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Biomedical subjects

G de Simone

Publications and source records attributed to G de Simone.

At least 55 records · Page 3Linked to original sources
PubMed1999

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.

Adult↗
PubMed1998

Relation of age to left ventricular function in clinically normal adults.

The extent to which age, independent of cardiovascular diseases, influences left ventricular (LV) function in adults is uncertain. Echocardiograms and simultaneous arterial pressure in 464 clinically normal adults aged 16 to 88 years were used to measure LV dimensions, endocardial and midwall LV fractional shortening, stroke volume, cardiac output, and circumferential end-systolic stress. The ratios of observed endocardial and midwall shortening to values predicted for observed end-systolic stress were used as measures of chamber and myocardial function. LV endocardial shortening increased slightly with age, as did an index of LV chamber performance, the end-systolic stress/volume index ratio (r = 0.11, p = 0.019, and r = 0.20, p <0.001). However, when age-related increases in LV wall thickness and blood pressure were controlled for by examining afterload-corrected endocardial shortening, no age relation was detected. Weak age-related declines were observed in midwall shortening (r = -0.09, p = 0.043) and afterload-corrected midwall shortening (r = -0.12, p <0.01). Cardiac index decreased slightly with advancing age (r = -0.14, mean -6.7 ml/min/m2/ year, p = 0.003). Total peripheral resistance and the pulse pressure/stroke volume ratio, a measure of arterial stiffness, increased more strongly with age (r = 0.27 and 0.38, both p <0.001). Thus, LV pump performance at rest measured by cardiac index is slightly lower in older than in younger clinically normal adults. Endocardial fractional shortening was slightly higher in older subjects, but the physiologically more appropriate midwall measures of myocardial function decreased slightly. The observed change in LV pump performance was related to smaller LV chamber size and higher total peripheral resistance in older subjects.

Adolescent↗
PubMed1998

Relation of insulin resistance to left ventricular hypertrophy and diastolic dysfunction in obesity.

OBJECTIVE: To assess relations of left ventricular (LV) geometry and function to insulin resistance in obesity-a condition associated with volume overload and abnormal LV relaxation. DESIGN: Cross-sectional relational study. SUBJECTS: 27 healthy overweight-obese subjects (18 women, body mass index (BMI) = 35.0+/-4.0 kg/m2) and 31 age-matched normal-weight controls (21 women, BMI = 22.6+/-2.4 kg/m2). MEASUREMENTS: Subjects were studied by Doppler-echocardiography the same day and hour (08.00 h) as measurements of fasting insulin and blood glucose were made. Insulin resistance was determined by the 'Homeostasis Assessment Model'. RESULTS: Twelve obese subjects with insulin resistance (IR) had higher body size than 15 patients without IR and higher blood pressure than normal-weight controls (all P < 0.01). Relative IR was related to isovolumic relaxation time. This relation was not maintained after controlling for age, blood pressure, weight and height. Isovolumic relaxation time was, however, positively related to diastolic blood pressure, a measure of load, in normal controls (r=0.44) and obese without IR (r=0.62) but not in insulin resistant subjects (r=0.14). CONCLUSION: IR does not independently influence myocardial relaxation in uncomplicated obesity, but modulates the effect of load on active diastole.

Adult↗
PubMed1998

Influence of cardiovascular risk factors on relation between angiotensin converting enzyme-gene polymorphism and blood pressure in arterial hypertension.

