Higher Relative Wall Thickness Research Articles

Antihypertensive treatment is associated with improved left ventricular geometry: the Rotterdam Study.

Left ventricular hypertrophy (LVH) increases the risk of cardiovascular disease. We evaluated the association between antihypertensive therapy and echocardiographically determined LVH. The Rotterdam Study is a population-based prospective cohort study among 7983 participants aged 55 years or over. Echocardiography was performed in 2823 participants. The study population consisted of 740 participants with grade 1 hypertension or antihypertensive monotherapy, without heart failure. Of these, 646 had an adequate echocardiogram for analysis of relative wall thickness (RWT) and 642 for left ventricular mass index. Participants were followed from 1 January 1991 until the date of echocardiography, between September 1992 and June 1993. Outcome measures were defined as being in the highest gender-specific quintile of left ventricular mass index and as having a RWT higher than 0.43. A Cox regression model with duration of use of antihypertensives defined as time-dependent covariates was used for data-analysis. Antihypertensive treatment lowered the risk of increased left ventricular mass index (RR 0.6, 95%CI 0.4-0.9). ACE-inhibitors, diuretics and beta-blockers all showed a risk reduction. Use of antihypertensives was also associated, although non-significantly, with a decrease of high RWT (RR 0.8, 95%CI 0.6-1.0). ACE-inhibitors, beta-blockers and calcium antagonists showed similar risk reductions, while diuretics seemed to increase the risk, possibly by reducing left ventricular end diastolic diameter. The use of antihypertensive drugs is associated with a decreased risk of echocardiographically determined LVH in a population-based setting.

Echocardiographic characteristics of professional football players

ObjectivesWe examined the echocardiographic characteristics of highly trained American football players. BackgroundIntense physical training is associated with morphologic and physiologic cardiac changes often referred to as the “athlete’s heart.” Echocardiographic features peculiar to elite football players have not been described. MethodsWe studied cardiac morphology and function as assessed by rest and stress echocardiography in 156 asymptomatic National Football League players. Resting and stress ejection fraction (EF), wall thickness, and diastolic left ventricular internal diameter (LVID) were measured. Left ventricular (LV) mass was calculated, as was relative wall thickness (RWT) defined as septal and posterior wall thickness divided by LVID. Control data were obtained from published studies. ResultsThe mean LVID (53 ± 0.5 mm) and maximal wall thickness (11.2 ± 0.2 mm) were increased over normal reported control subjects. There was a correlation between LVID and body weight (p = 0.01) and body surface area (BSA) (p = 0.01). The average LVID indexed to BSA was 23 ± 2 mm/M2. There was also a correlation between maximal wall thickness and body weight (p = 0.01) and BSA (p = 0.01). The average wall thickness indexed to BSA was 5.05 ± 0.88 mm/M2. Of the players, 23% had evidence of LV hypertrophy. Two players had an increased septal-to-posterior-wall-thickness ratio (≥1.3), although no player had an outflow gradient. The RWT for the players was 0.424 (± 0.1). The mean resting EF was 58% (± 4.4%), and every player undergoing exercise testing had an appropriate hyperdynamic response in cardiac function. ConclusionsBoth wall thickness and LVID of elite American football players are increased and correlate with body size. There is a high RWT, reflecting an emphasis on strength training. The LV EF was normal and not supranormal, as is sometimes believed. Regardless of the resting EF, all players had hyperdynamic cardiac responses with exercise.

