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Hypertension. 2001;37:1404-1409

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(Hypertension. 2001;37:1404.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Relation of Age to Left Ventricular Function and Systemic Hemodynamics in Uncomplicated Mild Hypertension

David J. Slotwiner; Richard B. Devereux; Joseph E. Schwartz; Thomas G. Pickering; Giovanni de Simone; Mary J. Roman

From the Department of Medicine and Hypertension Center, The New York Presbyterian Hospital–Weill Medical College of Cornell University, New York.

Correspondence to Dr Richard B. Devereux, Division of Cardiology, Box 222, The New York Presbyterian Hospital–Weill Medical College of Cornell University, 525 E 68th St, New York, NY 10021. E-mail rbdevere{at}mail.med.cornell.edu


*    Abstract
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Abstract—Previous studies in normotensive subjects have shown a slight decline in resting left ventricular pump function and midwall contractility with aging. We examined the relations of age to these variables and to peripheral resistance and vascular stiffness in 272 asymptomatic, unmedicated adults (25 to 80 years old) who had uncomplicated essential hypertension. Cardiac and carotid ultrasound and carotid pressure waveforms were obtained to measure left ventricular dimensions, endocardial and midwall left ventricular shortening, stroke index and cardiac index, end-systolic stress, and pulse pressure/stroke index and ß, pressure-dependent and independent measures of vascular stiffness, respectively. Endocardial and midwall stress-corrected left ventricular shortening assessed ventricular performance. Cardiac index and TPRI did not change with age in either gender, with age-related increases in systolic pressure offset by increasingly concentric ventricular geometry in women and enhanced ventricular systolic function in men. In contrast to the lack of age-related change in traditional hemodynamic indexes, pulse pressure/stroke volume and ß strongly increased with age (P<0.001). Thus, in uncomplicated, relatively mild essential hypertension, neither cardiac index nor peripheral resistance is associated with age. This hemodynamic stability is associated with age-related increased concentricity of ventricular geometry in women and increased ventricular performance indexes in hypertensive men. Vascular stiffness progressively increases with age, independent of change in mean pressure or resistance, possibly contributing to increased rates of cardiovascular events in older individuals.


Key Words: hypertension, mild • echocardiography • age • ventricular function • myocardium


*    Introduction
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Advancing age, increased left ventricular (LV) mass, and midwall but not endocardial fractional shortening have been shown to predict morbidity and mortality in hypertensive patients.1 2 3 4 5 6 7 Although reduced cardiac output and dysfunction of average myocardial fibers located at the LV midwall occur commonly in hypertension, it is not clear at what stage in the disease these changes develop.8 9 Previous cross-sectional and some longitudinal studies in hypertensive subjects have demonstrated elevated resting cardiac output (attributed to increased heart rate and/or stroke volume) in young, mildly hypertensive individuals.10 11 12 In contrast, low levels of invasively determined cardiac output and stroke index have been reported in older, often more severely hypertensive individuals.11 13 14

Nevertheless, uncertainty regarding the evolution of hemodynamic alterations persists.15 Results from invasive hemodynamic studies may be affected by an "alerting" response that may be greater at younger than older ages. Additionally, previous echocardiographic studies have used endocardial rather than midwall shortening to estimate LV function, thus measuring LV chamber performance accurately but tending to overestimate myocardial function in thick-walled hearts.

To reexamine these issues, we related echocardiographic measurements of cardiac output and total peripheral resistance (TPR) and arterial stiffness as well as LV systolic function and wall stress, measured at both the LV endocardium and midwall, to age in a large group of unmedicated hypertensive adults.


