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