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(Hypertension. 1997;30:777-781.)
© 1997 American Heart Association, Inc.

Articles

Systolic Function in Hypertensive Men With Concentric Remodeling

Diego B. Sadler; Gerard P. Aurigemma; David W. Williams; Domenic J. Reda; Barry J. Materson; ; John S. Gottdiener

From the Divisions of Cardiology of the University of Massachusetts Medical Center (D.B.S., G.P.A.), Worcester, and Georgetown University Hospital (J.S.G.), Washington, DC, and the Cooperative Studies Program, Department of Veterans Affairs (D.W.W., D.J.R., B.J.M.).

Correspondence to Gerard P. Aurigemma, MD, University of Massachusetts Medical Center, 55 Lake Ave North, Worcester, MA 01655. E-mail gerard.aurigemma{at}banyan.ummed.edu

	Abstract

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Abstract Hypertensive patients with concentric remodeling (relative wall thickness 0.45 and normal left ventricular [LV] mass index) may have poor outcomes. It is unclear whether systolic function abnormalities, shown to be present in some patients with concentric LV hypertrophy (increased LV mass index and relative wall thickness 0.45), are also present in patients with concentric remodeling. To assess LV pump, chamber, and myocardial function in hypertensive men with concentric remodeling, clinical and echocardiographic data of 118 hypertensive men with concentric remodeling were compared with data from 104 hypertensive men with normal relative wall thickness and normal LV mass index. Chamber function was assessed by relating endocardial fractional shortening to end-systolic circumferential stress, myocardial function was assessed by relating midwall fractional shortening to circumferential stress, and pump performance was assessed by stroke volume (Teichholz method). Compared with hypertensive men with normal relative wall thickness, concentric-remodeling patients had lower stroke volume (84±20 versus 111±20 mL, P<.001). Endocardial shortening was no different between the two groups (38±7% versus 40±7%, P=NS), but midwall shortening was lower in patients with concentric remodeling (20±3% versus 22±3%, P<.001), despite lower end-systolic stress (81±25 versus 117±37 g/cm², P<.001). Endocardial and midwall stress-shortening regression plots classified 28% and 42%, respectively, of the concentric remodeling patients below the fifth percentile of hypertensive patients with normal geometry. These data indicate that indexes of chamber and myocardial function are lower than those observed in hypertensive patients with normal geometry. Thus, indices of chamber, myocardial, and pump performance indicate potential abnormalities in systolic function in men with concentric remodeling.

Key Words: hypertrophy • systolic function • left ventricular mass

	Introduction

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Left ventricular hypertrophy, defined as an absolute increase in LV mass index, is an independent predictor of adverse outcome.^{1 2 3} In hypertensive patients with and without LVH, prognosis appears to be worse when the RWT (the ratio of wall thickness to LV cavity radius) is high.^{2 4} However, this issue is controversial.⁵ Recent work has shown that patients with concentric LVH (ie, increased LV mass index and high RWT) have depressed midwall and long-axis shortening, despite normal ejection fraction.^{6 7 8 9 10 11 12} It is possible that these subtle abnormalities in systolic function may be related to adverse outcome. Whether these abnormalities in systolic function relate to high RWT or to the presence of LVH is not clear. Accordingly, the purpose of the present study was to investigate systolic function in hypertensive patients with concentric remodeling (normal LV mass index but high RWT)¹³ who participated in a multicenter Veterans Affairs Cooperative Study of monotherapy in hypertension.¹⁴ Because earlier work has shown a high prevalence of obesity in this patient population,¹⁵ a secondary aim of the study was to assess the impact of obesity on systolic function parameters in patients with concentric remodeling.

	Methods

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Patient Population
The study population was part of a larger group of 1292 men who participated in a placebo-controlled, multicenter, double-blind, randomized, prospective trial of monotherapy in patients with uncomplicated mild to moderate hypertension (average blood pressure 152±14/99±3 mm Hg)¹⁴ and no evidence of cardiac or systemic disease. Of 1292 men who participated in the primary study, 994 (78%) had baseline (pretreatment) echocardiographic studies; studies in 690 men were considered technically adequate for analysis. Two hundred twenty-two men (32%) who comprised the study population had normal LV mass index using LV mass/height^2.7.¹⁶ The mean age was 56±1 years, and the mean baseline (pretreatment) blood pressure was 149±13/99±4 mm Hg.

To investigate the association between LV geometry and systolic function, the study population was classified by RWT,¹⁷ with a partition value of 0.45.¹³ Group 1 (n=118), which had concentric remodeling, had RWT 0.45; group 2 (n=104) had normal LV geometry (RWT <0.45) and served as the reference population.

