Alternans of the repolarization wave in a case of hypochloremic alkalosis with hypopotassemia.

A case of profound hypochloremic alkalosis with hypopotassemia is reported, showing electrocardiographic changes of electrical alternans of the repolarization wave (probably the U wave) without any change in the QRS complex. Transient concomitant P-pulmonale was noted. Hypopotassemia is discussed as a possible mechanism for the development of the electrical alternans.     

Isolated T wave alternans

Two patients with isolated T wave alternans are reported, with their vectocardiograms, their response to carotid sinus stimulation, and the response to calcium infusion in one of them with documented severe hypocalcemia. Eleven cases of the literature are briefly reviewed. The alternans of the T wave appears with severe QT prolongation, QT alternans, and an increased tendency to ventricular fibrillation. The findings are consistent with the hypothesis that T wave alternans may be the electrocardiographic manifestation of the transmembrane action potential alternans and could be related in some cases to hypocalcemia.     

Evaluation of postextrasystolic T wave alterations in identification of patients with coronary artery disease or left ventricular dysfunction

This study was performed (1) to assess the value of postextrasystolic T wave alterations in identification of patients with cardiac disease and (2) to determine if their frequency depends on length of compensatory pause. In 52 patients a pacing catheter was placed in the right ventricular (RV) apex, and premature beats were programmed to occur 30 msec beyond RV refractory period. Postextrasystolic T wave alterations occurred in 32 patients, 13 with an 19 without coronary artery disease (CAD) (NS). Such alterations were also not related to presence of abnormal left ventricular (LV) ejection fraction (less than 0.55) or end-diastolic pressure (greater than 12 mm Hg). In 33 patients, premature beats were also introduced 330 msec beyond the RV refractory period to compare effects of long and short compensatory pauses on frequency of postextrasystolic T wave alterations. When the pause was near maximal, 18 patients had alterations in 60 ECG leads; when it was shorter, seven patients had alterations in 10 leads (p less than 0.001). Thus, judging from provoked postextrasystolic T wave alterations, such spontaneous changes appear neither sensitive nor specific in the identification of patients with cardiac disease. The frequency of postextrasystolic T wave changes depends on the length of the compensatory pause.     

Postextrasystolic transient contractile alternans in canine hearts

Summary We found that postextrasystolic potentiated contractility after a spontaneous extrasystole most frequently decayed as a transient alternans over several beats in excised, cross-circulated, atrially paced canine hearts. This type of heart preparation, which we have been using consistently in mechanoenergetic studies, had normal coronary blood perfusion pressure as well as flow and mechanoenergetic performance. Spontaneous atrial and ventricular extrasystoles occurred occasionally in every heart. Arrhythmic changes in left ventricular (LV) pressure at a fixed volume reflected corresponding changes in contractility. We analyzed nearly 3,600 cases of postextrasystolic potentiation in 68 hearts; 84% decayed as transient alternans, 6% decayed exponentially, and 10% belonged to neither type. We found that a postextrasystolic compensatory pause always preceded the transient alternans after either an atrial or ventricular extrasystole at any constant atrial pacing rate (85–188 beats/min). The decay was either exponential or nonalternating when the pause did not exist after an atrial extrasystole during occasional pacing failure. Therefore, the compensatory pause after either an atrial or ventricular extrasystole seems essential for the postextrasystolic transient alternans of LV contractility in the type of canine heart preparation we have been using.Part of this study was presented in 1993 at a meeting of the Japanese Pathophysiology Society. The abstract of the presentation appeared in Jpn J Pathophysiol 1: 45, 1993.     

Postextrasystolic aortic pressure pulse response in coronary artery disease.

