Acute coronary syndrome versus cardiac memory: Unexpected cause of Pseudo-Wellens syndrome.

Pseudo-Wellens Syndrome (PWS) refers to absence of severe obstructive lesion in the proximal segment of the left anterior descending (LAD) despite having clinical and electrocardiography (ECG) features similar to Wellens Syndrome (WS). In previous reports, PWS most commonly caused by illicit drug use, stress cardiomyopathy, or unknown etiologies In this report, we aimed to present our case in which we detected the development of "memory T wave" secondary to Paroxysmal Supraventricular Tachycardia (PSVT) episodes as an interesting cause of PWS that has not been reported before.

Evaluation of T-wave memory after accessory pathway ablation in pediatric patients with Wolff-Parkinson-White syndrome.

BACKGROUND: T-wave memory (TWM) is a rare cause of T-wave inversion (TWI). Alterations in ventricular activation due to abnormal depolarization may cause repolarization abnormalities on the ECG, even if myocardial conduction returns to normal. These repolarization changes are defined as TWM. In our study, we aimed to determine the frequency of TWM development and the predictors affecting it in the pediatric population who underwent accessory pathway (AP) ablation due to Wolff-Parkinson-White (WPW) syndrome. METHODS: The data of patients with manifest AP who underwent electrophysiological studies and ablation between 2015 and 2021 were retrospectively analyzed. The study included 180 patients who were under 21 years of age and had at least one year of follow-up after ablation. Patients with structural heart disease, intermittent WPWs, recurrent ablation, other arrhythmia substrates, and those with less than one-year follow-up were excluded from the study. The ECG data of the patients before the procedure, in the first 24 h after the procedure, three months, and in the first year were recorded. The standard ablation technique was used in all patients. RESULTS: Postprocedure TWM was observed in 116 (64.4%) patients. Ninety-three patients (51.7%) had a right-sided AP, and 87 patients (48.3%) had a left-sided AP. The presence of posteroseptal AP was found to be significantly higher in the group that developed TWM. Of these patients, 107 (93.1%) patients showed improvement at the end of the first year. Preprocedural absolute QRS-T angle, postprocedural PR interval, and right posteroseptal pathway location were identified as predictors of TWM. CONCLUSION: The development of TWM is particularly associated with the right-sided pathway location, especially the right posteroseptal pathway location. The predictors of TWM are the preprocedural QRS-T angle, the postprocedural PR interval, and the presence of the right posteroseptal AP.

Rapid Pacing Decreases L-type Ca2+ Current and Alters Cacna1c Isogene Expression in Primary Cultured Rat Left Ventricular Myocytes.

The L-type calcium current (ICaL) is the first step in cardiac excitation-contraction-coupling and plays an important role in regulating contractility, but also in electrical and mechanical remodeling. Primary culture of cardiomyocytes, a widely used tool in cardiac ion channel research, is associated with substantial morphological, functional and electrical changes some of which may be prevented by electrical pacing. We therefore investigated ICaL directly after cell isolation and after 24 h of primary culture with and without regular pacing at 1 and 3 Hz in rat left ventricular myocytes. Moreover, we analyzed total mRNA expression of the pore forming subunit of the L-type Ca2+ channel (cacna1c) as well as the expression of splice variants of its exon 1 that contribute to specificity of ICaL in different tissue such as cardiac myocytes or smooth muscle. 24 h incubation without pacing decreased ICaL density by ~ 10% only. Consistent with this decrease we observed a decrease in the expression of total cacna1c and of exon 1a, the dominant variant of cardiomyocytes, while expression of exon 1b and 1c increased. Pacing for 24 h at 1 and 3 Hz led to a substantial decrease in ICaL density by 30%, mildly slowed ICaL inactivation and shifted steady-state inactivation to more negative potentials. Total cacna1c mRNA expression was substantially decreased by pacing, as was the expression of exon 1b and 1c. Taken together, electrical silence introduces fewer alterations in ICaL density and cacna1c mRNA expression than pacing for 24 h and should therefore be the preferred approach for primary culture of cardiomyocytes.

Dispersion of repolarization increases with cardiac resynchronization therapy and is associated with left ventricular reverse remodeling.