Myocardial function and geometry in hypertensive subjects with low levels of afterload

Background It has been hypothesized that the level of end-systolic wall stress (σm) is a feedback signal that regulates the level of hypertrophy. Thus, low levels of σm may signify inappropriate hypertrophy. Methods To characterize left ventricular (LV) structure and systolic function in hypertensive subjects with low levels of σm, we studied 763 patients. LV function was studied by midwall stress-shortening analysis. Partition values for σm were derived from a separate group of normal subjects, and the study population was divided into low stress (group I, n = 136), high stress (group III, n = 157), and intermediate stress group II (n = 470). LV chamber and myocardial function were characterized by relating shortening at the endocardium and at the midwall, respectively, to stress. Results As expected, group III patients had the highest values for systolic blood pressure and LV cavity size but the lowest values for wall thickness and relative wall thickness. Surprisingly, however, there were no significant differences among stress groups with regard to age or body mass index. Contrary to the hypothesis that low levels of stress are indicative of excessive hypertrophy, there were no significant differences among the 3 groups with regard to LV mass or any form of LV mass index. Furthermore, despite lower mean values for afterload, group I patients had significantly lower values for midwall shortening, and this finding was indicative of reduced myocardial function; stress-shortening plots demonstrated that 28% of group I patients fell below 95% CI compared with 10% of group II and only 5% of group III patients. Conclusions Hypertensive subjects with low values for σm have more concentric LV geometry (higher relative wall thickness) and, on average, reduced myocardial function. (Am Heart J 2002;143:546-51.)

Appropriate or inappropriate left ventricular mass in the presence or absence of prognostically adverse left ventricular hypertrophy.

To evaluate whether assessment of appropriateness of left ventricular mass (LVM) adds to the traditional definition of left ventricular hypertrophy (LVH). Cross-sectional, relational. Echocardiographic LVH and appropriateness of LVM were studied in 562 subjects (231 normotensive controls, aged 35+/-11 years, 142 women; 331 hypertensive patients, aged 47+/-11 years, 135 women) classified on the basis of either the presence or the absence of both LVH (LVM index > or = 51 g/m2.7) and inappropriate LVM (LVM > 128% of the value predicted by an equation including age, sex and stroke work). Body mass index was comparable in hypertensive patients and controls. Hypertensive patients without LVH but with inappropriate LVM (n = 21) had higher relative wall thickness and total peripheral resistance than all other groups, whereas cardiac output was lower (all P < 0.001). Midwall mechanics was normal with appropriate LVM, independently of presence of LVH, whereas it was depressed in inappropriate LVM, either with or without LVH (both P < 0.0001). There was no substantial difference in ejection fraction among controls and hypertensive groups. Stress-corrected midwall shortening was more closely related to deviation of LVM from the value appropriate for stroke work, body size and gender (r = -0.56, P < 0.0001) than to LVM index (r = -0.26). Inappropriate LVM is associated with concentric geometry, high peripheral resistance and depressed wall mechanics. The deviation of LVM from the value appropriate for stroke work, body size and sex correlates with measures of myocardial function better than LVM.

Left Ventricular Structure and Diastolic Function in Subjects with Two Hypertensive Parents

Purpose : To examine the influence of (i) strong predisposition to essential hypertension and (ii) insulin sensitivity and plasma levels of cardiomyotrophic hormones on echocardiographic parameters of left ventricular structure and function. Methods : 26 normotensive subjects (age 18–35) with bi-parental hypertension and 26 matched controls with normotensive parents. Families with non-insulin-dependent diabetes or morbid obesity were excluded. (i) Echocardiography; (ii) plasma concentrations of renin, angiotensin-II, aldosterone, epinephrine and norepinephrine; (iii) euglycaemic, hyperinsulinemic clamp study. Results (means - SD): Hypertension-prone subjects vs controls had (i) higher resting systolic (117.0 - 14.0 vs 107.1 - 11.9 mmHg), and 24-h diastolic blood pressure (77.9 - 7.1 vs 72.9 - 7.2 mmHg), (ii) higher relative wall thickness (RWT) (0.39 - 0.09 vs 0.34 - 0.06). They had similar left vetricular mass index, diastolic function parameters, insulin sensitivity and plasma concentrations of cardiomyotrophic hormones. The increased RWT was not attributable to any other factor than the systolic blood pressure. Conclusion : In a carefully selected group of subjects with two hypertensive parents compared to a control group, the only echocardiographic change demonstrated was an increased RWT. This remodelling was attributable to a higher systolic blood pressure in the hypertension-prone subjects, but not to insulin sensitivity or a selection of cardiomyotrophic hormones.

