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J Am Coll Cardiol, 2002; 40:1395-1400
© 2002 by the American College of Cardiology Foundation
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CLINICAL STUDY: SIGNIFICANCE OF ELECTROCARDIOGRAPHIC ABNORMALITIES

Quantitative assessment of electrocardiographic strain predicts increased left ventricular mass: the strong heart study

Peter M. Okin, MD, FACC*,*, Richard B. Devereux, MD, FACC*, Richard R. Fabsitz, MA{dagger}, Elisa T. Lee, PhD{ddagger}, James M. Galloway, MD, FACC§ and Barbara V. Howard, PhD||

* Division of Cardiology, Department of Medicine, Cornell Medical Center, New York, New York, USA
{dagger} National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
{ddagger} 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


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
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.

Abbreviations and Acronyms
  ASE
  American Society of Echocardiography
  CI
  confidence interval
  ECG
  electrocardiogram
  ESS
  end-systolic stress
  LV
  left ventricular
  LVH
  left ventricular hypertrophy
  ROC
  receiver operating characteristic
  STdep
  ST segment depression

The classic strain pattern of ST segment depression (STdep) and T-wave inversion in the lateral precordial leads of the rest electrocardiogram (ECG) is a well-recognized marker of the presence of anatomic left ventricular hypertrophy (LVH) (1–6) that has been associated with adverse prognosis in a variety of clinical populations (7–11). Indeed, lateral STdep and T-wave inversion is the strongest marker of morbidity and mortality when ECG LVH criteria have been utilized for risk stratification (8–10). Although the strain pattern can also reflect the presence of underlying coronary disease (2–4,8,10), the strong association of strain on the ECG with increased LV mass appears to be independent of the presence of coronary disease (2). Unfortunately, the fundamental qualitative nature of the strain pattern limits utility of this ECG criterion for the identification of LVH and for serial assessment of the severity of hypertrophy. Although quantitative assessment of the precise degree of STdep using computerized measurements has been demonstrated to predict mortality (12), the independent relationship of the measured degree of STdep in the lateral precordial leads to increased LV mass remains unclear. Thus, the present study examined the relation of quantitative measures of STdep in the lateral precordial leads on the rest ECG to LV mass and the presence of anatomic LVH, controlling for clinical and demographic variables that could potentially impact on this relationship.


   Methods
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Study population.   The Strong Heart Study is a community-based study of cardiovascular disease and its risk factors in American Indians from 13 communities in Arizona, Oklahoma, and North and South Dakota. Detailed information about the population, methods, and enrollment procedures for the study have previously been reported in detail (12–15). All participants underwent a personal interview, Rose questionnaire (16), physical examination, and fasting blood and urine sampling, and were categorized as having definite or possible coronary heart disease and diabetic as previously reported (14,15). The current study examined only the 1,595 participants in the second Strong Heart Study examination (65% women, mean age 59 ± 8 years) with digital ECG records in sinus rhythm with no bundle branch block, and with no clinical, ECG, or echocardiographic evidence of coronary artery disease. Participants were classified as having coronary disease and were excluded if they had myocardial infarction or definite coronary heart disease by diagnostic Q-waves by Minnesota code on the ECG, or segmental wall motion abnormalities on two-dimensional echocardiogram.

Electrocardiography
Standard 12-lead ECGs were performed with MAC-PC or MAC-12 digital ECG systems (GE Medical Systems) as previously described (12,13). Using the PR segment to define the isoelectric line, absolute ST segment deviation was measured by computer to the nearest 5 µV at the midpoint of the ST segment, defined as 1/8 the average R-R interval from the J-point on median complexes in lead V5 and V6. Participants were divided into quartiles based on the maximal magnitude of ST deviation in lead V5 or V6: quartile 1, ≥25 µV; quartile 2, 10 to 24 µV; quartile 3, –4 to 9 µV; and quartile 4, ≤–5 µV.