The response of the aortic systolic pressure after an extrasystole was evaluated in 100 consecutive patients with coronary artery disease. The patients were divided into four groups depending on the response of the first postextrasystolic beat. Group IA (45 patients), had lower systolic pressure, whereas group IB (40 patients), had a similar systolic pressure in the postextrasystolic beat, as compared to beats preceding the extrasystole. Group IIA (12 patients) and group IIB (3 patients), demonstrated an increased systolic pressure in the first postextrasystolic beat with subsequent beats in group IIB, also demonstrating pulsus alternans. Congestive heart failure and cardiomegaly were significantly more frequent in group II, as compared to group I patients. In group IIA and IIB, triple vessel disease was present in 83 and 100 per cent, respectively, as compared to 44 per cent in group I patients. Left ventricular end-diastolic pressure (mm. Hg) was 14 ± 6 and 12 ± 7 in group IA and IB respectively, as compared to 19 ± 9 (p < 0.025) in group IIA and 31 in group IIB. Comparing groups IA and IB with each other for cardiac output, stroke volume, end-diastolic volume and ejection fraction, revealed no significant difference. The cardiac output (L./min./M.²) was 2.2 ± 0.6 for group IIA, as compared (p < 0.01) to 2.8 ± 0.5 and 2.9 ± 0.5 in groups IA and IB. Stroke volume (ml./M.²) and ejection fraction were 30 ± 10 and 0.30 ± 0.08, respectively, for group IIA, which is signficantly less, as compared to group I patients. The end-diastolic volume (ml./M.²) in group IIA was 102 ± 28, which is significantly (p < 0.001) higher, as compared to group IA and IB. All patients in group IIB had an abnormal cardiac output, end-diastolic volume and ejection fraction. Thus, the differences in response between group I and group II patients to an extrasystole clearly define two distinct hemodynamic groups. The responses observed to an extrasystole are best explained by variable response of each group to postextrasystolic potentiation and aortic impedance.     

Myocardial mechanical restitution and potentiation partly underlie alternans decay of postextrasystolic potentiation: Simulation

Summary We have reported that the postextrasystolic potentiation (PESP) decays in alternans or monotonically, respectively, depending on whether the first postextrasystolic beat interval has a compensatory pause or not, in the canine left ventricle. To get better mechanistic insight into the alternans PESP decay, we hypothesized that the myocardial mechanical restitution and potentiation could partly account for both types of PESP decay. To test this hypothesis, we simulated PESP decay on a computer using a documented equation combining myocardial mechanical restitution and potentiation. We changed the first postextrasystolic beat interval after a fixed extrasystolic beat interval without changing regular and other postextrasystolic beat intervals. The simulated PESP decayed in alternans or monotonically as a function only of the first postextrasystolic beat interval. Thus, the myocardial mechanical restitution and potentiation could partly account for both alternans and monotonic decay of PESP. We conclude that myocardial mechanical restitution and potentiation may partly underlie the initial two alternating beats, the first beat being the most potentiated and the second beat being the most depressed, of alternans PESP decay in the canine heart. This study was partly supported by Grants-in-Aid for Scientific Research (07508003, 09470009, 10558136, 10770307, 10877006) from the Ministry of Education, Science, Sports and Culture, and 1997–1998 Frontier Research Grants for Cardiovascular System Dynamics from the Science and Technology Agency, all of Japan.     

U wave alternans in severe ischaemia

A patient with unstable angina and known heart failure, and marked U wave alternans on the electrocardiogram is reported. Alternans of the U wave with no change in the QRS complex is extremely rare. The relevant literature is reviewed.     

Linkage between mechanical and electrical alternans in patients with chronic heart failure

