Mieko Takasugi

Sleep apnoea induces cardiac electrical instability assessed by T-wave alternans in patients with congestive heart failure

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.

Continuous T-wave alternans monitoring to predict impending life-threatening cardiac arrhythmias during emergent coronary reperfusion therapy in patients with acute coronary syndrome

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.

Prevalence of Microvolt T-Wave Alternans in Patients With Long QT Syndrome and Its Association With Torsade de Pointes

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.

In-hospital monitoring of T-wave alternans in a case of amiodarone-induced torsade de pointes: clinical and methodologic insights

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.

Sudden reversible pacemaker failure in a patient with cardiac sarcoidosis: an unfortunate case of ventricular septal pacing

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.

'False-positive' intrathoracic impedance monitor alarm caused by amiodarone-induced hypothyroidism in a patient with cardiac resynchronization therapy-defibrillator.

A 78-year-old female received a cardiac resynchronization therapy-defibrillator equipped with an intrathoracic impedance (ITI) monitor and amiodarone therapy was initiated. A massive and long-lasting decrease in ITI occurred without heart failure (HF) deterioration. Pericardial effusion secondary to amiodarone-induced hypothyroidism may have caused the impedance reduction.

Relationship between T-wave alternans magnitude and T-wave amplitude before the onset of ventricular tachyarrhythmias during emergent reperfusion in acute coronary syndrome patients

We greatly appreciate Dr Madias’ remarks on our recent study demonstrating the usefulness of continuous T-wave alternans (TWA) monitoring in ultra-short-term prediction of impending life-threatening ventricular tachyarrhythmias (VTA) during emergent reperfusion therapy in acute coronary syndrome (ACS) patients.1 He raised an interesting question, namely, was there a relationship between the increase in TWA and the possible increase in T-wave amplitude prior to the occurrence of VTA?2 This question is based on his theory that TWA magnitude is affected …

Significance of T-wave inversion triggered by spontaneous atrial premature beats in patients with long QT syndrome

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.

Impact of T-wave amplitude on circadian variation in T-wave alternans

the T-wave amplitude have an effect on the calculated magnitude of the TWA, possibly irrespective of the changes in the arrhythmic propensity between day and night? The authors could provide some insight about the relationship of the calculated magnitude of the TWA and the corresponding T-wave amplitude in the two subgroups of the patients they studied. If such a relationship is found, one wonders whether we are witnessing circadian variation in the magnitude of the TWA due to a circadian variation in the amplitude of the corresponding T-waves. In such a scenario, a rise in the TWA magnitude at night in the patients with SA may not reflect a rise in their arrhythmogenic propensity, but merely the influence of the increased amplitude of the T-waves. Perhaps, this may be grounds for recommending adjustment of the values of measured TWA by the amplitude of the corresponding T-wave amplitudes. A multivariate analysis of the TWA magnitude and the T-wave amplitudes, as independent variables, with the values of AHI, as the dependent variable, may shed some light in this nagging problem. Could the authors help? References 1. Takasugi N, Nishigaki K, Kubota T, Tsuchiya K, Natsuyama K, Takasugi M, Nawa T, Ojio S, Aoyama T, Kawasaki M, Takemura G, Minatoguchi S. Sleep apnoea induces cardiac electrical instability assessed by T-wave alternans in patients with congestive heart failure. Eur J Heart Fail 2009;11:1063–1070. 2. Madias JE. A proposal for a T-wave alternans index. J Electrocardiol 2007;40:479–481.