PURPOSE: Cardiac resynchronization therapy (CRT) reduces ventricular activation times and electrical dyssynchrony, however the effect on repolarization is unclear. In this study, we sought to investigate the effect of CRT and left ventricular (LV) remodeling on dispersion of repolarization using electrocardiographic imaging (ECGi). METHODS: 11 patients with heart failure and electrical dyssynchrony underwent ECGi 1-day and 6-months post CRT. Reconstructed epicardial electrograms were used to create maps of activation time, repolarization time (RT) and activation recovery intervals (ARI) and calculate measures of RT, ARI and their dispersion. ARI was corrected for heart rate (cARI). RESULTS: Compared to baseline rhythm, LV cARI dispersion was significantly higher at 6 months (28.2 ± 7.7 vs 36.4 ± 7.2 ms; P = 0.03) but not after 1 day (28.2 ± 7.7 vs 34.4 ± 6.8 ms; P = 0.12). There were no significant differences from baseline to CRT for mean LV cARI or RT metrics. Significant LV remodeling (>15% reduction in end-systolic volume) was an independent predictor of increase in LV cARI dispersion (P = 0.04) and there was a moderate correlation between the degree of LV remodeling and the relative increase in LV cARI dispersion (R = -0.49) though this was not statistically significant (P = 0.12). CONCLUSION: CRT increases LV cARI dispersion, but this change was not fully apparent until 6 months post implant. The effects of CRT on LV cARI dispersion appeared to be dependent on LV reverse remodeling, which is in keeping with evidence that the risk of ventricular arrhythmia after CRT is higher in non-responders compared to responders.

Adaptation of ventricular repolarization time following abrupt changes in heart rate: comparisons and reproducibility of repeated atrial and ventricular pacing.

Adequate adaptation of ventricular repolarization (VR) duration to changes in heart rate (HR) is important for cardiac electromechanical function and electrical stability. We studied the QT and QTpeak adaptation in response to abrupt start and stop of atrial and ventricular pacing on two occasions with an interval of at least 1 mo in 25 study subjects with permanent pacemakers. Frank vectorcardiography was used for data collection. Atrial or ventricular pacing was performed for 8 min aiming at a cycle length (CL) of 500 ms. We measured the immediate response (IR), the time constant (τ) of the exponential phase, and T90 End, the time to reach 90% change of QT and QTpeak from baseline to steady state during and after pacing. During atrial pacing, the CL decreased on average 45% from mean (SD) 944 (120) to 518 (46) ms and QT decreased on average 18% from 388 (20) to 318 (17) ms. For QT, T90 End was 103 (24) s and 126 (15) s after start versus stop of atrial pacing; a difference of 24 (27) s (P = 0.006). The response pattern was similar for τ but IR did not differ significantly between pacing start and stop. The response pattern was similar for QTpeak and also for QT and QTpeak following ventricular pacing start and stop. The coefficients of variation for repeated measures were 7%-21% for T90 End and τ. In conclusion, the adaptation of VR duration was significantly more rapid following increasing than decreasing HR and intraindividually a relatively reproducible process.NEW & NOTEWORTHY We studied the duration of ventricular repolarization (VR) adaptation and its hysteresis, following increasing and decreasing heart rate by abrupt start and stop of 8-min atrial or ventricular pacing in study subjects with permanent pacemakers and repeated the protocol with ≥1 mo interval, a novel approach. VR adaptation was significantly longer following decreasing than increasing heart rate corroborating previous observations. Furthermore, VR adaptation was intraindividually a reproducible and, hence, robust phenomenon, a novel finding.

Reversion of cardiac memory during left bundle branch pacing.

Cardiac memory (CM) is identified as an altered T wave when normal ventricular activation resumes after an abnormal myocardial activation period. We present a case who initially underwent temporary right ventricular apex (RVA) pacing for one week which induced typical pseudo-primary T wave changes. The T wave inversion was observed after the end of RVA pacing when left bundle branch pacing (LBBP) was initiated, and the abnormal T waves gradually return to almost normal repolarization during LBBP 40 days later.

Surface ECG criteria can discriminate post-septal pacing cardiac memory from ischemic T wave inversions.

