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.     

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.     

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.     

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)>     

Effect of postextrasystolic potentiation on systolic bulging of ischemic myocardium

Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined. By 5 min after the left anterior descending coronary artery was occluded, there was regional bulging. Postextrasystolic potentiation diminished the extent of bulging by increasing both isovolumic and ejection percent systolic shortening (isovolumic -9.1 +/- 2.0% to -5.9 +/- 1.7%, p less than 0.008; ejection 2.2 +/- 0.7% to 4.3 +/- 2.0%, p less than 0.008). The tension-length loops after coronary occlusion showed an exponential upstroke and almost superimposed downstroke consistent with passive movement. The loops were unchanged by postextrasystolic potentiation. Wall tension data showed that bulging was reduced because of a shift down the tension-length curve as end-systolic wall tension was reduced by augmented nonischemic contraction. Similar results were seen at 60 min of coronary occlusion. This study demonstrates that the decrease in bulging seen with postextrasystolic potentiation is due to changes in loading conditions and not to contractile reserve.     

Direct stimulation of the sinus node in man. A possible explanation for an unusual finding during premature atrial stimulation.

An atypical behavior of the postextrasystolic pauses was observed in a 19-yr-old patient studied by His bundle electrography and programmed premature atrial stimulation. In the normal case there is a prolongation of the postextrasystolic pauses compared to the spontaneous cycle length allowing calculation of sinoatrial conduction time (SACT). In this case there were constant postextrasystolic pauses during the whole range of prematurity which were identical to the spontaneous cycle length. It is suggested that the catheter tip was accidentally positioned at the sinus node itself. The lengths of the spontaneous cycles, of the return cycles, and of the postreturn cycles showed no significant differences. Thus, one may assume that sinus node automaticity was not influenced in this case.     

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     

Effects of pacing rate and timing of defibrillation shock on the relation between the defibrillation threshold and the upper limit of vulnerability in open chest dogs

To test the relation between the defibrillation threshold and the upper limit of vulnerability, the shock strength associated with 50% probability of successful defibrillation (DFT50) and that associated with 50% probability of reaching the upper limit of vulnerability (ULV50) were determined in 20 open chest dogs with use of the delayed up-down method, with pacing drive cycle lengths of 150 to 500 ms and either single 6-ms shocks (10 dogs) or 12-ms biphasic shocks (10 dogs) given at the mid-upslope, peak and mid-downslope of the T wave of electrocardiographic lead II. The shocks were given by means of a patch-patch configuration on the anterior and posterior surfaces of the heart, which was paced from a stimulating electrode attached to the left ventricular apex. Analysis of variance showed no statistically significant differences in ULV50 as determined with different pacing cycle lengths. For monophasic shocks, DFT50 (331 +/- 66 V or 5.8 +/- 2.7 J) was not significantly different from ULV50 determined at the mid-upslope of the T wave (318 +/- 64 V or 5 +/- 2 J). The correlation coefficients between the two values were 0.74 (p = 0.014) for voltage and 0.67 (p = 0.034) for energy. In contrast, DFT50 was significantly higher than ULV50 as determined at the peak of the T wave (219 +/- 43 V or 2.3 +/- 1 J) and mid-downslope of the T wave (200 +/- 38 V or 1.9 +/- 0.9 J). In three dogs, ventricular fibrillation could not be induced at the mid-downslope of the T wave with any baseline pacing (Si) cycle length.(ABSTRACT TRUNCATED AT 250 WORDS)     

U wave alternans: an electrocardiographic sign of left ventricular failure

All postextrasystolic complexes seen over a twelve year period were carefully analyzed. Normally only the first complex is different, showing a slightly altered T and a larger U wave. Ten patients with left ventricular failure and postextrasystolic pulsus alternans consistently showed postextrasystolic U wave alternans. Besides introducing an electrocardiographic sign of heart failure, this provides some insight into the underlying etiology of the U wave.     

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.     

Cyclical changes in high-energy phosphates during the cardiac cycle by pacing-Gated 31P nuclear magnetic resonance.