INTRODUCTION: Progressive heart failure and ventricular fibrillation are major causes of death in patients with chronic heart failure. Mechanical alternans (pulsus alternans) has been observed in patients with severe congestive heart failure. Visible T wave alternans occasionally is a precursor of ventricular fibrillation. We investigated the occurrence of both cardiac alternans in 94 patients with chronic heart failure. Methods AND RESULTS: Mean left ventricular ejection fraction (LVEF) of the study population was 35 +/- 10%. Mechanical alternans was detected in left ventricular pressure during diagnostic cardiac catheterization. Only sustained mechanical alternans was included in the study. Visible T wave alternans, not microvolt alternans, was noted on standard surface ECG. Cardiac alternans was examined at rest, during physiologic tachycardia, and during stepwise dobutamine loading (2-4-8 microg/kg/min). Prevalences of mechanical and electrical alternans were 19.1% and 4.4% at rest, 45.5% and 8.0% during physiologic tachycardia, and 62.1% and 9.5% under dobutamine loading. Overall, 70 patients (74.5%) showed mechanical alternans and 10 patients (10.6%) showed T wave alternans. T wave alternans always appeared with large mechanical alternans. Among patients with mechanical alternans, cases with T wave alternans showed lower LVEF than those without (27.5 +/- 4.4 and 35.1 +/- 10.2, P < 0.002). CONCLUSION: Visible T wave alternans was detectable in patients with chronic heart failure, especially under tachycardia or catecholamine exposure. Investigating mechanical and mechanoelectrical alternans may bring new insights into the management of patients with chronic heart failure.     

Postextrasystolic U Wave Augmentation, a New Marker of Increased Arrhythmic Risk in Patients Without the Long QT Syndrome

Objectives. We attempted to determine the correlation between the presence of postextrasystolic changes in the STU segment and a history of sustained ventricular arrhythmias.

Background. Postextrasystolic U wave augmentation (a marked increment in U wave amplitude after premature ventricular complexes [PVCs]) is an adverse prognostic sign in the “pause-dependent long QT syndrome.” However, the prevalence of postextrasystolic changes in patients without the long QT syndrome is unknown.

Methods. We compared the configuration of the STU segment of the postextrasystolic beat (the sinus beat after a PVC) with the STU configuration during sinus rhythm in three patient groups: 1) 41 patients with spontaneous ventricular tachycardia/fibrillation (VT/VF) (VT/VF group), 2) 63 patients with heart disease and high grade ventricular arrhythmias (control group), and 3) 29 patients with high grade ventricular arrhythmias but no heart disease (reference group).

Results. Postextrasystolic T wave changes did not correlate with a history of ventricular tachyarrhythmias. However, postextrasystolic U wave changes were more common among the patients with VT/VF than among control subjects (39% vs. 8.7%, p < 0.001). By logistic multiple regression analysis, a low left ventricular ejection fraction (p < 0.001) and postextrasystolic U wave changes (p < 0.005) were independent predictors of ventricular tachyarrhythmias.

Conclusions. Postextrasystolic T wave changes are common and lack predictive value. Postextrasystolic U wave changes may be a specific marker of a tendency to the development of spontaneous ventricular arrhythmias. Prospective studies should be performed to confirm this association.

(J Am Coll Cardiol 1996;28:1746–52)>     

Postextrasystolic Repolarization Abnormalities in ST‐U Segment in Patients with Ventricular Arrhythmias

Background: Changes in U‐wave amplitude after premature ventricular contractions (PVC) are known as prognostic markers in the long QT syndrome dependent on bradycardia. The purpose of the study was to find correlation between postextrasystolic ST‐U segment changes and a history of sustained ventricular tachycardia or ventricular fibrillation (VT/VF). Methods: The ST‐U segment configurations were taken from the 24‐hour ambulatory ECG. The comparison of the morphology of these segments was performed between sinus beats preceding PVC's and first postextrasystolic beats. Population: Two groups of patients were evaluated: 1) 32 patients with VT/VF history (VT/VF group), and 2) 36 patients with potentially malignant arrhythmia (structural heart disease with frequent PVCs and/or nonsustained VT‐nsVT) tnon‐VT/VF group). Results: We found T‐wave changes in 8 patients (25%) from the VT/VF group and in 12 patients (33.3%) from the nonVT/VF group (P = NS) and U‐wave changes in 13 patients (40.6%) and 3 patients (8.3%), respectively (P < 0.05). Other ECG indexes related to PVC's were also considered: RR interval, coupling interval (Cl), prematurity index (Pl), and postextrasystolic pause (PP). The analysis of these ECG indices revealed, when compared with patients without T‐U‐wave changes, that the occurrence of U‐wave changes was significantly related to longer RR interval of the sinus rhythm preceding PVC: 1025 ± 211 vs 918 ± 200 ms (P < 0.05). The prematurity index was lowest in patients with U‐wave changes: 0.54 ± 0.12 vs 0.65 ± 0.16 (P < 0.01) while postextrasystolic pauses leading to the postextrasystolic U‐wave changes were significantly longer: 1383 ± 223 vs 1130 ± 247 ms (P < 0.001). Cl did not differentiate patients: 556 ± 108 vs 584 ± 117 ms (P = NS). Conclusions: Postextrasystolic changes in ST‐U segment configuration are dependent on bradycardia, low prematurity index of the PVC, and the lengthening of the postextrasystolic pause. U‐wave changes more frequently appeared in patients with malignant arrhythmias. Follow‐up study is needed to assess if they might be predictive for the occurrence or reoccurrence of arrhythmic episodes. A.N.E. 2002;7(1):17–21     

