Different impact of the metabolic syndrome on left ventricular structure and function in hypertensive men and women

Metabolic syndrome (MS) is increasingly recognized as an important cardiovascular risk factor in hypertension, but its influence on left ventricular (LV) mass and function in the 2 genders has not been specifically addressed. Among 618 nondiabetic, untreated hypertensive subjects, echocardiographically detected LV mass was significantly greater in subjects with MS. A significant interaction was observed between sex and the MS (P<0.003 for the multiplicative interaction term). Compared with women without the MS, those with the syndrome had a 24% greater LV mass (49.5+/-12 versus 40.0+/-10 g x m(-2.7); P<0.001), whereas the difference was only 9% in men (50.3+/-12 versus 46.1+/-10 g x m(-2.7); P=0.003). A greater prevalence of LV hypertrophy was found in women (37% versus 14%; P<0.001) but not in men (39% versus 29%; P=0.09) with the MS. After adjustment for the effect of age, body mass index, 24-hour systolic blood pressure, and several confounders, the MS was independently associated with a greater LV mass index in women (regression coefficient, 4.80; P<0.001) but not in men. Women with the MS also had a greater LV relative wall thickness (0.42+/-0.07 versus 0.39+/-0.07; P=0.004) and a depressed afterload-corrected midwall fractional shortening (94.0+/-12% versus 101.0+/-13%; P<0.001) than women without the syndrome, whereas no differences emerged in men. We conclude that, in untreated hypertension, MS has a different impact on LV hypertrophy and function in men and women. The effect of MS is more pronounced in women and is partly independent from the effect of several hemodynamic and nonhemodynamic determinants of LV mass.     

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Electrocardiographic (ECG) left bundle branch block (LBBB) is associated with left ventricular hypertrophy (LVH), but its relation to left ventricular (LV) geometry and function in hypertensive patients with ECG LVH is unknown. Echocardiograms were performed in 933 patients (548 women, mean age 66+/-7 years) with essential hypertension and LVH by baseline ECG in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. LBBB, defined by Minnesota code 7.1, was present in 47 patients and absent in 886 patients. Patients with and without LBBB were similar in age, gender, body mass index, blood pressure, prevalence of diabetes, and history of myocardial infarction. Despite similarly elevated mean LV mass (126+/-25 vs 124+/-26 g/m(2)) and relative wall thickness (0.41+/-0.07 vs 0.41+/-0.07, P=NS), patients with LBBB had lower LV fractional shortening (30+/-6 vs 34+/-6%), ejection fraction (56+/-10 vs 61+/-8%), midwall shortening (14+/-2 vs 16+/-2%), stress-corrected midwall shortening (90+/-13 vs 97+/-13%) (all P<0.001), and lower LV stroke index (38+/-7 vs 42+/-9 ml/m(2)) (P<0.05). Patients with LBBB also had reduced LV inferior wall and lower mitral E/A ratio (0.75+/-0.18 vs 0.87+/-0.38) (all P<0.05). The above univariate results were confirmed by multivariate analyses adjusted for gender, age, blood pressures, height, weight, body mass index, heart rate, and LV mass index. Among hypertensive patients at high risk because of ECG LVH, the presence of LBBB identifies individuals with worse global and regional LV systolic function and impaired LV relaxation without more severe LVH by echocardiography.     

Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives

OBJECTIVE: To evaluate the influence of obesity, per se or associated with hypertension, on left ventricular (LV) diastolic function. PATIENTS: Thirty-two obese newly-diagnosed never-treated hypertensives; 32 obese normotensives matched for age, sex and BMI with hypertensives; 32 lean newly diagnosed never-treated hypertensives and 32 lean normotensives, matched for age, sex and 24 h blood pressure (BP) with the obese subjects. METHODS: Twenty-four-hour ambulatory blood pressure monitoring and digitized M-mode LV echocardiograms. PARAMETERS EVALUATED: Twenty-four-hour, day-time and night-time BP and heart rate, percentage nocturnal BP fall; LV end-diastolic diameter index, septal and posterior wall thickness, LV mass index, peak shortening and lengthening rate of LV diameter, peak thinning rate of LV posterior wall. RESULTS: A main effect was found for obesity on LV diameter and LV mass and for hypertension on LV mass; LV systolic function was normal in all the subjects and similar among the four groups; LV diastolic function was significantly reduced in both obese groups with respect to lean ones. This difference persisted after correction of diastolic parameters for 24 h BP and heart rate, LV diameter and LV mass index and disappeared only after correction for body mass index. This latter was inversely related with diastolic parameters only in the obese groups. CONCLUSIONS: Obesity is associated with a preclinical impairment of LV diastolic function in both normotensives and hypertensives; the diastolic impairment is independent of haemodynamic factors, such as 24 h BP and heart rate, and bears no relation to LV geometry in normotensives and only little relation in hypertensives, having therefore to be ascribed to obesity itself.     

Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy

Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels.     

Effect of regression of left ventricular hypertrophy from systemic hypertension on systolic function assessed by midwall shortening (HOT echocardiographic study)

Depressed midwall shortening has been shown to be an independent predictor of cardiovascular morbid events in hypertensive patients with left ventricular (LV) hypertrophy despite normal endocardial fractional shortening. The effects of LV mass changes in hypertensive patients on midwall shortening are unclear. To determine the impact of LV hypertrophy regression on LV systolic function assessed at the endocardium and the midwall level, 508 patients (58% men, 57% Caucasians, mean age 60 +/- 7 years) participating in the Hypertension Optimal Treatment study were prospectively studied by serial echocardiography at baseline, year 1, year 2, and at the end of the study. The Hypertension Optimal Treatment study was designed to challenge the existence of the J-curve phenomenon in hypertension. This study enrolled men and women between 50 and 80 years of age with mild to moderate hypertension. Patients were treated with a regimen based on felodipine with the addition of other antihypertensive drug classes as needed to reduce the diastolic blood pressure to a predefined target of < or =80, < or =85, or < or =90 mm Hg. From baseline to year 1, year 2, and end of the study, body mass index was unchanged (30.4, 30.1, 30.2, and 30.5 kg/m(2)); however, diastolic blood pressure was significantly reduced (99, 83, 80, and 80 mm Hg, p <0.0001), as was systolic blood pressure (161, 139, 137, and 134 mm Hg, p <0.0001) and LV mass index (117, 119, 107, and 106 g/m(2), p <0.0001). Over the same period of observation the endocardial fractional shortening did not change significantly (40%, 42%, 43%, and 44%); however, shortening at the midwall level showed improvement (20%, 21%, 22%, and 30%, p <0.001). In conclusion, midwall shortening is a more sensitive index of systolic function in subjects with pressure-overload hypertrophy, and it identifies high-risk patients who may benefit from a more aggressive antihypertensive program. The disparity between midwall and endocardial shortening suggests reduced myofibril function in patients with hypertension-induced hypertrophy.     

Factors influencing left ventricular structure and stress-corrected systolic function in men and women with asymptomatic aortic valve stenosis (a SEAS Substudy)

To identify determinants of left ventricular (LV) structure and stress-corrected systolic function in men and women with asymptomatic aortic stenosis (AS), Doppler echocardiography was performed at baseline in 1,046 men and 674 women 28 to 86 years of age (mean 67 +/- 10) recruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS. LV hypertrophy was less prevalent in women despite older age, higher systolic blood pressure, and smaller aortic valve area/body surface area (all p values <0.05). In logistic regression analyses, LV hypertrophy was independently associated with male gender, severity of AS, hypertension, higher systolic blood pressure, and lower stress-corrected midwall shortening (scMWS) or stress-corrected fractional shortening (scFS; all p values <0.01). In men aortic regurgitation also was a predictor of LV hypertrophy (p <0.05). Women had greater scFS and scMWS when corrected for LV size or geometry (all p values <0.001). In multivariate analyses, female gender predicted 11% greater scFS and 4% greater scMWS independent of age, body mass index, heart rate, aortic valve area, LV mass, relative wall thickness, aortic regurgitation, hypertension, and end-systolic stress (R(2) = 0.23 and 0.59, respectively, p <0.001). In conclusion, the major determinants of LV hypertrophy in patients with asymptomatic AS are male gender, severity of AS, and concomitant hypertension. Women have higher stress-corrected indexes of systolic function independent of LV geometry or size, wall stress, older age, or more concomitant hypertension.     

