T-wave Alternans Magnitude Research Articles

Angerlike behavioral state potentiates myocardial ischemia-induced T-wave alternans in canines

OBJECTIVESThe main goal of this study was to determine whether induction of an angerlike state can result in significant levels of T-wave alternans, a marker of electrical instability, in the normal and ischemic heart.BACKGROUNDOutbursts of anger have been implicated in the occurrence of myocardial infarction and sudden cardiac death, but the pathophysiologic mechanisms remain unknown.METHODSA standardized behavioral challenge of eliciting an angerlike state was conducted before and during a 3-min period of coronary artery occlusion in six canines.RESULTSPrecordial T-wave alternans increased from 0.04 ± 0.02 at baseline to 1.40 ± 0.32 mV × ms (p < 0.05) during the angerlike response. When the angerlike state and myocardial ischemia were superimposed, the augmentation in T-wave alternans magnitude (to 3.27 ± 0.61 mV × ms, p < 0.05) exceeded their additive effects, increasing by 130% over the angerlike state alone (p < 0.05) and by 390% over occlusion alone (p < 0.05). Adrenergic influences were reduced by the beta1-adrenergic receptor blocking agent metoprolol (1.5 mg/kg, intravenous), which diminished T-wave alternans magnitude (p < 0.0004 for all) during the angerlike response (from 1.40 ± 0.32 to 0.80 ± 0.17 mV × ms) and during the combined intervention (from 3.27 ± 0.61 to 1.23 ± 0.13 mV × ms). In five additional normal anesthetized canines, atrial pacing at 180 beats/min did not increase T-wave alternans magnitude monitored from lead II electrocardiogram.CONCLUSIONSProvocation of an angerlike state results in T-wave alternans in the normal heart and potentiates the magnitude of ischemia-induced T-wave alternans. Elevation in heart rate during arousal does not appear to be the main factor in the development of alternans in the normal heart but may be an important component during myocardial ischemia. Enhanced adrenergic activity appears to mediate the effects in both the normal and ischemic hearts. T-wave alternans may constitute a useful electrophysiologic measure for clinical use in conjunction with behavioral stress testing or ambulatory monitoring.

T wave alternans and ventricular arrhythmias in arterial hypertension.

Patients with a positive microvolt-level T wave alternans (TWA) are characterized by an increased risk of ventricular tachyarrhythmias. Arterial hypertension leads to an increase of sudden cardiac death risk, particularly if left ventricular hypertrophy is present. The aim of this study was to investigate the value of TWA in patients with arterial hypertension. Fifty-one consecutive patients were included in the study. TWA analysis was performed with patients sitting on a bicycle ergometer and exercising with a gradual increase of workload to maintain a heart rate of at least 105/min. After recording 254 consecutive low-noise-level heartbeats, the exercise test was stopped. The ECG signals were digitally processed by a spectral analysis method. The magnitude of TWA was measured at a frequency of 0.5 cycle per beat. A TWA was defined as positive if the ratio between TWA and noise level was >3.0 and the amplitude of the TWA was >1.8 microV. Eight of the 51 patients (16%) showed a positive TWA. If left ventricular hypertrophy was present, the prevalence of TWA was higher (33.3% versus 8.3%; P:<0.05). Sensitivity concerning a previous arrhythmic event was 73%, and specificity was 100%. The alternans ratio was significantly higher in patients with a previous event (39.3+/-62.3 versus 2.4+/-4.6; P:<0.001), as was the cumulative alternans voltage (4.7+/-4.1 versus 1.6+/-1.9 microV; P:<0.001). In 16 patients invasively investigated by an electrophysiological study, a significant correlation between inducibility of tachyarrhythmias and a positive TWA result was found (Spearman R:=0.36, P:=0.01). We conclude that the arrhythmic risk of patients with arterial hypertension is markedly increased if microvolt-level TWA is present. The prevalence of TWA is higher in patients with left ventricular hypertrophy.

