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    Influence of obesity on left ventricular midwall mechanics in arterial hypertension

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    The evaluation of the effect of obesity on left ventricular systolic performance may differ in relation to the method used to measure left ventricular function and to the type of study population. Whether obesity worsens left ventricular midwall mechanics in arterial hypertension has never been investigated. Accordingly, we assessed echocardiographic left ventricular midwall shortening-circumferential end-systolic stress relations in 156 normotensive and normal-weight (reference) adults, 94 normotensive and overweight (1985 National Institutes of Health partition values) to obese (body mass index > 30 kg/m(2)) adults, 263 hypertensive and normal-weight adults, and 224 hypertensive and overweight-to-obese adults. There was an inverse relation of midwall shortening to circumferential end-systolic stress in all groups (all P < .005). Left ventricular performance as a ratio of observed to predicted midwall shortening fell below the fifth percentile in 4 of 94 (4%) of overweight-to-obese normotensive individuals. Eighty-eight of 487 hypertensive subjects (18.1%) exhibited depressed midwall shortening as a percentage of the value predicted from wall stress, with no difference between normal-weight (50 of 263 [19%]) and overweight (38 of 224 [17%]) subjects. Sixty-one normotensive and 131 hypertensive subjects were frankly obese. After adjustment for sex and age, midwall shortening, as either absolute values or a percentage of predicted, was not statistically different among obese, overweight, and normal-weight subjects in both normotensive and hypertensive groups. For each quartile of observed-to-predicted midwall shortening ratio, obese subjects had greater left ventricular end-diastolic volume than normal-weight subjects among both normotensive and, more evidently, hypertensive subjects. A predicted midwall shortening was generated from both wall stress and left ventricular volume with the use of multiple regression analysis. High body mass index, mean blood pressure, aging, and male sex independently predicted low afterload and left ventricular volume-independent midwall left ventricular performance (multiple R = .31, P < .0001). Thus, (1) midwall left ventricular systolic performance in asymptomatic overweight or frankly obese individuals is comparable to that in normal-weight individuals in both the presence and absence of arterial hypertension; (2) however, maintenance of normal left ventricular performance in obese individuals is associated with the use of Starling reserve; and (3) this compensatory mechanism is especially evident when arterial hypertension and obesity coexist

    Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight.

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    This study was designed to determine the most appropriate method to normalize left ventricular mass for body size. BACKGROUND: Left ventricular mass has been normalized for body weight, surface area or height in experimental and clinical studies, but it is uncertain which of these approaches is most appropriate. METHODS: Three normotensive population samples--in New York City (127 adults), Naples, Italy (114 adults) and Cincinnati, Ohio (444 infants to young adults)--were studied by echocardiography. Relations of left ventricular mass to body size were similar in all normal weight groups, as assessed by linear and nonlinear regression analysis, and results were pooled (n = 611). RESULTS: Left ventricular mass was related to body weight to the first power (r = 0.88), to body surface area to the 1.5 power (r = 0.88) and to height to the 2.7 power (r = 0.84), consistent with expected allometric (growth) relations between variables with linear (height), second-power (body surface area) and volumetric (left ventricular mass and body weight) dimensions. Strong residual relations of left ventricular mass/body surface area to body surface area (r = 0.54) and of ventricular mass/height to height (r = 0.72) were markedly reduced by normalization of ventricular mass for height2.7 and body surface area1.5. The variability among subjects of ventricular mass was also reduced (p < 0.01 to p < 0.002) by normalization for body weight, body surface area, body surface area1.5 or height2.7 but not for height. In 20% of adults who were overweight, ventricular mass was 14% higher (p < 0.001) than ideal mass predicted from observed height and ideal weight; this increase was identified as 14% by left ventricular mass/height2.7 and 9% by ventricular mass/height, whereas indexation for body surface area, body surface area1.5 and body weight erroneously identified left ventricular mass as reduced in overweight adults. CONCLUSIONS: Normalizations of left ventricular mass for height or body surface area introduce artifactual relations of indexed ventricular mass to body size and errors in estimating the impact of overweight. These problems are avoided and variability among normal subjects is reduced by using left ventricular mass/height2.7. Simple nomograms of the normal relation between height and left ventricular mass allow detection of ventricular hypertrophy in children and adults