Longitudinal mitral annulus velocities are reduced in hypertensive subjects with or without left ventricle hypertrophy

Normotensive and hypertensive subjects with and without left ventricular (LV) hypertrophy (LV mass index [LVMI] >51 g/m(2.7)) were examined by conventional echocardiography and tissue Doppler imaging of mitral annulus motion. The subgroups included nonobese normotensive subjects (n=16; age 51+/-9 years; 11 female; systolic blood pressure [SBP] 109+/-11 mm Hg, body mass index [BMI] 24+/-2.7 kg/m2; LVMI 32+/-5.5 g/m(2.7)), nonobese hypertensive subjects without LV hypertrophy (n=16; age 54+/-12 years; 12 female; SBP 166+/-15 mm Hg; BMI 25+/-2.7 kg/m2; LVMI 42+/-5.5 g/m(2.7)), and hypertensive subjects with LV hypertrophy (n=22; age 56+/-10 years; 10 female; SBP 181+/-19 mm Hg; BMI 26+/-2.3 kg/m2; LVMI 69+/-16 g/m(2.7)). Ejection fraction was comparable among the subgroups, but midwall fractional shortening was reduced in hypertensive subjects with LV hypertrophy (approximately 26%). Isovolumic relaxation time was increased in subjects with LV hypertrophy, whereas mitral wave A velocity was increased in hypertensive subjects with and without LV hypertrophy. Tissue Doppler imaging mitral annulus systolic (SM) and diastolic (EM) velocities were reduced in subjects with and without LV hypertrophy compared with normotensive subjects. There was a positive correlation between SM and EM (r=0.68; P<0.0001) and negative correlations between these 2 variables and LVMI (SM, r=-0.41; P=0.002; EM, r=-0.56; P<0.0001). Thus, reductions in mitral annulus systolic and diastolic velocities parallel increases in LV mass in hypertensive subjects, beginning at LV mass within the clinically defined normal values.     

Gender differences in systolic left ventricular function in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study)

Echocardiography was performed in 944 untreated hypertensive patients (391 women and 553 men, mean age 66 years) who had electrocardiographic left ventricular (LV) hypertrophy at baseline in the Losartan Intervention For End point reduction in hypertension (LIFE) study to evaluate gender-associated differences in systolic LV function. Women had significantly lower diastolic blood pressure (175/97 vs 173/99 mm Hg) and body surface area and a higher body mass index (all p < 0.01). Women also had higher LV ejection fraction (EF), endocardial and midwall fractional shortening (63% vs 60%, 35% and 33%, and 16% vs 15%, respectively, all p < 0.01), higher stress-corrected midwall fractional shortening (98% vs 96%, p < 0.05), and lower circumferential end-systolic wall stress (178 vs 187 kdynes/cm(2), p < 0.01). There was no difference in age or LV mass indexed for height(2.7), but relative wall thickness was higher in women (0.42 vs 0.41, p < 0.05). In multiple regression analyses: (1) EF and endocardial fractional shortening were 2% to 3% higher in women than men, independent of the effects of LV stress, body mass index, and height (multiple r = 0.77 and 0.75, respectively, gender p < 0.02 in both models); (2) midwall fractional shortening was 0.5% higher in women, independent of the effects of age, body mass index, circumferential end-systolic stress, and absence of diabetes (multiple r = 0.36, p = 0.014 for gender); and (3) stress-corrected LV midwall fractional shortening was 2% higher (p = 0.004) in women, independent of the effects of age, height, heart rate, body mass index, and diabetes (multiple r = 0.33). Thus, female gender is an independent predictor of higher systolic LV function in hypertensive patients with electrocardiographic LV hypertrophy.     

Effect of weight loss on cardiac chamber size, wall thickness and left ventricular function in morbid obesity

