Correlation Of Left Ventricular Mass Research Articles

Importance of 24h ambulatory blood pressure monitoring in patients with acromegaly and correlation with cardiac magnetic resonance findings.

Arterial hypertension (AH) is prevalent in acromegaly, but few studies using 24-h ambulatory blood pressure monitoring (24h-ABPM) suggest that its frequency may be different from office blood pressure (OBP). Left ventricular hypertrophy (LVH) is one of the most frequent cardiac abnormalities. Cardiac magnetic resonance (CMR) is considered the gold standard to evaluate the heart. To compare the frequency of AH when measured by 24h-ABPM and by OBP and to correlate BP with cardiac mass. Patients over 18years of age with acromegaly underwent OBP evaluation and were later referred to the 24h-ABPM. Treatment-naïve patients were submitted to CMR. We evaluated 96 patients. From 29 non hypertensive patients by OBP, 9 had AH on 24h-ABPM. In the group of patients with a previous diagnosis of AH by OBP, 25 had controlled BP and 42 had abnormal BP on 24h-ABPM, when analyzed by OBP there were 28 with controlled BP. We observed a positive correlation between diastolic BP measured in 24h-ABPM and IGF-I levels, but we did not observe the same correlation with age, sex, body mass index and GH levels. The CMR was performed in 11 patients. We found a positive correlation of left ventricular mass (LVM) and BP of 24h-ABPM. In contrast, there was no correlation of OBP with CMR parameters. We observed, that 24h-ABPM in acromegaly allows the diagnosis of AH in some patients with normal BP in OBP and also to allow a better treatment. 24h-ABPM shows a better correlation with VM by CMR.

Correlation of Left Ventricular Mass with Biochemical Variables in Hypertensive Subjects

Correlation of Left Ventricular Mass with Biochemical Variables in Hypertensive Subjects

ADHERENCE TO ANTIHYPERTENSIVE MEDICATION AND LEFT VENTRICULAR HYPERTROPHY IN RESISTANT ARTERIAL HYPERTENSION

Objective: According to current registry data, 37% of hypertensive patients reach target blood pressure level. The failure to achieve target blood pressure level cause cardiovascular complications and mortality. Poorly treated arterial hypertension is long-term asymptomatic condition leading to hypertension-mediated organ damage (HMOD), that can be detected by imaging methods and laboratory tests. The aim of our study was to find out the difference in left ventricular (LV) mass values in nonadherent and adherent hypertensive patients. Design and method: We determined adherence to therapy by measuring serum levels of antihypertensive drugs in 329 subjects with resistant arterial hypertension. The full adherence was defined by presence of antihypertensive agents in serum. Non-adherent patients had at least one antihypertensive agent absent. All subjects had transthoracical echocardiographic examination. LV mass (LVM) was calculated by the cubic method and indexed to body surface area to obtain LV mass index (LVMI). The relation of adherence to LVM and LVMI was analysed with Mann-Whitney test and Spearman correlation test. Supported by IGA_LF_2018_045. Results: 240 subjects (73%) were assessed as adherent, the remaining 89 (27%) as non-adherent. Median LVM in adherent patients was 228 g, in non-adherent 245 g (P = 0.105). Median LVMI in adherent patients was significantly lower (106 g/m2) compared to non-adherent patients (120 g/m2) (P = 0.019). LVMI showed weak but statistically significant negative correlation with adherence, correlation coefficient r = −0.123 (P = 0.025). The correlation of LVM with adherence had r = −0.079 (P = 0.134). Conclusions: Non-adherent patients with resistant arterial hypertension have higher prevalence of left ventricular hypertrophy in comparison to adherent patients. Early detection of nonadherence can define a group of patients at high risk for developing hypertension modified organ damage (HMOD).

Transesophageal Echocardiography Guidance of Antegrade Cardioplegia Delivery for Cardiac Surgery.