Whether cyclical changes in energy-related phosphate metabolites arise during a cardiac cycle in isolated rat hearts and are affected by differences in myosin isozyme composition was determined. Myocardial adenosine triphosphate (ATP), phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH in normal, hypothyroid and hyperthyroid rat hearts were measured using the pacing-gated 31P nuclear magnetic resonance technique. Maximal decrease in ATP and PCr, and maximal increase in Pi at the peak-systole in normal rat hearts were observed. In hypothyroid and hyperthyroid rats, similar cyclical changes in phosphate metabolites were observed during the cycle. However, the magnitude of fluctuations was smaller in hypothyroid rats and larger in hyperthyroid rats compared with that observed in normal rats. Cardiac myosin isozyme patterns were also different amongst the experimental groups. The results suggest that cyclical changes and the magnitude of fluctuations in energy-related phosphate metabolites during a cardiac cycle may depend on the cardiac workload and the intrinsic properties in the enzyme kinetics of myosin.     

Regional, age-dependent, and genotype-dependent differences in ventricular action potential duration and activation time in 410 Langendorff-perfused mouse hearts

Although numerous studies have reported the effects of genetic alterations on murine electrophysiology, the range of normal values for ventricular activation, repolarization, and arrhythmias in mouse hearts is not known. We analyzed right ventricular (RV), left ventricular (LV), and septal activation times, monophasic action potential durations (APD), and right ventricular effective refractory periods during spontaneous rhythm, induced AV nodal block, right ventricular pacing (100–300 ms paced cycle length), and programmed stimulation in 410 beating, Langendorff-perfused, wild-type mouse hearts of CD1, DBAC3H, FVBN, C57/Bl6, and hybrid backgrounds (age 203 ± 132 days). Action potential duration was longer at longer cycle lengths. LV-APD prolonged more than RV-APD, resulting in an increased heterogeneity of APD at longer pacing cycle lengths. Higher heart weight/body weight ratio and DBAC3H and FVB/N backgrounds were associated with long APD, C57Bl/6 background was associated with short APD. Activation times were longer in older hearts. There were no clear-cut sex-dependent APD differences. Sustained spontaneous arrhythmias occurred in 1% of hearts, non-sustained arrhythmias in 18%. Induction of AV block and C57Bl/6 genetic background were associated with spontaneous arrhythmias. Programmed stimulation induced arrhythmias in 51% of hearts. Inducible arrhythmias were associated with advanced age and shorter refractory periods. Ventricular APD in beating mouse hearts show rate- and site-dependent changes comparable to man and large animals. Bradycardia provokes spontaneous arrhythmias in mouse heart, while age-dependent conduction slowing and short refractory periods predispose to induced arrhythmias. Genetic background influences repolarization and arrhythmogenesis. These findings provide systematic data for the design and interpretation of arrhythmia studies in murine disease models.     

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.     

A Role for the Renin-Angiotensin System in the Evolution of Cardiac Memory

INTRODUCTION: We studied the role of the cardiac renin-angiotensin II system in the genesis of cardiac memory, in which T wave changes induced by ventricular pacing (VP) accumulate and persist during subsequent sinus rhythm. METHODS AND RESULTS: Anesthetized dogs were instrumented via a thoracotomy and three 20-minute runs of VP were interspersed with periods of normal sinus rhythm sufficient to permit T wave recovery to 90% of control. Memory was quantified as the change (delta) in T wave vector angle showing accumulation over the three monitoring periods. In five control dogs T wave vector = -27 +/- 49 degrees, and this shifted by 104 degrees (P < 0.05) over the three postpacing recovery periods. In seven dogs infused with the receptor blocker saralasin, five infused with the angiotensin-converting enzyme inhibitor captopril, and four infused with the tissue protease inhibitor chymostatin, there were significant reductions in the incidence and the accumulation of memory. In four other experiments, we used isolated, blood-perfused canine hearts to demonstrate that VP used to induce memory alters the contractile pattern of the left ventricle. CONCLUSIONS: We propose that the alteration in myocardial stretch induced by pacing activates angiotensin II synthesis by cardiac cells. We propose, further that the endogenous cardiac renin-angiotensin II system (blocked by saralasin, captopril and by chymostatin) is an important contributor to the induction of memory.     

Is all Ventricular Fibrillation the Same?