BACKGROUND: The angiotensin-converting enzyme gene insertion (I)/deletion (D) polymorphism might be involved in the development of several cardiovascular diseases, but its role in humans remains controversial. OBJECTIVE: To investigate the relation between the angiotensin converting enzyme gene polymorphism and extent of blood pressure elevation in arterial hypertension, taking into account the influence of cardiovascular risk factors. METHODS: We studied 171 patients (aged 49 +/- 9 years, 61 women) with abnormal clinic and 24 h ambulatory blood pressures, after a 3-week wash-out. RESULTS: We found no significant difference in clinic and ambulatory blood pressures among homozygotic D (DD), heterozygotic D (ID) and homozygotic I (II) angiotensin converting enzyme genotypes and between homozygotic D (DD) and pooled heterozygotic D (ID) plus homozygotic I (II) (non-DD) angiotensin converting enzyme genotypes. At least one additional cardiovascular risk factor (smoking, hypercholesterolaemia or diabetes) was present for 103 patients (33 DD and 70 non-DD). Non-DD subjects (n = 43) without additional cardiovascular risk factors exhibited lower values of 24 h, daytime systolic and pulse blood pressures than did members of all other groups (all P < 0.04). In the presence of risk factors, DD and non-DD subjects exhibited similar systolic and pulse ambulatory blood pressures, in that we found higher values in non-DD genotype subjects with risk factors than we did for non-DD subjects without additional risk factors. In multivariate analysis, the combination of non-DD genotype and absence of cardiovascular risk factors was associated with the lowest values of systolic and pulse blood pressures. CONCLUSIONS: Angiotensin converting enzyme insertion allele appears clustered with lower ambulatory systolic and pulse blood pressures in hypertensive patients when the potential interference of additional cardiovascular risk factors is eliminated. A high prevalence of cardiovascular risk factors in population studies might blunt a possible biological association of blood pressure with DD genotype by contributing to raising of blood pressures also in subjects with non-DD genotypes.

Adult↗
PubMed1998

Clinical impact of various geometric models for calculation of echocardiographic left ventricular mass.

BACKGROUND: M-mode echocardiographic left ventricular mass calculated using a thick-wall prolate ellipsoidal model is widely used in clinical and epidemiologic studies. Doubts regarding the ability of this approach to obtain a precise estimate of left ventricular weight across a wide range of values have recently been raised and an alternate thin-wall ellipsoidal model has been proposed to gain greater precision. OBJECTIVE: To compare thin-wall and thick-wall (American Society of Echocardiography and Penn convention) models for calculation of left ventricular mass. DESIGN: Validation, cross-sectional, and longitudinal studies. PARTICIPANTS: Necropsy data and living cohorts from Naples, New York City, and Umbria region of Italy (PIUMA registry). RESULTS: The average thin-wall left ventricular mass was slightly greater than the necropsy left ventricular weight (mean 225 versus 220 g), whereas no difference was detected using regression-adjusted thick-wall methods. Use of the thin-walled model slightly overestimated left ventricular mass relative to both thick-wall models at the lowest left ventricular mass while slightly underestimating the highest values. Comparison of Cox proportional hazard models in two longitudinal studies demonstrated that there was a substantial equivalence among methods, with a marginally better performance of thick-wall models for cardiovascular risk stratification (P < 0.05 in one study). CONCLUSIONS: Although it is imperfect, because it is based on simplifying geometric assumptions, computation of left ventricular mass on the basis of M-mode echocardiographic left ventricular dimensions using thick-wall prolate-ellipsoidal models is valuable for identification of left ventricular hypertrophy and for cardiovascular risk stratification of patients with essential hypertension. Calculation of left ventricular mass by use of a thin-wall prolate-ellipsoidal geometry does not yield appreciably different results than those which are obtained by use of thick-wall models.

Cardiovascular Diseases↗
PubMed1998

Relation of left ventricular midwall function to cardiovascular risk factors and arterial structure and function.

Left ventricular (LV) midwall shortening (MWS) is subnormal in relation to LV circumferential end-systolic stress (ESS) (ESS-corrected MWS) in many hypertensive patients with normal LV chamber function and predicts subsequent morbidity and mortality. However, little is known of the relations of LV midwall function to demographic and metabolic variables or to arterial geometry. Asymptomatic, unmedicated normotensive (n=366) or hypertensive (n=282) adults were assessed with echocardiography and carotid ultrasound. In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P<.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03). Among hypertensive patients, lower values for both midwall function indices were associated independently with higher peripheral resistance (P<.00001), heart rate (P<.00005), body mass index (P<.01), and arterial RWT (P=.04), as well as male gender (P<.0002). In the entire population, lower LV MWS was independently related to higher peripheral resistance, heart rate (both P<.00001), body mass index (P=.0006) and arterial RWT (P=.009); male gender (P<.00001); and lower age (P=.004), diastolic pressure (P=.042), and systolic carotid artery expansion (P=.032). Lower ESS-corrected MWS in the entire population was independently associated with higher peripheral resistance and heart rate (both P<.00001), body mass index (P=.0006), arterial RWT (P=.004); male gender; and lower diastolic pressure (both P<.00001), age (P<.00005), arterial expansion in systole (P=.006), and serum HDL cholesterol levels (P=.04). Among a subset (n=60), ESS-corrected MWS was positively related to apolipoprotein A1 (P=.004) and negatively to hemoglobin A1c (P<.01). Thus, higher LV midwall function is associated with female gender and more favorable profiles of hemodynamics, metabolic pattern, and arterial structure and function.

