and (b) beta-adrenergic transmembrane signalling in CHF is also impaired at the level of the guanine nucleotide regulatory proteins.

Adenylyl Cyclases↗
PubMed1989

Influence of allopurinol plus verapamil treatment on myocardial tissue necrosis during permanent coronary occlusion in canine hearts with small infarcts.

We previously showed that combined treatment with allopurinol plus verapamil had a salutary effect on tissue necrosis during 24-h permanent coronary occlusion. The present study was undertaken to determine whether cardioprotection with allopurinol plus verapamil as compared with either allopurinol or verapamil treatment alone could be sustained in dog hearts during 48-h permanent coronary occlusion. In 46 dogs, coronary occlusion was induced using a closed-chest embolization procedure. Four groups were studied: (a) untreated controls, (b) dogs receiving allopurinol, (c) dogs receiving verapamil, and (d) dogs receiving allopurinol plus verapamil. Tissue necrosis was evaluated using triphenyltetrazolium staining and was related to two major baseline predictors of infarct size: anatomic risk zone size and coronary collateral flow. In untreated controls, the ratio of infarct to risk zone was inversely related to coronary collateral flow; analysis of covariance (ANCOVA) indicated that treatment with allopurinol or verapamil alone and combined allopurinol plus verapamil shifted this relationship downward. In conclusion, combined treatment with allopurinol plus verapamil did not afford additional limitation of tissue necrosis as compared with either allopurinol or verapamil treatment alone; however, considerable and statistically significant limitation of tissue necrosis was observed even during 48-h permanent coronary occlusion without reperfusion.

Allopurinol↗
PubMed1989

Beta-adrenergic receptor number and adenylate cyclase function in denervated transplanted and cardiomyopathic human hearts.

To test the hypothesis that there is up-regulation of beta-adrenergic receptor density or supersensitivity of beta-adrenergic receptor-stimulated adenylate cyclase in the denervated transplanted human heart, we studied myocardium from transplanted, normal, and failing hearts. Myocardium was obtained from 10 patients 9 +/- 3 months after cardiac transplantation, from 10 patients without cardiac disease, and from eight patients with symptomatic congestive heart failure due to idiopathic cardiomyopathy. beta-Adrenergic receptor density in transplanted myocardium (15 +/- 3 fmol/mg protein, 1.20 +/- 0.14 fmol/mg DNA) was not different from that in normal myocardium (22 +/- 3 fmol/mg protein, 1.46 +/- 0.13 fmol/mg DNA; p = NS for both). In myocardium from cardiomyopathic hearts, beta-adrenergic receptor density was markedly reduced (8 +/- 2 fmol/mg protein, 0.84 +/- 0.13 fmol/mg DNA; p less than 0.05 and p less than 0.01 vs. normal myocardium, respectively). Likewise, the response of adenylate cyclase to isoproterenol in transplanted myocardium was not significantly different from that in normal myocardium, but the response was markedly depressed in cardiomyopathic myocardium. Although forskolin-stimulated adenylate cyclase activity was similar in all three groups, guanine nucleotide-stimulated adenylate cyclase activity was markedly reduced in transplanted myocardium (20 +/- 17 vs. 78 +/- 13 pmol/mg/min for normal myocardium, p less than 0.01) and to a lesser degree in cardiomyopathic myocardium (39 +/- 14 pmol/mg/min, p less than 0.03 vs. normal myocardium). Thus, there is no evidence of beta-adrenergic receptor up-regulation or supersensitivity in denervated transplanted human myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1989

Electrophysiological and anatomic differences between canine hearts with inducible ventricular tachycardia and fibrillation associated with chronic myocardial infarction.