INTRODUCTION: Little information is available on the relationship between the mode of induction of ventricular fibrillation (VF) to VF characteristics. METHODS AND RESULTS: VF was induced from the anterior left ventricle by programmed electrical stimulation, burst pacing, alternating current (AC), high current S2 at a site remote from S1, T wave shock, and intersecting wavefronts in seven normal dogs and seven dogs with chronic myocardial infarction. Using two electrode arrays, 112 electrograms were recorded from the anterior and lateral wall. Cycle lengths were analyzed and activation vectors were created by summing orthogonally recorded bipolar electrograms. The magnitude of the vector loops was integrated over time to produce an "ensemble vector" index (EVI) whose magnitude is high when beat-to-beat activation direction is consistent and low when activation direction is variable. T wave shock-induced VF had a significantly longer cycle length 1 to 5 seconds after VF onset than other modes of induction (P < 0.05). The frequency-corrected EVI was significantly larger for AC current and T wave shock-induced VF as opposed to all other modes of VF induction in early VF (P < 0.0001). After 10 seconds of VF, these differences persisted only on the anterior wall. CONCLUSION: VF induced in animals by T wave shock and AC current had different characteristics than VF induced by other methods. These findings may have implications for our understanding of VF pathophysiology.     

Cardiac function and myocardial contractility: a perspective

An experimental study was designed to validate postextrasystolic potentiation assessment of myocardial viability or functional reserve of cardiac segments after acute coronary occlusion. Segmental systolic fractional area changes and wall thickening in pacing-induced postextrasystolic beats were mapped in 12 closed chest dogs by two-dimensional echocardiography during a control period and from 20 minutes to 3 hours after occlusion of the left anterior descending coronary artery. The extent of myocardial ischemic and necrotic zones was evaluated in left ventricular slices and subsegements corresponding to echographic cross sections. During two-dimensional echocardiography, left ventricular segments that were found to be neither ischemic nor necrotic always exhibited a significant augmentation of both fractional area change and wall thickening during the postextrasystolic beat that followed an induced premature contraction with a 42.4% coupling interval. In segments without necrosis but with varying degrees of ischemia, significant postextrasystolic potentiation was also demonstrated, even after 3 hours of occlusion. In contrast, segments that developed more than 80% necrosis failed to potentiate systolic fractional area change after 2 hours, and systolic wall thickening, even after 20 minutes of coronary occlusion. Statistical evaluation revealed a characteristic threshold at 41 to 60% necrosis, beyond which no potentiation of function could be elicited 3 hours after occlusion. Extrapolation from the experimental data suggests that when two-dimensional echographic studies in myocardial ischemia indicate postextrasystolic augmentation of segmental left ventricular function, the latter segments may be assumed to contain only small infarcts or to consist of reversibly ischemic and normal myocardium. Conversely, segments that fail to exhibit postextrasystolic potentiation can be assumed to be more than 60% necrotic.     

In vivo detection of reperfused myocardium by nuclear magnetic resonance imaging

To assess the potential of in vivo nuclear magnetic resonance imaging for the detection of reperfused myocardium, in vivo T2-weighted spin echo images were obtained of dogs at 0.15 tesla. Imaging was done during 3 hours of coronary occlusion (group I), and during 3 hours of coronary occlusion followed by 1 hour of reperfusion (group II). On sacrifice, the hearts were drained of blood and imaged in situ to determine the effect of in vivo imaging on myocardial signal intensity. The hearts were then excised and imaged at 1.4 tesla to compare the effect of high resolution imaging on image quality. Of the six hearts in group I and the eight hearts in group II with a myocardial infarction and suitable image quality, four of the former hearts and six of the latter demonstrated a small but visible increase in infarct signal intensity at 3 hours of occlusion on the time to echo [TE] = 60 ms, single echo images. The T2 (transverse) relaxation time of the infarct (measured in vitro by spectrometer) increased by 13% when compared with normal tissue. In contrast, the reperfused infarct was more easily visualized, with signal intensity increasing by 31 +/- 17% and infarct T2 increasing by 20%. Imaged at 1.4 tesla, the excised hearts showed the infarct to be subendocardial during occlusion and extending transmurally with reperfusion. It is concluded that, although visualized, the increase in infarct signal intensity at 3 hours of coronary occlusion is small and this is consistent with the small increase in infarct signal intensity and T2 relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of intramyocardial hemorrhage using high-field proton (1H) nuclear magnetic resonance imaging