The initial volume of antegrade cardioplegia used to induce asystole during aortic cross-clamp still is based on empiric methods and may be excessive, potentially leading to hyperkalemia, myocardial edema, and acute left ventricular distention from aortic regurgitation. The objectives were to determine whether the volume of cardioplegia required to induce asystole is proportional to left ventricular mass, and whether the degree of left ventricular distention is proportional to the severity of aortic regurgitation. Prospective observational study. Two tertiary university hospitals. Transesophageal echocardiography was used to estimate left ventricular mass (prolate ellipse revolution formula), quantify aortic regurgitation, and monitor for distention during initial antegrade cardioplegia delivery. The volume of cardioplegia required for asystole was recorded. Fifty-eight patients aged over 18 years scheduled for cardiac surgery requiring aortic cross-clamping. There was a weak correlation of left ventricular mass and antegrade cardioplegia volume required for asystole (r = 0.35, p = 0.047). The degree of left ventricular distention correlated moderately with the severity of aortic regurgitation (r = 0.55, p = 0.007) and was excessive and stopped early (aborted) in 24% of all patients, including 18% of 39 patients without aortic regurgitation. An aortic regurgitation vena contracta of 0.3 cm predicted aborted cardioplegia with modest accuracy (AUC 0.81, 0.66-0.99, p = 0.02, sensitivity 71%, specifity 81%). Estimated left ventricular mass is not a useful predictor of the initial volume of antegrade cardioplegia required to induce asystole. However transesophageal echocardiography can predict and monitor for left ventricular distention, which is common.

Correlates of left ventricular mass in chronic hemodialysis recipients

We aimed to clarify the correlates of left ventricular mass and secondarily, left ventricular volume, in a cohort of prevalent hemodialysis recipients. Left ventricular hypertrophy is common and left ventricular mass is a widely-accepted surrogate for clinical outcomes in dialysis recipients, who are often subjected to chronic pressure and volume overload. However, the precise pathophysiologic mechanisms of left ventricular hypertrophy in this unique population have not been well understood. This was a cross-sectional study of patients receiving conventional thrice-weekly dialysis in Toronto, Canada. Left ventricular mass and volume were assessed with cardiac magnetic resonance and indexed to the patient's height to the power of 2.7. Fibroblast growth factor-23 concentration was measured using a C-terminal enzyme-linked immunosorbent assay. Patient demographics, comorbidities, dialysis-associated blood pressures and ultrafiltration volumes, biochemical and hematologic parameters, vascular access and medications were extracted from clinical records. Multivariable linear regression was used to identify independent correlates of left ventricular mass index (LVMI) and the left ventricular end diastolic volume index (LVEDVI). We enrolled 56 patients, of whom 23 (41.1 %) were women with mean age 54 ± 12 years. Mean LVMI was 31.1 ± 6.8 g/m(2.7). In multivariable analyses, systolic blood pressure and LVEDVI were the only factors significantly associated with LVMI. Post-dialysis weight, percent reduction in urea and the presence of a permanent form of vascular access were associated with LVEDVI. Fibroblast growth factor-23 was not associated with either LVMI or LVEDVI. Blood pressure and left ventricular dilatation are independent determinants of elevated left ventricular mass. Aggressive blood pressure reduction and avoidance of volume overload may confer LVM regression and improve clinical outcomes.

Left Ventricular Hypertrophy in Hypertensive Children and Adolescents: Predictors and Prevalence

Left ventricular hypertrophy is an independent predictor of cardiovascular morbidity and mortality in adults. In children, the primary correlate of left ventricular mass (LVM) is lean body mass, but fat mass, gender and systolic blood pressure are also contributors. LVM can be estimated from echocardiographic measurements, and by indexing this allometrically to height to the 2.7 power, the left ventricular mass index (LVMI) can be calculated. LVMI optimizes detection of left ventricular hypertrophy with established normal curves for children from birth to 18 years. In children with sustained hypertension, 8-41 % have LVMI above the 95th percentile and in 10-15.5 % of these, LVMI is elevated above levels associated with increased mortality in adults. The presence of obesity is associated with higher LVMI than is found in children with hypertension alone. In children with chronic kidney disease, left ventricular hypertrophy develops relatively early and becomes more prevalent as kidney function decreases. In summary, left ventricular hypertrophy is a sensitive marker of target organ damage in children with BP elevation, obesity and chronic kidney disease providing important management information.

What Can Genetic Studies of Left Ventricular Mass Tell Us?