This study examined electrophysiological and anatomic differences between dogs with ventricular tachycardia (VT) and fibrillation (VF) inducible by programmed ventricular stimulation 7-21 days after left anterior descending coronary artery ligation. Of 106 dogs studied, 40 had inducible VT, 19 had inducible VF, and 47 had no inducible arrhythmias. Differences between these three groups of animals were examined with cardiac mapping (to determine ventricular activation time in sinus rhythm) and post-mortem pathology (to measure infarct size and to reconstruct the anatomy at the infarct edge). Animals with inducible VT had longer maximal epicardial activation time (127 +/- 8 msec) than did animals with inducible VF (91 +/- 8 msec, p less than 0.05) or animals with no inducible arrhythmias (75 +/- 2 msec, p less than 0.001). Delayed epicardial activation occurred in 90% of animals with VT, 42% of animals with VF, and in only 6% of animals with no inducible arrhythmias. Endocardial and myocardial activation times were similar for the VT and VF groups. Infarct size was 18 +/- 2% of the ventricles for the VT group, much higher than for the VF group (11 +/- 2%, p less than 0.001) or for the group with no inducible arrhythmias (9 +/- 1%, p less than 0.001). The maximum diameter of viable muscle bundles interdigitating with scar tissue at the infarct edge was much larger in animals with VT (2.4 +/- 0.2 mm) than in animals with VF (1.8 +/- 0.2 mm, p less than 0.05) or animals with no inducible arrhythmias (1.7 +/- 0.1 mm, p less than 0.01). Thus, when compared with animals with inducible VF, animals with inducible VT had longer epicardial activation time, larger infarct size and viable muscle bundles of larger diameter at the infarct edge.

Animals↗
PubMed1988

Differences between patients with ventricular tachycardia and ventricular fibrillation as assessed by signal-averaged electrocardiogram, radionuclide ventriculography and cardiac mapping.

This study examined 65 patients with ventricular tachycardia or fibrillation late after myocardial infarction to determine whether they differed with respect to duration of ventricular activation in sinus rhythm and left ventricular ejection fraction. Patients with spontaneous ventricular tachycardia had a longer ventricular activation time in sinus rhythm than did patients with spontaneous ventricular fibrillation. This difference was detected with the signal-averaged electrocardiogram (ECG) (tachycardia 181 +/- 33 ms, fibrillation 152 +/- 23 ms, p less than 0.001) and at epicardial mapping (tachycardia 210 +/- 17 ms, fibrillation 192 +/- 17 ms, p less than 0.02). Left ventricular ejection fraction was lower in patients with spontaneous ventricular tachycardia (0.22 +/- 0.09) than in patients with spontaneous ventricular fibrillation (0.27 +/- 0.09) (p less than 0.05). The patients with both spontaneous and inducible ventricular fibrillation had a shorter ventricular activation time on the signal-averaged ECG (129 +/- 17 ms) and a higher ejection fraction (0.36 +/- 0.05) than did either patients with spontaneous ventricular fibrillation and inducible ventricular tachycardia (158 +/- 21 ms and 0.25 +/- 0.08, respectively, each p less than 0.01) or patients with both spontaneous and inducible ventricular tachycardia (181 +/- 33 ms and 0.22 +/- 0.09, respectively, each p less than 0.001). Of the patients with inducible ventricular tachycardia, presentation with tachycardia rather than fibrillation was associated with a longer ventricular activation time on the signal-averaged ECG (181 +/- 33 versus 158 +/- 21 ms, p less than 0.02) and a longer cycle length of inducible ventricular tachycardia (290 +/- 61 versus 259 +/- 44 ms, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Quantitation of day to day variability in mode of induction of ventricular tachyarrhythmias by programmed stimulation.

Spontaneous day to day variability in the mode of induction of ventricular tachycardia at programmed stimulation in the drug-free state has been described but not quantitated. To quantitate this variability, this study employed a new protocol of programmed stimulation in which the number of extrastimuli required for tachycardia induction was the only major stimulation variable. This protocol was applied to 18 consecutive patients with previously documented sustained ventricular tachyarrhythmia due to coronary artery disease. One to seven extrastimuli were available for arrhythmia induction if required. Each patient underwent programmed stimulation in the absence of antiarrhythmic drugs on 3 separate days with a mean interval of 5 +/- 2.7 days between studies. A sustained ventricular tachyarrhythmia was inducible in all studies with less than or equal to 4 extrastimuli; the mean number of extrastimuli required was 2.4 +/- 0.8. Day to day variability in the number of extrastimuli required for tachycardia induction was observed in the majority of patients (72%). Eleven patients (61%) varied by one extrastimulus over the three control studies, and two patients (11%) varied by two extrastimuli. At analysis of variance, the 95% confidence interval for the degree of day to day variability was +/- 1 extrastimulus from the mean number required in the three studies. Multiple configurations of induced ventricular tachycardia were frequently observed at repeat studies and occurred in 15 patients (83%). In conclusion, spontaneous day to day variability in mode of induction of ventricular tachycardia in the absence of drugs is common.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1988

Effect of repetition of extrastimuli on sensitivity and reproducibility of mode of induction of ventricular tachycardia by programmed stimulation.