Apolipoproteins↗
PubMed1998

Interaction between body size and cardiac workload: influence on left ventricular mass during body growth and adulthood.

The development of the left ventricle parallels body growth. During infancy, the relation between body size and left ventricular (LV) mass is very close. With advancing age, variability of LV mass in relation to body size markedly increases. To test the hypothesis that the age-related increase in variability of LV mass is due to the progressive impact of hemodynamic stimuli on LV growth, quantitative M-mode echocardiograms were obtained in 766 normal-weight, normotensive individuals over a range of ages from 1 day to 85 years (330 female subjects, 373 subjects younger than 18 years). LV mass was linearly related to height2.7 (r2=.69). Prediction of values of LV mass by body size was more accurate at birth and progressively less precise with increasing age. Stroke work (stroke volume times systolic pressure) was closely related to LV mass (r2=.74). The explained variance of LV mass increased from 69% in the univariate regression with height2.7 to 82% in a multivariate model including height2.7, stroke work, and gender. In children and adolescents (younger than 18 years), height2.7 was the main determinant of LV mass, whereas during adulthood stroke work and gender were more important predictors of LV mass than height2.7. Thus (1) the influence of body growth on development of LV mass decreases after early infancy because of both the variability of hemodynamic load and the increasing effect of gender; (2) after adolescence, during adulthood, in normotensive, normal-weight individuals, the impact of hemodynamic load and male gender on LV mass is greater than the one of body size; and (3) an appreciable proportion of variability of LV mass remains unexplained with the studied models. This might be due to genotypic variations and/or measurement error.

Adult↗
PubMed1997

Relations of left ventricular mass to demographic and hemodynamic variables in American Indians: the Strong Heart Study.

BACKGROUND: Previous studies have identified associations of left ventricular (LV) mass with demographic (body habitus and sex) and hemodynamic variables (blood pressure, stroke volume [SV], and myocardial contractility), but the relative strength and independence of these associations remain unknown. METHODS AND RESULTS: We examined the relations of echocardiographically determined LV mass to demographic variables, blood pressure, Doppler SV, and measures of contractility (end-systolic stress [ESS]/end-systolic volume index and midwall fractional shortening [MFS] as a percentage of predicted for circumferential end-systolic stress [stress-independent shortening]) in 1935 American Indian participants in the Strong Heart Study phase 2 examination without mitral regurgitation or segmental wall motion abnormalities. Weak positive relations of LV mass with systolic and diastolic pressures (r=.22 and r=.20) were exceeded by positive relations with height (r=.30), weight (r=.47), body mass index (r=.31), body surface area (r=.49), and Doppler SV (r=.50) and negative relations with ESS/volume index ratios (r= -.33 and -.29) and stress-independent MFS (r= -.26, all P<.0001). In multivariate analyses that included blood pressure, SV, and a different contractility measure in each model, systolic pressure, stroke volume, and the contractility measure were independent correlates of LV mass (multiple R=.60 to .66, all P<.0001). When demographic variables were added, LV mass was more strongly predicted by higher SV and lower afterload-independent MFS than by greater systolic pressure, height, and body mass index (each P<.00001, multiple R=.71). CONCLUSIONS: Additional characterization of volume load and contractile efficiency improves hemodynamic prediction of LV mass (R(2)=.30 to .44) over the use of systolic blood pressure alone (R(2)=.05), with a further increase in R(2) to .51 when demographic variables are also considered. However, nearly half of the ventricular mass variability remains unexplained.

Aged↗
PubMed1997

Usefulness of subnormal midwall fractional shortening in predicting left ventricular exercise dysfunction in asymptomatic patients with systemic hypertension.

