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BACKGROUND: Little is known about the role of atrial arrhythmias (AAs) in triggering Torsade de Pointes (TdP) in patients with long-QT syndrome (LQTS). The aim of this study was to examine the contribution of AAs to the development of TdP in acquired LQTS patients. METHODS: The initiation patterns of 81 episodes of TdP obtained from 34 consecutive acute acquired LQTS patients (14 men, median age, 69 years; median QTc, 645.5 ms) with documented TdP were analyzed. The initiation mode of TdP was divided into 3 categories: (1) preceding short-long sequence (SLS); (2) sudden R-on-T phenomenon without preceding SLS; and (3) increased atrial rate. The patients were divided into 2 groups based on the presence or absence of AAs-induced TdP; AAs-induced (n=18) and non-AAs-induced (n=16) groups. The association of clinical/ECG characteristics and TdP frequency after initiating conventional therapy with AAs-induced TdP was evaluated. The groups were compared using the Mann-Whitney U test or Fisher exact test. RESULTS: AAs-induced group comprised 52.9% (18/34) of the patients studied. TdP was preceded by AAs-initiated SLSs in 41.2% (14/34) of the patients and was directly induced by R-on-T AAs (AAs coincidentally encountered a vulnerable repolarizing region during the T wave) in 23.5% (8/34). AAs triggered 48 (59.3%) of the 81 TdP episodes. AAs-initiated SLSs in 67.8% (40/59) of the SLS-induced TdP episodes. R-on-T AAs accounted for 23.5% (19/81) of the TdP episodes. AAs-induced group experienced TdP after initiating therapy more frequently than non-AAs-induced group (2.5 versus 1 event, P=0.008). AAs-induced group exhibited macroscopic T-wave alternans more frequently than non-AAs-induced group (6 versus 0, P=0.02). CONCLUSIONS: AAs play a key role in triggering TdP in more than half of patients with acute acquired LQTS and can increase TdP frequency after initiating therapy. Thus, AAs are not benign but rather can be life-threatening in patients with acute acquired LQTS.

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BACKGROUND: Ambulatory electrocardiogram (ECG)-based microvolt T-wave alternans values measured by the modified moving average method (MMA-TWA) can be disrupted by T-wave changes that mimic true repolarization alternans. METHODS: We investigated potential sources of measurement error by studying 19 healthy subjects (12 men; median age, 25) free of known heart disease with 36-month follow-up to establish freedom from significant arrhythmia or syncope. All participants underwent 24-hr continuous 12-lead ECG monitoring. Causes of automated MMA-TWA ≥42 µV episodes were classified based on visual inspection. RESULTS: A total of 2,189 episodes of automated MMA-TWA episodes ≥42 µV were observed in all subjects (peak MMA-TWA: median, 94 µV; interquartile range, 81-112 µV). All episodes included one or more beats with T-wave deformation which lacked "repeating ABAB pattern" and therefore were identified as TWA measurement error. Causes of such error were categorized as: (a) artifact [72.6% (1,589/2,189), observed in 19 (100%) subjects], more frequently in limb than precordial leads; (b) T-wave changes due to changes in heart/body position [25.5% (559/2,189), observed in 14 (73.7%) subjects], frequently observed in leads V1-2; and (c) postextrasystolic T-wave changes [1.9% (41/2,189), observed in 2 (10.5%) subjects]. CONCLUSIONS: Relying only on automated MMA-TWA values obtained during ambulatory ECG monitoring can lead to incorrect measurement of TWA. Our findings offer the potential to reduce false-positive TWA results and to achieve more accurate detection of true repolarization alternans.

