abstract
presented
at the 1997 NASPE
New Orleans, Louisiana
May 7-10, 1997
Is T-wave Alternans
Caused by Left Ventricular Hypertrophy?
PACE 1997;20:II-691
David M. Strasser, MD, Lee A. Biblo, MD, Jason
K. Smith, MD, Siavash Yazdanfar, BS, Michel G. Farah, MD, Michael
C. Smith, MD, Touraj Taghizadeh, MD, David S. Rosenbaum, MD, University
Hospitals of Cleveland, Case Western Reserve University, Cleveland,
Ohio
Previously, a relationship between microvolt-level
T-wave alternans (TWA) and susceptibility to ventricular arrhythmias
has been established in patients with hypertrophic cardiomyopathy
and in patients with ischemic heart disease. Because left ventricular
hypertrophy (LVH) is also a significant risk factor for sudden
cardiac death (SCD), it is possible that TWA simply reflects the
degree of LVH. To determine if LVH causes TWA, we measured TWA
and left ventricular mass index (LVMI) in a young (age 40 ±
10 years) chronic hemodialysis population, as these patients have
an increased risk for SCD and a high incidence of LVH in the absence
of tother structural heart disease.
Eighteen (12 men, 6 women) chronic hemodialysis patients
(mean duration 39 months) with preserved left ventricular systolic
function (LVEF >0.40) underwent echocardiography and
bicycle exercise testing to 70% of age-predicted maximal heart
rate. Microvolt-level beat to beat fluctuations in T wave amplitude
were measured with sensitive spectral analysis techniques using
software and hardware designed to minimize exercise related noise.
A test was positive if there were sustained alternans >1.9
µV during exercise or >1.0 µV during rest,
and the alternans could not be attributed to artifact. Left ventricular
mass was measured using standard 2D/M-mode echocardiographic methods.
Twelve patients (67%) met established criteria for LVH. All
patients with LVH had concentric hypertrophy with LVMI ranging
from 137 to 324 g/m2 for men (normal <132 g/m2)
and 127 to 233 g/m2 for women (normal < 109 g/m2).
Only one of twelve patients with LVH (LVMI 137 g/m2)
demonstrated TWA with an alternans magnitude of 3.3 µV.
One of the six patients without LVH (LVMI 87 g/m2)
exhibited TWA with a magnitude of 2.9 µV.
Conclusions: These data
demonstrate that T-wave alternans is not solely dependent on LVH.
This implies that TWA in patients with hypertrophic cardiomyopathy
or ischemic heart disease involves additional factors and cannot
be explained by coexisting LVH. Further studies are necessary
to determine if TWA can predict myocardial electrical instability
and SCD in the chronic hemodialysis population.
1 Oak Park Drive
Bedford, MA 01730
617-271-1200