Concealment of electrocardiographically based diagnosis of left ventricular hypertrophy by anasarca

Diagnosis of left ventricular hypertrophy (LVH) is primarily based on measurements of R- and S-waves from various electrocardiographic (ECG) leads. Recent information has shown that anasarca peripheral edema (AN) (defined as fluid accumulation diagnosed by weight gain, positive fluid intake/output records, and pitting edema in the lower extremities and rest of the body, particularly in the dorsal region) leads to attenuation in the amplitude of QRS complexes and consequently could interfere with the diagnosis of LVH. The objective of this study was to evaluate whether the diagnosis of LVH is concealed by AN.

Conventional ECG measurements and diagnostic binary characterization according to the Cornell, Sokolow-Lyon, and Romhilt-Estes systems were carried out in 14 patients with LVH (six patients with AN and eight patients admitted contemporaneously who did not gain weight during their hospitalization and who served as control subjects). The patients with AN were evaluated on admission (before the development of AN), and on the days of half of peak weight (HF-W) gain, peak weight (P-W) gain, and the lowest subsequent weight (L-W). The control subjects were evaluated on admission and at discharge. Analyses included the following: characterization by the three LVH diagnostic instruments mentioned previously; QRS amplitude measurements for the assessment of LVH before and after development of AN; and comparisons of the AN patients with the control subjects.

Measurements and binary characterization was diagnostic of LVH on admission by design for all 14 patients. However, although such characterization remained unaltered for the control subjects, the patients with AN revealed statistically significant drops in all ECG measurements on the days of HF-W gain (P = .016 to .0005) and P-W gain (P = .02 to .0005), at which points the diagnosis of LVH could no longer anymore substantiated.

The results of this study indicate that AN interferes with electrocardiographically based diagnosis of LVH. This has clinical implications because accurate characterization of the presence or absence of LVH is unattainable in patients with AN and should await abatement of the edematous state. The previously stated can be extrapolated to the patients with congestive heart failure who have gone on to develop right heart failure and AN, or to patients with end-stage renal failure who also reveal attenuation of the ECG QRS potentials at the stage of poor compensation of their edematous state.