Influence of age on left atrial appendage function in patients with nonvalvular atrial fibrillation.

Age is an independent risk factor for thromboembolism in nonvalvular atrial fibrillation (NVAF). An association between low left atrial appendage (LAA) Doppler velocities and thromboembolic risk in NVAF has been reported. The study was undertaken to identify age-related differences in LAA function that may explain the higher thromboembolic rates in older patients with NVAF. Forty-two consecutive patients (age 69+/-2 years [range 42-92], 24 [57%] men) with NVAF underwent transthoracic and transesophageal echocardiography. The following were compared in 22 patients younger and 20 older than 70 years: left ventricular (LV) diameter, mass and ejection fraction, left atrial (LA) diameter and volume, LAA area and volume, LAA peak emptying (PE) and peak filling (PF) velocities, presence and severity of spontaneous echo contrast (SEC) and mitral regurgitation (MR). Left atrial diameter (4.6+/-0.1 vs. 4.5+/-0.2 cm), LA volume (105+/-10 vs. 92+/-8 ml), LAA area (6.8+/-0.6 vs. 5.2+/-0.8 cm2), and LAA volume (5.6+/-0.9 vs. 3.9+/-1.0 ml) were similar (p>0.05) in both groups. Older patients had lower LAA PE (26+/-2 vs. 34+/-3 cm/s, p = 0.02) and PF (32+/-2 vs. 41+/-4 cm/s, p = 0.04) velocities, lower LV mass (175+/-13 vs. 234+/-21 gm, p = 0.02), higher relative wall thickness (0.52+/-0.02 vs. 0.43+/-0.03, p = 0.02), smaller LV diastolic diameter (4.3+/-0.1 vs. 5.2+/-0.2 cm, p < 0.001), and higher LV ejection fraction (62+/-2 vs. 55+/-2%, p = 0.025). Frequency and severity of SEC and MR were similar in both groups. Multivariate analysis identified older age as the only significant predictor of reduced LAA velocities. Compared with younger patients, older patients with NVAF have lower LAA velocities despite higher LV ejection fraction, smaller LV size, and similar LA and LAA volumes. These findings may explain the higher thromboembolic rates in older patients with NVAF.

Impact of arterial elastance as a measure of vascular load on left ventricular geometry in hypertension.

Effective arterial elastance (Ea), integrating the pulsatile component of left ventricular (LV) afterload, is an estimate of aortic input impedance. We evaluated relationships of Ea with left ventricular anatomy and function in essential hypertension. A cross-sectional analysis in 81 normotensive and 174 untreated hypertensive individuals enrolled in a referral hypertension centre. Using echocardiography we determined left ventricular mass index (LVMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FSe) and midwall (FSm) fractional shortening and total peripheral resistance (TPR). Carotid pressure waveforms were obtained by arterial tonometry, and end-systolic pressure (Pes) was measured at the dicrotic notch. Ea index (EaI) was calculated as Pes/(SV index); LV elastance (Ees) was estimated as Pes/LV end-systolic volume, and ventriculo-arterial coupling was evaluated by the Ea/Ees ratio. EaI was higher in hypertensives than in normotensives (3.02 +/- 0.63 versus 2.40 +/- 0.52 mmHg/l per m2; P< 0.0001). Using the 95% upper confidence limit in normotensives, hypertensives were divided in two groups with normal or elevated EaI. The 38 hypertensives with elevated EaI had higher RWT (0.41 +/- 0.06 versus 0.37 +/- 0.05), lower LVMI (87.5 +/- 18.5 versus 96.8 +/- 19.3 g/m2), higher TPR (2247 +/- 408 versus 1658 +/- 371 dynes/cm s(-5)) and lower FSe and FSm (35 +/- 5 versus 39 +/- 5 and 16 +/- 2 versus 18 +/- 2%; all P< 0.05) than patients with normal EaI. Ea/Ees ratio was increased and cardiac output was reduced in hypertensives with elevated EaI. High values of EaI identify a minority of hypertensive patients characterized by elevated TPR, left ventricular concentric remodelling, depressed left ventricular systolic function and impaired ventriculo-arterial coupling.

