John E. Madias

Anasarca-mediated attenuation of the amplitude of electrocardiogram complexes: a description of a heretofore unrecognized phenomenon

OBJECTIVESnThe relationship between the changes of weight (WT) and electrocardiogram (ECG) QRS amplitude in patients with anasarca (AN) was evaluated.nnnBACKGROUNDnAttenuation of the ECG voltage occurs as the electrical current spreads from the epicardium to the body surface. The voltage registered is a function of the cardiac potentials, the electrical resistivities of the intervening tissues and the orientation of the ECG leads with respect to the direction of propagation of excitation. Lung congestion and pericardial and pleural effusions can cause attenuation in the ECG potentials; additionally, a similar change was recently observed in patients with AN.nnnMETHODSnA prospective study of this phenomenon in 28 patients with a critical illness was carried out. Electrocardiograms and patients WTs were recorded daily. Pericardial effusions were excluded by serial echocardiograms. The sums of the amplitude of QRS complexes from the 12 ECG leads (Sigma QRS) were correlated with the corresponding WTs. Intracardiac ECGs, done in three patients, were correlated with surface ECGs.nnnRESULTSnAdmission WT was 148.9 +/- 37.8 lbs, and it peaked to 197.8 +/- 52.3 lbs (p = 0.0005). Admission Sigma QRS was 120.2 +/- 41.6 mm and dropped to 54.8 +/- 26.9 mm at time of peak WT (p = 0.0005). Regression of Sigma QRS on WT revealed an r = 0.61 and a p = 0.0005. Subsequent WT loss in 13 patients (from 219.0 +/- 40.7 lbs to 179.5 +/- 41.7 lbs, p = 0.001) led to an increase of Sigma QRS from 53.5 +/- 24.5 mm to 86.8 +/- 38.2 mm (p = 0.001). Intracardiac ECGs remained stable, while surface ECGs changed with perturbations of WT.nnnCONCLUSIONSnAttenuation of ECG voltage in patients with AN correlates with WT gain, and it can be attributed to a shunting of the cardiac potentials due to the low resistance of the AN fluid.

Are the T-Wave Alternans Amplitude “Zones” Related to T-Wave Amplitude “Zones” in ECG Ambulatory Recordings?

To the Editor, The contribution by Burattini et al., published ahead of print in the Journal, dealt with an identification of four ‘‘zones’’ of amplitude/duration of T-wave alternans (TWA) in 200 patients with coronary artery diseased and 176 healthy subjects. The four ‘‘zones’’ or ‘‘subzones’’ as the authors called them were formed by considering low and high amplitude of the TWA signal, of short or long duration, with magnitude of the TWA defined as the product of amplitude and duration of TWA signals, from ambulatory ECG tracings. This is a methodological study, which did not set out to evaluate the performance of the authors’ method in predicting clinical events or ICD-based therapeutic shocks. Nevertheless, it is of interest that the study used thresholds from healthy subjects to determine what should be considered abnormal or normal in the patients with coronary artery disease. This should be commended and should be emulated by other workers who may also elect to study healthy subjects along with their target pathological populations, instead of relying on lV thresholds established previously (e.g., ‡1.9 lV), or decided upon based on the best negative predictive performance of arrhythmic events. The amplitude of TWA is viewed with increasing frequency as an important aspect in the assessment of TWA in patients, and this applies both to the time domain analysis (e.g., modified moving average) and the frequency domain spectral analytic method, in-spite the customary employment of the ‡1.9 lV threshold. What is refreshing in the study of Burattini et al. is that the duration of the TWA and its derived amplitude/ duration product are also employed as variables. The value of these needs to be corroborated, and if found meaningful, vigorously exploited in clinical studies. It would be fascinating to be able to predict specific arrhythmic behaviors depending on the four combinations of amplitude/duration of TWA the authors have formulated. To shift the matter to another concern, it has been postulated that the amplitude of TWA may be T-wave amplitude dependent. Ample experience in ambulatory ECG recordings reveal that the amplitude of the T-wave and the morphology, amplitude, and polarity of the entire J–T interval is quite variable throughout the duration of the recordings in both normal subjects and patients. One wonders as to the impact of such T-wave perturbations on the amplitude of the corresponding measured values of TWA. The authors could provide some insight on this by exploring for a relationship between the amplitude of the TWA and the amplitude of the corresponding T-waves in the leads X, Y, and Z, which they employed in the measurements of the TWA. Also it would be contributory to the above expressed concept to evaluate the influence of the changes in the T-wave amplitude, noted during the ambulatory ECG recordings, and the corresponding amplitude of the TWA in the individual leads X, Y, and Z. This boils down to the notion, that if the TWA amplitude depends, to some degree, on the amplitude of the T-wave that was used for its calculation, a correction or adjustment is in order, as previously theorized. Relevant to the notion that TWA magnitude may be T-wave dependent is recent experimental work on the spatial distribution of TWA, where a 64-lead body surface potential map (BSPM) set outperformed in the detection of TWA the orthogonal XYZ lead set and the 12-lead ECG; it would be of interest to evaluate in this study whether the leads showing the larger TWA magnitude were the ones also showing large corresponding T-wave amplitudes, independent of the overall characterization of TWA+ and TWA status, based on a threshold clinically significant value, exceeded in ‡1 ECG lead(s). Intuitively one wonders whether the ‘‘best ECG leads’’ showing the greater Address correspondence to John E. Madias, Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, USA. Electronic mail: madiasj@nychhc.org Annals of Biomedical Engineering, Vol. 38, No. 1, January 2010 ( 2009) pp. 223–224 DOI: 10.1007/s10439-009-9806-y

Microvolt T-Wave Alternans: Is There Anything That Can Be Done to Save It?

The sobering results reported in the contribution of Chow et al. ([1][1]), published in the November 11, 2008, issue of the Journal , calls for a serious and in-depth reassessment of microvolt T-wave alternans (MTWA) technology for its role in the identification of patients with ischemic and

Multiple bioelectric impedance vectors in the monitoring of congestive heart failure.

I was delighted to read the report by Khoury et al. ([1][1]) in the March 24, 2009, issue of the Journal , related to an area I have been interested in since 1998, namely, using electrocardiography in monitoring the edematous state of patients with varying pathologic features, including congestive

T-wave alternans and intraventricular conduction delays.

I read with great interest the study by Cantillon et al. ([1][1]) on the utility of microvolt T-wave alternans (MTWA) in predicting total mortality and arrhythmia-free survival in patients with a left ventricular ejection fraction ≤30% who had been referred for invasive electrophysiological

Anasarca and low electrocardiogram voltage: Reply

I am grateful to Dr. Brennan for directing me to literature describing a direct correlation of albumin and amplitude of QRS complexes [(1)][1]. To respond to his inquiry I have modeled an analysis of our data after the study of Dr. Heaf [(1)][1]. Our patients were critically ill, were followed for a