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J Am Coll Cardiol, 2002; 40:1395-1400 © 2002 by the American College of Cardiology Foundation |



* Division of Cardiology, Department of Medicine, Cornell Medical Center, New York, New York, USA
National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
University of Arizona, Tucson, Arizona, USA
|| MedStar Research Institute, Washington, DC, USA.
Manuscript received March 22, 2002; revised manuscript received May 23, 2002, accepted May 31, 2002.
* Reprint requests and correspondence: Dr. Peter M. Okin, Cornell Medical Center, 525 East 68th Street, New York, New York 10021, USA.
pokin{at}med.cornell.edu
OBJECTIVES: This study was designed to examine the relation of computer-measured ST depression (STdep) in the lateral precordial leads to the presence of left ventricular hypertrophy (LVH).
BACKGROUND: Qualitative abnormalities of repolarization in the lateral precordial leads of the electrocardiogram, as manifested by the strain pattern of T-wave inversion and STdep, are markers for LVH and adverse prognosis. However, the independent relationship of increased left ventricular (LV) mass to quantitative measures of STdep in these leads remains unclear.
METHODS: Electrocardiograms and echocardiograms were examined in the second Strong Heart Study examination in 1,595 American Indian participants without evident coronary disease. The absolute magnitude of ST segment deviation above or below isoelectric baseline was measured by computer in leads V5 and V6, and participants were grouped according to gender-specific quartiles of maximal STdep. Left ventricular hypertrophy was defined by indexed LV mass >49.2 g/m2.7 in men and >46.7 g/m2.7 in women.
RESULTS: Increasing STdep was associated with older age, greater pulse pressure, serum fibrinogen levels and urinary albumin/creatinine ratios, and with stepwise increases in LV mass (145 ± 28 vs. 150 ± 33 vs. 156 ± 36 vs. 164 ± 43 g, p < 0.001), indexed LV mass (38.2 ± 7.7 vs. 39.3 ± 8.7 vs. 40.5 ± 9.4 vs. 44.0 ± 11.0 g/m2.7, p < 0.001), and prevalence of LVH (11.6 vs. 19.1 vs. 21.5 vs. 31.2%, p < 0.001). After controlling for clinical differences, increasing STdep remained strongly associated with increased prevalence of LVH (p = 0.0001).
CONCLUSIONS: In the absence of evidence of coronary disease, increasing STdep in the lateral precordial leads is associated with increasing LV mass and increased prevalence of anatomic LVH.
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