This study examined the effect of repeating the delivery of a programmed extrastimulus that previously failed to induce ventricular tachycardia, without the usual practice of concurrently altering other stimulation variables such as pacing site or basic cycle length. The impact of such repetition on both sensitivity and day to day variability in mode of arrhythmia induction was assessed in 24 patients with documented sustained ventricular tachycardia or fibrillation. Programmed stimulation in the absence of drugs was performed in each patient on 3 separate days. In the first 12 patients, each extrastimulus was scanned through diastole to refractoriness four times if no ventricular tachyarrhythmia was induced (longitudinal repetition); in the second 12 patients, each extrastimulus was delivered four times at a particular coupling interval before the interval was decreased in 10 ms steps to a closer coupling interval (lateral repetition). Day to day reproducibility of the mode of arrhythmia induction was compared with reproducibility in a control group of 18 similar patients studied previously on 3 separate days without repetition. A sustained ventricular tachyarrhythmia was inducible in all studies with four or fewer extrastimuli. In the group studied with longitudinal repetition, there was a 25% increased yield of induced ventricular tachycardia due solely to repetition of each extrastimulus scan, and the 95% confidence limit for tachycardia induction with any extrastimulus was achieved by delivering that extrastimulus three times. In the group studied with lateral repetition, there was also an increased yield of induced ventricular tachycardia at any extrastimulus coupling interval achieved by repetitive delivery of that coupling interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Randomized controlled trial of prophylactic antiarrhythmic therapy in patients with inducible ventricular tachyarrhythmias after recent myocardial infarction.

Survivors of acute myocardial infarction who had inducible sustained ventricular tachyarrhythmias at programmed stimulation 1-4 weeks after infarction were recruited to a randomized pilot trial of Class I antiarrhythmic drugs, in an attempt to determine whether their mortality and risk of spontaneous ventricular tachycardia and fibrillation could be reduced by treatment. Of 136 eligible patients, 96 (71%) joined the trial and 47 were randomized to 'no treatment' and 49 were randomized to 'treatment' (quinidine, disopyramide or mexiletine given to attain 'therapeutic' serum levels). During follow-up, the two groups fared similarly. For the 'treatment' and 'no treatment' groups, the respective 3-year probabilities of remaining incident-free were:cardiac death, 0.91 vs 0.89; instantaneous death + non-fatal ventricular tachyarrhythmias, 0.87 vs 0.87; cardiac death + non-fatal ventricular tachyarrhythmias, 0.83 vs 0.85. The highest risk patients with inducible ventricular tachycardia fared similarly in the 'treatment' and 'no treatment' groups. The respective probabilities of remaining incident-free were: cardiac death, 0.89 vs 0.88; instantaneous death + non-fatal ventricular tachyarrhythmias, 0.79 vs 0.84; cardiac death + non-fatal ventricular tachyarrhythmias, 0.76 vs 0.77. We conclude that prophylactic Class I antiarrhythmic drug therapy with quinidine, disopyramide or mexiletine given to achieve a 'therapeutic' serum level does not appear to alter the prognosis of patients with inducible ventricular tachyarrhythmias after myocardial infarction.

Actuarial Analysis↗
PubMed1988

Intracoronary infusion of dobutamine to patients with and without severe congestive heart failure. Dose-response relationships, correlation with circulating catecholamines, and effect of phosphodiesterase inhibition.