Echocardiography
Studies were performed using fundamental imaging with commercially available phased-array echocardiographs as previously described (15,17,18). Left ventricular internal dimensions and wall thicknesses were measured at end-diastole by American Society of Echocardiography (ASE) recommendations (19) on up to three cycles. When M-mode recordings could not be optimally oriented, correctly oriented linear dimension measurements were made using two-dimensional imaging by leading-edge ASE convention (20). Relative wall thickness was calculated as end-diastolic posterior wall thickness/LV radius; LV mass was calculated and was indexed for height2.7 to take into account the normal allometric relation of LV mass to body size (21). Left ventricular hypertrophy was considered present if LV mass index was >46.7 g/m2.7 in women or >49.2 g/m2.7 in men (22). Hypertrophy was considered concentric if LV relative wall thickness was >0.430 and eccentric if relative wall thickness was normal; patients with normal LV mass were considered to have normal LV geometry if relative wall thickness was ≤0.430 or to have concentric remodeling if relative wall thickness was increased (17,22). Myocardial contractile performance was assessed by examining LV systolic shortening in relation to circumferential end-systolic stress (ESS) (23). To estimate myocardial oxygen demand, the ESS-LV mass-heart rate product was calculated as previously described (24).

Data and statistical analyses
Data were analyzed with SPSS, release 10.0 (SPSS Inc., Chicago, Illinois). Data are presented as mean ± SD for continuous variables and as proportions for categorical variables. Differences in mean values according to quartiles of ST deviation were compared using analysis of variance and were further compared using analysis of covariance to adjust for differences in age, gender, pulse pressure, albuminuria, and fibrinogen levels across quartiles, using standard analysis of variance in which quartiles are assumed to be nominal. Differences in prevalences across quartiles were compared by {chi}2 tests. The independent relation of echocardiographic LVH to increasing STdep was determined using forward stepwise logistic regression analyses in which the Wald {chi}2 with 3 df was used to assess the significance of increasing STdep across quartiles and with odds ratios calculated using the first quartile of ST deviation as the reference group. Overall test accuracy of STdep for the detection of LVH was assessed by receiver operating characteristic (ROC) curve analysis. For all tests, a two-tailed p value <0.05 was considered significant.


   Results
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Mean ST segment deviation was 14 ± 14 µV, STdep of any magnitude was present in 29.5% and only 0.1% of the study population had ≥100 µV (0.1 mV) of STdep. Clinical and demographic characteristics of participants according to quartiles of increasing magnitude of STdep in leads V5 or V6 are shown in Table 1. Increasing STdep in these leads was associated with older age, higher systolic and pulse pressures, greater serum fibrinogen levels, and greater urinary albumin/creatinine ratios. Prevalences of female gender, diabetes, and current smoking were similar across quartiles and there was no association of diastolic blood pressure with increasing magnitude of STdep.


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  		Table 1 Clinical and Demographic Characteristics According to the Magnitude of ST Depression in Leads V5 or V6

 
Relations of LV structure and function to increasing STdep in the lateral precordial leads are examined in Table 2. Increasing STdep was associated with greater LV wall thicknesses, increased LV internal dimension, and consequently with greater LV mass and LV mass indexed for body size. Because increasing STdep was associated with parallel increases in LV wall thicknesses and internal dimension, relative wall thickness remained constant across quartiles of STdep. Increasing STdep was associated with increased wall stress and with evidence of increasing myocardial oxygen demand, as reflected by increasing ESS-LV mass-heart rate product.


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  		Table 2 Echocardiographic Characteristics According to the Magnitude of ST Depression in Leads V5 or V6

 
Prevalences of echocardiographic LVH and abnormal LV geometry according to increasing magnitude of STdep in leads V5 or V6 are shown in Table 3. The prevalence of LVH increased across quartiles of ST deviation, ranging from only 11.6% in those with ≥25 µV of ST elevation to 31.2% in participants with true STdep of ≥–5 µV. Left ventricular geometry varied in a similar fashion with increasing STdep; participants with greater STdep were less likely to have normal geometry, but were more likely to have either eccentric or concentric hypertrophy than those with less STdep. However, the prevalence of concentric remodeling remained stable across STdep quartiles.