Left ventricular hypertrophy (LVH), whether measured by electrocardiography, echocardiography, or at autopsy, is associated with increased risk of cardiovascular morbidity and mortality.1,2 Although LVH has been associated with several clinical characteristics such as age, sex, body mass index, and hypertension, the effects and their directionality have varied according to the criteria for LVH.3 Aggregation within families suggests a heritable component due to genetics,4 although a recent study of echocardiographic left ventricular mass in a large sample was unable to identify common genetic factors.5 Treatment of hypertensives with LVH can lead to its regression and with it reduction in risk of cardiovascular disease.6 Thus, it appears to be a modifiable risk factor, although LVH induced by exercise training is thought to be benign. Thus, LVH is a complex trait with diverse definitions, has multiple clinical and genetic contributors and is a modifiable risk factor in some but not all settings. Article see p 626 It is not surprising therefore that the (patho-) physiological mechanisms that underlie LVH remain incompletely characterized. Human genetics offers one opportunity to expose mechanisms not previously recognized to play a role in the development of LVH. Shah et al report in this issue of Circulation Cardiovascular Genetics a genetic screen to identify common genetic variants related to electrocardiographic correlates of left ventricular mass (ECG LVM): 2 reflecting simple voltage measures—Sokolow-Lyon voltage and 12-lead QRS voltage sum—and 2 incorporating QRS duration—Cornell product and QRS voltage product.7 The investigators genotyped gene-focused single-nucleotide polymorphisms (SNPs) found on the ITMAT-Broad-CARE (IBC) array, marketed by Illumina as the HumanCVD BeadChip 50K array, with ≈35 000 SNPs passing quality control. The array includes SNPs at 2100 candidate genes selected for being implicated in processes thought to be involved in cardiovascular disease as well as some …

Concordance analysis of left ventricular mass by transthoracic echocardiography versus 64-slice multidetector computed tomography

Left ventricular mass (LVM) is considered an independent cardiovascular risk factor. Today we have new cardiac imaging methods for its calculation, which are incorporated into the already established classic. The aim of the study was to assess a comprehensive analysis of the correlation of LVM between two different diagnostic techniques, transthoracic echocardiography (TTE) and 64-slice multidetector computed tomography (MDCT).

Comparison of Methods to Measure Heart Size Using Noncontrast-Enhanced Computed Tomography

Left ventricular (LV) mass is a useful independent predictor of cardiovascular events. We sought to develop a new correlate of LV mass using noncontrast-enhanced cardiac computed tomography (NCE-CCT). We assessed 22 different ventricular measurements made with NCE-CCT in 60 participants in the Multi-Ethnic Study of Atherosclerosis. The primary outcome was the correlation between the NCE-CCT measurements and magnetic resonance imaging (MRI)-derived LV mass. Correlation coefficients (r) for the 22 NCE-CCT techniques in comparison to MRI-derived LV mass ranged from 0.12 to 0.80, with 14 of the 22 techniques having r > 0.7. The highest correlation was achieved using the modified Simpson Rule method to determine the biventricular volume (r = 0.80; P < 0.001). Interrater reliability was good, with intraclass correlation coefficients of 0.84 to 0.90 for the best (r > 0.75) NCE-CCT methods. Noncontrast-enhanced cardiac computed tomography measurements of both biventricular volume and LV volume correlated well with MRI-derived LV mass in a population free of clinical cardiovascular disease.

One clinic measure of light exercise central blood pressure is a stronger correlate of left ventricular mass than 24 hour ambulatory blood pressure monitoring

Background Twenty four hour ambulatory blood pressure (24ABPM) is the gold standard for assessing blood pressure (BP) control. However, central BP during daily activity may be a stronger determinant of cardiovascular risk. This study aimed to compare 24ABPM with light exercise central BP (mimicking daily activity) for predicting left ventricular (LV) mass. Methods Study population comprised 54 patients (aged 58±7 years; 20 men) including those with treated hypertension (n=16), untreated masked hypertension (n=23) and normotensive controls (n=15). Subjects underwent 2D echocardiography for determination of LV mass (indexed; g/m2.7), resting brachial BP, 24ABPM and estimated central BP by radial tonometry during graded cycle ergometry. Central systolic BP (SBP) was estimated from the radial second systolic peak (P2) as well as the derived central waveform. Results The range of LV mass index and 24ABPM SBP were 17.8-55.1 g/m2.7 and 107-153 mmHg respectively. As expected, 24ABPM SBP was significantly associated with LV mass index (r=0.30, p=0.02), but not with clinic resting brachial (r=0.21; p=0.14) or central SBP (r=0.20; p=0.14). However, the strongest correlates of LV mass index were light exercise (50% heart rate reserve) radial P2 (r=0.54, p<0.001) and central SBP (r=0.47; p<0.001). On multiple regression analysis, radial P2, but not 24ABPM SBP, was independently associated (β=0.45; p<0.01) with LV mass index after accounting for other confounding variables. Conclusion A one-off clinic estimate of light activity central SBP outweighs 24ABPM for predicting LV mass. This rapid, noninvasive technique may provide a superior measure of BP control compared with the current gold standard.