Cardiac memory (CM) refers to transient T wave changes that appear after cessation of a period of abnormal ventricular activation, such as right ventricular (RV) pacing. ECG criteria for differentiating post-pacing CM from ischemia-induced T wave changes were previously published only for apical, but not for septal RV pacing. AIM: To find ECG criteria for discriminating post-septal pacing CM from ischemic T wave inversions. METHODS: ECGs were analyzed in 2 groups: CM (n = 23) and ischemia (n = 26). CM was induced by 2 weeks of DDD pacing with a short AV delay. Ischemic patients were grouped by culprit vessel: left anterior descending (LAD), circumflex (Cx), right coronary artery (RCA). RESULTS: CM was visible on the ECG after 1 week of ventricular pacing, started to disappear in <1 week after pacing cessation and was completely reversible within 4 weeks of pacing cessation. T wave axis differed between CM (75.8 ±â€¯18.5°) and Cx (-25.2 ±â€¯25.5°, p < 0.01) and RCA (-18.3 ±â€¯18.9°, p < 0.01) groups, but not compared to LAD group (96.4 ±â€¯65.0°, p = 0.17). The combination of (1) positive T wave in aVF; and (2) (i) T wave amplitude in aVF ≥ the absolute value of the most negative precordial T wave, or (ii) positive T wave in V5 and positive or isoelectric T wave in lead I identified CM from all ischemia with a sensitivity of 91% and a specificity of 92%. CONCLUSION: ECG criteria can discriminate post-septal RV pacing CM from ischemic changes with high sensitivity and specificity.

T-wave changes of cardiac memory caused by frequent premature ventricular contractions originating from the right ventricular outflow tract.

INTRODUCTION: Cardiac memory is recognized as altered T-waves when the sinus rhythm resumes after an abnormal myocardial activation period that recovers slowly over several weeks. The T-wave changes after ablation of frequent premature ventricular contractions (PVCs) as cardiac memory was not known. OBJECTIVE: This study identified whether cardiac memory exists after successful ablation of PVCs from the right ventricular outflow tract (RVOT). METHODS: We investigated 45 patients who underwent successful ablation of PVCs from RVOT and 10 patients who underwent unsuccessful ablation. We analyzed the amplitude of the T-wave, QT intervals, and QRST time-integral values of a 12-lead electrocardiogram before ablation and 1 day, 3 days, and 1 month after ablation. RESULTS: In the successful ablation group, the amplitude of the T-wave and QRST time-integral values of lead II, III, aVR, aVL, and aVF significantly changed after ablation and gradually normalized within 1 month. In addition, if the number of pre-ablation PVCs was small, then the corresponding impact was also small. However, the greater the number of pre-ablation PVCs, the more prominent the changes. Significant changes were not observed in the unsuccessful ablation group. CONCLUSION: When ablation of PVCs from RVOT was successful, primary T-wave changes because of cardiac memory and the gradual normalization of the amplitude of the T-wave were observed. No significant T-wave changes were detected after unsuccessful ablation.

Multiple myocardial bridges associated with left-ventricular dysfunction, intermittent left bundle branch block, and cardiac memory: A case report.

Myocardial bridges are a congenital anomaly in which a segment of the coronary artery takes a "tunneled" intramuscular course. Few reports have associated myocardial bridges with left-ventricular dysfunction in patients with ischemia. Intermittent left bundle branch block is a conduction disturbance that has been described to be associated with myocardial bridges and cardiac memory. This study reports unusual associations of multiple myocardial bridges, angina, left-ventricular dysfunction, intermittent left bundle branch block, and cardiac memory.

Cardiac Memory: A Case Report and Review of the Literature.

BACKGROUND: A variety of clinical syndromes can cause T-wave inversion (TWI), ranging from life-threatening events to benign conditions. One benign cause of TWI is cardiac memory, which is characterized by the transient inversion of T-waves following abnormal activation of the ventricles, commonly due to intermittent left bundle branch block (LBBB), tachydysrhythmias, electrical pacing, or ventricular pre-excitation. CASE REPORT: A 72-year-old man presented to the emergency department with chest pain, nausea, vomiting, and headache. Upon arrival, his electrocardiogram (ECG) showed new-onset LBBB with appropriate secondary ST-T wave changes. A subsequent ECG showed disappearance of LBBB and newly inverted T-waves in precordial leads V1-V5, followed by a repeat ECG that again showed LBBB. Serial troponin testing was unremarkable. During hospitalization, echocardiogram and nuclear perfusion stress test were normal. The transient TWIs in this patient were believed to be due to cardiac memory. We performed a literature review and identified 39 published cases of cardiac memory. The most common etiology for cardiac memory was after cardiac pacemaker placement, followed by intermittent LBBB (as was seen in our patient), and post-tachydysrhythmia. Patient ages ranged from 21 to 88 years, with an equal number of cases reported in men and women. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Cardiac memory is a poorly understood, rarely observed phenomenon that can occur in the setting of intermittent LBBB. Testing for acute cardiac ischemia and underlying coronary artery disease is still recommended, as the diagnosis of cardiac memory can only be made after negative workup.