Left ventricular hypertrophy in hypertension: stimuli, patterns, and consequences.

Left ventricular (LV) size in childhood closely parallels body size, whereas in adulthood LV mass is increasingly affected by effects of obesity, hypertension, the level of cardiac volume load, and the level of LV myocardial contractility. Recently, additional independent associations of diabetes, arterial structure and function and as yet unknown genes with higher LV mass have been defined; angiotensin II and insulin have also been suggested to be additive stimuli to LV hypertrophy. Consideration of the level of LV mass and of the LV wall thickness/chamber radius ratio (relative wall thickness) has identified four different geometric patterns of LV adaptation to hypertension, including concentric LV hypertrophy (increased mass and wall thickness), eccentric hypertrophy (increased mass, normal relative wall thickness), concentric remodeling (increased relative wall thickness with normal mass) and normal LV geometry. Concentric hypertrophy is associated with especially high arterial pressure while eccentric hypertrophy is associated with obesity and elevated volume load. Numerous studies show that increased LV mass predicts cardiovascular events and death independently of all conventional risk factors; initial studies have also identified adverse implications of low LV midwall function and high relative wall thickness. Pioneer studies strongly suggest that reversal of LV hypertrophy is associated with an improved prognosis.

Effects of chronic adenosine uptake blockade on adrenergic responsiveness and left ventricular chamber function in pressure overload hypertrophy in the rat.

Increased sympathetic activity contributes to the progression of heart failure. Adenosine counteracts sympathetic activity by inhibition of presynaptic norepinephrine release and attenuation of the metabolic and contractile responses to beta-adrenergic stimulation. In this study, we tested the hypothesis that the adenosinergic effects (uptake blockade) of dipyridamole may retard the progression of pressure overload hypertrophy in the rat. To verify that the administration of dipyridamole increases myocardial adenosine levels in the rat, epicardial adenosine concentrations were measured from 12 isolated, perfused rat hearts exposed to 10(-7) and 10(-6) mol/l dipyridamole. Adenosine concentrations were increased with both doses of dipyridamole. Also, 9 weeks of dipyridamole treatment resulted in decreased sensitivity to the adenosine A1-receptor agonist, 2-chloro-N6-cyclopentyl adenosine, suggesting that dipyridamole increases adenosine levels in the intact rat. In the second part of the study, rats were divided into either abdominal aortic-banded or sham-operated groups and were treated with either dipyridamole or saline. After 9 weeks of treatment, two-dimensional Doppler echocardiographic studies were performed and the adrenergic responsiveness to 10(-8) mol/l isoproterenol was assessed in vitro. The saline-treated banded group demonstrated concentric left ventricular hypertrophy, abnormal diastolic filling, increased wet lung weights and attenuation of adrenergic responsiveness. In contrast, the dipyridamole-treated banded rats exhibited more concentric geometry (higher relative wall thickness with similar left ventricular mass), normal left ventricular filling characteristics and preserved adrenergic responsiveness. Systolic left ventricular chamber and myocardial function, as assessed by stress-endocardial and midwall shortening relationships, were not significantly altered by banding or dipyridamole treatment. Dipyridamole treatment prevented the development of abnormal left ventricular chamber filling, preserved adrenergic responsiveness and appeared to attenuate detrimental chamber remodeling in rats with pressure overload hypertrophy.