*    Methods
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Study Population
Patients included 162 hypertensive patients undergoing clinical evaluation at the New York Presbyterian Hospital Hypertension Center or in work site–based clinics, 54 subjects undergoing baseline evaluation for a treatment trial,16 and 10 volunteers found to be hypertensive during evaluation as part of a neighborhood outreach program. Criteria for inclusion were (1) arterial pressure >=140/90 (or 160/90 in individuals >65 years of age) by the first and fifth Korotkoff phases by arm cuff and mercury manometer, by multiple clinic measurements, (2) absence of cardioactive medication, (3) good-quality echocardiograms, (4) absence of clinical or laboratory evidence of secondary hypertension, and (5) absence of clinical or echocardiographic evidence of coronary artery or valvular disease. Antihypertensive medication had been discontinued from 3 weeks to 6 years previously by 68% of women and 58% of men (P=NS) who were similar in age to never-treated individuals (mean=56 versus 53 years, P=NS). Obesity was defined as body mass index >30 kg/m2 in both genders.17

Echocardiography
Two-dimensionally guided M-mode echocardiograms were recorded by previously described procedures to visualize LV structures.18 Tracings were coded and read blindly. End-diastolic LV internal dimensions and wall thicknesses were measured by the Penn Convention to calculate LV mass.19 20 LV measurements by the American Society of Echocardiography (ASE) method21 were used to determine LV relative wall thickness (2xposterior wall thickness/LV diastolic internal dimension), diastolic and systolic chamber volumes,22 and, with blood pressure measurements, to calculate LV end-systolic circumferential wall stress.23 24 LV contractile function was evaluated by assessment of midwall and endocardial ventricular mechanics.25

LV mass was indexed for height,2,7 as has been demonstrated to be a sensitive and specific method to identify LV hypertrophy26 27 and predict an adverse prognosis.28

Measurements of LV chamber dimensions at end diastole and end systole by ASE recommendations21 were used to calculate endocardial (e) fractional shortening (FS). Circumferential end-systolic stress (ESS) calculated at the midwall at the level of the LV minor axis using a cylindrical model24 was used as the primary measure of myocardial afterload. Midwall shortening was calculated by taking into account the epicardial migration of the midwall during systole, as described previously.25 Equations relating LV endocardial shortening and midwall shortening to circumferential ESS in 140 apparently normal adults25 were used to predict endocardial and midwall shortening for observed ESS. Observed/predicted midwall and endocardial shortening were used as stress-corrected measures of LV performance.7 25

Pulse pressure/stroke index was used as an estimate of overall systemic arterial stiffness. Common carotid artery dimensions and pressure waveforms acquired by applanation tonometry were used to calculate ß, a pressure-independent measure of vascular stiffness29 30 as ß=ln(Ps/Pd)/[(Ds-Dd)/D0), where Ps and Pd are the systolic and diastolic pressure, Ds and Dd are the systolic and diastolic dimensions, and D0 is the arterial dimension at a standardized blood pressure.31

Statistical Analysis
Data were analyzed with SPSS software. Data are presented as mean±SD. Partial correlation coefficients were used to study relations between age and other characteristics, with adjustment for prior antihypertensive medication use. For purposes of comparison, the population was divided into 3 approximately equal-sized groups 25 to 49, 50 to 60, and >=61 years of age; because of a disproportionate number of women in the oldest age group, cardiovascular variables were analyzed separately in women and men. The general linear model with the Sidak post hoc test was used to identify differences between age groups, with entry of an indicator variable for prior medication use to determine whether there were nonlinear changes with age of variables under study. The null hypothesis was tested with a 2-tailed {alpha}<0.05 criterion.


*    Results
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Subject Characteristics
The 170 men and 102 women in the study ranged in age from 25 to 85 years of age (mean, 55±12); 179 patients were white, 76 African-American or African-Caribbean, 12 Hispanic, and 5 Asian (Table 1). One hundred forty-six subjects had never smoked, 102 were former smokers, and 24 smoked currently. Total cholesterol was 224±43 mg/dL; HDL cholesterol, 54±16 mg/dL; triglycerides, 139±100 mg/dL; and total cholesterol/HDL, 4.21±1.45. Obesity was present in 21% of the population. The proportion of current smokers was lowest in the oldest age group, whereas the youngest age group had the highest proportion of never-smokers (P=0.01). Modest positive relations with age were observed for total cholesterol level (r=0.24, P<0.001) but not for total cholesterol/HDL (r=0.14), HDL cholesterol (r=0.07), or triglyceride levels (r=0.03) in partial correlations adjusting for gender and prior antihypertensive therapy.