Relationship of left ventricular mass to insulin sensitivity and body mass index in healthy individuals

Objective— The objective of this study was to investigate the contribution of insulin resistance, hyperinsulinaemia and obesity, independently of other major factors, to changes in left ventricular mass a cardiovascular risk indicator, in a healthy population without co-morbid states such as diabetes or hypertension.Methods and results— This cross-sectional relational study was perfomed in 153 healthy subjects, comprising 76 men and 77 women with ages ranging from 23 to 67 years. All of them were normotensive and had a normal oral glucose tolerance test, none had cardiovascular disease and none were taking any medication.Weight, height and waist circumference were measured and BMI was calculated.A blood sample was drawn in the fasting state: plasma glucose, insulin, serum total and high density lipoprotein (HDL), low density lipoprotein cholesterol and triglycerides were measured. Insulin resistance was determined by the ‘Homeostasis Assessment Model’ (HOMA-IR). Subjects were studied by echocardiography. The left ventricular mass was calculated by using the anatomically validated formula of Devereux et al.Results— Left ventricular mass significantly and positively correlated with BMI, age, systolic and diastolic blood pressure and fasting blood glucose. The correlation of left ventricular mass with fasting blood glucose was not maintained after controlling for BMI. BMI, fasting blood glucose, HOMAIR, systolic and diastolic blood pressure showed significant differences with higher values for people with left ventricular hypertrophy.The logistic regression analysis showed a strong association between left ventricular hypertrophy and BMI (p < 0.05).Conclusion— Insulin resistance and fasting insulin is not associated with left ventricular hypertrophy in healthy people, independent of obesity. Obesity appears to be an independent risk factor for left ventricular hypertrophy.

Correlation between left ventricular mass and urinary sodium excretion in specific genotypes of CYP11B2

Aldosterone has essential roles in regulating intravascular volume and blood pressure, and is suggested to influence cardiac structure. However, the association of polymorphisms in the aldosterone synthase gene (CYP11B2) with hypertension or cardiac hypertrophy remains controversial. To evaluate the distribution of polymorphisms in the CYP11B2 gene and the possible associations between genotypes and blood pressure, urinary excretion of aldosterone or electrolytes and echocardiographic measurements, in a Japanese population. We examined the association of two common diallelic polymorphisms within CYP11B2, one in the promoter -344T/C and the other an intron 2 gene conversion, with blood pressure, 24-h urinary excretion of aldosterone and electrolytes, and echocardiographic measurements, in a Japanese population. We confirmed significant linkage disequilibrium between these polymorphic loci and ethnic differences in frequency of the alleles. The -344C and -344T haplotypes apparently diverged before the intron conversion polymorphism was generated on the latter haplotype. Allele frequencies did not differ between 535 normotensive and 360 hypertensive individuals or between hypertensive individuals with higher and lower concentrations of renin. The only significant correlation was a positive correlation of left ventricular mass with 24-h urinary excretion of sodium, which occurred only in individuals with the -344CC genotype or the intron 2 conversion (-/-) genotype. The -344CC or intron 2 conversion (-/-) genotype in CYP11B2 may be a risk factor for developing sodium-sensitive cardiac hypertrophy. Ethnic differences in the distribution of CYP11B2 genotypes combined with differences in salt intake might account for inconsistencies between previous reports.

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.

Sibling correlation of left ventricular mass and geometry in hypertensive African Americans and whites: the HyperGEN study

Background Evidence suggests that left ventricular (LV) mass is under genetic control, independently of risk factors known to influence LV size and geometry. Methods As part of the HyperGEN study, four field centers recruited African American and white hypertensive siblings ( n = 1664), aged 23 to 87 years. Two-dimensionally guided M-mode echocardiography was performed, and LV mass and relative wall thickness (RWT) were measured at a central reading center. Familial correlations were calculated separately for each ethnic group using maximum likelihood methods, adjusted for the potential confounding influences of age, gender, systolic blood pressure, and obesity. Results In African Americans, brother-sister, brother-brother, and sister-sister correlation coefficients and standard errors for LV mass were 0.29 (0.08), 0.44 (0.10), and 0.33 (0.05). In whites, the corresponding correlations were lower than in African Americans at 0.05 (0.08), 0.12 (0.11), and 0.22 (0.09), respectively. Sibling correlation of LV geometry, assessed by RWT, was less in African Americans than in whites: brother-sister, 0.04 (0.10) v 0.21 (0.10), brother-brother, 0.12 (0.22) v 0.28 (0.09), and sister-sister, 0.11 (0.07) v 0.19 (0.11). Conclusions: LV mass is strongly correlated in hypertensive African American siblings, and modestly correlated in their white counterparts, whereas RWT has stronger sibling correlation in whites. The patterns of familial correlation of echocardiographic LV mass and RWT suggest that the genetic underpinnings of LV hypertrophy and geometric remodeling may differ among ethnic groups.