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  		Table 3 Prevalence of Echocardiographic Left Ventricular Hypertrophy and Abnormal Left Ventricular Geometry in Relation to Increasing Magnitude of ST Segment Depression in Leads V5 or V6

 
Because increasing STdep was associated with increasing age, greater systolic and pulse pressure, and with higher levels of fibrinogen and albuminuria (Table 1), and because of the known gender differences in LV dimensions and mass, independent relations of echocardiographic findings to increasing magnitude of STdep were examined using analysis of covariance (Table 4). After adjusting for the possible impact of these clinical and demographic differences, increasing STdep remained associated with increased LV wall thicknesses and internal dimension, LV mass, and LV mass indexed for height2.7. Because of slightly greater increases in LV internal dimension than in wall thickness after adjusting for these covariates, the highest quartile of STdep was associated with a slight reduction in relative wall thickness. End-systolic stress remained higher with increasing STdep even after adjusting for differences in pressure, and the strong association between increasing STdep and the ESS-LV mass-heart rate product increased stepwise across quartiles of STdep after adjusting for clinical differences. Of note, additional adjustment by the ESS-heart rate component of the mass-stress heart rate product, as a measure of myocardial oxygen demand, did not alter the relation of increasing LV mass to greater magnitude of STdep.


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  		Table 4 Echocardiographic Characteristics According to the Magnitude of ST Depression in Leads V5 or V6 Adjusted for Differences in Age, Gender, Systolic and Pulse Pressure, Fibrinogen Levels, and Albuminuria

 
In parallel fashion, the relation of echocardiographic LVH to increasing STdep was further examined using logistic regression analyses (Table 5). In univariate analyses, increasing magnitude of STdep in the lateral precordial leads was strongly associated with an increased odds ratio of echocardiographic LVH. The odds of LVH remained strongly associated with increasing magnitude of STdep after adjusting for baseline differences, with a >2.5-fold increased prevalence of hypertrophy in participants in the highest quartile of STdep, and with significantly increased risk of LVH associated with the presence of minimal-to-no STdep (quartile 3) and decreasing amplitude of ST elevation (quartile 2). The magnitude of STdep in the lateral precordial leads alone had moderate, but highly significant, test accuracy for the detection of LVH (Fig. 1), with an area under the ROC curve of 0.726 ± 0.025 (p < 0.001). Of note, an STdep partition of ≤–10 µV identified LVH with a specificity of 85.0% and sensitivity of 38.1%, statistically similar to the 86.9% specificity (p = 0.133) and 41.2% sensitivity (p = 0.749) of Cornell voltage-duration product criteria ([RavL+SV3*QRS duration) (25).


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  		Table 5 Logistic Regression Analyses to Assess the Predictive Value of Increasing Magnitude of ST Segment Depression in Leads V5 or V6 for the Presence of Left Ventricular Hypertrophy

 


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  		Figure 1 Receiver operating characteristic (ROC) curve illustrating overall accuracy of the absolute magnitude of ST segment deviation in leads V5 and V6 for the identification of echocardiographic left ventricular hypertrophy. The area of 0.726 ± 0.25 under the ROC curve was highly significant for the detection of hypertrophy (p < 0.001). Representative partition values of ST deviation are illustrated alongside the ROC curve at the points corresponding to their sensitivity and specificity.

 

   Discussion
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 Abstract
 Methods
 Results
 Discussion
References
 
This study demonstrates that the presence of small but measurable increases in the magnitude of STdep in leads V5 and/or V6 in subjects with no evidence of underlying coronary disease is associated with greater LV mass and higher likelihood of having anatomic LVH, even after controlling for the higher blood pressure and other clinical differences associated with increased STdep. The increased LV mass and higher prevalence of LVH in participants with greater magnitudes of STdep offer insights into the known association of all-cause and cardiovascular mortality with even minimal amounts of STdep on the rest ECG (12). These findings, together with the strong association of the more qualitative ECG strain pattern with LVH (1–6), suggest that quantitative measures of the absolute magnitude of STdep in the lateral precordial leads, reflecting even minimal degrees of LV "strain," should be incorporated into the ECG assessment of the presence and prognostic severity of LVH.

Previous studies have demonstrated a strong relation between the ECG strain pattern and anatomic LVH (1–6), and that the prevalence of strain rises with increasing severity of hypertrophy (3). The present study extends these observations to a large, prospectively examined population-based sample, confirming the strong association between lateral repolarization abnormalities and the presence of LVH and further demonstrating that gradual decreases in the amplitude of the ST segment in leads V5 and/or V6, even when still above the isoelectric baseline, significantly increase the odds of LVH. In this context, it is important to note that the association between STdep and LVH in the current study does not reflect the impact of the typical strain pattern on the magnitude of STdep, as only two participants had >0.1 mV (100 µV) of STdep, which would be considered to reflect strain on the ECG. However, the greatest LV mass and highest prevalence of hypertrophy was seen in those participants with true, although mostly minimal, STdep (quartile 4), confirming the association between greater STdep and LV mass found when body surface mapping techniques were employed (26). Overall accuracy of the absolute magnitude of ST deviation in the lateral leads for detection of LVH was modest by ROC curve analysis (Fig. 1), suggesting that incorporation of additional ECG findings along with ST deviation will improve clinical detection of LVH using the ECG (26).

