Showing papers on "QRS complex published in 1991"

A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.

Abstract: BACKGROUNDIn the differential diagnosis of a tachycardia with a wide QRS complex (greater than or equal to 0.12 second) diagnostic mistakes are frequent. Therefore, we investigated the reasons for failure of presently available criteria, and we identified new, simpler criteria and incorporated them in a stepwise approach that provides better sensitivity and specificity for making a correct diagnosis.METHODS AND RESULTSA prospective analysis revealed that current criteria had a poor specificity for the differential diagnosis. The value of four new criteria incorporated in a stepwise approach was prospectively analyzed in a total of 554 tachycardias with a widened QRS complex (384 ventricular and 170 supraventricular). The sensitivity of the four consecutive steps was 0.987, and the specificity was 0.965.CONCLUSIONSCurrent criteria for the differential diagnosis between supraventricular tachycardia with aberrant conduction and ventricular tachycardia are frequently absent or suggest the wrong diagnosis. The...

Spectral turbulence analysis of the signal-averaged electrocardiogram and its predictive accuracy for inducible sustained monomorphic ventricular tachycardia☆

Abstract: This study was designed to assess the accuracy of a new noninvasive frequency analysis method for predicting patients with inducible sustained monomorphic ventricular tachycardia (VT) at electrophysiologic study and hence the risk of spontaneous ventricular tachyarrhythmias. Signal-averaged electrocardiograms from 3 orthogonal bipolar surface leads were evaluated using a microcomputer-based frequency analysis system that performs analysis of conventional time-domain late potentials as well as incorporating a new technique for spectral analysis of relatively short, overlapping signal segments spanning the whole QRS complex. The spectral analysis technique measured abnormalities anywhere in the entire QRS complex and did so without dependence on any arbitrarily defined frequency, duration or amplitude cutoffs. The hallmark of arrhythmogenic abnormality was hypothesized to be frequent and abrupt changes in the frequency signature of the QRS wave front velocity as it propagates throughout the ventricle around areas of abnormal conduction, resulting in a high degree of spectral turbulence. One-hundred forty-two subjects were studied, including 71 totally normal control subjects ("true negatives"), 33 with both late potentials by time-domain analysis and inducible sustained monomorphic VT ("true positives"), 28 with late potentials but no evidence of spontaneous or inducible sustained monomorphic VT ("false positives") and 10 with inducible sustained monomorphic VT but absence of time-domain late potentials ("false negatives"). The frequency analysis technique correctly classified 100% of the true negatives, 97% of the true positives, 86% of the late potentials false positives and 60% of the late potentials false negatives. The total predictive accuracy of frequency analysis for all groups was 94%, compared with 73% for time-domain late potential analysis. The results suggest that a high degree of spectral turbulence of the overall QRS signal during sinus rhythm may provide a more accurate marker for the anatomic-electrophysiologic substrate of reentrant tachyarrhythmias than detection of late potentials in the terminal QRS region by either time- or frequency-domain analysis. Spectral turbulence analysis is applicable to patients irrespective of the QRS duration and the presence or absence of bundle branch block.

Method and apparatus for ECG signal analysis and cardiac arrhythmia detection

Abstract: A method and apparatus for arrhythmia detection comprise steps and means for acquiring at least one continuous analog signal produced by an ECG system, producing at least one digital signal based on the analog signal, producing a plurality of scalar signals from the at least one digital signal, extracting features from the scalar signal, and plotting the extracted features in a feature space having a number of dimensions equal to the number of extracted features. A normal QRS complex is identified based on the population of QRS complexes located within clusters of QRS features within the feature space. Subsequent QRS complexes acquired after identification of the normal QRS complex are labeled based on a plurality of rules and the location of each subsequent QRS complex with respect to both prior and subsequent normal QRS complexes.

Simulation of high-resolution QRS complex using a ventricular model with a fractal conduction system. Effects of ischemia on high-frequency QRS potentials.