Similar effects of isolated systolic and combined hypertension on left ventricular geometry and function: the LIFE study

Echocardiograms of 143 patients with isolated systolic hypertension were compared to 808 patients with combined (systolic and diastolic) hypertension. All patients met electrocardiographic criteria for left ventricular hypertrophy and were evaluated off medication. Patients with isolated systolic hypertension were older, shorter, weighed less, and were mostly women, but body mass index (BMI) was similar in both groups. Systolic blood pressure (SBP) was 172 mm Hg in isolated systolic hypertension, 174 mm Hg in combined ( P = not significant). Diastolic blood pressure was 83 and 101 mm Hg, respectively ( P < .001). Despite having mean arterial pressure 12 mm Hg lower than patients with combined hypertension, the group with isolated systolic hypertension had equally severe abnormalities of left ventricular mass, left ventricular geometric patterns, and measures of systolic and diastolic function. Peripheral resistance was lower and pulse pressure/stroke volume ratio (arterial stiffness index) was higher and the isovolumic relaxation time shorter in isolated systolic hypertension. Multiple regression analyses identified age, height, BMI, stress-corrected mid wall shortening, stroke volume, male gender, and systolic or mean blood pressure (but not isolated systolic hypertension) as independent correlates of left ventricular mass. Relative wall thickness was independently associated with isolated systolic hypertension ( P = .001) in addition to mean pressure and other covariates. The present results add support to the concept that systolic blood pressure (SBP) is a stronger determinant than diastolic pressure of cardiac target organ damage in hypertension.

Genetic and environmental influences on left ventricular mass. A family study.

The relations between left ventricular mass (LVM) with age, gender, body size, and blood pressure were investigated in healthy adults and children from 149 nuclear families. LVM was strongly correlated with overall weight, especially in the children. Genetic analysis indicated that the segregation of LVM was compatible with an additive polygenic model, with a heritability estimate of 34% before adjustment for weight and 28% after adjustment for weight. Genetic and/or familial environmental factors played a strong role in the correlation of LVM and weight; they accounted for all of the correlation between the 2 traits in adults and 59% of the correlation in children. Spouses exhibited a strong correlation in their weight, which suggested that common family environment may contribute to the family correlations and to the observed heritability of the trait. LVM was strongly correlated with blood pressure before adjustment for weight, but this correlation could be attributed to nonfamilial environment rather than genetic factors. After adjustment for weight, the intertrait correlations between LVM and blood pressure were nonsignificant. Thus, adjustment for weight accounts for all common determinants of LVM and blood pressure.

Static and pulsatile blood pressure correlates of left ventricular structure and function in black and white young adults: The CARDIA study

Objective: To determine the unbiased relative strength of the association of static (systolic and diastolic) and pulsatile (pulse pressure) blood pressure components with left ventricular mass and function. Background: Blood pressure is correlated with left ventricular mass; however, the unbiased relative strength of static and pulsatile blood pressure components with left ventricular mass and function is unknown in young adults. Methods: Cross-sectional analyses of 3918 young adult participants at 4 community-based CARDIA clinical centers during 1990 and 1991. Results: Left ventricular mass positively correlated (P < .01) with systolic, diastolic, and pulse pressure in all ethnicity-sex groups except for diastolic blood pressure in white men (P = .19). The association rank ordered as systolic blood pressure > pulse pressure > diastolic blood pressure except in white men, in whom pulse pressure and systolic blood pressure reversed positions in this hierarchy. Systolic blood pressure was the third and fourth strongest independent correlate of left ventricular mass in men and women, respectively. Body mass index, followed by height, was the strongest correlate of left ventricular mass in both sexes. Left ventricular wall thickness/chamber radius ratio positively correlated with diastolic and systolic blood pressure (women only) (P < .05) but not with pulse pressure. In all groups, stroke volume positively correlated (P < .05) with pulse pressure but was unrelated to static blood pressure measures, except for systolic blood pressure in black men. Left ventricular mass and the ventricular wall thickness/chamber radius ratio were greater in blacks compared with whites. Conclusions: Although systolic blood pressure was consistently the strongest unbiased blood pressure correlate of left ventricular mass, this relation varied by ethnicity and sex. Pulse pressure correlated with favorable left ventricular function and geometry, suggesting an opposite meaning to the ominous prognosis of wide pulse pressure in hypertensive, older adults. (Am Heart J 1999;138:856-64.)