To determine cardiac chamber size, wall thickness and left ventricular (LV) systolic function in morbidly obese patients, M-mode and cross-sectional echocardiography was performed in 62 patients whose body weight was greater than or equal to twice their ideal weight but who were free from underlying organic heart disease and systemic hypertension. The initial clinical protocol consisted of a medical history, physical examination, electrocardiogram at rest, chest x-ray and echocardiogram. Thereafter, each patient underwent gastric restriction. Thirty-four patients returned for follow-up echocardiography 4.3 +/- 0.3 months after substantial weight loss was achieved. For the whole group (n = 62) and LV internal dimension in diastole was enlarged in 24 (39%), the right ventricular internal dimension was enlarged in 20 (32%), the left atrial dimension was enlarged in 25 (40%) and the ventricular septal and LV posterior wall thickness was increased in 35 (56%). In the 34 patients who returned for follow-up, mean body weight decreased significantly, from 135 +/- 8 to 79 +/- 6 kg (73 +/- 4% of the amount over ideal body weight). In the subgroup with low preoperative LV fractional shortening (n = 13), mean LV fractional shortening increased from 22 +/- 2% to 31 +/- 2% (p less than 0.01). This was accompanied by a significant decrease in the mean LV internal dimension in diastole and mean blood pressure. The results indicate that cardiac chamber enlargement, LV hypertrophy and LV systolic dysfunction occur frequently in morbidly obese patients and that LV systolic dysfunction in such persons may improve following substantial weight loss.     

Ambulatory blood pressure and metabolic abnormalities in hypertensive subjects with inappropriately high left ventricular mass

Appropriateness of left ventricular (LV) mass to cardiac workload can be evaluated by the ratio of observed LV mass to the value predicted for an individual's gender, height(2.7), and stroke work at rest (%PLVM). It is unclear which pathophysiological factors are associated with inappropriately high LV mass in hypertensive subjects. Adequate LV mass was defined by the 90% confidence interval (73% to 128%) of the distribution of %PLVM in 393 normal-weight normotensive subjects. In 185 hypertensive subjects (aged 56+/-11 years; 60% male, 29% black), according to %PLVM, 164 (88%) had adequate LV mass, 16 (9%) had inappropriately high LV mass (%PLVM >128%), and 5 (3%) had %PLVM <73% (low LV mass). Age, gender, smoking habit, proportion of never-treated subjects, total cholesterol, triglycerides, and creatinine levels did not differ significantly between subjects with adequate and inappropriately high LV mass. Body mass index, fasting glucose, and proportion of black subjects were higher (all P<0.05), while HDL cholesterol was lower (P<0.05) in subjects with inappropriately high LV mass. Blood pressure at the echocardiogram was comparable between subjects with adequate and inappropriately high LV mass, but the latter group had higher ambulatory blood pressure (P<0.01). Subjects with inappropriately high LV mass also had higher aortic root dimension and LV relative wall thickness and relatively lower LV systolic performance than those with adequate LV mass (all P<0.001). Larger aortic root diameter and lower systolic function were also found in hypertensive subjects with inappropriate LV hypertrophy compared with those with adequate LV hypertrophy. In an exploratory case-control study that compared subjects with low %PLVM with age-matched counterparts with adequate LV mass, low %PLVM was associated with lower body mass index, more favorable metabolic profile, and higher LV myocardial contractility. Higher body mass index, larger aortic root, and black race were independent correlates of increased %PLVM. Thus, in arterial hypertension, levels of LV mass inappropriately high for gender, cardiac workload, and height(2.7) are associated with higher body mass index, higher ambulatory blood pressure, larger aortic root diameters, and relatively low myocardial contractility.     

Obstructive sleep apnea-dependent and -independent adrenergic activation in obesity

No agreement exists as to the mechanisms responsible for the sympathetic hyperactivity characterizing human obesity, which has been ascribed recently to a chemoreflex stimulation brought about by obstructive sleep apnea rather than to an increase in body weight, per se. In 86 middle-age normotensive subjects classified according to body mass index, waist-to-hip ratio, and apnea/hypopnea index (overnight polysomnographic evaluation) as lean and obese subjects without or with obstructive sleep apnea, we assessed via microneurography muscle sympathetic nerve traffic. The 4 groups were matched for age, gender, and blood pressure values, the 2 obese groups with and without obstructive sleep apnea showing a similar increase in body mass index (32.4 versus 32.0 kg/m2, respectively) and waist-to-hip ratio (0.96 versus 0.95, respectively) compared with the 2 lean groups with or without obstructive sleep apnea (body mass index 24.3 versus 23.8 kg/m2 and waist-to-hip ratio 0.77 versus 0.76, respectively; P<0.01). Compared with the nonobstructive sleep apnea lean group, muscle sympathetic nerve activity showed a similar increase in the obstructive sleep apnea lean group and in the nonobstructive sleep apnea obese group (60.4+/-2.3 and 59.3+/-2.0 versus 40.9+/-1.8 bs/100 hb, respectively; P<0.01), a further increase being detected in obstructive sleep apnea subjects (73.1+/-2.5 bursts/100 heart beats; P<0.01). Our data demonstrate that the sympathetic activation of obesity occurs independently in obstructive sleep apnea. They also show that this condition exerts sympathostimulating effects independent of body weight, and that the obstructive sleep apnea-dependent and -independent sympathostimulation contribute to the overall adrenergic activation of the obese state.     