Abstract: Recent studies have analyzed the high-fidelity surface electrocardiographic signal, and efforts have been made to increase the diagnostic sensitivity of the electrocardiogram by observing its high-frequency components. It was found that the high-frequency (150-250-Hz) electrocardiogram appears to detect evidence of transient ischemia with greater sensitivity than visual inspection of the surface electrocardiogram. A finite-element three-dimensional model of the ventricles with a self-similar (fractal) conduction system has been introduced as a bridge to the understanding of electrocardiographic phenomena related to high-frequency potentials. The model was activated, and the dipole potential generated by adjacent activated and resting cells was calculated to obtain a high-resolution QRS complex. Normal and ischemic activation processes was stimulated by regional reduction in conduction velocity. It was found that although the resulted low-frequency QRS complex was not significantly altered from normal conditions, the high-frequency components exhibited morphological changes similar to the ones observed during animal experiments and human studies. Based on the results obtained from the model, it can be concluded that these morphological changes can be attributed to a slowing of conduction velocity in the region of ischemia and that the model is adequate for meeting the challenges imposed by the requirements of high-frequency methods applied in clinical cardiology.

Myotonic heart disease: a clinical follow-up.

Abstract: We followed 37 patients with myotonic dystrophy for a mean of 6 years. Two developed atrial flutter or fibrillation, 6 developed a new bundle branch block, 1 developed complete heart block requiring a pacemaker, and another with progressive 1st-degree heart block and a widening QRS interval had a sudden death. Most patients had predictable, gradually progressive disease of their cardiac conduction system. We recommend that patients with progressive atrioventricular block or widening QRS interval due to myotonic heart disease have yearly ECGs and be questioned about syncope or presyncope to determine the need for a cardiac pacemaker.

Dynamic qrs-complex and st-segment monitoring in acute myocardial infarction during recombinant tissue-type plasminogen activator therapy

Abstract: Changes of the QRS complex are the electrocardiographic expression of irreversible injury of the myocardium. In humans, the process of infarction occurs over several hours. A more rapid development of QRS changes has been reported in patients treated with thrombolytic agents. Patients with strongly suspected acute myocardial infarction (AMI) included in a placebo-controlled trial of 100 mg of recombinant tissue-type plasminogen activator (rt-PA) were monitored for 24 hours with continuous, on-line vectorcardiography. The magnitude of the QRS vector changes correlated with infarct size estimated by the maximal value of lactate dehydrogenase-1 (r = 0.69, p less than 0.001) as well as with left ventricular ejection fraction 30 days after randomization (r = 0.49, p less than 0.001). Treatment with intravenous rt-PA limited total QRS vector change but the QRS vector changes observed occurred more rapidly and reached a plateau 131 minutes earlier in patients treated with rt-PA than in those receiving placebo (p less than 0.01). A certain pattern of highly variable ST vector magnitude was identified and was associated with higher maximal lactate dehydrogenase-1 values (23 +/- 13 vs 14 +/- 10 mu kat/liter, p less than 0.001) and a tendency to higher 1-year mortality (24 vs 9%, p = 0.08) than in patients without this pattern. In patients with this pattern, rt-PA did not affect maximal lactate dehydrogenase-1, time to maximal creatine kinase and final magnitude of QRS vector change.

Identification of first acute Q wave and non-Q wave myocardial infarction by multivariate analysis of body surface potential maps.

Abstract: BACKGROUNDPatients with acute non-Q wave myocardial infarction (NQMI) appear to have more jeopardized residual myocardium at high risk for subsequent angina, reinfarction, or malignant arrhythmias than patients with acute Q wave myocardial infarction (QMI). Unfortunately, conventional electrocardiographic (ECG) criteria have limited utility in recognizing NQMI.METHODS AND RESULTSThe present study combines the increased information content of body surface potential maps (BSPM) over the 12-lead ECG with the power of multivariate statistical procedures to identify a practical subset of leads that would allow improved diagnosis of NQMI. Discriminant analysis was performed on 120-lead data recorded simultaneously in 159 normal subjects and 308 patients with various types of myocardial infarction (MI) by using instantaneous voltages on time-normalized P, PR, QRS, and ST-T waveforms as well as the duration of these waveforms as features. Leads and features for optimal separation of 159 normals from 183 patients ...

Multivariate analysis to simplify the differential diagnosis of broad complex tachycardia.