    Assessment of left ventricular function by the mid-wall fractional shortening-end-systolic stress relation: effects of gender, hypertension and left ventricular geometric pattern

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    Objectives. This study examined left ventricular performance in relatively unselected hypertensive patients by use of physiologically appropriate midwall shortening/end-systolic stress relations. Background. Supranormal left ventricular function has been reported in hypertensive patients, possibly due to an artifact of mismatching endocardial rather than midwall fractional shortening to mean left ventricular end-systolic stress. Methods. Samples of 474 hypertensive patients (150 women, 324 men) and 140 normal subjects (68 women, 72 men) were drawn from a large urban employed population. The inverse relations (p < 0.0001) of both echocardiographic endocardial and midwall fractional shortening to end-systolic stress in normal subjects were used to calculate the ratios of observed to predicted endocardial and midwall fractional shortening in hypertensive patients. Midwall shortening was calculated from an elliptic model, taking into account the epicardial migration of the midwall during systole. Results. Use of midwall fractional shortening in hypertensive patients reduced the proportion of patients with function above the 95th percentile of normal from 22% to 4% (p < 0.0001) and fractional shortening as a percent of predicted from 107% (p < 0.001 vs. 100% in normotensive control subjects) to 95% (p < 0.0001; p < 0.001 vs. 101% in normotensive control subjects). Midwall shortening was below the 5th percentile of normal in 16% of hypertensive patients instead of 2% with endocardial shortening (p < 0.0001): They tended to be older than other hypertensive patients and had concentric left ventricular hypertrophy. Among hypertensive patients, those with concentric left ventricular hypertrophy or remodeling had reduced midwall shortening as a percent of predicted from end-systolic stress (p < 0.0001). Conclusions. Use of the physiologically more appropriate midwall shortening/end-systolic stress relation 1) markedly reduces the proportion of hypertensive subjects identified as having high endocardial left ventricular function; and 2) identifies a substantial subgroup of patients with reduced left ventricular function who have concentric geometry of the left ventricle, a pattern associated with high cardiovascular risk

    Relation of Age to Left Ventricular Structure, Function, and Systemic Hemodynamics in Normotensive and Hypertensive Employed Adults.

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    To determine the effect of age on left ventricular status and systemic hemodynamics, we evaluated by echocardiogram older (age at or above 60 years, n equals 148) and younger (age is less than 60 years, n equals 472) employed adults. Using World Health Organization criteria, the population was divided into the following blood pressure strata: normotensive (n equals 142), borderline hypertensive (n equals 194), and sustained hypertensive (n equals 284). Older subjects were compared to younger subjects in each blood pressure stratum. Older subjects with borderline hypertension and sustained hypertension had a higher systolic blood pressure and wider pulse pressure than younger individuals. Older subjects with borderline hypertension had higher left ventricular mass index (106.7Â+/-28.7 vs 93.9Â+/-22.4, P equals 0.03), and greater wall thicknesses and relative wall thicknesses than younger subjects. Older borderline hypertensive patients had greater left ventricular wall thicknesses and mass, but closely resembled both age groups of sustained hypertensive patients in this regard. Older and younger individuals with borderline hypertension had similar mean cardiac outputs, stroke volumes, and peripheral resistances. In contrast, older patients with sustained hypertension had a lower stroke volume, stroke volume index, cardiac output, cardiac index, and fractional shortening, and a higher total peripheral resistance than their younger counterparts. There were no significant relations between age and any echocardiographic measurement in normotensive subjects. Borderline hypertensive individuals exhibited weak relationships between age and left ventricular wall thicknesses (r equals 0.17; 23) and left ventricular internal dimensions (r equals -0.19 and -0.21). Very weak negative relationships were identified between age and cardiac output for both hypertensive groups. In conclusion, increasing age had relatively little effect on cardiac status in either normotensive or sustained hypertensive employed adults, but was associated with greater left ventricular hypertrophy among individuals with borderline hypertension according to the World Health Organization classification. These results are consistent with the independent value of age and left ventricular mass as predictors of hypertensive complications, but also suggest that under some circumstances, greater age or longer exposure to hypertension may magnify the target-organ effects at a given degree of blood pressure elevation
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