Relation of left ventricular geometry and function to systemic hemodynamics in hypertension: the LIFE Study. Losartan Intervention For Endpoint Reduction in Hypertension Study

OBJECTIVES: To clarify the relations of systemic hemodynamics to left ventricular (LV) geometric patterns in patients with moderate hypertension and target organ damage. BACKGROUND: LV geometry stratifies risk in hypertension, but relations of LV geometry to systemic hemodynamic patterns in moderately severe hypertension have not been fully elucidated. DESIGN: Cross-sectional case-control study. SETTING: Baseline findings in the echocardiographic substudy of the Losartan Intervention For Endpoint Reduction in Hypertension Study (LIFE) and in a normotensive reference group. PATIENTS/PARTICIPANTS: Nine hundred and sixty-four patients with Stage I-II hypertension and LV hypertrophy by Cornell voltage duration criteria ((SV3 + RaVL [+ 6 mm in women]) x QRS > 2440 mm x ms) or modified Sokolow- Lyon voltage criteria (SV1 + RV5/RV6 > 38 mm), and 366 apparently normal adults. INTERVENTIONS: None. METHODS: Two-dimensional and Doppler echocardiograms were used to classify hypertensive patients into groups with normal geometry, concentric remodelling and concentric and eccentric hypertrophy, and to measure stroke volume (SV), cardiac output, peripheral resistance and pulse pressure/SV as a measure of arterial stiffness. Comparisons were adjusted for covariates by general linear model with the Sidak post-hoc test RESULTS: Mean SV was higher in patients with eccentric hypertrophy (83 ml/beat) and lower with concentric remodeling (68 ml/beat) than in normal adults (73 ml/ beat). Cardiac output was highest in patients with eccentric LV hypertrophy and lower with concentric remodeling than eccentric hypertrophy; mean pressure and peripheral resistance were equally high in all hypertensive subgroups, whereas pulse pressure/SV was most elevated (by a mean of 47% versus reference subjects) with concentric remodeling and least so (mean + 15%) with eccentric hypertrophy. In multivariate analysis (Multiple R + 0.68), LV mass was independently related to higher systolic pressure, older age, SV, male gender and body mass index (all P< 0.001). Relative wall thickness was independently related (Multiple R + 0.50) to older age, higher systolic pressure, lower SV (all P< 0.001) and higher body mass index (P + 0.007). SV and cardiac output were lower in patients with low stress-corrected midwall shortening. CONCLUSION: In patients with moderate hypertension and ECG LV hypertrophy, the levels of SV and pulse pressure/ SV, are associated with, and may be stimuli to different LV geometric phenotypes.     

Obstructive sleep apnea, hypertension, and their interaction on arterial stiffness and heart remodeling

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) and hypertension are independently associated with increased stiffness of large arteries that may contribute to left ventricular (LV) remodeling. We sought to investigate the impact of OSA, hypertension, and their association with arterial stiffness and heart structure. DESIGN: We studied 60 middle-aged subjects classified into four groups according to the absence or presence of severe OSA with and without hypertension. All participants were free of other comorbidities. The groups were matched for age, sex, and body mass index. MEASUREMENTS AND RESULTS: Full polysomnography, pulse-wave velocity (PWV), and transthoracic echocardiography were performed in all participants. Compared with normotensive subjects without OSA, PWV, left atrial diameter, interventricular septal thickness, LV posterior wall thickness, LV mass index, and percentage of LV hypertrophy had similar increases in normotensive OSA and patients with hypertension and no OSA (p < 0.05 for all comparisons), with a significant further increase in PWV, LV mass index, and percentage of LV hypertrophy in subjects with OSA and hypertension. Multivariate regression analysis showed that PWV was associated with systolic BP (p < 0.001) and apnea-hypopnea index (p = 0.002). The only independent variable associated with LV mass index was PWV (p < 0.0001). CONCLUSIONS: Severe OSA and hypertension are associated with arterial stiffness and heart structure abnormalities of similar magnitude, with additive effects when both conditions coexist. Increased large arterial stiffness contributes to ventricular afterload and may help to explain heart remodeling in both OSA and hypertension.     