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BACKGROUND: The aim of study was to investigate effects of beta-blockade on microvolt T-wave alternans (TWA), a precursor of lethal arrhythmia, in patients with long QT syndrome (LQTS). METHODS: Eleven consecutive LQTS patients, types 1 (n = 6), 3 (n = 2), and "non-1, non-2, non-3" (n = 3) were enrolled. All patients underwent 24-hr continuous 12-lead ECG monitoring before and after initiation of beta-blockade therapy. TWA was measured using the modified moving average method. RESULTS: Seven (63.6%) of the 11 patients studied were symptomatic, with history of cardiac arrest or documented Torsade de Pointes (TdP) in 4 and syncope in three patients. After a median follow-up of 34 months, beta-blockade reduced the number of symptomatic patients to 1 with TdP (p < 0.02), in whom TdP frequency decreased from 25 events/60 months (0.42 event/month) to seven events/69 months (0.1 event/month). In association with this reduction in symptoms, peak TWA decreased by 47% in the cohort after a median of eight months of beta-blockade therapy [from 95 (74-130) to 50 (39.5-64.5) µV, p = 0.01]. All patients exhibited TWA ≥42 µV before beta-blockade therapy, which eliminated these episodes in four patients. Daily frequency of TWA ≥42 µV episodes decreased by 87% [from 15 (6-26) to 2 (0-5) episodes/day, p = 0.009]. CONCLUSIONS: This study is limited by the small sample size and is mainly hypothesis generating. TWA monitoring deserves further evaluation as a risk marker and a guide to therapy in LQTS patients in future large-scale studies.

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BACKGROUND: In patients with the long QT syndrome (LQTS), a sudden increase in heart rate can cause T-wave alternans (TWA) with beat-to-beat alternating polarity of T wave. We hypothesized that LQTS patients at high risk for torsades de pointes (TdP) may exhibit momentary atrial or sinoatrial premature beat-induced T-wave inversion (APB-TWI). OBJECTIVE: The purpose of this study was to assess the association of APB-TWI with TdP history and with microvolt TWA. METHODS: Twenty-four-hour continuous 12-lead electrocardiograms (ECGs) were recorded in 18 healthy subjects and 39 consecutive patients with LQTS types 1 (n = 21), 2 (n = 4), 3 (n = 4), and unidentified (n = 10). Peak TWA was determined by the modified moving average method. RESULTS: The 39 LQTS patients were divided into 2 groups: 10 LQTS patients with TdP history (TdP group) and 29 without (non-TdP group). None of the healthy subjects showed APB-TWI, whereas 38.5% of the LQTS patients (15/39) exhibited APB-TWI. The incidences of APB-TWI and TWA ≥42 µV were significantly higher in the TdP group than in the non-TdP group (APB-TWI: 80% vs 24.1%, P = .006; TWA ≥42 µV: 100% vs 65.5%, P = .04). APB-TWI was inferior in sensitivity for an association with TdP history to TWA ≥42 µV (80% vs 100%) but superior in specificity (75.9% vs 51.7%). Patients with APB-TWI exhibited significantly higher TWA values than those without [median (interquartile range) 73 (55-106.5) vs 48 (37.5-71.8) µV, P = .02]. CONCLUSION: APB-TWI is an easily measurable ECG pattern and is strongly associated with TdP history as well as TWA ≥42 µV in LQTS patients. APB-TWI and TWA may share pathophysiological mechanisms.

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BACKGROUND: Prevalence of microvolt T-wave alternans (TWA) and the strength of its association with torsade de pointes (TdP) history have not been fully investigated in patients with long QT syndrome (LQTS). METHODS AND RESULTS: Twenty-four-hour continuous 12-lead ECGs were recorded in 10 healthy subjects (5 men; median age, 21.5 years) and 32 patients (13 men; median age, 13 years) with LQTS types 1 (n=18), 2 (n=4), 3 (n=4), and unidentified (n=6). Peak TWA was determined by the Modified Moving Average method. None of the healthy subjects had TWA ≥42 µV. All 8 (100%) LQTS patients with a history of TdP exhibited TWA ≥42 µV, whereas only 14 (58.3%) of the 24 LQTS patients without TdP history reached ≥42 µV (p=0.04). Thus, the 42-µV cut point provided 100% sensitivity and 41.7% specificity for an association with TdP history. In the 22 (68.8%) LQTS patients with TWA ≥42 µV, only 2 (median; interquartile range, 1-3) leads exhibited TWA ≥42 µV. Highest TWA levels were recorded in precordial leads (V1-V6) in 30 (93.8%) patients, most frequently in lead V2 (43.8%). A single ECG lead detected only ≤63.6% of TWA ≥42 µV episodes, whereas the combined leads V2 to V5 detected 100% of TWA ≥42 µV. CONCLUSIONS: Microvolt TWA is far more prevalent in LQTS patients than previously reported and is strongly associated with TdP history. TWA should be monitored from precordial leads in LQTS patients. The use of a limited set of ECG leads in conventional monitoring has led to underestimation of TWA and its association with TdP.

