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J Am Coll Cardiol, 2001; 38:514-520
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY

Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study

Peter M. Okin, MD, FACC*, Richard B. Devereux, MD, FACC*, Markku S. Nieminen, MD, PhD, FACC{dagger}, Sverker Jern, MD{ddagger}, Lasse Oikarinen, MD, PhD{dagger}, Matti Viitasalo, MD, PhD{dagger}, Lauri Toivonen, MD, PhD{dagger}, Sverre E. Kjeldsen, MD, PhD§, Stevo Julius, MD, ScD, FACC||, Björn Dahlöf, MD, PhD{ddagger} for the LIFE Study Investigators

* Department of Medicine, Division of Cardiology, Cornell University Medical Center, New York, New York, USA
{dagger} Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland
{ddagger} Sahlgrenska University Hospital/Östra, Göteborg, Sweden
§ Ullevål University Hospital, Oslo, Norway
|| University of Michigan Medical Center, Ann Arbor, Michigan, USA

Manuscript received November 10, 2000; revised manuscript received March 1, 2001, accepted April 10, 2001.

Reprint requests and correspondence: Dr. Peter M. Okin, Cornell University Medical Center, 525 East 68th Street, New York, New York 10021
pokin{at}mail.med.cornell.edu

OBJECTIVES

This study was designed to assess the relation of electrocardiographic (ECG) strain to increased left ventricular (LV) mass, independent of its relation to coronary heart disease (CHD).

BACKGROUND

The classic ECG strain pattern, ST depression and T-wave inversion, is a marker for left ventricular hypertrophy (LVH) and adverse prognosis. However, the independence of the relation of strain to increased LV mass from its relation to CHD has not been extensively examined.

METHODS

Electrocardiograms and echocardiograms were examined at study baseline in 886 hypertensive patients with ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage enrolled in the Losartan Intervention For End point (LIFE) echocardiographic substudy. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite to the QRS axis in leads V5 and/or V6.

RESULTS

Strain occurred in 15% of patients, more commonly in patients with than without evident CHD (29%, 51/175 vs. 11%, 81/711, p < 0.001). When differences in gender, race, diabetes, systolic pressure, serum creatinine and high density lipoprotein cholesterol were controlled, strain on baseline ECG was associated with greater indexed LV mass in patients with (152 ± 33 vs. 131 ± 32 g/m2, p < 0.001) or without CHD (131 ± 24 vs. 119 ± 22 g/m2, p < 0.001). In logistic regression analyses, strain was associated with an increased risk of anatomic LVH in patients with CHD (relative risk 5.14, 95% confidence interval [CI] 1.16 to 22.85, p = 0.0315), without evident CHD (relative risk 2.91, 95% CI 1.50 to 5.65, p = 0.0016), and in the overall population when CHD was taken into account (relative risk 2.98, 95% CI 1.65 to 5.38, p = 0.0003).

CONCLUSIONS

When clinical evidence of CHD is accounted for, ECG strain is likely to indicate the presence of anatomic LVH. Greater LV mass and higher prevalence of LVH in patients with strain offer insights into the known association of the strain pattern with adverse outcomes.

Abbreviations and Acronyms
  ASE = American Society of Echocardiography
  CHD = coronary heart disease
  ECG = electrocardiogram, electrocardiographic
  ESS = end-systolic stress
  HDL = high density lipoprotein
  LIFE = Losartan Intervention For End point study
  LV = left ventricular
  LVH = left ventricular hypertrophy




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