Effect of Heart Rate on T Wave Alternans

T wave alternans (TWA) is a promising technique for detecting arrhythmia vulnerability. Previous studies in animals demonstrated that the magnitude of TWA is dependent on heart rate. However, the effects of heart rate on TWA in humans and the clinical relevance of this effect remain controversial. This was a prospective evaluation of pacing rate and monitoring lead configuration on TWA in subjects undergoing electrophysiologic study. Measurements of TWA were performed on 45 patients in the absence of antiarrhythmic drugs. Recordings were made in normal sinus rhythm and during atrial pacing at 100 and 120 beats/min. Sustained monomorphic ventricular tachycardia (VT) was induced in 29 patients with programmed stimulation. TWA in the vector magnitude lead increased with heart rate, independent of VT inducibility (0.4 +/- 0.7 microV, 1.6 +/- 1.9 microV, and 2.4 +/- 2.1 microV in sinus rhythm and at 100 and at 120 beats/min, respectively; P < 0.001). In addition, the diagnostic performance of TWA for inducible VT was dependent on heart rate (sensitivity 4%, 42%, and 65%, and specificity 100%, 93%, and 63% at 77, 100, and 120 beats/min, respectively). By analyzing orthogonal leads rather than the vector magnitude lead, the sensitivity is increased from 42% to 59% at 100 beats/min, but the specificity is reduced from 93% to 72%. These results indicate that TWA in humans is strongly dependent on heart rate with regard to both magnitude and diagnostic performance. The optimal heart rate for the measurement of TWA is between 100 and 120 beats/min and multiple leads should be monitored.

ECG features of microvolt T-wave alternans in coronary artery disease and long QT syndrome patients

T-wave alternans (TWA) is a marker of myocardial electrical instability. We compared ECG features of microvolt TWA in coronary artery disease (CAD) and long QT syndrome (LQTS) patients. Method. The study populations consisted of 43 CAD and 39 LQTS patients. TWA was detected in resting Hotter recordings using the new correlation method (CM). After preprocessing to adjust for RR variability and respiratory modulation, CM was used to quantify TWA amplitude (A CM), duration (N CM), and magnitude (MAG CM; defined as the product of A CM and N CM). Results. TWA was detected in 19 (44%) CAD and 17 (44%) LQTS patients. TWA was associated with longer RR intervals ( P = 0.006) and had larger magnitudes ( P = 0.067) in LQTS than CAD patients. The TWA was identified as transient (nonstationary) in 15 of 19 (79%) TWA-positive CAD patients, and in 8 of 17 (47%) TWA-positive LQTS patients ( P = 0.047). Conclusions. The frequency of TWA detected with CM is similar in LQTS and CAD patients. TWA is larger in LQTS than in CAD patients, whereas TWA is more frequently transient (nonstationary) in LAD than LQTS patients. In LQTS patients, but not in CAD patients, a longer RR is associated with TWA, indicating different electrophysiologic mechanisms in the two pathologies.

1027-40 How to Detect ECG T-Wave Alternans in Patients at Risk for Sudden Cardiac Death

We have shown previously that subtle and visually inapparent T wave alternans (TWA) is a marker of susceptibility to sudden cardiac death (SCD). Since the characteristics of TWA in patients with SCD are poorly understood. the optimal technique for detecting TWA remains controversial. To resolve this problem, high-fidelity orthogonal ECGs were recorded during atrial pacing (100 bpml from 35 patients undergoing EP testing. TWA measured by fast Fourier transform (FFT) and complex demodulation (CD) techniques were compared in two groups of patients; 1. High Risk Group (n = 15); Inducible sustained monomorphic VT at EP testing or SCD during 20 month follow up, and 2. Low Risk Group (n = 20); Negative EP test and no SCD during 20 month follow up. With FFT. beat-to-beat T wave amplitude oscillations occurring at the alternans frequency are measured relative to spectral noise. With CD, beat-to-beat T wave amplitude oscillations were modeled as a sinusoid whose amplitude is assumed to be a measure of TWA without regard to noise levels. The magnitude of TWA measured by FFT and CD correlated well (r 2 = 0.97) when TWA levels were relatively high (&gt;5 μ V). However, the detection of very low level (1 μ V – 5 μ V), but prognostically important TWA differed considerably between the two techniques. Using a cutoff TWA level of 2 μ V to define TWA positivity, FFT predicted high risk for SCD with a sensitivity of 70% and specificity of 80%, whereas CD had a sensitivity of 90% and specificity of only 5%. Computer simulations performed with an idealized alternans wave form demonstrated that the poor specificity of CD was due to an inability of CD to selectively discriminate TWA from noise. When the phase of TWA was reset on random beats (to simulate ectopic beats), TWA was measured more accurately by CD than FFT. However, phase resetting was found in only 2.7% of ECG complexes analyzed from patients and its presence did not substantially obscure the detection of TWA by FFT compared to CD. Very low level TWA is a prognostically significant marker for SCD and is more accurately measured using the FFT technique. The enhanced specificity of FFT compared to CD results from the capability of FFT to discriminate low level TWA from noise.