Long-term follow-up study after closure of secundum atrial septal defect in children: An echocardiographic study

Serial echocardiography was performed in 51 children with isolated secundum atrial septal defect before and after surgery to measure the effects of chronic right ventricular overload on ventricular function. Right ventricular dilation increased dramatically with growth and with size of the left to right shunt only in the youngest children (body surface area less than 0.5 m²). A lesser effect of growth and no significant effect of shunt size were noted in older children.Although an initial decrease in right ventricular size occurred in the first 3 months after operation, persistent right ventricular dilation remained up to 5 years after closure of the interatrial defect in more than 80 percent of patients. Preoperatively, the ratio of the right ventricular preelection period to ejection time was significantly less than that of normal children. This ratio increased dramatically after operation, exceeding normal values early in the postoperative period in 18 of 48 children and persisting in 6 of 22 after 3 months. Left ventricular dimensions were normal early and late after operation. Left ventricular function was apparently normal, although] an exceptionally high shortening fraction was noted in 22 (44 percent) of 51 children after operation. Aortic systolic time interval ratios decreased after operation from high normal to low normal values.It is hypothesized that the persistent enlargement of the right ventricle after operation may be due to the chronic preoperative dilation secondary to chronic interatrial shunting. The abnormally high shortening fraction after operation may result from an abnormal left ventricular geometric configuration or abnormality of filling. It is suggested that surgical closure of the atrial defect in the first 3 years of life may prevent these abnormalities.     

Spontaneous compared with induced onset of sustained ventricular tachycardia

Electrophysiological characteristics of the modes of initiation of 16 episodes of spontaneously occurring sustained ventricular tachycardia recorded in 16 patients by two-channel ambulatory electrocardiographic monitoring were compared with the characteristics of ventricular tachycardia induced by programmed electrical stimulation. Eleven episodes of spontaneous ventricular tachycardia began after a single ventricular premature depolarization (VPD), three episodes after two VPDs, and two episodes after five VPDs. By comparison, only four episodes of sustained ventricular tachycardia were induced with a single VPD. Each episode of spontaneous ventricular tachycardia was initiated by a late coupled VPD (RR':QT ratio greater than 1.0). The VPD was often morphologically similar to the ensuing ventricular tachycardia (eight of 11 episodes that began after a single VPD). No correlation was found between the modes of initiation of spontaneous and induced ventricular tachycardia. We hypothesize that concealed decremental slow conduction, reflected in the long coupling intervals of VPDs initiating ventricular tachycardia, is of critical importance in initiating ventricular tachycardia. We conclude that major differences exist in the timing and number of VPDs associated with the onsets of spontaneous and induced sustained ventricular tachycardia.     

Serial changes in left ventricular relaxation and chamber stiffness after large myocardial infarction in rats

To determine the time course of changes in left ventricular diastolic properties after a large myocardial infarction, we serially measured left ventricular relaxation, chamber stiffness, and the ratio of left ventricular cavity to wall volume (V/VW) after coronary artery ligation in rats. Left ventricular relaxation was measured during the occlusion and then both relaxation and chamber stiffness were measured at 3 hr, 24 hr, and 3, 5, and more than 22 days after infarction. Left ventricular pressures and left ventricular dP/dt were recorded with micromanometer-tipped catheters. Left ventricular relaxation was measured by computer digitization of the left ventricular pressure tracings and averaged over 100 to 150 cardiac cycles. Five chamber stiffness constants were calculated from pressure-volume curves that were obtained ex vivo. We found ventricular relaxation prolonged for the first hour after coronary occlusion; relaxation was maximally prolonged at 10 to 15 min after onset of occlusion. After 1 hr relaxation returned to normal. However, by 5 days ventricular relaxation was again prolonged. Left ventricular stiffness constants were increased at 3 and 24 hr, resulting in a shift of the left ventricular pressure-volume relation to the left. At 3 days after coronary artery ligation, all stiffness constants and the pressure-volume relation returned to normal. At more than 22 days the pressure-volume relation was shifted to the right and the stiffness constant for low filling pressures was decreased. V/VW was significantly decreased from 0.603 +/- 0.021 at 3 and 24 hr to 0.379 +/- 0.024 and 0.362 +/- 0.032, respectively. V/VW was significantly increased at more than 22 days (0.921 +/- 0.094).(ABSTRACT TRUNCATED AT 250 WORDS)     