The postextrasystolic T wave change

Microelectrophysiologic studies of canine and human ventricular myocardium demonstrate characteristic changes in the configuration of the transmembrane action potential upon abrupt rate change. Additional studies have shown also that these action potential changes, involving cellular repolarization (phase 2 and phase 3), correlate closely with the magnitude of the concurrent postextrasystolic contractile changes. Further experiments in normal anesthetized dogs demonstrate that the postextrasystolic T wave change relates significantly to the magnitude of the postextrasystolic contractile potentiation. In addition, depression of the contractile state by pentobarbital enhanced the relative magnitude of postextrasystolic contractile change, whereas enhancement of the contractile state by acetylstrophanthidin yielded a lessening of the relative magnitude of postextrasystolic contractile potentiation. However, the associated T wave relation persists, as a result of which the postextrasystolic T wave change is more prominent in the presence of myocardial depression of contractility. It has therefore been suggested that the postextrasystolic T wave change is basically a normal phenomenon correlating with the magnitude of postextrasystolic contractile change. The observed association of the postextrasystolic T wave change with myocardial disease may reflect the relatively greater postextrasystolic contractile change associated with depression of the contractile state. A review of clinical electrocardiograms appears to corroborate this contention, demonstrating that when other variables are excluded exhibition of the postextrasystolic T wave change relates significantly to the closeness of the coupling of the premature complex and the magnitude of the base line T wave.     

Effects of stable and changing rates and premature ventricular beats on transient tachycardia-, pseudobradycardia-, and bradycardia-dependent bundle branch block alternans.

New circumstances under which bundle block (BBB) alternans may appear or disappear are described. 1) Tachycardia-dependent as well as bradycardia-dependent BBB alternans may begin after constant BBB is interrupted by a premature ventricular beat. Tachycardia- and bradycardia- dependence may be differentiated by the shape of the first beat after the pause. 2) When BBB alternans disappears during a constant ventricular rate, tachycardia-dependent BBB alternans changes to persistent normal or more normal intraventricular conduction, whereas bradycardia-dependent BBB alternans changes to a persistently greater degree of BBB. 3) BBB alternans appears to be tachycardia- or pseudobradycardia-dependent in relation to the cycle length and antegrade and retrograde refractory periods in the involved bundle branch. 4) BBB alternans may be recognized during persistent irregular ventricular action in atrial fibrillation. Here the recognition of BBB alternans depends upon the sequence of contours as well as upon the cycle lengths.     

Postextrasystolic T wave changes in normal canine hearts

Premature ventricular beats were induced at variable coupling intervals and postextrasystolic T wave changes were observed following various postextrasystolic cycle lengths in 19 closed chest dogs with normal hearts. Following relatively longer postextrasystolic cycle lengths, reversal of the T wave polarity was seen in six dogs (31%), only T wave amplitude changes were seen in 6 dogs (31%), and no significant T wave changes were seen in seven dogs (38%). It was concluded that postextrasystolic T wave changes occur in normal hearts and have no useful diagnostic values.     