Previous findings on the relationship between the stain pattern and LV geometry have been less consistent (2,3,11). In hypertensive patients in the LIFE study (2), strain was associated with a predominance of the concentric pattern of LVH because of increased wall thicknesses out of proportion to slightly increased LV chamber size. Two other studies (3,11), including one that exclusively examined patients with pure aortic regurgitation associated with increases in LV dimension out of proportion to increases in LV wall thicknesses (11), found that ECG strain was associated with a greater prevalence of eccentric LVH. The present study extends these observations by relating small decreases in ST segment amplitude to stepwise increases in the prevalence of eccentric LVH, with an increased prevalence of concentric hypertrophy observed only in the quartile of participants with the greatest STdep (Table 3). These differing associations between lateral repolarization abnormalities and patterns of LV geometry could in part reflect differences among study populations, with the selected hypertensive patients in the LIFE study being at increased risk for concentric LV geometry (2). In addition, the increased prevalence of concentric LVH in the highest quartile of STdep in the present study suggests that only true ST depression, as opposed to decreased amplitude of ST elevation, may be associated with concentric LVH. Further study will be necessary to address this issue.

Although participants with clinical evidence of coronary disease were excluded from the present study, we cannot completely exclude the presence of coronary disease among the selected participants. Indeed, STdep on the ECG in itself is a strong predictor of underlying coronary disease and there is a strong association between coronary disease and LVH (27) that could in part contribute to the observed relation between STdep and LV mass. However, the finding of strong associations between the strain pattern and increased LV mass in hypertensive patients enrolled in the LIFE study (2) with and without evidence of coronary heart disease suggests that the observed relation between STdep and LVH is not predominantly a function of subclinical coronary disease. Indeed, coronary disease need not be invoked to account for the ST changes associated with hypertrophy (28–30). The association between STdep and increased wall thickness suggests a possible effect of myocardial cell hypertrophy on repolarization abnormalities, consistent with the distributed dipole model of the ECG response to hypertrophy proposed by Thiry et al. (28). Additionally, ST depression could reflect true subendocardial ischemia even in the absence of coronary disease, possibly through inadequate increases in coronary artery size in response to hypertrophy (29,30) and/or secondary to increased myocardial oxygen demand as manifest by higher wall mass-stress-heart rate products with greater STdep. However, the continued association of increased LV mass with increasing STdep, after further adjusting for the ESS-heart rate component of the stress-mass-heart rate product as a marker of myocardial oxygen demand using analysis of covariance, further suggests that the relationship between LV mass and STdep occurs independent of the possible effects of subclinical ischemia in this population.

There are several possible limitations to this study. First, as noted earlier, the possibility that subclinical coronary disease is affecting these results cannot be completely excluded. Second, although it is unclear to what degree these findings in American Indians can be generalized to other ethnic populations, the parallels between the present results and those in an international study of hypertensive patients (2) suggest that similar relationships of LV mass and LVH to STdep will be present in other patient populations.

These findings have several important implications. First, the strong association between even minor degrees of STdep and increasing LV mass strongly suggests that incorporation of computerized measures of lateral repolarization abnormalities can increase diagnostic accuracy of the ECG for the detection of anatomic LVH (26). Because both the strain pattern and quantitative STdep on the ECG are strong markers of increased morbidity and mortality (7–12), and in light of preliminary data suggesting that resolution of the strain pattern can be associated with regression of anatomic hypertrophy (31), these findings provide further impetus for evaluation of serial changes in STdep for assessment of regression versus progression of LVH and for additional refinement of risk stratification.


   Footnotes
 
This work was supported by grants HL-41642, HL-41652, HL-41654, and HL-65521 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland; by grant M10RR0047-34 (GCRC) from the National Institutes of Health, Bethesda, Maryland; and by a grant from The Michael Wolk Heart Foundation, New York, New York. The views expressed in this article are those of the authors and do not necessarily reflect those of the Indian Health Service.


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