比索洛尔联合苯那普利对脑出血后室性心律失常的疗效观察

目的分析比索洛尔联合苯那普利对脑出血后室性心律失常的治疗效果。 方法选取2016年5月至2017年6月荣成市人民医院收治的60例脑出血后室性心律失常患者,按随机数表法分为对照组与研究组。对照组患者接受比索洛尔治疗,研究组患者接受比索洛尔联合苯那普利治疗。采用24 h动态心电图对患者用药治疗前后心率、室性期前收缩次数进行监测,于治疗前后进行NIHSS评分。 结果治疗后,两组患者心率均较治疗前降低(P<0.05),研究组患者心率低于对照组(P<0.05)。研究组患者治疗后室性期前收缩的发生次数低于对照组,差异有统计学意义(P<0.05)。治疗后,两组患者NIHSS评分均较治疗前降低(P<0.05);观察组治疗后NIHSS评分低于对照组(P<0.05)。 结论比索洛尔联合苯那普利可以减少脑出血后室性心律失常患者室性期前收缩发生次数,有效治疗脑出血后室性心律失常,有利于神经功能的改善,可以进一步推广应用。     

Change in filling pattern with preload reduction reflects left ventricular relaxation

BACKGROUND: The early diastolic mitral valve pressure gradient and the rate of left ventricular filling are determined by the rate of left ventricular relaxation and left atrial pressure at the time of mitral valve opening. Accordingly, we hypothesized that the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved systolic function. METHODS: We evaluated the relationship between the logistic time constant of left ventricular relaxation and left ventricular filling pattern calculated from the time derivative of left ventricular volume using a microtipmanometer and a conductance catheter in 26 consecutive patients with preserved left ventricular ejection fraction (>45%). Left ventricular filling patterns were determined from the maximal rates of early diastolic left ventricular filling (E velocity) and atrial filling (A velocity) before and after preload reduction by inferior venal caval occlusion. RESULTS AND CONCLUSIONS: There was no significant relationship between the logistic time constant of left ventricular relaxation and the E/A velocity ratio at baseline. However, the time constant was correlated with the E/A velocity ratio after venal caval occlusion (r=-0.47, p=0.02). Furthermore, the time constant was correlated with %E/A velocity change, which was defined as the rate of change of E/A before and after caval occlusion divided by E/A after caval occlusion, more significantly (r=-0.67, p<0.01) than with the E/A velocity ratio after caval occlusion. Thus, the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved left ventricular ejection fraction.     

Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices

Implantable defibrillators use algorithms based on ventricular electrographic data to detect the onset and termination of arrhythmias, but these algorithms do not always differentiate hemodynamically stable from unstable arrhythmias. Although, ideally, left ventricular function should be used to assess the hemodynamic state, right ventricular pulse pressure can be assessed in humans on a long-term basis with a transvenous lead. The potential utility of right ventricular pulse pressure to assess hemodynamic stability was studied in 22 patients with induced ventricular arrhythmias. Right ventricular pressure was measured with use of a transvenous right ventricular endocardial pacing lead with a piezoelectric bender pressure sensor 3 cm from its tip. Single ventricular premature paced beats administered in up to a bigeminal frequency did not alter the mean right ventricular pulse pressure (control 33.7 +/- 26, bigeminy 35.7 +/- 26 mm Hg). Twenty-one episodes of induced ventricular tachycardia were studied in the electrophysiology laboratory. Five seconds after tachycardia induction, hemodynamically stable ventricular tachycardia had a longer cycle length (294 +/- 41 ms) and the right ventricular pulse pressure ratio was higher (0.55 +/- 0.26) than that in unstable ventricular tachycardia (cycle length 256 +/- 55 ms, p = 0.06; pulse pressure ratio 0.26 +/- 0.09, p less than 0.05). Twenty episodes of ventricular fibrillation were induced in eight patients. One second after induction, right ventricular pulse pressure decreased from 25 +/- 5 to 6 +/- 3 mm Hg (p less than 0.05). On the first beat after defibrillation, right ventricular pulse pressure increased to 24 +/- 14 mm Hg, a level not significantly different from that before the induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of the mitral complex in left ventricular contraction--an analysis of the results of mitral valve replacement with preservation of the posterior mitral complex