Negative concordant T waves during paced ventricular rhythm: An honest enemy is better than a false friend.

The ECG diagnosis of myocardial infarction and ischemia in pacemaker patients is often challenging. The three criteria, proposed by Sgarbossa et al. in 1996, useful to suspect myocardial ischaemia in patient with left bundle branch block were demonstrated to be valid also in pacemaker patients. In the last years, concordant negative T waves in patients with ventricular paced rhythm were linked to various expressions of acute myocardial injury. If available, comparison with previous ECG is crucial. Partial persistence of cardiac memory during fusion beats created an anomalous concordance between negative T waves and QRS axis and could induce erroneous suspicions. AV delay modification could help to unmask this situation.

Episodic Left Bundle Branch Block-A Comprehensive Review of the Literature.

Episodic (transient/ intermittent) left bundle branch block (LBBB) has been associated with different conditions such as bradycardia, tachycardia, anesthesia, acute pulmonary embolism, changes in intrathoracic pressure, chest trauma, cardiac interventional procedures, mad honey poisoning, and in other clinical settings. Of note, exclusion of an acute coronary syndrome in the setting of episodic LBBB is of great importance. Moreover, episodic LBBB is sometimes symptomatic and may be associated with left ventricular systolic and/or diastolic dysfunction or conduction disturbances leading to syncope. This review article provides a comprehensive overview of the conditions associated with episodic LBBB and discusses the clinical impact of this phenomenon.

Differences between cardiac memory T wave changes after idiopathic left ventricular tachycardia and ischemic T wave inversion induced by acute coronary syndrome.

BACKGROUND: Cardiac memory (CM) after idiopathic left ventricular tachycardia (ILVT) mimics ischemic T wave inversion (TWI) induced by acute coronary syndrome (ACS). We aimed to establish electrocardiography criteria for differentiating the CM from ischemic TWI. METHODS AND RESULTS: We evaluated 16 ILVT and 48 ACS patients. We identified TWI after ILVT in 9/16 patients (CM group), typically in leads II, III, aVF, aVR, and V4-6. The characteristics of CM were similar to TWI induced by ACS involving right coronary artery, but the CM group had more TWI in V4 and shorter QTc. The criteria of (1) positive T in aVL, (2) negative or isoelectric T in II, and (3) negative T in V4-6 or (4) QTc <430ms were 100% sensitive and 96% specific for the CM group. CONCLUSION: CM after ILVT can be differentiated in most cases from ischemic TWI by the distribution of TWI and the QTc.

Electrical remodeling reflected by QRS and T vector changes following cardiac resynchronization therapy is related to survival in heart failure patients with left bundle branch block.

INTRODUCTION: We investigated changes in electrocardiographic spatial QRS and T vectors as markers of electrical remodeling before and after cardiac resynchronization therapy (CRT) and their association with altered outcome. METHODS AND RESULTS: In 41 patients with LBBB, ECGpost was recorded during intrinsic rhythm after interrupting CRT pacing and compared to the pre-implant ECGpre and the ECG during CRT (ECGCRT). Mean spatial angles between QRS and T vectors were determined with the Kors matrix conversion. Left ventricular ejection fraction (LVEF) was determined with nuclear isotope ventriculography before CRT implantation (LVEFpre) and at inclusion (LVEFpost). Following CRT, LVEF improved significantly from 26 ± 10 to 36 ± 14% (p=0.01). Duration of QRSpre (168 ± 15 ms) was not different from QRSpost (166 ± 15 ms). A smaller angle between QRSCRT and Tpost was related to a greater angle between Tpre and Tpost (Pearson's R -0.61 - p<0.001). During follow-up (30 ± 2 months) 9 patients (22%) died. Univariate Cox regression revealed higher mortality in the patients with lower LVEFpost (HR 1.10, p=0.01), a larger angle QRSCRTTpost (HR 1.03, p=0.03), a smaller angle QRSpreQRSpost (HR 0.97, p=0.03) and smaller angle TpreTpost (HR 0.95, p<0.01). After adjusting for LVEFpost, only smaller angle TpreTpost was associated with mortality (HR 0.96, p=0.03). CONCLUSIONS: Electrical remodeling can be quantified by measuring the angles between spatial QRS and T vectors before, during and after CRT. In absence of QRS duration changes, more extensive electrical remodeling is associated with a significantly better survival. QRS and T vector changes deserve further investigation to better understand the individual response to CRT.