We have recently shown that a subgroup of asymptomatic hypertensive patients exhibit subnormal left ventricular (LV) midwall fiber shortening at rest and that this finding predicts morbidity and mortality independently of age, blood pressure (BP), or the presence of LV hypertrophy. However, it is unknown whether abnormal midwall fractional shortening predicts either subnormal LV functional reserve or extracardiac damage in asymptomatic hypertensive patients. Accordingly, we compared radionuclide cineangiographic LV ejection fraction at rest and maximum exercise as well as clinical findings between 89 patients with normal and 16 patients with subnormal midwall fractional shortening by echocardiogram. Patients with low midwall fractional shortening were similar in gender, age, and systolic BP to those with normal shortening but had higher mean diastolic BP and body mass indexes (both p < 0.05). The 2 groups also had similar resting ejection fraction (56 +/- 9% vs 55 +/- 15%, with normal or subnormal shortening, respectively, p = NS). Patients with subnormal midwall fractional shortening had higher LV mass and tended to have higher urinary protein excretion and serum creatinine levels. Subnormal LV ejection fraction with exercise (< 54%) was observed in 13 of 89 patients (15%) with normal midwall fractional shortening but in 7 of 16 patients (44%) with subnormal shortening (p < 0.05). Multiple linear regression analysis revealed that midwall fractional shortening independently predicted exercise performance (p < 0.001). Thus, subnormal midwall fractional shortening predicts depressed LV fractional reserve in asymptomatic hypertensive patients and may contribute to identification of patients with extracardiac target-organ damage.

Adult↗
PubMed1997

Stroke volume and cardiac output in normotensive children and adults. Assessment of relations with body size and impact of overweight.

BACKGROUND: Relations between organs and body size are not linear but rather follow allometric (growth) relations characterized by their powers (exponents). METHODS AND RESULTS: Stroke volume (SV) by M-mode echocardiography was related to height, weight, body surface area (BSA), and ideal BSA (derived from ideal body weight for given height) in 970 normotensive individuals (1 day to 85 years old; 426 < 18 years old; 204 overweight to obese; 426 female). In normal-weight children, adults, and the entire population, SV was related by allometric relations to BSA (power = 0.82 to 1.19), body weight (power = 0.57 to 0.71), and height (power = 1.45 to 2.04) (all P < .0001). Relations of cardiac output to measures of body size had lower allometric powers than those for SV in the entire population (0.41 for body weight, 0.62 for BSA, and 1.16 for height). In overweight adults, observed SVs were 17% greater than predicted for ideal BSA, a difference that was approximated by normalization of SV for height to age-specific allometric powers. Similarly, observed cardiac output was 19% greater than predicted for ideal BSA, a difference that was accurately detected by use of cardiac output/height to age-specific allometric powers but not of BSA to the first power. CONCLUSIONS: Indices of SV and cardiac output for BSA are pertinent when the effect of obesity needs to be removed, because these indices obscure the impact of obesity. To detect the effect of obesity on LV pump function, normalization of SV and cardiac output for ideal BSA or for height to its age-specific allometric power should be practiced.

Adolescent↗
PubMed1997

Relation of left ventricular longitudinal and circumferential shortening to ejection fraction in the presence or in the absence of mild hypertension.

OBJECTIVES: To study left ventricular longitudinal shortening in arterial hypertension and the relative contribution of longitudinal and circumferential fiber shortening to ventricular ejection. METHODS: Two-dimensional and M-mode echocardiograms were obtained for 50 normotensive subjects (aged 49 +/- 12 years) and 50 never-treated mild hypertensive patients (aged 49 +/- 11 years), to measure the minor-axis endocardial and midwall shortening, long-axis shortening and ejection fraction. RESULTS: The midwall shortening was lower in hypertensive than it was in normotensive subjects (P < 0.001) and was related inversely to the circumferential wall stress for both groups (P < 0.04 and 0.0001, respectively). The long-axis shortening in hypertensive patients (22.2 +/- 4.2%) and in normotensives (23.6 +/- 5.4%) was not statistically different, and was not related either to the meridional or to the circumferential wall stress. The ejection fraction was also similar for the two groups (68.2 +/- 6.3 versus 68.6 +/- 5.6%). Both for normotensive and for hypertensive subjects, the ejection fraction was influenced mainly by the midwall shortening (61 and 40% of the variance for normal and hypertensive individuals, respectively), with a minor contribution from the long-axis shortening, which was 7% for normotensive subjects and 18% for hypertensive patients, a statistically significant difference (P < 0.001). The combined effect of midwall and longitudinal shortenings on the ejection fraction was regulated by the relative wall thickness, and was maximal for hypertensive patients with an ejection fraction greater than that predicted by the midwall shortening. CONCLUSIONS: Left ventricular ejection is produced principally by circumferential shortening and is related independently to the relative wall thickness. In the presence of arterial hypertension and an altered cardiac load, longitudinal shortening becomes an important mechanism by which to augment ejection, thereby offsetting the reduction in midwall shortening.