The importance of the mitral complex in left ventricular contraction was studied in seventy-five patients who underwent mitral valve replacement (MVR) with preservation of the posterior mitral complex (modified MVR:mMVR), and in one hundred and twenty-two patients who had conventional mitral valve replacement (cMVR). Mechanical heart valves (Medtronic Hall or St. Jude Medical valves) were used in MVR. Patients after mMVR showed lower left atrial pressures, higher left ventricular stroke work indexes, and better left ventricular function curve using less catecholamines than those after cMVR during the initial 24 hours following cardiopulmonary bypass. M-mode echocardiographic analysis revealed that the sequential apex-to-base contraction of the ventricular wall was better preserved after mMVR than after cMVR. This tendency was more prominent in mitral regurgitation (MR) than in mitral stenosis (MS) patients. Echocardiographic analysis revealed that the posterior mid left ventricular segment began to contract and reached maximal contraction earlier than the basal segment in patients before and after mMVR. After cMVR, this tendency was less noticeable, and the contraction processed and peaked almost simultaneously in all segments. The mitral complex plays an important role in left ventricular contraction, and modified MVR can be said to be an excellent procedure for preserving left ventricular function.     

Echocardiographic pressure-dimension analysis following anatomically corrective operation of d-transposition of the great arteries

The major theoretical advantage of anatomic correction of transposition of the great arteries compared with intraatrial repair is that the left ventricle becomes the systemic pump. In 10 patients we analysed 5-12 months after anatomic correction the left ventricular echocardiographic pressure-dimension loop, meridional wall stress and left ventricular stiffness from the simultaneous recordings of the left ventricular pressure and M-mode echocardiogram. The low left ventricular diameters, left ventricular hypertrophy in 4 patients, and increased peak meridional wall stress in 3 patients indicate that left ventricular adaption to systemic impedance is still incomplete 5-12 months after anatomic correction. The cycle efficiency was reduced in 2 patients, indicating incoordinate left ventricular contraction and relaxation. In one of these patients the left ventricular stiffness was severely increased, while in another patient there was a slight increase in left ventricular stiffness. In all patients the right ventricular internal diameter was increased due to the long-standing preoperative pressure and volume overload.     

右心室流入道间隔部起搏血流动力学研究

目的本文旨在对右心室流入道间隔部起搏的血流动力学进行分析,以确立右心室流入道间隔部起搏的临床地位。方法本研究通过射频消融房室结建立Ⅲ°房室传导阻滞模型,结合影像学及心电图定位方法于右心室流入道间隔部置入螺旋电极导线,并分别比较右心室心尖部、右心室流出道及右心室流入道间隔部起搏后急性血流动力学指标变化,并随访右心室流入道间隔部起搏2周后的血流动力学指标。结果即刻血流动力学研究结果显示,右心室流入道间隔部较心尖部和右心室流出道起搏心排血量高(P<0.05),左心室舒张末期压力较低(P<0.05),而右心室流入道间隔部起搏前后各项血流动力学无显著变化。结论右心室流入道间隔部起搏具有良好的血流动力学效应,可作为右心室心尖部起搏的替代起搏部位。     

Treatment of ventricular tachycardia-induced cardiomyopathy by transcatheter radiofrequency ablation.

Catheter ablation of ventricular tachycardia was successfully performed in a patient with dilated cardiomyopathy (ejection fraction 38%) and a long history of repetitive palpitations. Holter monitoring showed ventricular tachycardia that had a left bundle branch block QRS configuration with inferior axis deviation and was present for about one third of the daytime hours. At electrophysiological testing, ventricular tachycardia was reproduced by isoprenaline infusion. Radiofrequency energy delivered to the right ventricular outflow tract was successful at preventing the induction of ventricular tachycardia. Left ventricular ejection fraction had improved from 38% to 48% one month after ablation. During the follow up period of one year the patient remained free from arrhythmia on no medication. The ejection fraction was 61% one year after ablation. This report confirms that dilated cardiomyopathy can be induced by ventricular tachycardia and demonstrates that dilated cardiomyopathy can be reversed if the tachycardia is abolished by radiofrequency catheter ablation.     