Echocardiography
Details of the methodology used for obtaining echocardiographic measurements in this patient population have been previously published.¹⁵ Briefly, standard American Society of Echocardiography (ASE) measurement criteria¹⁹ were used. LV mass was calculated by both the ASE criteria^{19 20} and the Cornell-Penn convention.¹⁷ In view of the high prevalence of obesity in the study population,¹⁵ it was decided that the most appropriate means for LV mass indexation was LV mass/height^2.7.¹⁶ We used the partition value of 51 g/m^2.7 as a cutoff for LV hypertrophy¹⁶ and excluded any patient with a LV mass index equal to or exceeding this value. RWT of the LV was expressed as the ratio of twice the posterior wall thickness to the end-diastolic cavity dimension.¹⁸ LV volumes were derived from M-mode data by the Teichholz formula.²¹

LV Wall Stress
End-systolic circumferential wall stress (c) was calculated according to the following formula:

This formula uses measurements of LV dimensions and blood pressure as determined by sphygmomanometry, where P is end-systolic pressure, a is the internal (endocardial) radius, b is the epicardial radius, and r is the midwall radius.²² End-systolic pressure was calculated as one third of the sum of systolic pressure plus twice the diastolic pressure.²³

LV Pump, Chamber, and Myocardial Function
Pump function was defined by stroke volume and was expressed as the difference between end-diastolic and end-systolic volumes.

Chamber function was assessed as percent FS at the endocardium, calculated as the difference between the end-diastolic and end-systolic circumference multiplied by 100. Myocardial function was assessed by percent circumferential FS at the midwall and was calculated using a two-shell cylindrical model, which does not require the conventional assumption that inner- and outer-wall thickening fractions are equal.^{10 11} Data provided by this method reflect shortening of a theoretical circumferential midwall fiber; in contrast to endocardial FS, midwall FS is not influenced by relative wall thickness.¹² The formulas needed to calculate midwall FS are shown in "Appendix 1."

Endocardial and midwall FS were related to circumferential end-systolic wall stress by use of linear regression so that LV chamber and myocardial function, respectively, could be assessed. The relation of FS to end-systolic stress has been postulated to be a relatively afterload-independent index of contractile state.^{24 25}

Obesity
To investigate the interaction between obesity and geometry, body mass (Quetelet) index, a measure of adiposity,^{26 27} was calculated as weight (kg) divided by height (m) squared. Normal weight was defined by body mass index <27 kg/m², overweight as 27 to 30 kg/m², and obesity as >30 kg/m².¹⁵

Statistical Analysis
Data are expressed as mean±SD. Comparisons of continuous variables between the concentric remodeling and normal geometry groups were performed by Student's t test for independent groups.

A two-way ANOVA with interaction was used to address the relation between midwall and endocardium shortening indexes (dependent variables) and RWT, Quetelet index, and their interaction (independent variables). Regression coefficients of endocardial and midwall FS versus circumferential end-systolic stress were obtained for patients with concentric remodeling and those with normal RWT. Ninety-five percent confidence intervals were then established for subjects with normal geometry, who were used as a reference population. Subjects with concentric remodeling and values for LV functional parameters below the fifth percentile of the reference population were considered to have depressed chamber and myocardial function relative to hypertensive patients with normal geometry.

A value of P<.05 was considered to be statistically significant. All tests were two-sided.

	Results

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Population Demographics
Data for demographics of the study population are shown in Table 1. Patients with concentric remodeling (group 1) were slightly older (P=.054) than those individuals with normal geometry (group 2). There were no differences in systolic or diastolic blood pressure, heart rate, body surface area, Quetelet index, or racial distribution between these two groups.

View this table: [in this window] [in a new window]   Table 1. Demographic Data

Echocardiographic Data
The principal echocardiographic data are displayed in Table 2. Group 1 patients had smaller LV diastolic and systolic cavity dimensions and larger septal and posterior wall thickness than group 2 patients. LV mass index, by both ASE and Cornell-Penn conventions, did not differ between the two groups.

View this table: [in this window] [in a new window]   Table 2. Left Ventricular Size and Systolic Function

Systolic Function
There was no difference in the endocardial FS between the two groups (P=.09). By contrast, midwall FS was significantly lower in group 1 than in group 2 (P<.001), despite decreased afterload; end-systolic circumferential stress for group 1 was lower than that for group 2 (P<.0001), suggesting that myocardial function in group 1 patients is reduced as compared with hypertensive control patients with normal geometry. Pump function, as determined by stroke volume, was also reduced in group 1 compared with group 2 (P<.001).