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  		Table 1. Demographic Findings in Subjects Grouped by Age

When the several age groups were compared, with control for gender and prior treatment (Table 1), the proportion of women rose and height, weight, and body surface area decreased with age, without change in body mass index or heart rate. Systolic blood pressure increased, diastolic pressure decreased, and pulse pressure rose most strongly with age, without difference among age groups in mean arterial pressure.

Relation of LV Performance and Geometry to Age
Among hypertensive women (Table 2), there were no significant differences between age groups in any measure of LV systolic function or afterload to age; however, end-systolic stress and stress-adjusted LV chamber function rose slightly with age when considered as continuous variables. In contrast, LV wall thicknesses, relative wall thickness, and mass all showed positive relations to age in both between-group comparisons and partial correlations (Table 2).


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  		Table 2. Relation of LV Chamber and Myocardial Performance to Age in Women1

Among hypertensive men (Table 3), both endocardial and midwall LV shortening rose with age, with no change in end-systolic stress. As a result, stress-corrected midwall shortening increased with age, as did the end-systolic stress/volume index ratio in continuous analyses. In contrast to the findings in women, there was no association between age and any of the measures of LV geometry.


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  		Table 3. Relation of LV Chamber and Myocardial Performance to Age in Men1

Relations of Systemic Hemodynamics to Age
Among hypertensive women (Table 4), heart rate, mean arterial pressure, and stroke index were not related to age. As a result, there were no associations between age and absolute or indexed values of cardiac output or TPR. In contrast, stiffness of the systemic arterial tree as measured by the ratios of pulse pressure to stroke volume or to stroke index, as well as the pressure-corrected stiffness index (ß), all had highly significant increases with age.


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  		Table 4. Relation of Systemic Hemodynamics to Age in Women1

Among hypertensive men (Table 5), there was a slight downward trend with age in heart rate, with no change in mean arterial pressure and a small increase in stroke index. As a result, there were no associations between age and absolute or indexed cardiac output or peripheral resistance. Similar to findings in women, stiffness of the systemic arterial tree as measured by the ratios of pulse pressure to stroke volume or stroke index as well as the pressure-corrected stiffness index (ß) all increased strongly with age.


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  		Table 5. Relation of Systemic Hemodynamics to Age in Men1

Comparison to Normotensive Adults
Compared with findings in normal subjects concurrently studied in our laboratory,32 hypertensive patients had marginally higher mean endocardial fractional shortening (39% versus 38%, P=0.086), lower midwall shortening (mean, 17.8% versus 18.5%, P<0.001) and marginally lower stress-corrected midwall shortening (105% versus 107%, P=0.06), higher cardiac index (2.87±0.70 versus 2.68±0.57 L · min-2 · m-2, P<0.001), peripheral resistance index (3339±846 versus 2792±648 dyne · s-5 · cm-5 · m-5, P<0.0001), pulse pressure/stroke index (1.51 versus 1.16 mm Hg · mL-2 · m-2, P<0.001) and ß (6.1 versus 5.0, P=0.007).


*    Discussion
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 *Discussion
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The results of the present study indicate that LV pump performance at rest, as measured by cardiac output and its index, are similar in younger, middle-aged, and older unmedicated women and men with uncomplicated, relatively mild essential hypertension. This stability of cardiac pump function is paralleled by a lack of association between age and TPR or its index in either gender. However, this stability of major hemodynamic features of hypertension across a wide range of age appeared to be attained by different patterns of LV adaptation in women and men. Among women, the age-related increase in systolic blood pressure was offset by increasing LV wall thicknesses and mass, similar to the pattern observed previously with aortic stenosis,33 with no change in measures of LV endocardial or midwall shortening. In contrast, hypertensive men showed no association between age and LV geometric variables, whereas age was positively associated with LV endocardial and midwall shortening both as absolute values and after adjustment for end-systolic stress. Our finding of stable TPR index (TPRI) and cardiac index but progressive increase with age in measures of vascular stiffness identifies a dissociation between a progressive effect of age on conduit artery function and a lack of age-associated change in resistance vessels in hypertensive patients with similar levels of mean arterial pressure.