We infused dobutamine into the left main coronary artery of 24 patients with severe congestive heart failure (CHF) and 8 normal subjects without hemodynamic dysfunction. The maximal +dP/dt response to intracoronary (IC) dobutamine in CHF patients was only 37% of that in normals. This decrease in maximal response was not associated with a rightshift in the EC50 for dobutamine's effect on +dP/dt, or a decrease in the affinity of myocardial beta adrenergic receptors for dobutamine determined in vitro. In nine of the CHF patients, IC dobutamine infusion was followed by IC infusion of the phosphodiesterase inhibitor milrinone, and subsequently, by a second IC infusion of dobutamine. After IC milrinone, the increase in +dP/dt caused by IC dobutamine (74 +/- 10%) was significantly greater than that caused by the first infusion of dobutamine (52 +/- 11%; P less than 0.003) or milrinone (42 +/- 6%; P less than 0.001). Resting plasma norepinephrine was markedly elevated in CHF patients (837 +/- 208 ng/liter), but not in normal subjects (142 +/- 32 ng/liter); and the increase in +dP/dt caused by IC dobutamine was inversely related to resting plasma norepinephrine levels (r = -0.653; P less than 0.001). IC dobutamine caused a dose-related decrease in plasma norepinephrine (maximal effect, -160 +/- 31 ng/liter; P less than 0.001). Thus, (a) the maximal inotropic response to dobutamine is markedly depressed in patients with severe CHF, and is significantly greater after pretreatment with the phosphodiesterase inhibitor milrinone; (b) the impairment in inotropic response to dobutamine is inversely related to circulating norepinephrine levels; and (c) myocardial stimulation by dobutamine results in withdrawal of sympathetic tone.

Catecholamines↗
PubMed1987

Changes in ventricular activation time on the signal-averaged electrocardiogram in the first year after acute myocardial infarction.

Repeat signal-averaged electrocardiograms were used in 40 patients to document changes in ventricular activation time and delayed potentials in the first 12 months after acute myocardial infarction. Beta-blocking and antiarrhythmic drug use was stopped for 1 week before each recording. Patients with reinfarction during follow-up were excluded. Signal-averaged electrocardiograms were first performed 1 to 4 weeks after infarction. They were repeated at 6 and 12 months in 31 patients in whom spontaneous ventricular tachycardia (VT) did not develop and were repeated after VT in the other 9 patients. Of the 9 patients in whom VT developed, all had delayed potentials at initial study and 8 (89%) still had delayed potentials at restudy after VT. In the VT patients, mean ventricular activation time was similar before and after VT (178 ms and 174 ms, respectively). In the 11 patients who had delayed potentials initially and in whom VT did not develop, the proportion with delayed potentials was 55% (6 of 11) at 6 months and did not change (55%) at 12 months. Mean ventricular activation time in these patients was 164 ms at initial study, decreasing to 147 ms at 6 months (p less than 0.05) and 148 ms at 12 months. In 20 patients with no delayed potentials initially, none had delayed potentials at 6 months and only 2 (10%) had delayed potentials detectable at 12 months. Mean ventricular activation time in these patients increased slightly, from 120 ms at initial study to 128 ms at 12 months (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias.

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group I), ventricular activation time averaged 115 +/- 2 ms, compared with 166 +/- 3 ms (p less than 0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 +/- 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 +/- 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p less than 0.001), but lower than that for group II (p less than 0.001). The incidence of delayed ventricular activation was 89% for group II, 26% for group III and 18% for group IV. Sustained VT was not inducible in group I patients, but was inducible in 78% of group II (p less than 0.001 vs group I) and 20% of group III (p less than 0.05 vs group I; p less than 0.001 vs group II) (group IV was not studied).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Effect of excision of ventricular myocardium on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia.

The ability of surgical excision of electrically abnormal ventricular myocardium to either abolish delayed potentials or modify their timing was investigated in 21 patients with spontaneous ventricular tachycardia (VT) late after myocardial infarction. This study also examined whether modification of delayed potentials after surgery was associated with loss of ability to induce VT or improvement in left ventricular function. Signal averaging of the electrocardiogram (ECG), programmed stimulation and radionuclide ventriculography were performed preoperatively and were repeated 10 to 14 days postoperatively. At preoperative investigation, all patients had delayed potentials on the signal-averaged ECG and inducible VT at programmed stimulation. In 7 patients (33%), delayed potentials were abolished by surgery, exceeding the baseline variability of 8.5% for detection of delayed potentials. VT was no longer inducible postoperatively in 16 patients (76%), including the 7 in whom delayed potentials were no longer detectable. In the patients in whom VT was no longer inducible, mean ventricular activation time decreased from 178 ms preoperatively to 151 ms postoperatively (standard error of the mean difference = 6 ms, p less than 0.001). In the 5 patients with inducible VT postoperatively, no significant change in mean ventricular activation time was seen, 181 vs 171 ms (standard error of mean difference = 9 ms). Reductions in ventricular activation time were not associated with an improvement in left ventricular ejection fraction unless aneurysmectomy was performed in addition to excision of electrically abnormal myocardium. Thus, the signal-averaged ECG may have a role in assessing the efficacy of antiarrhythmic surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Limitation of infarct size for 24 hours by combined treatment with allopurinol plus verapamil during acute myocardial infarction in the dog.