Gender differences in left ventricular function at rest and with exercise in asymptomatic aortic stenosis

In 29 women and 53 men with asymptomatic aortic stenosis, two-dimensional (2-D) and Doppler echocardiography were performed at rest and immediately after treadmill exercise testing to examine gender difference in left ventricular geometry, systolic and diastolic function, functional status, and exercise capacity. Aortic stenosis severity was similar between men and women. Women reported more functional impairment than men (88% ± 14% vs 95% ± 7%; p = 0.02). When indexed to body surface area, women had a smaller end-diastolic volume (39 ± 14 vs 50 ± 15 ml/m 2; p = 0.002), end-systolic volume (13 ± 6 ml/m 2 vs 18 ± 9 ml/m 2; p = 0.01) and left ventricular mass (73 ± 26 gm/m 2 vs 84 ± 21 gm/m 2; p = 0.05), but a higher relative wall thickness in systole (1.5 ± 0.4 cm vs 1.3 ± 0.4 cm; p = 0.05), and fractional shortening (43% ± 7% vs 39% ± 10%; p = 0.03). Women had higher early and late transmitral velocities than did men (early, 92 ± 24 cm/sec vs 79 ± 29 cm/sec; p = 0.05; late, 97 ± 30 cm/sec vs 68 ± 23 cm/sec; p < 0.0001), a higher time-velocity integral in early diastole (18.2 ± 4.8 cm vs 15.1 ± 4.3 cm; p = 0.006), a significantly shorter exercise duration (4.5 ± 4.1 minutes vs 8.0 ± 3.9 minutes; p < 0.0001), a greater degree of functional aerobic impairment (25% ± 48% vs 2% ± 33%; p = 0.02), and a smaller increase in cardiac output with exercise (5.4 ± 3.5 L/min vs 8.0 ± 4.3 L/min; p = 0.01), in spite of similar peak heart rate and blood pressure responses. In these asymptomatic subjects with aortic stenosis, women had smaller, relatively hypercontractile ventricles, a different diastolic filling profile, more exercise limitation, and poorer functional capacity. These findings demonstrate the importance of gender in the response of the left ventricle to chronic pressure overload.

Reduced left ventricular systolic pump performance and depressed myocardial contractile function in patients > 65 years of age with normal ejection fraction and a high relative wall thickness

We studied the relation between relative wall thickness, left ventricular systolic pump performance, and myocardial contractile function in 77 older patients with normal ejection fraction who were free of valvular and myocardial ischemic disease. Group 1 comprised 49 patients with relative wall thickness ≥0.45; group 2 (n = 28) had normal relative wall thickness. Pump performance was characterized by stroke volume index, cardiac index, and stroke work; myocardial function was characterized by midwall shortening and circumferential stress versus shortening relations. Group 1 patients had lower end-diastolic volume (83 ± 3 vs 124 ± 5 ml, p < 0.05), cardiac index (2.6 ± 0.2 vs 3.5 ± 0.1 L/min/m 2, p < 0.05), and stroke work/100 g left ventricular mass (43 ± 2 vs 53 ± 3 g-m/100 g, p < 0.005). Although there was no significant difference with regard to ejection fraction or fractional shortening at the endocardium, fractional shortening at the midwall was significantly lower in group 1 than in group 2 (16 ± 1% vs 19 ± 1%, p < 0.005). This lower value for midwall shortening was observed despite lower values for end-systolic stress, implying decreased myocardial contractile function. Lower stroke volume index in group 1 patients, likely due to small chamber size, was not offset by increased heart rate, resulting in a low-normal cardiac index; in 33% of group 1 patients, cardiac index was < 2.2 L/min/m 2, indicating reduced pump performance. Our data indicate an abnormality in pump performance and myocardial function in patients who have high relative wall thickness and normal ejection fraction.