Relative wall thickness is an independent predictor of left ventricular systolic and diastolic dysfunctions in essential hypertension.

The objective of this study was to elucidate the relationship between left ventricular geometry and left ventricular (LV) function in patients with untreated essential hypertension. We evaluated LV systolic and diastolic functions by M-mode echocardiography in 24 normotensive control subjects (NC) and 129 patients with essential hypertension. Patients were divided into four groups according to the relative wall thickness and LV mass index: a normal left ventricle (n=57), a concentric remodeling (n=7), a concentric hypertrophy (n=31), and an eccentric hypertrophy (n=34) group. LV systolic function as measured by midwall fractional shortening (FS) was significantly decreased in both the concentric remodeling and concentric hypertrophy groups; no differences were observed for endocardial FS. LV diastolic function as measured by isovolumic relaxation time (IRT) was also decreased in both the concentric remodeling and concentric hypertrophy groups. In multivariate analysis, relative wall thickness (p<0.0001), end-systolic wall stress (p<0.0001), and systolic blood pressure (p=0.002) were independently associated (r2=0.72) with midwall FS in a model including age, LV mass index, body mass index, diastolic blood pressure and IRT. In addition, relative wall thickness (p=0.0008) and age (p<0.0001) were independently associated (r2=0.31) with IRT in a model including LV mass index, end-systolic wall stress, body mass index, systolic and diastolic blood pressures and midwall FS. We conclude that LV geometry as evaluated by relative wall thickness may provide a further independent stratification of LV systolic and diastolic functions in essential hypertension.     

Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients: a losartan intervention for endpoint reduction in hypertension (LIFE) cardiovascular magnetic resonance and echocardiographic substudy

Concentric hypertensive left ventricular (LV) hypertrophy is presumed to be a symmetrical process. Using MRI-derived intramyocardial strain, we sought to determine whether segmental deformation was also symmetrical, as suggested by echocardiography. High echocardiographic LV relative wall thickness in hypertensive LV hypertrophy allows preserved endocardial excursion despite depressed LV midwall shortening (MWS). Depressed MWS is an adverse prognostic indicator, but whether this is related to global or regional myocardial depression is unknown. We prospectively compared MWS derived from linear echocardiographic dimensions with MR strain(in) in septal and posterior locations in 27 subjects with ECG LV hypertrophy in the Losartan Intervention for Endpoint Reduction in Hypertension Study. Although MRI-derived mass was higher in patients than in normal control subjects (124.0+/-38.6 versus 60.5+/-13.2g/m(2); P<0.001), fractional shortening (30+/-5% versus 33+/-3%) and end-systolic stress (175+/-22 versus 146+/-28 g/cm(2)) did not differ between groups. However, mean MR(in) was decreased in patients versus normal control subjects (13.9+/-6.8% versus 22.4+/-3.5%), as was echo MWS (13.4+/-2.8% versus 18.2+/-1.4%; both P<0.001). For patients versus normal control subjects, posterior wall(in) was not different (17.8+/-7.1% versus 21.6+/-4.0%), whereas septal(in) was markedly depressed (10.1+/-6.6% versus 23.2+/-3.4%; P<0.001). Although global MWS by echocardiography or MRI is depressed in hypertensive LV hypertrophy, MRI tissue tagging demonstrates substantial regional intramyocardial strain(in) heterogeneity, with most severely depressed strain patterns in the septum. Although posterior wall 2D principal strain was inversely related to radius of curvature, septal strain was not, suggesting that factors other than afterload are responsible for pronounced myocardial strain heterogeneity in concentric hypertrophy.     

Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects

OBJECTIVE: To investigate the prevalence of sleep breathing disorders, loud snoring and excessive daytime sleepiness in a group of obese subjects, and to identify the predictors of obstructive sleep apnea (OSA) severity in these patients. SUBJECTS: A total of 161 consecutive obese patients (body mass index (BMI)> or =30.0 kg/m(2)), ranging between 30.0 and 67.3, represented by 57 men and 104 women, aged 16-75 y. Forty (15 men and 25 women) age-matched (20-70 y) nonobese (BMI<27 kg/m(2)) volunteers were also recruited for the study. MEASUREMENTS: Respiratory function parameters, nocturnal sleep quality (evaluated by a specific questionnaire), nocturnal hypoventilation and OSA (evaluated by night polysomnography) were examined in all subjects. Anthropometric parameters (neck circumference, waist circumference, waist-to-hip ratio) were also investigated. RESULTS: Eighty-three obese patients (51.5% of the obese group) had a respiratory disturbance index (RDI)> or =10, corresponding to a moderate or severe sleep apnea. In particular, 24.8% (40/161), ie a quarter of all obese patients, were affected by severe OSA and this alteration was present in 42.1% of obese men (24/57) and in 15.4% (16/104) of obese women. When a stepwise multiple regression analysis was performed, neck circumference in men and BMI in women were shown to be the strongest predictors of sleep apnea. Twenty-nine percent of all obese subjects (40.3% of men and 23.1% of women) showed nocturnal hypoventilation; however, it was present as a unique breathing alteration in only 5% of the obese population. The percentage of patients having excessive daytime sleepiness was significantly higher than in nonobese subjects, even when only nonapneic obese patients were considered (P<0.001). CONCLUSION: This study shows that OSA is present in more than 50% of a population of obese patients with a mean BMI higher than 40.0, this percentage being much higher than that commonly reported in previous studies, particularly in women. Neck circumference in men and BMI in women seem to be the strongest predictors of the severity of OSA in obese patients. Nocturnal hypoventilation seems to be present in more than 29% of a severe obese population. Moreover, this study indicates that morbid obesity can be associated with excessive daytime sleepiness even in the absence of sleep apnea.     

Left ventricular hypertrophy in hypertension: functional aspects

The purpose of this study was to detect the anatomical and functional response of the left ventricle in essential, uncomplicated hypertension. Fifty outpatients, whose hypertension (DBP greater than 95 mmHg on three separate visits) had been documented from few weeks to a maximum of 5 years, showing neither electrocardiographic abnormalities nor other signs referable to target organ damage, underwent an M-mode, computerised echocardiographic study. Twenty-seven patients has never been treated, and 23 patients were withdrawn from previous treatments for at least one month. Echocardiographic data of the left ventricle were compared with those of 38 normals, matched by sex, age and body surface area. Hypertensives showed a significant increase in both LV mass index (p less than 0.001) and relative wall thickness (p less than 0.001), a pattern of concentric hypertrophy, which prevented an inappropriate rise in wall tension. Twenty-four patients, whose LV mass was above the mean normal value plus two standard deviations, were considered to have left ventricular hypertrophy. The remaining 26 patients were classified as non hypertrophic, for their mass resulted lower than the mean value of controls plus 2 SD: left ventricular mass was 152 +/- 32 g/m2 and 97 +/- 19 g/m2, respectively (p less than 0.001). Systolic performance was enhanced in both subgroups of hypertensives, since their values of fractional shortening and those of mean-Vcf were both above the line which represents the normal relationship with end-systolic stress. Diastolic relaxation, evaluated by means of time to peak filling rate, was impaired only in the hypertensive subjects with increased LV mass (p less than 0.001 vs. normotensive), being retained in the non-hypertrophic patients. In the whole hypertensive group, LV mass index poorly correlated with casual systolic blood pressure (r = 0.31; p less than 0.05), while time to peak filling rate showed a good correlation with LV mass index (r = 0.76; p less than 0.001). We conclude that: 1) in essential hypertension without electrocardiographic abnormalities or target organ damage, echocardiographic left ventricular hypertrophy is a rather frequent finding; 2) the pattern of concentric hypertrophy, by reducing the increase in wall tension due to pressure load, contributes to the retained, or enhanced, systolic performance seen in our series; 3) on the other hand, left ventricular filling seems to be impaired in relation to the degree of myocardial hypertrophy.     