Interaction of platelets with the vessel wall in the pathophysiology of sudden cardiac death

The occurrence of ventricular fibrillation after occlusion of the circumflex coronary artery in the conscious dog was examined as one preparation for sudden cardiac death arising from coronary artery disease. The incidence of ventricular fibrillation after after circumflex occlusion was reduced from 53% to 6% (p less than .01) by the infusion of prostacyclin in doses that do not alter cardiac output or peripheral resistance. This effect of prostacyclin led to the evaluation of two structurally different inhibitors of thromboxane synthase in this preparation; RO 22-4679 and U-63557A reduced ventricular fibrillation by 82% and 100%, respectively (p less than .05). The inhibition of ventricular fibrillation by U-63557A was abrogated by pretreatment with indomethacin, suggesting that a metabolite of the endoperoxide that accumulated during thromboxane synthase inhibition was responsible for the protection from ventricular fibrillation.     

Changes in left ventricular torsion during ischemia-reperfusion

We aimed to characterise the alterations of left ventricular twist during ischaemia-reperfusion and to study their relationship to global left ventricular function. Systolic left ventricular twist was measured at the mid-papillary muscle level by colour tissue Doppler echocardiography in 7 anaesthetised open-chest dogs at baseline, 90 min-occlusion of the left anterior descending, and 180 min after reflow. Tissue Doppler was also performed in 34 patients after anterior infarct and in 20 controls. In controls, rotation occurred counterclockwise when viewed from the base. In a random subset of subjects, the assessment of ventricular twist by tissue Doppler was validated against magnetic resonance myocardial tagging. Myocardial ischaemia led to a decrease in ventricular twist in dogs and infarct patients (p < 0.01). This decrease was correlated with the extent of the asynergic area and global left ventricular function (p < 0.001). In dogs, cardiac twist was higher after reflow relative to ischaemia (p < 0.01). Thus, acute myocardial ischaemia is responsible for a decrease in left ventricular twist that is related to global ventricular function. Colour tissue Doppler echocardiography provides straightforward assessment of left ventricular twist in humans.     

Relationship between shock energy and postdefibrillation ventricular arrhythmias in patients with implantable defibrillators

BACKGROUND: The relationship between postdefibrillation ventricular arrhythmias and shock strength is poorly understood in patients with implantable defibrillators. The purpose of this study was to characterize the relationship between postdefibrillation ventricular arrhythmias and shock strength. METHODS AND RESULTS: Forty-three patients with an implanted defibrillator underwent six separate inductions of ventricular fibrillation (VF) after a step-down defibrillation energy requirement (7.3 +/- 4.6 J) was determined. For each of the first three inductions of VF, the first two shocks were low energy and equal to approximately 75% of the defibrillation energy requirement (5.4 +/- 3.3 J), or to the defibrillation energy requirement plus 10 J (17.5 +/- 4.3 J). After the first two shocks, subsequent shocks were programmed to the maximum available energy (29.0 +/- 2.5 J). The alternate technique was used for the subsequent three inductions of VF. Postdefibrillation ventricular arrhythmias were noted. Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec were more frequent after a low-energy shock (19%), than after a high-energy shock (1.5%; P = 0.005). Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec were more frequent after a high-energy shock (32%), than after a low-energy shock (7.1%; P = 0.002). A relationship between the cycle length of the postdefibrillation ventricular arrhythmias and the absolute defibrillation energy was observed (P < 0.001; r = 0.6), and ventricular arrhythmias with a cycle length > 300 msec were uncommon after shocks < or = 10 J (P = 0.001). The characteristics of ventricular arrhythmias after maximum-energy shocks were similar to those that occurred after high-energy shocks. CONCLUSIONS: Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec are more common after shocks of strength associated with a low probability of successful defibrillation. Postdefibrillation ventricular arrhythmias with a cycle length of > 300 msec are more common after high- and maximum-energy shocks, and are directly related to the absolute defibrillation energy.     

Daily serial evaluation of left ventricular function with equilibrium radionuclide ventriculography following thrombolysis during acute myocardial infarction

The changes in ventricular function after reperfusion by coronary thrombolysis are important when deciding about further definitive treatment necessary to ensure long-term vessel patency. The purpose of this study was to evaluate the early changes in left ventricular function after reperfusion. Left ventricular function was serially evaluated for 10 days in a group of 18 patients receiving intracoronary thrombolytic therapy for an acute myocardial infarction. Comparison of the global ventricular function in the successfully and unsuccessfully reperfused groups of patients showed significantly better function in the successful group than the unsuccessful group after the first day, which was maintained for the entire study period. Global and regional ventricular function in the successfully reperfused patients showed significant early improvement during the initial 72 h with maintenance of this improvement for the study period of 10 days. In the patients in whom reperfusion was unsuccessful, regional ventricular function showed no change, while the global function declined from day 5 to day 8 of the study period. This study then confirms the significant improvement in ventricular function after successful reperfusion. The time course pattern of the change in ventricular function indicates that the most significant improvement occurs within the first 72 h after reperfusion. These changes are similar to those previously reported in experimental animals.     