Proton (1H) nuclear magnetic resonance (NMR) imaging has been used to define zones of myocardial infarction (MI), which appear as areas of relatively increased signal intensity (SI). However, zones of decreased SI have been observed within the areas of infarction and have been postulated to result from intramyocardial hemorrhage. To explore this phenomenon further, ex vivo spin-echo 1H NMR imaging at 1.5 Tesla was performed in 17 dogs after 24 hr (n = 9) and after 72 hr (n = 8) of coronary artery occlusion. In all dogs, a zone of increased SI (118 +/- 9% compared with normal myocardium) was observed in the distribution of the occluded coronary artery. In 12 of the 17 dogs, zones of decreased SI (92 +/- 8% compared with normal) were seen within or around the central zone of increased SI. Gross inspection and histological assessment of sliced myocardium usually disclosed hemorrhage in the regions of decreased SI. In three of the five dogs with no apparent zones of decreased SI on NMR, the infarct was small, and only minor hemorrhage was observed by gross inspection, whereas in the remaining two dogs no hemorrhage was seen. Myocardial flow in the hemorrhagic regions was significantly higher than in the necrotic core (59 +/- 29% vs. 31 +/- 24% compared with control, P less than 0.05). Image-derived calculation of T2 relaxation times in the different infarcted regions revealed a significant shortening of T2 in the infarcted hemorrhagic zones with decreased SI compared with the infarct zones with increased SI (49 +/- 8 msec vs. 66 +/- 8 msec, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

T wave changes persisting after ventricular pacing in canine heart are altered by 4-aminopyridine but not by lidocaine. Implications with respect to phenomenon of cardiac 'memory'.

BACKGROUND. Cardiac "memory" refers to changes in T wave polarity induced by ventricular pacing that persist long after resumption of normal atrioventricular conduction. METHODS AND RESULTS. We studied the occurrence and mechanism of T wave changes in the open-chest anesthetized dog subjected to three discontinuous 20-minute periods of right ventricular pacing. ECG changes were recorded in the standard limb leads during normal conduction (prepacing) and three trains (T1, T2, and T3) of right ventricular pacing at a rate 50% higher than normal (pacing), each followed by a period of normal conduction (postpacing) lasting as long as necessary for T wave changes to return to control values. During each of these phases, heart rate, QRS, corrected QT (QTc) duration, and T wave amplitude were measured. In the first group (control), T wave inversions occurred during normal atrioventricular conduction after a period of right ventricular pacing. These T wave anomalies appeared in the absence of any change in heart rate, QRS, or QTc duration. The magnitude of the T wave amplitude change was significantly greater after each successive pacing period. Furthermore, the changes in T wave morphology persisted for a longer period after each successive pacing train. In a second experimental group, lidocaine, which depresses the sodium window current, was administered to six dogs that were subjected to the same pacing protocol. Lidocaine decreased the QTc interval and prolonged QRS duration but did not alter the magnitude of changes in T wave amplitude and time to recovery described in control animals during the three postpacing intervals. In contrast, in the third group, 4-aminopyridine, a drug that blocks the transient outward current (ito), abolished the changes in T wave morphology that occurred during any postpacing interval. CONCLUSIONS. These results demonstrate that the manifestation of cardiac memory in the in situ dog heart is not altered by lidocaine but is abolished by 4-aminopyridine. Thus, cardiac memory may be based on a physiological property of the myocardium that is related to specific K+ channels.     

Response of the left ventricle in coronary artery disease to postextrasystolic potentiation.

Left ventricular volumes and contractile patterns were evaluated during the first sinus beat after a compensatory pause resulting from ventricular arrhythmia and were compared to the second sinus beat (control beat) in order to evaluate the effect of postextrasystolic potentiation. Twelve patients had no evidence of heart disease (group I). Fifty patients had coronary artery disease and included 14 patients (group IIa) with no prior myocardial infarction and a normal left ventricular contractile pattern and 19 pateints (group IIb) with an abnormal contractile pattern. Seventeen pateints (group IIc) had a documented transmural myocardial infarction as well as an abnormal left ventricular contractile pattern. In all patients the first postextrasystolic sinus beat, when compared to the second sinus beat, demonstrated increases in stroke volume and ejection fraction and decrease in end-systolic volume. There were no qualitative changes in the contractile pattern in the immediate postextrasystolic beat in the patients with normal left ventricular function. In both group IIb and group IIc the changes in end-systolic volume, stroke volume and ejection fraction were significantly greater than observed in groups I and IIa. Abnormal wall segments present in the control beat in groups IIb and IIc demonstrated after postextrasystolic potentiation a normal contractile pattern, improved pattern or no change when compared to the control beat. Abnormal wall segments were more likely to revert to normal as a result of postextrasystolic potentiation in group IIb than group IIc. Akinesia was less likely to revert completely to normal than hyposinesia. In 20 of 24 patients the changes in contractile pattern after aortocoronary bypass surgery corresponded to those observed as a result of postextrasystolic potentiation.