Abstract: Univariate analysis has identified several criteria that aid the differential diagnosis of broad complex tachycardia. In this study of 102 consecutive patients multivariate analysis was performed to identify which of 15 clinical and 11 electrocardiographic variables were independent predictors of ventricular tachycardia. These were shown to be a history of myocardial infarction, the QRS waveforms in leads aVF and V1, and a change in axis from sinus rhythm to tachycardia of more than 40 degrees. If none of the criteria was met, the diagnosis was almost certainly supraventricular tachycardia. If one criterion was met the diagnosis was probably supraventricular tachycardia. If two criteria were met then the diagnosis was probably ventricular tachycardia. If three or four criteria were met, the diagnosis was almost certainly ventricular tachycardia. The predictive accuracy was 93%. This was increased to 95% by including two other criteria--definite independent P wave activity and ventricular extrasystoles with the same QRS configuration as that in tachycardia. These criteria were not included in the multivariate analysis because though they were 100% specific they were seldom seen. These four criteria can be used as simple rules in determining the origin of a broad complex tachycardia.

Electrocardiographic body surface potential mapping in the Wolff-Parkinson-White syndrome. Noninvasive determination of the ventricular insertion sites of accessory atrioventricular connections.

Abstract: BACKGROUND A reliable, noninvasive procedure to determine the location of accessory atrioventricular connections in patients with Wolff-Parkinson-White syndrome would add an important diagnostic tool to the clinical armamentarium. METHODS AND RESULTS Body surface potential mapping (BSPM) using 180 electrodes in various-sized vests and displayed as a calibrated color map was used to determine the ventricular insertion site of the accessory atrioventricular (AV) connections in 34 patients with Wolff-Parkinson-White syndrome. Attempts were made to determine the 17 ventricular insertion sites described by Guiraudon et al. All 34 patients had an electrophysiologic study (EPS) at cardiac catheterization, and 18 had surgery so the ventricular insertion sites could be accurately located using EPS at surgery. A number of physiologic observations were also made with BSPM. CONCLUSIONS The following conclusions were drawn: 1) BSPM using QRS analysis accurately predicts the ventricular insertion site of accessory AV connections in the presence of a delta wave in the electrocardiogram; 2) the ventricular insertion sites of accessory AV connections determined by BSPM and by EPS at surgery were identical or within one mapping site (1.5 cm or less) in all but four of 18 cases; three of the four exceptions had more than one accessory AV connection, and the other had a very broad ventricular insertion; 3) BSPM and EPS locations of the accessory AV connections correlated very well in the 34 cases despite the fact that BSPM determines the ventricular insertion site and EPS determines the atrial insertion site of the accessory AV connection; 4) as suggested by the three cases of multiple accessory AV connections, EPS and BSPM may be complementary since BSPM identified one pathway and EPS identified the other (in the case with a broad ventricular insertion, BSPM and EPS demonstrated different proportions of that insertion); 5) BSPM using ST-T analysis is very much less accurate in predicting the ventricular insertion site of accessory AV connections unless there is marked preexcitation; 6) standard electrocardiography using the Gallagher grid methodology (but with no attempt at stimulating maximal preexcitation) was not as accurate as QRS analysis of BSPM in predicting the ventricular insertion site of the accessory AV connection; however, exact comparison is hampered by the different number and size of the Gallagher and Guiraudon insertion sites; 7) BSPM using QRS analysis appears to be very accurate in predicting right ventricular versus left ventricular posteroseptal accessory AV connections; 8) typical epicardial right ventricular breakthrough, indicative of conduction via the specialized AV conduction system, occurs in all patients with left ventricular free wall accessory AV connections; 9) epicardial right ventricular breakthrough was not observed in cases with right ventricular free wall or anteroseptal accessory AV connections; 10) epicardial right ventricular breakthrough can occur in the presence of posteroseptal accessory AV connections, whether right or left ventricular; and 11) the delay in epicardial right ventricular breakthrough in cases with left ventricular insertion may provide a marker to estimate the degree of ventricular preexcitation.

Electrocardiographic findings in athletic students and sedentary controls.