Effects of ventricular fibrillation and defibrillation on pacing threshold in the anesthetized dog

The effects of transthoracic and internal defibrillation on the bipolar ventricular pacing threshold in 20 anesthetized dogs were examined. Ventricular pacing was accomplished with a computer-controlled, constant voltage pacemaker that permitted rapid determination of pacing threshold. Defibrillation at various energy levels was administered during ventricular pacing and after ventricular fibrillation of 5, 15, 30, 45, 60 or 120 s duration in the 20 dogs. Defibrillation during pacing or within 15 s after initiation of ventricular fibrillation did not significantly increase threshold, regardless of defibrillation energy or mode of delivery. Defibrillation after ventricular fibrillation lasting greater than or equal to 30 s increased (p less than 0.05) threshold determined 6 s after defibrillation. The increase in threshold (in volts) determined 6 s after defibrillation was an exponential function of fibrillation duration (30 s = 0.30 +/- 0.09 V; 45 s = 0.53 +/- 0.13 V; 60 s = 2.24 +/- 1.05 V), but was independent of defibrillation energy or mode of delivery. Threshold returned to control values 15 to 30 s after defibrillation. Cardiopulmonary bypass to maintain coronary perfusion prevented the increase in pacing threshold even after ventricular fibrillation of up to 2 min duration. Pacing threshold is not increased by transthoracic or internal defibrillation, but is increased by ventricular fibrillation of sufficient duration to create substantial myocardial hypoxemia.     

Doppler tissue imaging analysis of ventricular function after surgical and transcatheter closure of atrial septal defect

The long-term ventricular function of children after surgical and transcatheter closure of secundum atrial septal defects was assessed by Doppler tissue imaging and compared with that of age-matched controls. Long-term right ventricular function was impaired in patients after surgical repair, as reflected by decreased systolic and diastolic tricuspid annular velocities and an increased Tei index. In contrast, right ventricular function was preserved after transcatheter device closure.     

Atrial and ventricular volume and function evaluated by magnetic resonance imaging in patients with persistent atrial fibrillation before and after cardioversion

Atrial fibrillation (AF) is the most common cardiac arrhythmia and 25% of those >40 years old will experience AF. Left atrial size and left ventricular function are independently related to cardiovascular morbidity and mortality. Our aim was to evaluate cardiac volume and function using magnetic resonance imaging in patients with persistent AF and to describe the changes after cardioversion (CV). Sixty consecutive patients with persistent AF and 19 healthy volunteers had cardiac volumes evaluated by cinematographic breath-hold magnetic resonance imaging. Patients with AF were evaluated before CV and at 1, 30, and 180 days after CV, if still in sinus rhythm. All atrial and ventricular volumes and left ventricular mass decreased and ejection fractions increased significantly after CV (p <0.0001 for all variables). Atrial and ventricular diastolic volumes increased significantly the day after CV. The atrial diastolic volumes had decreased significantly at 30 days and ventricular volumes at 180 days. The atrial systolic volumes decreased significantly the day after CV, but the ventricular systolic volumes remained constant the day after CV and decreased thereafter. Only the right atrial volumes were normalized 180 days after CV. The same results were found in a subgroup of patients with lone AF. In conclusion, reversal of atrial dimensions and function happened earlier than ventricular reversal after CV in persistent AF. Atrial reversal began immediately and ventricular reversal was not seen before 30 days after CV. Our results suggest that the changes to the left atrium and both ventricles caused by AF could be permanent and that CV of AF may be preferable.     