Adult↗
PubMed1997

Left ventricular filling in arterial hypertension. Influence of obesity and hemodynamic and structural confounders.

We assessed the relations of left ventricular filling to load and geometry by Doppler echocardiography in 80 normotensive subjects (40 normal-weight [36 +/- 12 years, 24 women] and 40 obese [35 +/- 13 years, 24 women]) and 61 hypertensive subjects without silent coronary heart disease (29 normal-weight [43 +/- 13 years, 15 women] and 32 obese [42 +/- 13 years, 19 women]) and comparable left ventricular midwall performance. Left ventricular mass divided by height to the 2.7 power was higher in all groups than in normotensive normal-weight subjects (all P < .0001) and in hypertensive than normotensive obese subjects (P < .001). After controlling for age, sex, blood pressure, and heart rate, isovolumic relaxation time was prolonged in hypertensive subjects and normotensive obese subjects compared with normotensive normal-weight subjects (all P < .0001). Body mass index, left ventricular dimension and mass, and circumferential end-systolic stress did not influence these differences. In pooled groups, prolonged isovolumic relaxation time was predicted by high mean blood pressure (beta = 0.52, P < .001), low end-systolic stress (beta = -0.33, P < .001), increased left ventricular mass (beta = 0.24, P < .004), and high body mass index (beta = 0.14, P < .05, multiple R = .72, SEE = 16.5 milliseconds, P < .0001). Between-group differences in peak early transmitral flow velocity, the deceleration time of early filling velocity, and the ratio of early to late left ventricular filling disappeared after controlling for left ventricular mass. Thus, (1) isovolumic relaxation time is prolonged in both arterial hypertension and obesity; (2) the presence of obesity does not significantly increase isovolumic relaxation time in hypertension; and (3) abnormalities of left ventricular filling in arterial hypertension are offset after controlling for left ventricular mass.

Adult↗
PubMed1997

Age-related changes in total arterial capacitance from birth to maturity in a normotensive population.

We evaluated the effect of body growth and aging on the ratio of echocardiographic (Teichholz) stroke volume to pulse pressure (SV/PP ratio) in 373 normal-weight, normotensive children to adolescents (1 day to 17 years old; 166 girls, 87 nonwhite) and 393 normal adults (17 to 85 years old; 164 women, 112 nonwhite). Stroke volume increased with age in children (r = .64, P < .0001) and was stable in adults; pulse pressure decreased slightly with age in children (r = -.10, P = .06) and increased in adults (r = .29, P < .0001). As a consequence, SV/PP ratio increased with age in children (r = .51, P < .0001) and decreased in adults (r = -.18, P = .0004). To control for changes in body size that influence the size of the arterial tree, we used ANCOVA to adjust SV/PP for body size. Body size-adjusted SV/PP ratio was no longer related to age in children, whereas the negative relation with aging in adults remained statistically significant (r = -.19, P < .0002). Heart rate was negatively related to SV/PP ratio in both children and adolescents and adults, but this relation did not influence the relation with age. In multivariate analysis, high SV/PP ratio was predicted by greater height (P < .002) and weight (P < .04) and nonwhite race (P < .001) in children and adolescents and by younger age (P < .0001), greater weight (P < .0001), and low heart rate (P < .001) in adults. Sex did not enter the regression models. Thus, (1) SV/PP ratio is a measure of increasing capacity of the arterial tree during growth, whereas it depends on arterial compliance during adulthood through old age; (2) arterial compliance decreases progressively with aging; (3) the apparent difference between males and females might be due to their different body sizes.

Adolescent↗