This study examined whether combination therapy with allopurinol plus verapamil would enhance limitation of myocardial infarct size compared with either allopurinol or verapamil alone in closed-chest dogs subjected to 24 hr of permanent coronary occlusion. Four groups were studied: control, dogs receiving allopurinol (400 mg po 24 and 2 hr before coronary occlusion and 10 mg/kg iv 6 hr after occlusion), dogs receiving verapamil (200 micrograms/kg iv bolus, then continuous administration of 5 micrograms/kg/min), and dogs receiving allopurinol plus verapamil as indicated above. The anatomic risk zone and regional myocardial blood flow were measured with radioactive microspheres administered intraventricularly 1 min after coronary occlusion. Necrotic tissue was visualized by triphenyl tetrazolium chloride staining and the risk zone by autoradiography of the microspheres. Infarct size, expressed as a percentage of the risk zone, was 75.9 +/- 13.7% (mean +/- SD) in the control group, 44.1 +/- 13.3% in the allopurinol group (p less than .05 vs control), 40.6 +/- 11.1% in the verapamil group (p less than .05 vs control), and 37.9 +/- 13.6% in the allopurinol plus verapamil group (p less than .05 vs control; p = NS vs drug-treated groups). In controls, there was a close correlation (r = -.83) between infarct size and subepicardial collateral blood flow. As a result the expected infarct size in the treatment group that would have occurred without drug-treatment could be reliably predicted based on the correlation between infarct size and subepicardial collateral blood flow. The ratio of the actual and predicted infarct size provides a "salvage index".(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1986

Effect of antiarrhythmic therapy on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia after acute myocardial infarction.

The ability of class I and class II antiarrhythmic drugs to either abolish delayed potentials or modify their timing was investigated in 39 patients with spontaneous ventricular tachycardia (VT) after myocardial infarction. Before the study all patients had delayed potentials on the signal-averaged electrocardiogram and inducible VT with programmed stimulation. These investigations were repeated during 67 trials of oral antiarrhythmic therapy (mexiletine 25, quinidine 24, metoprolol 13, disopyramide 2, procainamide 1, drug combinations 2). Delayed potentials were abolished in only 5 trails (7%), which was within the baseline variability of 8.5% for detection of delayed potentials. In the 7 trials in which VT inducibility was suppressed, delayed potentials persisted in 6 and mean ventricular activation time was virtually unchanged (151 ms before drug therapy, 152 ms after). Quinidine, mexiletine and metoprolol caused no consistent change in ventricular activation time. There was also no change in mean ventricular activation time (164 ms before and 163 ms after drug treatment) in patients in whom spontaneous VT did not recur with drug therapy during follow-up. Thus, the tested antiarrhythmic drugs had no consistent effects on presence or timing of delayed potentials on the signal-averaged electrocardiogram, even when VT inducibility was suppressed or recurrence of spontaneous VT was prevented.

Action Potentials↗
PubMed1986

Reproducibility of measurements of ventricular activation time using the signal-averaged Frank vectorcardiogram.

Interobserver and day-to-day variability in detecting delayed potentials and in measuring duration of ventricular depolarization using the signal-averaged Frank vectorcardiogram were investigated in 20 patients, 12 with and 8 without ventricular tachycardia (VT). No patients were taking antiarrhythmic medications, digoxin or beta blockers at the time of study. The presence of delayed potentials and duration of ventricular activation were measured 2 times a mean of 5 days apart by 2 observers. Analysis of variance showed no significant interobserver variability in ventricular activation time. Day-to-day differences in ventricular activation times were small in patients without VT, none of whom had delayed potentials at either study. Delayed potentials were present in all 12 patients with VT at the first recording and in 11 at the repeat recording. However, significant (p less than 0.01) day-to-day variability was found in ventricular activation times, and 3 of the 12 patients had marked (more than 20 ms) day-to-day changes. It is concluded that in the absence of medical or surgical intervention, delayed potentials detected on 1 day have a high chance of being present at a repeat recording. However, the exact timing of these delayed potentials shows marked day-to-day variation in some patients. Interobserver variability is not significant with this method of detecting delayed potentials.

Adult↗