Relations of preoperative hemodynamics and coronary blood flow to improved left ventricular function after valve replacement for aortic regurgitation

In this study of the limits of reversibility of left ventricular function after aortic valve replacement for aortic regurgitation, measurements were made of pre- and postoperative coronary blood flow and left ventricular volumes. Eighteen patients who had undergone aortic valve replacement for pure aortic regurgitation using the Bj?rk-Shiley valve or the Bicerval valve were restudied an average of 8 +/- 3 months after surgery. Postoperative left ventricular end-systolic and end-diastolic volumes returned to near normal values. The slight left ventricular wall thickening apparent before surgery remained unchanged after surgery and, consequently, left ventricular mass, though somewhat reduced, remained abnormally high. Ejection fraction, which was low preoperatively, returned to normal postoperatively. Total coronary sinus blood flow decreased after surgery, but coronary sinus blood flow per 100 g of left ventricular mass increased. This recovery of coronary flow per unit mass was believed to cause the improvement in left ventricular function. A significant correlation was found between postoperative systolic function and preoperative left ventricular end-systolic and end-diastolic volumes, wall thickness and, especially, left ventricular mass, the latter indicating that, if preoperative left ventricular mass is less than 350 g/m2, postoperative improvement of systolic function is attainable. Another significant correlation was indicated by measurements of coronary sinus blood flow per 100 g of left ventricular mass. If this is greater than 35 ml/min before surgery, a postoperative improvement in systolic function to within the normal range may be expected.     

Proarrhythmic effects of ventricular electrical catheter ablation in dogs

Electrical catheter ablation of arrhythmogenic sites is a new therapy for ventricular tachycardia that is still being investigated. Recent studies have shown, however, that the procedure itself can provoke serious ventricular arrhythmias. The incidence, course and mechanism of these arrhythmias were studied in 10 beagles treated with a single R wave-synchronized cathodal shock delivered to the endocardial ventricular wall (5 dogs left ventricular, 5 dogs right ventricular). Shocks were delivered at 30 (four dogs), 80 (two dogs) or 250 J (four dogs). Each dog underwent programmed electrical stimulation at or near the ablation site before, within 1 hour after and 1 week after the shock. Holter electrocardiographic monitoring (24 hours) was performed during day 1 and 7 after the shock in all the dogs, and extended Holter monitoring was done during the first 5 days in four dogs. All dogs survived for 1 week. Within 10 minutes after the shock, a sustained ventricular tachycardia was recorded in nine dogs; deterioration into ventricular fibrillation occurred in two dogs. In nine dogs, 60 to 169 monomorphic ventricular tachycardia episodes (mean 101) occurred on day 1 and 0 to 11 (mean 3) occurred on day 7; Holter monitoring failed for technical reasons in one dog. Extended Holter monitoring showed a marked decline in the incidence of tachycardia during the first 3 days. Early activation during ventricular tachycardia was always derived at or near the ablation site, and the QRS configuration during pre- and postablation pacing at this site was identical to the tachycardia configuration. Ventricular tachycardia was never inducible with programmed stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Altered ventricular stretch contributes to initiation of cardiac memory.

BACKGROUND: Cardiac memory is a change in T-wave morphology induced by ventricular pacing or arrhythmias that persist after resumption of normal AV conduction. Changing the pacemaker site from atrium to ventricle alters ventricular activation and the mechanical pattern of ventricular contraction. Either or both alterations affect T-wave configuration. OBJECTIVE: The purpose of this study was to study the role of altered contractile patterns on initiation of cardiac memory. METHODS: Isolated rabbit hearts were immersed in Tyrode's solution (37 degrees C) and aortically perfused at a constant pressure of 70 mmHg. Three orthogonal quasi-ECG leads were recorded via six Ag-AgCl electrodes located on the walls of the bath. Hearts were paced at a constant cycle length from either the right atrial appendage or left ventricle lateral wall. The pulmonary artery was sealed, and both ventricles contracted isovolumetrically. Cardiac memory was quantified as T-wave vector displacement expressed as distance between T-wave vector peaks during atrial pacing before and after ventricular pacing. RESULTS: Five minutes of ventricular pacing induced significant T-wave vector displacement that returned to control in 5 to 10 minutes. No significant changes in intraventricular pressure occurred during and after ventricular pacing. Interventions that decreased ventricular load (shunting both ventricles to the bath) or contractility (excitation-contraction uncoupler blebbistatin) significantly decreased developed pressure and eliminated T-wave vector displacement. Neither intervention affected ventricular activation during ventricular pacing. Locally applied left ventricular epicardial stretch induced T-wave vector displacement similar to that induced by ventricular pacing. CONCLUSION: Altered ventricular activation during ventricular pacing initiates cardiac memory via induction of altered contractile patterns and altered stretch.