Stress-shortening relations at the endocardium and midwall (Figs 1 and 2) were examined to analyze chamber and myocardial functions, respectively. Endocardial FS was inversely related to circumferential end-systolic stress both in individuals with normal geometry (r=-.90, P=.0001) and in patients with concentric remodeling (r=-.89, P<.0001). Similarly, the inverse relation of midwall fractional shortening to end-systolic stress was significant in both subjects with normal RWT (r=-.76, P=.0001) and in subjects with concentric remodeling (r=-.44, P=.0001). Stress-shortening relation values are summarized in Table 3.

View larger version (18K): [in this window] [in a new window]   Figure 1. Endocardial fractional shortening/end-systolic circumferential stress regression plot indicates that 28% of concentric remodeling hypertensive patients fall below the 95% CI of normal-geometry individuals.

View larger version (17K): [in this window] [in a new window]   Figure 2. Midwall fractional shortening/end-systolic circumferential stress regression plot shows that 42% of patients with concentric remodeling fall below the 95% CI of hypertensive patients with normal geometry.

View this table: [in this window] [in a new window]   Table 3. Endocardial and Midwall Shortening in Relation to Circumferential End-Systolic Stress

Relative to the control population, 28% of patients with concentric remodeling (Fig 1) had chamber function determined by endocardial stress-shortening relation below the fifth percentile. Likewise, 42% of patients with concentric remodeling had midwall stress-shortening coordinates below the fifth percentile.

Relation Between Obesity, Hypertension, LV Geometry, and Midwall Shortening
On a two-way ANOVA with interaction, the relation between RWT and midwall FS was the same across all three levels of the Quetelet index. Adjustment for systolic blood pressure did not change this relation. Thus, there did not appear to be a significant influence of obesity on myocardial function as determined by midwall shortening.

	Discussion

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Echocardiographic and MRI-tagging studies have shown that patients with concentric LVH and normal ejection fraction have depressed circumferential fractional shortening at the midwall.^{6 7 8 9 10 11 12} However, it is uncertain whether the abnormal geometry (increased RWT) or the hypertrophy per se is responsible for reduced systolic function. The present study shows that by stress-shortening analyses, a substantial percentage of patients with mild to moderate hypertension and high RWT but normal LV mass index have lower chamber (28%) and myocardial (42%) function indexes compared with hypertensive patients with normal geometry. These lower values for endocardial and midwall shortening, relative to stress, are paralleled by decreased stroke volume, which we used as a descriptor of pump function. Because this study included only patients with normal LV mass index and high RWT, our results indicate that increased RWT, rather than hypertrophy, is related to lower values for indexes of systolic function.

Our midwall-shortening data qualitatively agree with those of de Simone et al,⁶ who studied 50 patients with concentric remodeling and found that midwall FS was reduced compared with normotensive control patients (15±2% versus 17±2%, P<.01). However, our chamber function data (endocardial FS) differ from those of de Simone et al; whereas the mean value for endocardial FS in our study was not different in patients with concentric remodeling compared with hypertensive patients with normal LV mass and RWT (38% versus 40%, P=.10), when endocardial FS was plotted against end-systolic stress, 28% of the patients fell below the fifth percentile, suggesting depressed chamber function in those individuals. This finding of depressed chamber function differs from that of de Simone et al,⁶ who reported a normal observed-to-predicted endocardial stress-shortening relation in hypertensive patients with concentric remodeling compared with normotensive control patients. It is likely that our results differ from those of de Simone et al⁶ because our reference population comprised hypertensive patients with normal LV RWT, whereas de Simone et al's reference population comprised normotensive individuals with normal LV structure. It has been argued that hypertensive patients with normal LV mass and normal RWT have "enhanced" endocardial shortening for the level of afterload.^{28 29 30} Therefore, relative to these individuals, concentric-remodeling patients may appear to have reduced endocardial shortening. Support for this conclusion may be found in the data recently reported by Verdecchia et al,⁴ who compared hypertensive patients with concentric remodeling to hypertensive patients with normal RWT and found a lower observed-to-predicted endocardial FS (101% versus 110%, P<.01) in the concentric remodeling group. Concentric remodeling subjects and hypertensive subjects with normal RWT in the series of Verdecchia et al had similar endocardial FS, despite 20% lower values for meridional end-systolic wall stress (57 versus 71 g/cm², P<.01) in the concentric remodeling group.⁴ It is also possible that subjects who fall below the confidence limits of the endocardial stress-shortening relation actually have an abnormality in LV chamber performance. Unfortunately, the lack of a normotensive control group does not permit us to fully evaluate this intriguing possibility.