Abstract: We have investigated resting electrocardiograms from 1,299 athletic students taken in the same laboratory during the years 1973-1982 and compared them with electrocardiograms recorded in 151 age- and sex-matched sedentary controls. Fifty-two parameters were recorded for each electrocardiogram and computerized. We found that athletic students had a significant lower heart rate, longer PQ time and a prolonged QTc compared to control subjects. Athletes had higher maximal Q amplitudes in precordial leads, higher R in V1, and higher indices of right ventricular hypertrophy (RV1 + SV5) and left ventricular hypertrophy (Sokolow-Lyon and Grant indices). Furthermore, the athletes had higher maximal ST elevation and higher maximal T wave amplitudes in precordial leads. Sinus bradycardia was more frequent in athletes. All control subjects were in sinus rhythm whereas 0.9% of the athletes had other rhythms (nodal, coronary sinus or wandering pacemaker). Athletes and control subjects did not differ significantly with regard to premature beats, atrioventricular block, bundle branch block or the Wolff-Parkinson-White pattern. We conclude that training induces significant changes in heart rate, conduction times, ST elevation. QRS and T voltage, slow rhythm disturbances and atrioventricular and sinoatrial block were infrequent in the resting electrocardiogram taken in the supine position and disappeared immediately on sitting and during exercise. Training-induced electrocardiographic changes may partly be due to alterations in autonomic tone and partly to structural changes in the myocardium. Different normal criteria for left ventricular hypertrophy may be warranted in athletes.

A Comparison of QRS Complexes Resulting From Unipolar and Bipolar Pacing: Implications for Pace-Mapping

Abstract: KADISH, A.H,, ET AL.: A Comparison of QRS Complexes Resulting From Unipolar and Bipolar Pacing: Implications for Pace-Mapping. To examine differences in QRS configuration produced by bipolar versus unipolar pacing, 12-lead electrocardiograms recorded during bipolar (distaJ cathode] pacing with 5- and 10-mm intereJectrode distances were compared to electrocardiograms recorded during unipolar cathodal pacing from the distal catheter pole. Pacing was performed at a cycle length of 500 msec using each of the two bipolar configurations at current strengths equal to late diastolic threshold, twice threshold and 10 mA. The pacing site was at the right ventricular apex in 15 patients and at various left ventricular locations in 14 patients. The electrocardiograms recorded during bipolar and unipolar pacing were compared by two independent observers for minor QRS configuration changes, major configuration changes and amplitude changes. Minor configuration differences between unipolar and bipolar pacing occurred occasionally when the interelectrode distance during bipolar pacing was 5 mm (mean ± S.D. 0.5 ±1.2 leads per electrocardiogram]. However, when the interelectrode distance was 10 mm, minor configuration differences were seen more commonly (1.3 ± 2.0 leads per electrocardiogram; P < 0.05 vs 5-mm distance]. Major configuration differences were uncommon with either configuration at all current strengths. Pacing at 10 mA produced a larger number of configuration differences than pacing at either threshold or twice threshold [P < 0.05). Amplitude differences were seen in a mean of 1.9 ± 2.1 leads per electrocardiogram with the 5-mm interelectrode distance and a mean of 2.9 ± 2.1 leads using the 10-mm interelectrode distance (P < 0.05J. In conclusion: fl] bipolar ventricular pacing can result in QRS complexes that are different from those obtained with unipolar pacing at the same catheter iocation, presumably due to an anodal contribution during bipolar pacing; (2) increasing the interelectrode distance and stimulus intensity increases these differences; and (3] because the proximal electrode's contribution to depolarization can alter the QRS configuration during pacing in a variable way, the use of bipolar pace-mapping to localize sites of origin of ventricular tachycardia may result in less spatial resolution than unipolar pace-mapping. (PACE, Vol. 14, May, Part I 1991]

Atrial pacing as an adjunct to the management of post-surgical His bundle tachycardia.