Cardiac memory in cardiac resynchronization therapy: A vectorcardiographic comparison of biventricular and left ventricular pacing.

INTRODUCTION: "Cardiac memory" (CM) refers to a change in repolarization induced by an altered pathway of activation, manifested after resumption of spontaneous ventricular activation (SVA). AIMS: To investigate for the first time in humans the effects of left ventricular (LV) pacing on CM development through vectorcardiography (VCG). METHODS: We studied 28 patients with heart failure (HF) and left bundle branch block (LBBB) treated with cardiac resynchronization therapy (CRT). Fourteen patients underwent biventricular (BIV) stimulation; the other 14 underwent LV stimulation only. VCG was acquired during SVA at baseline and during AAI and DDD pacing immediately after and 7 and 90 days after the implant. RESULTS: At baseline, in both groups, the QRS and T vectors angles were those specific of LBBB pattern. During DDD pacing, QRS vector angle changed to the right and upward in BIV patients while no significant differences were observed in LV patients. During AAI pacing, T vector angle changed significantly in BIV patients, following the direction of the paced QRS and amplitude significantly increased. In LV patients no significant differences in T vector angles were observed. Only T vector amplitude significantly increased at 7 days (p=0.03) and at 90 days (p=0.008 vs baseline). CONCLUSION: In patients with LBBB, BIV pacing induces cardiac memory development as a significant change in T vector magnitude and angle, while LV pacing doesn't induce significant modifications in QRS and T vector angles and CM is manifested only as a significant T vector amplitude change.

Cardiac memory during rather than after termination of left bundle branch block.

An 83-year-old woman with chronic left bundle branch block and remote history of pacemaker implantation for intermittent AV block was hospitalized for fatigue and leg swelling. She had no cardiac complaints. Routine 12-lead electrocardiogram showed sinus rhythm with left bundle branch block. There were diffuse negative T waves in the inferior and anterolateral leads that were concordant with the QRS complexes. Echocardiogram was normal and nuclear perfusion heart scan showed no abnormality. It was noted that the negative T waves during left bundle branch block were in the exact same leads as were the deep negative QRS complexes during ventricular pacing. The electrocardiographic changes were consistent with cardiac memory. This case is unique because cardiac memory in patients with intermittent left bundle branch block typically occurs when the QRS complexes normalize and not during left bundle branch block itself. Our findings indicate that memory Ts can develop not only after normalization of wide complex rhythms but also with alternating wide complex rhythms as in the presented case where a ventricular paced rhythm was replaced by left bundle branch block.

THE CHATTERJEE PHENOMENON: A DEMONSTRATION OF CARDIAC MEMORY IN PACED RHYTHMS.

Introduction: While T-wave inversions (TWI) are associated with various pathologies, they are rarely associated with cardiac memory, termed the Chatterjee phenomenon. Case: A 76-year-old man with sick sinus syndrome with a pacemaker presented with chest tightness and new onset TWI in his precordial leads. On admission, he tested positive for COVID-19, but remained stable and only required minimal supplemental oxygen. His troponin was only slightly elevated, and EKG showed TWI throughout his precordial leads. A previous EKG had shown normal sinus rhythm without a paced rhythm or ST wave abnormalities. Interrogation of his pacemaker revealed an AV-paced rhythm. Given his chest tightness without dynamic changes in his troponin or EKG, the symptoms were considered more likely related to his COVID-19 infection, and he was discharged home. Discussion: Aberrancies in normal cardiac conduction can result in altered electrical activation, especially for those with AV pacemakers, leading some patients to develop cardiac memory, manifesting as TWI. Conclusion: AV-paced rhythm and narrow QRS complexes with TWI localized to precordial leads without evidence of active cardiac ischaemia may suggest cardiac memory, termed the Chatterjee phenomenon, requiring no invasive interventions. LEARNING POINTS: In patients with T-wave inversions, various conditions should considered in the differential diagnosis, including left bundle branch block and sick sinus syndrome, although T-wave inversions in V1-V3 are non-specific and benign.Cardiac memory, termed the Chatterjee Phenomenon, is one of the causes of T-wave inversions which is sometimes ignored.No invasive interventions are needed for T-wave inversions with the Chatterjee phenomenon.