Postextrasystolic T wave changes and angiographic coronary disease.

The significance of postextrasystolic T wave changes in beats following induced extrasystoles was assessed by angiography in 55 patients. These T wave changes were found in 81 per cent of coronary artery disease patients but also in 68 per cent of patients with normal coronary arteries (PNS). All patients with normal baseline electrocardiograms and normal coronary arteries showed postextrasystolic T wave changes. In electrocardiographic leads corresponding to the distribution of major coronary arteries, T wave changes occurred just as frequently when the artery was normal (54%) as when the artery was stenosed (55%). Left ventricular asynergy was not associated with an increased frequency of postextrasystolic T wave changes and in fact ejection fraction was greater end-diastolic pressure lower in patients with T wave changes. Thus, postextrasystolic T wave changes appear not to be useful in diagnosing or localising coronary artery disease.     

The influence of ectopic beats and tachyarrhythmias on stroke volume and cardiac output

The potentially adverse influence of premature ectopic beats or tachyarrhythmias on cardiac performance was studied by assessing the echocardiographic left ventricular stroke volume in 21 patients with cardiac rhythm disturbances. The beat to beat stroke volume correlated closely with end-diastolic volume in each patient, (averge R=.9). Premature ventricular contractions decreased stroke volume by an average of 48±8 ml (−71%) compared with sinus beats; whereas the postextrasystolic beats, although preceded by a pause and higher end-diastolic volume, increased stroke volume by only 16±7 ml (18%) over the sinus, beats. Those postextrasystolic beats with equivalent timing and end-diastolic volume to the sinus beats had a mean stroke volume only 8 ml higher, suggesting that postextrasystolic potentiation plays only a minor role in augmenting stroke volume. Transient aberrant ventricular conduction of intermittent left bundle branch block, ectopic beats or atrial fibrillation failed to alter stroke volume. Ventricular bigeminy, trigeminy and quadrigeminy lowered cardiac output by 1.3, .9 and .7 l/min. The onset, of tachyarrhythmias was oftentimes associated with a continuously changing end-diastolic volume and stroke volume, with either alternation or progressive increment of these variables.It is apparent that premature contractions decrease stroke volume by virtue of their infringement on diastolic, filling, the principle beat to be determinant of stroke volume in arrhythmias being left ventricular end-diastolic volume. Since premature beats decrease stroke volume to an extent greater than postextrasystolic beats increase it, they may reduce cardiac outpout by a substantial degree, depending on their frequency of occurrence and degree of prematurity.     

Statistical analysis of the different factors which could affect postextrasystolic potentiation in the human heart.

The effect of different coupling indices and intervals that could theoretically affect postextrasystolic potentiation has been investigated. A total of 150 ventricular premature beats corresponding to 20 patients submitted to routine cardiac catheterization were studied. Only single ventricular premature contractions following at least four regular sinus beats were considered. Percentage changes in left ventricular systolic pressure, end-diastolic pressure, and max dp/dt were correlated against seven indices and intervals. Index 2 (coupling interval/coupling interval + postextrasystolic pause) gave the better correlations. Besides, this Index includes two intervals that were demonstrated to have statistical significance when individually considered. It has been proved that in the first postextrasystolic beat the highest values of max dt/dt, or left ventricular systolic pressure occurred in early ventricular premature beats, giving a negative regression with Index 2, while in the second postextrasystolic beat the highest values of max dp/dt and left ventricular systolic pressure corresponded to late prematuring beats, giving therefore positive regressions with Index 2 (slope inversion phenomenon). The third and fourth postextrasystolic beats had similar positive regressions but with progressively smaller slopes. Correlations between left ventricular end-diastolic pressure and Index 2 were very poor. It is suggested that variations in baroreceptor activity could account for the different forms of potentiation observed in early and late extrasystoles. In five cases, there were no consistent differences in potentiation when premature beats were elicited from either right or left ventricles.     