Left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is an important cardiovascular risk factor. The presence of LVH carries risk independent of hypertension. LVH can be detected non-invasively using electrocardiography or echocardiography. Clinical studies have consistently shown that ambulatory blood pressure is a stronger correlate of left ventricular mass than office blood pressure. Furthermore, treatment-induced decreases in left ventricular mass index are also more tightly related to reductions in ambulatory blood pressure than reductions in office blood pressure. The primary intervention for subjects with hypertension and LVH is optimal blood pressure control. Several small studies now suggest that therapeutic changes resulting in regression of left ventricular mass also confer a reduction in cardiovascular risk. Therefore, LVH is a serious negative risk factor that is more closely related ambulatory rather than office blood pressure. Fortunately, current evidence suggests that optimal antihypertensive therapy resulting in regression of hypertrophy will reduce at least short-term cardiovascular events. Physicians need to be more aware of LVH as a cardiovascular risk factor.

Plasma angiotensin II, predisposition to hypertension, and left ventricular size in healthy young adults.

We studied the correlates of left ventricular mass (LVM) in 84 healthy young adults aged 16 to 24 years from the general population. Subjects were selected according to predisposition to hypertension into four groups with either high or low personal blood pressures and either high or low parental blood pressures. LVM was measured by echocardiography, and measurements of blood pressure, heart rate, body dimensions, and plasma concentrations of components of the renin-angiotensin system were made under resting conditions. LVM was similar in individuals predisposed to hypertension (high personal and parental blood pressures) and those with contrasting predisposition (low personal and parental pressures). Regression analysis of the combined groups showed that LVM correlated closely with body size, particularly lean body mass (r=.69, P<.0001) and systolic (r=.35, P<.0001) but not diastolic blood pressure. Plasma angiotensin II (r=.39, P<.0001), renin (r=.302, P<.01), and angiotensin-converting enzyme (r=.22, P<.05) showed significant correlation with LVM. Multiple regression analysis revealed that plasma angiotensin II was the most important component of the renin-angiotensin system and that its effect was independent of systolic blood pressure and body size. These findings provide evidence in humans that angiotensin II exerts a direct on myocardial size. This association may have important implications for the complications and treatment of left ventricular hypertrophy.

Effect of lean body mass, fat mass, blood pressure, and sexual maturation on left ventricular mass in children and adolescents. Statistical, biological, and clinical significance.

Left ventricular hypertrophy has been established as an independent risk factor for the development of cardiovascular morbidity and mortality. It is clear that left ventricular mass increases during childhood and adolescence with body growth. The extent to which other factors, such as obesity, stage of sexual maturation, and level of blood pressure, determine left ventricular mass has been controversial. The study was a cross-sectional evaluation of the relationship of left ventricular mass determined by echocardiography with lean body mass and fat mass determined by dual-energy x-ray absorptiometry, which is the most valid and reliable method for determination of body composition in children and adolescents. The relationship of left ventricular mass with the stage of sexual maturation and with systolic and diastolic blood pressure was also evaluated. Two hundred one subjects (105 boys, 96 girls; 103 white and 98 black) 6 to 17 years old were studied. Age (r = .72), height (r = .81), weight (r = .84), body surface area (r = .87), sexual maturation (r = .75), lean body mass (r = .86), fat mass (r = .54), systolic BP (r = .58), and diastolic BP (r = .48) were all univariate correlates of left ventricular mass. In a multiple regression analysis, only lean body mass, fat mass, and systolic blood pressure were statistically significant independent correlates of left ventricular mass. Lean body mass alone explained 75% of the variance of left ventricular mass, whereas fat mass and systolic blood pressure explained only 1.5% and 0.5% of the variance, respectively. Lean body mass was the strongest determinant of left ventricular mass in all four race-sex groups. This study provides an opportunity to separate the effects on left ventricular mass of lean body mass resulting from linear growth from those of fat mass resulting from obesity. Lean body mass, fat mass, and systolic blood pressure all have a statistically significant independent association with left ventricular mass, suggesting that all three play an important biological role in determining left ventricular mass. However, fat mass and systolic blood pressure have only a small impact on left ventricular mass. This indicates that fat mass and blood pressure would be expected to be of only minor clinical importance in determining left ventricular mass in normal children and adolescents.