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We report a case of macroscopic T-wave alternans occurring 30 min before the onset of amiodarone-induced torsade de pointes, illustrating a means to monitor for proarrhythmia.

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We report a case of sudden marked deterioration of ventricular stimulation threshold resulting in pacemaker failure 16 months after a ventricular septal lead implantation for atrioventricular block. Echocardiography revealed septal wall thinning at the electrode-tissue interface, which was not detected pre-operatively. Endomyocardial biopsy confirmed cardiac sarcoidosis. The increased threshold was reversible with prednisolone.

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AIMS: T-wave alternans (TWA) can precede onset of ventricular tachyarrhythmia (VTA). We evaluated the usefulness of continuous TWA monitoring in ultra-short-term prediction of impending life-threatening VTA upon emergent reperfusion in acute coronary syndrome (ACS) patients. METHODS AND RESULTS: Twenty consecutive ACS patients undergoing emergent reperfusion therapy were studied. Continuous ambulatory electrocardiograms (ECGs) (leads V1 and V5) were recorded during emergency room visit and therapy. Peak TWA was determined before and after reperfusion by the modified moving average method. Coronary balloon angioplasty/stenting was successfully performed in 19 patients and intracoronary vasodilator was administered in 1 patient with coronary spasm. Three (15.0%) patients developed VTA requiring cardioversion soon after reperfusion. Peak TWA before reperfusion was higher in patients with VTA than in those without (33.0 ± 4.4 vs. 15.8 ± 4.0 µV, P < 0.001). Two patients with arrhythmia exhibited an upsurge in TWA to 75 and 105 µV before onset of VTA. In the third patient, macroscopic TWA appeared in leads V1-V4 in a 12-lead ECG prior to VTA upon pharmacological resolution of vasospasm, although the ambulatory ECG field of view could not detect the upsurge. CONCLUSION: Acute coronary syndrome patients at risk of developing VTA soon after reperfusion exhibit premonitory episodes of increased TWA. Thus, TWA monitoring may be useful for ultra-short-term prediction of life-threatening cardiac arrhythmia risk upon emergent reperfusion in ACS patients. Continuous 12-lead ECGs may be required to optimize detection of TWA, which is regionally specific.

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AIMS: To assess the involvement of sleep apnoea in nocturnal sudden cardiac death (SCD) by evaluating cardiac electrical instability using T-wave alternans (TWA), a risk marker for lethal cardiac arrhythmias, and severity of sleep apnoea in congestive heart failure (CHF) patients. METHODS AND RESULTS: A total of 40 CHF patients simultaneously underwent overnight simplified respiratory polygraphy and 24 h continuous electrocardiography. Peak TWA during both daytime and nighttime were calculated by the modified moving average method. The patients were divided into two groups; 30 patients with daytime predominant TWA (whose peak TWA was higher during daytime than during nighttime) and 10 with nighttime predominant. Apnoea-hypopnoea index (AHI) was significantly higher in patients with nighttime predominant TWA than in those with daytime predominant (35.9 +/- 8.1 vs. 23.9 +/- 14.4 events/h, P = 0.02), and was an independent predictor of nighttime predominant TWA (odds ratio, 1.08; 95% confidence interval, 1.01-1.16; P = 0.03). Moreover, peak TWA during the night was correlated positively with AHI (P < 0.001), and AHI was an independent determinant of nocturnal TWA value (r(2) = 0.27, P = 0.009). CONCLUSION: In CHF patients, sleep apnoea induces cardiac electrical instability manifested as TWA, reflecting increased risk of nocturnal SCD. Moreover, some CHF patients with sleep apnoea exhibit nighttime predominant TWA. Therefore, TWA should also be evaluated during the night.

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