In a recent study involving a small number of older hypertensive individuals with concentric LV geometry,⁷ we found that approximately one third of patients with normal ejection fraction but abnormal RWT have a substantial abnormality in systolic pump performance that is characterized by low stroke volume and low cardiac output. The present study extends that observation to a much larger group of patients with high relative wall thickness and normal LV mass index. Thus, the smaller stroke volume associated with high RWT observed in the present study is likely to be related to chamber size, suggesting that concentric geometry develops at the expense of a smaller cavity volume.

Obesity
Obesity is an independent predictor of LVH in patients with mild to moderate hypertension.¹⁵ Furthermore, the effects of systolic blood pressure on LV mass are amplified by obesity.¹⁵ There are conflicting data, however, concerning the relation among LV geometry, hypertrophy patterns, and obesity.^{15 31 32 33} Data from the Veterans Affairs Cooperative Study show that concentric LVH is highly prevalent in obese patients.¹⁵ In contrast, de Simone et al reported that eccentric hypertrophy was the most common pattern in obese patients and that concentric remodeling was less prevalent among obese patients than among normal-weight subjects.³³ There were several reasons for investigating the relation of obesity to systolic function in our study population. We wanted to determine whether there were subtle indications of reduced systolic function in obese subjects because midwall mechanics may be abnormal when ejection fraction is normal and RWT is high. Because indexing LV mass to body surface area in a population with a high prevalence of obesity might misclassify some obese subjects with concentric LVH as having concentric remodeling, we chose, as our indexation method, LV mass/height^2.7. In addition, we also analyzed our data by the Quetelet index to determine whether reduced myocardial function is related to geometry or hypertrophy. Our results show that in this population, reduced midwall shortening (relative to hypertensive patients with normal geometry) is independent of obesity because the interaction between midwall shortening, RWT, and systolic blood pressure was the same for all levels of body mass index.

Clinical Implications
Koren et al² were the first to report that patients with the concentric remodeling pattern suffered higher mortality than subjects matched for LV mass and blood pressure. These findings were confirmed recently by Verdecchia et al,⁴ who studied a larger series of subjects with essential hypertension and reported that concentric remodeling was associated with an increased rate of cardiovascular morbid events compared with patients with normal RWT (RR, 2.56; 95% CI, 1.20 to 5.45; P<.01). In contrast, Krumholz et al,⁵ reporting on the Framingham Heart Study population, found that geometry was not an independent predictor of cardiovascular events after adjustment for LV mass, although there was a trend toward more events in men. The study population in the report by Krumholz et al⁵ differed from the previously mentioned studies^{2 4} in hypertension status and racial composition. It is interesting to note that the Framingham Heart Study subjects were less likely to be black and that blacks have a higher prevalence of concentric geometry.³⁴ It is also important to point out that the study by Krumholz et al⁵ was a general population study. In contrast, the study populations of Koren et al² and Verdecchia et al⁴ comprised referred hypertensive subjects who were judged to be free of heart disease. It is not certain how the findings reported here relate to prognosis. A recent study by de Simone et al³⁵ suggests that reduced midwall shortening is, like LVH, an independent predictor of cardiovascular events. It is possible, therefore, that the subjects with reduced midwall FS represent a group at high risk for cardiac morbid events. It is also possible that the development of concentric geometry may indicate an early stage of transition to overt systolic dysfunction as seen in animal models of pressure-overload hypertrophy.³⁶ To that extent, the development of concentric geometry may serve to maintain normal pump performance despite depressed myocardial function.^{7 37}

	Selected Abbreviations and Acronyms

 

FS = fractional shortening LV = left ventricle LVH = left ventricular hypertrophy RWT = relative wall thickness

	Acknowledgments

 
We wish to thank Lynn Stewart for assistance in manuscript preparation.

	Appendix 1

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Formulas for Midwall Shortening Calculations
1. End-systolic endocardial radius (a)=(LV dimension sys-tole)/2 or Ds/2, where Ds is LV dimension SYS.

2. End-systolic epicardial radius (b)=(Ds/2)+PW SYS or (Ds/2)+hes, where hes is PW SYS and Ds is LV dimension SYS.

3. End-systolic midwall "increment"= a'=-{Ds-square root (Ds² +[hes(2 · Dd+hd)(Ds+hes)]/(Dd+hd)}/2

where hd is posterior wall DIAS, Ds is LV dimension SYS, hes is PW SYS, and Dd is LV dimension DIAS.

4. End systolic midwall radius (r)=a+a'.

5. Midwall fractional shortening (%)=[(Dd+hd)–(Ds+2 · a')]/[Dd+hd] · 100.

Received October 23, 1996; first decision November 14, 1996; accepted March 6, 1997.

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