Geometric changes allow normal ejection fraction despite depressed myocardial shortening in hypertensive left ventricular hypertrophy

This study of hypertensive left ventricular hypertrophy 1) assessed myocardial shortening in both the circumferential and long-axis planes, and 2) investigated the relation between geometry and systolic function. In hypertensive left ventricular hypertrophy, whole-heart studies have suggested normal systolic function on the basis of ejection fraction-systolic stress relations. By contrast, isolated muscle data show that contractility is depressed. It occurred to use that this discrepancy could be related to geometric factors (relative wall thickness). We studied 43 patients with hypertensive left ventricular hypertrophy and normal ejection fraction (mean +/- SD 69 +/- 13%) and 50 clinically normal subjects. By echocardiography, percent myocardial shortening was measured in two orthogonal planes; circumferential shortening was measured at the endocardium and at the midwall, and long-axis shortening was derived from mitral annular motion (apical four-chamber view). Circumferential shortening was related to end-systolic circumferential stress and long-axis shortening to meridional stress. Endocardial circumferential shortening was higher than normal (42 +/- 10% vs. 37 +/- 5%, p < 0.01) and midwall circumferential shortening lower than normal in the left ventricular hypertrophy group (18 +/- 3% vs. 21 +/- 3%, p < 0.01). Differences between endocardial and midwall circumferential shortening are directly related to differences in relative wall thickness. Long-axis shortening was also depressed in the left ventricular hypertrophy group (18 +/- 6% in the left ventricular hypertrophy group, 21 +/- 5% in control subjects, p < 0.05). Midwall circumferential shortening and end-systolic circumferential stress relations in the normal group showed the expected inverse relation; those for approximately 33% of the left ventricular hypertrophy group were > 2 SD of normal relations, indicating depressed myocardial function. There was no significant relation between long-axis shortening and meridional stress, indicating that factors other than afterload influence shortening in this plane. High relative wall thickness allows preserved ejection fraction and normal circumferential shortening at the endocardium despite depressed myocardial shortening in two orthogonal planes.

Gender differences in left ventricle geometry and function in patients undergoing balloon dilatation of the aortic valve for isolated aortic stenosis. NHLBI Balloon Valvuloplasty Registry.

Gender differences in cardiac size have been described in normal humans and animals and in response to pressure overload. To examine the influence of gender on the left ventricular response to pressure overload, clinical, haemodynamic, and echocardiographic data were analysed in the 232 adults with isolated aortic stenosis enrolled in the Balloon Valvuloplasty Registry. There were 92 men (mean (SD) age 75 (11) years) and 140 women (79 (9) years; P = 0.002). Women had similar symptoms (New York Heart Association class) but lower overall functional status than men (P = 0.008). Catheterisation data showed similar valve area indices (mean (SD) (0.30 (0.09) in men and 0.31 (0.13) cm/m2 in women) but higher peak and mean gradients in women (peak 74 (30) v 63 (22) mm Hg; mean 61 (21) v 54 (18) mm Hg; both P < or = 0.01). On M mode echocardiography women had greater septal and posterior wall thickness but similar cavity diameter, after normalising dimensions to body surface area, resulting in higher relative wall thickness (0.60 (0.20) v 0.50 (0.15); P = 0.0002). Left ventricular mass index was similar in women and men (166 (59) v 159 (50) gm/m2 respectively), however, the prevalence of left ventricular hypertrophy according to sex specific criteria was 54% in men and 81% in women (P = 0.0001). Multiple logistic regression models that adjusted for age, functional status, fractional shortening, and left ventricular systolic pressure found the presence or absence of hypertrophy to be independently associated with gender (P < or = 0.002). Left ventricular systolic function tended to be better in women, who had a higher cardiac index (2.5 (0.8) v 2.3 (0.6) 1/min/m2; P = 0.01), left ventricular peak systolic pressure (211 (36) v 192 (35) mm Hg; P = 0.0001), and echo fractional shortening (32 (13) v 28 (12)%; P = 0.05); however, these differences were reduced when patients with regional wall motion abnormalities were excluded. In this population of elderly patients undergoing balloon dilatation of isolated aortic stenosis, left ventricular chamber geometry was different in men and women. Because this was a selected population, gender should be further evaluated as a possible determinant of the cardiac adaptation to chronic pressure overload.