Left ventricular mass and systolic dysfunction in essential hypertension

A relation between left ventricular (LV) hypertrophy and depressed midwall systolic function has been described in hypertensive subjects. However, a strong confounding factor in this relation is concentric geometry, which is both a powerful determinant of depressed midwall systolic function and a correlate of LV mass in hypertension. To evaluate the independent contribution of LV mass to depressed systolic function, 1827 patients with never-treated essential hypertension (age 48 +/- 12 years, men 58%) underwent M-mode echocardiography under two-dimensional guidance. Relative wall thickness was the strongest determinant of low midwall fractional shortening (r = -0.63, P < 0.0001). The significant inverse relation observed between LV mass and midwall fractional shortening (r = -0.43, P < 0.0001) persisted after taking into account the effect of relative wall thickness (partial r = -0.27, P < 0.0001). Within each sex-specific quintile of relative wall thickness, prevalence of subnormal afterload-corrected midwall systolic function was greater in subjects with, than in subjects without, LV hypertrophy (P < 0.05 for the first, third, fourth and fifth quintile). In a multiple linear regression analysis, both LV mass (P < 0.0001) and relative wall thickness (P < 0.0001) were independent predictors of a reduced midwall fractional shortening. In conclusion, the inverse association between LV mass and midwall systolic function is partly independent from the effect of relative wall thickness. LV hypertrophy is a determinant of subclinical LV dysfunction independently of the concomitant changes in chamber geometry.     

Left ventricular mass and function in young obese women.

OBJECTIVE: Obesity is associated with a high mortality rate due to cardiovascular disease. Left ventricular (LV) hypertrophy has been described in relation to obesity. The aim of this study was to evaluate echocardiographically the LV mass and function in young obese women as compared to lean women with similar characteristics. DESIGN: Prospective study. SUBJECTS: Eighty-two young women (< or =40 y), with obesity degree varying from I to III (BMI from 30 to 50 kg/m2) were compared to eighty young lean women. All of them were normotensive, none had cardiovascular complaints or any previous history of pulmonary disease, and none were taking any medication. The LV mass was calculated by the Devereux and Reichek formula. RESULTS: The LV mass was strongly increased in all obese groups (P<0.00003 to 0.000005) compared to lean subjects. LV mass adjusted indexes for height, BMI or volume were also increased compared to lean subjects and when adjusted for weight it was decreased. However when comparing LV mass/body surface area index this difference was not statistically significant. The linear regression analysis showed a strong association between the degree of obesity and LV mass, (r=0.52, P<0.001). Systolic and diastolic function in obese patients were similar to lean subjects, except for a lower E/A ratio in the obese group (P=0.005). CONCLUSION: In asymptomatic young obese women, there are some echocardiographic findings suggesting early cardiac involvement that seems to be related to the degree of obesity.     

Association of subclinical right ventricular dysfunction with obesity.

OBJECTIVES: The purpose of this research was to identify the determinants of right ventricular (RV) dysfunction in overweight and obese subjects. BACKGROUND: Right ventricular dysfunction in obese subjects is usually ascribed to comorbid diseases, especially obstructive sleep apnea. We used tissue Doppler imaging to identify the determinants of RV dysfunction in overweight and obese subjects. METHODS: Standard and tissue Doppler echocardiography was performed in 112 overweight (body mass index [BMI] 25 to 29.9 kg/m2) or obese (BMI >30 kg/m2) subjects and 36 referents (BMI <25 kg/m2), including 22 with obstructive sleep apnea but no obesity. Tissue Doppler was used to measure RV systolic (s(m)) and diastolic (e(m)) velocities and strain indexes. RESULTS: Obese subjects with BMI >35 kg/m2 had reduced RV function compared with referent subjects, evidenced by reduced s(m) (6.5 +/- 2.4 cm/s vs. 10.2 +/- 1.5 cm/s, p < 0.001), peak strain (-21 +/- 4% vs. -28 +/- 4%, p < 0.001), peak strain rate (-1.4 +/- 0.4 s(-1) vs. -2.0 +/- 0.5 s(-1), p < 0.001), and e(m) (-6.8 +/- 2.4 cm/s vs. -10.3 +/- 2.5 cm/s, p < 0.001), irrespective of the presence of sleep apnea. Similar but lesser degrees of reduced systolic function (p < 0.05) were present in overweight (BMI 25 to 29.9 kg/m2) and mildly obese (BMI 30 to 35 kg/m2) groups. Differences in RV e(m), s(m), and strain indexes were demonstrated between the severely versus overweight and mildly obese groups (p < 0.05). Body mass index remained independently related to RV changes after adjusting for age, log insulin, and mean arterial pressures. In obese patients, these changes were associated with reduced exercise capacity but not the duration of obesity and presence of sleep apnea or its severity. CONCLUSIONS: Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.