Abstract: OBJECTIVE--To examine the benefits of restoring atrioventricular synchrony to children with His bundle tachycardia after operation for congenital heart disease. DESIGN--Review of clinical outcome of adopting the technique of R wave synchronised atrial pacing as an adjunct to the management of His bundle tachycardia from September of 1987 till June of 1990. PATIENTS--Eleven consecutive children (aged between 3 days and 13 years) with haemodynamically significant His bundle tachycardia after cardiopulmonary bypass surgery. INTERVENTIONS--Atrial pacing synchronised either manually or automatically to the R wave of the His bundle tachycardia was implemented so that atrial depolarisation preceded the following R wave by an appropriate PR interval. RESULTS--An immediate and sustained increase in mean systemic blood pressure (average 15 mm Hg, range 6-30 mm Hg) was seen with the onset of atrial pacing in 10 of the 11 children. One child, who had undergone a Fontan procedure, developed atrial flutter shortly after the onset of atrial pacing and required direct current cardioversion. Four children died. Of the seven survivors, six have sustained sinus rhythm which returned between two and 10 days after the onset of tachycardia. One of the survivors has severe neurological impairment attributed to a period of low cardiac output during tachycardia; the others are alive and well. In those children who did badly the mean time between arrhythmia occurrence and the start of atrial pacing or cooling or both was nine hours; in those who did well it was one hour. CONCLUSIONS--Atrial pacing synchronous with the His bundle is a useful adjunct in the management of children with His bundle tachycardia after surgery for congenital cardiac disease.

Ventricular tachycardia and accelerated ventricular rhythm presenting in the first month of life.

Abstract: Fourteen infants aged less than 1 month presented to our institution during the last 22 years with ventricular tachycardia (VT) or accelerated ventricular rhythm and a structurally normal heart. In 2, VT was associated with long QT syndrome. Both are alive on beta-blocker therapy, 1 with an implanted pacemaker. Twelve infants had accelerated ventricular rhythm, and 2 of these died in the first 2 months of life of unrelated conditions. The other 10 are alive at a median age of 4 years (range 2 months to 11 years), and none were lost to follow-up. Hemodynamic compromise did not occur with accelerated ventricular rhythm. The ventricular rate was very close to the sinus rate in all 12, less than 12% above the sinus rate. The mean QRS duration during accelerated ventricular rhythm was 92.5 ms, and averaged twice the QRS duration during sinus rhythm. Fusion beats were seen in all 12, and there was atrioventricular dissociation with capture beats in 10. In 2, ventriculoatrial conduction was present. Treatment was attempted in 5 of the 10 survivors with accelerated ventricular rhythm, and was thought to be successful in 4. Treatment was later successfully withdrawn in all 5, so that all 10 survivors were free of accelerated ventricular rhythm and were not receiving antiarrhythmic medications at last follow-up. Because of the excellent long-term outcome and the lack of hemodynamic compromise during the rhythm, it seems reasonable to withhold antiarrhythmic therapy in infants with accelerated ventricular rhythm and await resolution of the rhythm.

The antifibrillatory actions of UK-68,798, a class III antiarrhythmic agent.

Abstract: The electrophysiologic and antifibrillatory properties of UK-68,798 were studied in vivo in a conscious canine model of sudden coronary death. Electrophysiologic testing was performed on conscious male mongrel dogs (14.5-21.5 kg) 3 to 5 days after surgical induction of an anterior myocardial infarction by occlusion (2 h)-reperfusion of the left anterior descending coronary artery. Compared to saline-treated control animals, UK-68,798 at a dose of 0.9 mg/kg i.v. did not (P = .083) suppress the induction of ventricular tachycardia by programmed electrical stimulation. Six of 12 UK-68,798-treated dogs remained inducible, whereas 10 of 12 vehicle-treated dogs responded to electrical induction of arrhythmia. When compared to predrug inducibility, UK-68,798 significantly (P = .007) reduced the incidence of programmed electrical stimulation-induced ventricular tachycardia. In five of the six dogs inducible after UK-68,798 administration, the cycle length of the induced ventricular tachycardia was prolonged (P = .007) compared to the predrug cycle length. Heart rate, PR interval and QRS duration were not affected by UK-68,798 administration. The rate-corrected QT interval was prolonged (P less than .05) by UK-68,798. The ventricular effective refractory period was increased by UK-68,798 (158 +/- 7 msec, predrug vs. 185 +/- 7 msec, postdrug). Subsequent to programmed electrical stimulation, a 150 microA anodal current was applied to the luminal surface of the left circumflex coronary artery to induce transient episodes of posterolateral ischemia in response to electrolytic injury of the vessel wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Antiarrhythmic efficacy of a new class III agent, UK-68,798, during chronic myocardial infarction: evaluation using three-dimensional mapping.