LV Pump Performance and Systemic Hemodynamics in Relation to Age
As seen in Table 6, this study suggests a "middle ground" between earlier studies that found either an increase34 35 36 37 38 39 40 or no change10 11 13 14 41 42 43 in LV function with age in hypertension and subsequent studies that favored the conclusion that cardiac output decreased in sustained hypertension after a brief initial period of increased LV function.15 44 45 Our results indicate that pump function is similar across a range of age groups in asymptomatic patients with relatively mild hypertension who are either unmedicated or can safely be taken off medication. However, our cross-sectional study evaluates patients with similar calculated mean arterial pressures in the 3 age groups 25 to 49, 50 to 60, and >=61 years and hence does not provide insight into hemodynamic changes that would occur if early-onset hypertension were left untreated and became progressively more severe by the time individuals reached the age of our older patients. Previous invasive studies also may have been affected by an "alerting response" to catheterization techniques that may be greater in the young, leading to higher cardiac output in this age group.


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  		Table 6. Changes in LV Function With Age in Previous Studies of Hypertensive Subjects

Despite the lack of change in mean pressure with age, systolic pressure showed the expected age-related increase. Separate analyses in women and men revealed gender differences in apparent mechanisms of adaptation to the rising systolic pressure. In women, concentric remodeling of LV geometry blunted but did not completely prevent an increase in myocardial afterload, assessed by circumferential end-systolic stress, in older subjects, whereas no change in LV chamber or myocardial function was observed. In contrast, the larger group of hypertensive men showed positive associations of age with several measures of LV systolic function but not with LV geometric variables. The explanation for these gender differences in LV adaptive changes is uncertain but could include selective withdrawal caused by prior morbid events of men at especially high risk because of abnormal LV geometry in addition to their gender and hypertension status.

Previous studies have shown a range of results including increased, decreased, or constant cardiac index and peripheral resistance in older hypertensive patients. Much of the discrepancy among these reports may be due to examination of subjects with different severities of hypertension. Data from available longitudinal studies10 13 14 37 46 suggest that, on average, progression from mild to moderate to severe hypertension is paralleled by evolution of the hemodynamic profile from increased cardiac index with normal peripheral resistance to normal cardiac index with increased resistance to decreased cardiac index with markedly increased resistance. Vascular stiffness has not been considered in these studies, yet a steady increase with age in both normal and hypertensive patients has been well described.29 47 Whether increased vascular stiffness occurs as an early hemodynamic change in hypertension or whether our patients represent a sample of subjects in transition between the above first and second stages of hemodynamics is unclear. In either situation, vascular stiffening appears to play a role independent of TPRI in the pathophysiology of mild essential hypertension. This is not surprising, considering that arterial stiffening may result from both arterial wall hypertrophy and atherosclerosis. It has also been shown that vascular stiffness is related to LV geometry in normotensive and hypertensive adults.48 49

Conclusions
Resting LV pump performance and peripheral resistance are not significantly related to age into the eighth decade in unmedicated adults with relatively mild, uncomplicated hypertension. This functional stability is sustained in hypertensive women by increased concentricity of LV geometry and in men by enhanced LV systolic function. Although cardiac index and TPR index (TPRI) remain stable across a range of age in relatively mild essential hypertension, vascular stiffness rises significantly.


*    Acknowledgments
 
This study was supported in part by grants HL-18323, HL-30605, and HL-47540 from the National Heart, Lung and Blood Institute, Bethesda, Md. We would like to thank Mariane C. Spitzer, RDMS, for technical expertise in performance of echocardiograms, Michael J. O’Grady for assistance with data analysis, Drs Stevo Julius and Per Lund-Johansen for critical reading of the manuscript, and Virginia Burns for assistance in preparation of the manuscript.

Received September 27, 2000; first decision October 11, 2000; accepted November 21, 2000.


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