Postextrasystolic T wave changes and angiographic coronary disease.

The significance of postextrasystolic T wave changes in beats following induced extrasystoles was assessed by angiography in 55 patients. These T wave changes were found in 81 per cent of coronary artery disease patients but also in 68 per cent of patients with normal coronary arteries (PNS). All patients with normal baseline electrocardiograms and normal coronary arteries showed postextrasystolic T wave changes. In electrocardiographic leads corresponding to the distribution of major coronary arteries, T wave changes occurred just as frequently when the artery was normal (54%) as when the artery was stenosed (55%). Left ventricular asynergy was not associated with an increased frequency of postextrasystolic T wave changes and in fact ejection fraction was greater end-diastolic pressure lower in patients with T wave changes. Thus, postextrasystolic T wave changes appear not to be useful in diagnosing or localising coronary artery disease.     

Alternating atrial electromechanical dissociation as contributing factor for pulsus alternans.

Ten patients with mechanical pulsus alternans were studied by echocardiography and mechanocardiography. All had been or were in congestive heart failure. An atrial mechanism for pulsus alternans could be identified in two patients: one with primary congestive cardiomyopathy and one after aortic valve replacement for calcific aortic stenosis. Each strong systole was preceded by an "a" wave, while each weak systole was not. This was documented on both the apexcardiogram and the M-mode echocardiogram. Since both patients were in normal sinus rhythm with regular PP intervals, it was concluded that alternating atrial electromechanical dissociation was either the underlying mechanism or contributed to the pulsus alternans. Thus, alternating atrial electromechanical dissociation exists and may cause pulsus alternans. Pulsus alternans is not necessarily the result of left ventricular myocardial dysfunction alone.     

Occult T Wave Alternans in Long QT Syndrome

T Wave Alternans in LQTS. T wave alternans that is visually apparent on the ECG is a known risk factor for sudden death in idiopathic long QT syndrome (LQTS). To determine if occult and visually undetectable forms of T wave alternans are also present in LQTS, we measured T wave alternans from a 16-year-old girl with LQTS during exercise using spectral analysis methods and a recording system designed to minimize exercise-related noise. While there was no alternans at rest, statistically significant, yet visually inapparent T wave alternans were measured both during exercise and recovery. Using identical recording techniques, no significant T wave alternans was detected from the subject's mother, who had a prolonged QT interval but was not experiencing arrhythmias, nor from five healthy volunteers with normal QT intervals. This report suggests that electrocardiographically occult, yet prognostically important forms of T wave alternans may be present in patients with LQTS.     

T wave alternans is a predictor of death in patients with congestive heart failure

Few data are available about the prognostic role of T wave alternans in patients with congestive heart failure. To assess the ability of T wave alternans, used alone or in combination with other risk markers, to predict cardiac death in decompensated patients, we enrolled 46 patients, mean age 59+/-9, males 89%, ischemic etiology 61%, NYHA class III 35%, left ventricular ejection fraction 29+/-7%. After 1.6 years follow-up, seven patients died from cardiac death (16%), non-sudden in six (86%) and sudden in one (14%). T wave alternans was positive in 24 (52%), negative in 13 (28%), indeterminate in nine patients (20%). T wave alternans was positive in all patients with events (100%) but only in 16 of 37 patients without (41%) (P=0.02). Other predictors of cardiac death were O(2) consumption at the peak of exercise (P=0.03), standard deviation of all NN intervals (P=0.05) and Wedge pressure (P=0.03). When receiver operator characteristics curves were calculated, the highest area (0.73) was found for O(2) consumption at the peak of exercise considering the single variables and for O(2) consumption at the peak of exercise plus T wave alternans (0.79) for combination of them; the comparison of the two receiver operator characteristics curves did not reach statistical difference (P=0.5). In conclusion, this is the first study reporting that T wave alternans can predict cardiac death, with a marginal additional prognostic power when used in combination with measurement of O(2) consumption at the peak of exercise.