Abstract: UK-68,798 is a potent class III antiarrhythmic agent that selectively lengthens the effective refractory period (ERP) in isolated tissue without affecting conduction velocity. The present study was performed to evaluate the antiarrhythmic efficacy of UK-68,798 (30 micrograms/kg i.v.) in dogs with a previous myocardial infarction. UK-68,798 did not alter the PQ interval or QRS duration of the surface electrocardiogram but did increase the Q-Tc interval significantly. The ventricular ERP was increased significantly (P less than .01) at a basic cycle length of stimulation of either 300 ms (ERP increased 24 +/- 10 ms) or 250 ms (ERP increased 20 +/- 12 msec), indicating that the response was preserved at more rapid rates. UK-68,798 prevented the induction of sustained ventricular tachycardia in six of seven animals (86%, P = .03). However, UK-68,798 failed to prevent the induction of ventricular fibrillation (VF) in dogs where VF was the only arrhythmia induced. To evaluate the mechanisms responsible for the prevention of ventricular tachycardia and lack of efficacy against inducible VF, detailed three-dimensional activation mapping of the heart in vivo was used. Induction of ventricular tachycardia was prevented by UK-68,798 due to a lengthening of the ERP in the epicardial region surrounding the infarct with no effect on conduction velocity even in periinfarct regions bordering the infarct. In contrast, the induction of VF was dependent on a rapid nonreentrant or focal mechanism that was not altered by the lengthening of ERP with UK-68,798. Thus, UK-68,798 is a selective class III antiarrhythmic agent that is likely to be efficacious in preventing arrhythmias due to a reentrant mechanism in patients with a previous myocardial infarction.

Copper deficiency in a genetically hypertensive cardiomyopathic rat: electrocardiogram, functional and ultrastructural aspects.

Abstract: The effect of copper deficiency on cardiac function and structure was studied in a strain of rats (SHHS/Mcc-cp) known to develop cardiac failure as adults. Restriction of dietary copper (less than or equal to 1 mg/kg vs. 6 mg/kg in adequate diets) at weaning in both sexes for a 6-wk period produced cardiac hypertrophy. Male rats developed more severe copper-deficiency symptoms than their female counterparts. In both sexes of copper-deficient rats, there was an increase in cardiac length, width, free ventricular wall thickness and septum thickness. Electrocardiographic tracings revealed greater QRS height among male copper-deficient rats. Heart rate also was substantially reduced in this group. The increased volume of myocardium occupied by mitochondria in the copper-deficient male rats might result in increased electrical resistance that would increase the QRS height; hypertrophy or anemia also could be contributory. Some male copper-deficient rats had prolongation of the QRS in a bundle branch block pattern. Maximal rates of rise and fall for left ventricular pressure were reduced in male copper-deficient rats. The gross histology indicated that this type of heart failure was more concentric than eccentric. The copper-deficient male rat may serve as a useful model for studying the concentric cardiac hypertrophy that occurs in humans.

Beat-to-beat electrocardiographic morphology variation in healed myocardial infarction

Abstract: Using high-fidelity electrocardiographic (ECG) amplifiers, we measured subtle beat-to-beat ECG morphologic variations at different phases of the ECG complex. The electrocardiograms were recorded from 49 men with a documented Q-wave myocardial infarction and from 30 age-matched normal men. Forty consecutive beats were averaged to achieve an average ECG signal from which variance could be calculated. The relative variance, defined as the ratio between the integrated variance of the examined window and the integrated variance of the ECG signal that was close to full cycle length, was calculated at QRS onset and at offset in 2 frequency bands (4 to 40 and 60 to 120 Hz). Patients with healed infarction had a relative variance of 2.1 +/- 0.5 (mean +/- standard deviation [SD]) at QRS offset (a window of 40 ms), which was significantly lower than that of the healthy volunteers: 2.5 +/- 0.33 (mean +/- SD; p less than 0.02) at the low-frequency band. At the high-frequency band, patients with healed infarction had a significantly higher relative variance than the control subjects at QRS onset: 1.95 +/- 0.58 vs 1.55 +/- 0.35 (mean +/- SD; p less than 0.005). A model based on the numerous minor conduction abnormalities that exist in the chronically ischemic myocardium is presented to explain the changes in variance at the onset and offset of the QRS. The variance changes described can eventually serve as quantitative indexes of myocardial injury and electrical stability in patients with ischemic heart disease.