Impact of chamber geometry and gender on left ventricular systolic function in patients >60 years of age with aortic stenosis

In aortic stenosis, gender and other differences in the adaptive remodeling of the left ventricle have been described, but the influence of left ventricular (LV) geometry on systolic function is not widely appreciated. This study tested the hypothesis that the increased ejection fraction seen in some elderly women with aortic stenosis is due to changes in LV geometry, not increased myocardial mass or enhanced myocardial function. We therefore investigated gender-related differences in LV and myocardial function by analysis of end-systolic circumferential stress versus shortening relations in 65 patients (29 men and 36 women) with aortic stenosis who underwent cardiac catheterization and echocardiography. Despite similar degrees of aortic stenosis, there were significant differences between men and women with regard to LV geometry and function. When compared with men, women had higher peak LV pressures (205 ± 27 vs 188 ± 27 mm Hg, p < 0.01), higher ejection fractions (66 ±14% vs 57 ± 18%, p < 0.05), smaller LV end-diastolic dimensions (43 ± 8 vs 51 ± 6 mm, p < 0.01) and higher relative wall thickness (0.66 ± 0.27 vs 0.50 ± 0.10, p < 0.01). LV mass was similar in the 2 groups. Mean values for stress were lower in women and there was a predominance of women at extremely low levels of stress; this subgroup had very high values for relative wall thickness and endocardial shortening, but overall stress-shortening relations were normal. In contrast to chamber function (i.e., endocardial shortening), myocardial function was depressed compared with age-matched control subjects; the midwall shortening analysis, however, showed no difference in circumferential shortening between men and women. Differences between endocardial and midwall shortening were directly related to differences in relative wall thickness. Thus, exaggerated endocardial fractional shortening and high ejection fraction in elderly women with aortic stenosis is due to alterations in LV geometry, not increased LV mass or enhanced myocardial function.

Relation of concentric left ventricular hypertrophy and extracardiac target organ damage to supranormal left ventricular performance in established essential hypertension

Increased cardiac performance has been documented in patients with early systemic hypertension, but its prevalence and determinants in patients with uncomplicated sustained essential hypertension have not been characterized. Radionuclide cineangiography in 116 patients with uncomplicated essential hypertension showed that 12 of 116 (10%) had supranormal resting left ventricular (LV) ejection fraction (>70%, above the highest value in normal subjects), while 104 patients had a normal resting ejection fraction (45 to 70%). Patients with a high resting ejection fraction had higher systolic and diastolic blood pressure compared with patients with normal resting ejection fraction (182 mm Hg vs 169, p < 0.01, and 110 vs 103, p < 0.05, respectively), markedly greater echocardiographic LV mass (136 vs 94 g/m2, p < 0.01), smaller ventricular dimensions in systole (2.5 vs 3.1, p < 0.01) and diastole (4.4 vs 4.9, p < 0.05), and higher relative wall thickness (0.61 ± 0.20 vs 0.39 ± 0.98, p < 0.001). Patients with supranormal resting ventricular performance had lower end-systolic wall stress than normal volunteers or patients with normal resting LV function (48 vs 64 vs 74 × 103 dynes/cm2, respectively). Patients with an elevated LV ejection fraction also had significantly more abnormal funduscopic examinations and greater proteinuria. Thus, a subset of essential hypertensive patients with moderately to severely elevated blood pressure developed marked concentric LV hypertrophy associated with subnormal end-systolic stress and supranormal LV performance. These patients manifested greater peripheral target organ damage than patients with lower ejection fraction but lesser hypertrophy, suggesting that the severity of their hypertensive cardiovascular disease is more accurately reflected by indexes of cardiac hypertrophy than of LV performance.