Electrocardiographic prediction of myocardial area at risk.

Abstract: The 12-lead electrocardiogram in 23 patients with an evolving first myocardial infarction (12 anterior and 11 inferior) was correlated with the myocardial area at risk measured by tomographic perfusion imaging with technetium-99m sestamibi. Of several electrocardiographic factors, only the extent and quantity (with and without R-wave normalization) of ST depression differed significantly between inferior and anterior evolving infarction. The myocardial area at risk was greater in anterior than in inferior evolving infarction. The extent of the myocardium at risk correlated modestly (r = 0.58) with total ST displacement in anterior evolving infarction and with total ST depression normalized to the R wave (r = 0.70) in inferior evolving infarction. Because of the large standard errors (9 to 15% of the left ventricle), estimates of the myocardial area at risk based on these electrocardiographic variables have minimal clinical value in the individual patient.

Narrow QRS Ventricular Tachycardia

Abstract: Objective: To determine the frequency and clinical characteristics of narrow QRS ventricular tachycardia (QRS duration ≤ 0.11 seconds). Design: Consecutive survey of patients with ventricular tachy...

Spontaneous myocardial ischemia and the signal-averaged electrocardiogram

Abstract: The effects of transient myocardial ischemia on the signal-averaged electrocardiogram were investigated in 13 patients with coronary artery disease and spontaneous angina undergoing 3-channel ambulatory electrocardiography. Ischemia was seen as ST elevation in 2 patients or ST depression in 11; it was anterior in 5 patients, inferior in 4 and undefined in 4. Signal-averaged electrocardiograms with noise levels ≤1 μV were obtained from Holter tapes during 54 of 61 ischemic attacks recorded in the study group (88%), and compared with 54 tracings recorded within 60 minutes of the index attacks. Baseline tracings were normal in 8 patients (62%), showed a long QRS duration in 2 (15%), and both a long QRS duration and a late potential in the remaining 3 (23%). Comparison of recordings at baseline and during ischemic attacks revealed no significant changes in signal-averaged electrocardiographic parameters. Absence of significant differences was also noted when analysis was performed according to the type of ischemic attacks (associated with ST elevation [n = 14] or ST depression [n = 40]), their location (anterior [n = 21] or inferior [n = 23]), their duration (>10 minutes [n = 29] or ≤10 minutes [n = 25]), and their magnitude (>2 mm [n = 18] or ≤2 mm [n = 36]). It is concluded that spontaneous transient myocardial ischemia, independent of its type, location, duration and magnitude, does not generate a substrate for late potentials on the signal-averaged electrocardiogram.

In vivo effect of bradykinin during ischemia and reperfusion: improved electrical stability two weeks after myocardial infarction in the pig.

Abstract: In this study, the effect of bradykinin or saline infusion during ischemia and reperfusion on electrical stability, 2 weeks after myocardial infarction, was assessed. Acute myocardial infarction was induced in 21 pigs by a transluminal occlusion of the left coronary artery with a catheter balloon, inflated for 45 min. Bradykinin was administered by a 30-min infusion that started after 30 min of coronary occlusion and was continued until 15 min after reperfusion. Although creatine kinase levels in bradykinin-treated animals were significantly lower (p <0.001), 2 week survival was not different between groups. In survivors, the filtered QRS (ventricular deflection) duration (detected using signal-averaged electrocardiography) was significantly prolonged in saline-treated pigs, whereas in bradykinin- treated pigs this prolongation was prevented. The terminal voltage of the QRS complex was significantly lower in saline-treated pigs than in bradykinin-treated pigs. These two parameters signify an improved electrical stability after bradykinin treatment. Refractory periods in saline-treated hearts were longer than in bradykinin-treated hearts (106 +/- 10% vs. 95 +/- 13%, p <0.05). Also, current thresholds in the infarct border zones showed a greater variance in saline-treated hearts (p <0.001), pointing toward more tissue heterogeneity of the infarct border zone. Programmed electrical stimulation showed a trend toward reduced inducibility of sustained ventricular tachycardia in bradykinin-treated hearts. Therefore, bradykinin improves electrical stability 2 weeks after experimental myocardial infarction.