Independent Predictors Of Left Ventricular Mass Research Articles

Cardiac Structure and Function in 8- to 12-Year-Old Children Following In-Utero Exposure to Preeclampsia (FINNCARE Study).

We evaluated how elevated blood pressure in children exposed to preeclampsia (PE) impacted on their cardiac structure and function, as well as relations with maternal, gestational, and perinatal factors and child body size and composition. A total of 182 PE (46 early-onset preeclampsia) and 85 unexposed (non-PE) children were examined in the FINNCARE study 8 to 12 years after the index pregnancy with echocardiography; office, central, and 24-hour ambulatory blood pressures; and body anthropometrics and composition. PE children had lower right ventricular basal sphericity index (mean difference, -0.26 95% CI, -0.39 to -0.12) and lower mitral lateral E'-wave peak velocity (-1.4 cm/s [95% CI, -2.1 to -0.6]), as well as higher E to E' ratio (0.40 [95% CI, 0.15-0.65]) and indexed tricuspid annular plane systolic excursion (0.03 [95% CI, 0.01-0.05]) compared with non-PE children. These differences were accentuated in early-onset PE children. Left ventricular mass (LVM) or left atrial volume were not different between PE and non-PE children. Lean body mass, body fat percentage, and 24-hour systolic blood pressure were independent predictors of LVM. Lean body mass and body fat percentage were independent predictors of left atrial volume. No significant associations between LVM or left atrial volume and maternal, gestational, or perinatal parameters were found. Preadolescent PE children display a more globular-shaped right ventricle with higher longitudinal systolic displacement as well as mildly altered diastolic indices, with the alterations being pronounced in early-onset preeclampsia. Lean body mass and adiposity are independently related with LVM and left atrial volume, and systolic blood pressure with LVM in both PE and non-PE children. These unfavorable associations indicate remodeling of cardiac structure in young children also reflected in mild functional changes in PE children. URL: https://www.clinicaltrials.gov; unique identifier: NCT04676295.

Abstract 51: Ambulatory Blood Pressure Phenotype And Cardiovascular Risk In Youth: The Ship-ahoy Study

We investigated whether blood pressure (BP) phenotype based on clinic & 24-hour ambulatory BP (ABP) was associated with intermediate markers of cardiovascular disease (CVD) in 374 adolescents enrolled in a study of the relationship of BP to CV risk. Clinic BP was measured by auscultation and categorized using the 2017 AAP guideline. ABP was measured for 24 hours by an oscillometric device and analyzed using the adult ABP wake SBP cut-point (130 mmHg). This created 4 BP phenotype groups: normal BP (n=224), white coat hypertensive (n=48), ambulatory hypertensive (n=57) & masked hypertensive (n=45). Echocardiographic parameters & carotid-femoral pulse wave velocity (PWVcf) were measured to assess CVD risk. Left ventricular mass (LVM) was lowest in the normal BP group, whereas multiple measures of cardiac function and PWVcf were worse in the masked and ambulatory hypertensive groups: Generalized linear models adjusted for body mass index (BMI) were constructed to examine the associations between BP phenotype and the measured CVD variables. ABP phenotype was an independent predictor of LVM, diastolic and systolic function and PWVcf in the unadjusted model. ABP phenotype remained significantly associated with diastolic function (E/e’, e’/a’), systolic function (ejection fraction) and increased arterial stiffness (PWVcf) after adjustment for BMI percentile (all p<=0.05). We conclude that BP phenotype is an independent predictor of markers of increased CVD risk in adolescents, including impaired cardiac function and increased vascular stiffness. ABP monitoring has an important role in CVD risk assessment in youth.

Coronary artery calcification, carotid intima-media thickness and cardiac dysfunction in young adults with type 2 diabetes mellitus

AimsCardiovascular diseases (CVD) are the major causes of mortality in patients with type 2 diabetes mellitus (T2DM). There is paucity of information on prevalence of subclinical atherosclerosis and cardiac dysfunction in young adults with T2DM. This study aimed to assess the prevalence of subclinical atherosclerosis and cardiac dysfunction in young adults with T2DM, asymptomatic for CVD. MethodsSixty-two patients with T2DM, age between 30 and 50 years were evaluated for coronary artery calcium (CAC) score, carotid intima-media thickness (CIMT) and flow-mediated dilatation (FMD) at the brachial artery. All were subjected to 2D-color Doppler echocardiography, electrocardiography and testing for serum N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity C-reactive protein (hsCRP). The results were compared with those in 60 age, sex and BMI-matched healthy controls. ResultsPrevalence of a positive CAC score was comparable among subjects with and without T2DM (14.5% vs 11.7%). Patients with T2DM had a significantly higher CIMT (0.54 ± 0.15 vs 0.49 ± 0.10 mm, p = 0.01), left ventricular (LV) mass (170 ± 36 vs 147 ± 23 g, p < 0.001), heart rate (83 ± 13 vs 74 ± 11, p < 0.001) and QTc interval (402 ± 20 vs 382 ± 21 ms, p < 0.001) compared to controls. FMD was lower in patients with T2DM compared to controls (9.1 ± 4.4% vs 10.7 ± 3.9%, p = 0.04). There was a higher prevalence of LV hypertrophy (37% vs 7%, p < 0.001) and diastolic dysfunction (7% vs 0) in patients with T2DM compared to controls. None of the participants had systolic dysfunction. Hypertension (42 vs 7%, p < 0.001) and metabolic syndrome (76 vs 35%, p < 0.001) were more prevalent in the patient group. In the multivariate analysis, age was the lone predictor of CIMT and FMD; while T2DM and male gender were the independent predictors of LV mass. ConclusionsYoung adults with T2DM, asymptomatic for CVD had a higher prevalence of CVD risk factors, LV hypertrophy and diastolic dysfunction. A higher CIMT and LV mass, and a lower FMD were noted in patients with T2DM. CAC score was comparable between the groups and thus may not be a useful tool for assessment of subclinical atherosclerosis in this cohort, where CIMT and FMD may be more appropriate.

The relationship of alcohol consumption with left ventricular mass in people 35 years old or older in rural areas of Western China

The aim of this study was to investigate the association between alcohol intake and left ventricular mass (LVM) independent of the effects of blood pressure and other factors in rural areas of Western China. The present study included 1007 subjects (487 men and 520 women) aged ≥35 years from the Tongan district, Chongqing, China. The quantity and frequency of alcohol consumption were estimated from a validated questionnaire. Echocardiography was used to assess left ventricular dimensions. Drinkers was associated with higher LVM compared with nondrinkers (β = 6.9, 95% confidence interval: 1.3–12.5, P = .015). A dose-dependent higher LVM across increasing alcohol consumption was observed (P < .05). LVM was significantly correlated with regular drinking (β = 10.0, 95% confidence interval: 3.6–16.4). In subjects with hypertension, quantity of alcohol consumption (P for interaction = .013) and frequency of alcohol consumption (P for interaction = .025) were strongly associated with higher LVM when stratified by blood pressure. However, interactions linked to age, body mass index, and gender were found to be no significant difference. These results indicate that both quantity and frequency of alcohol consumption are independent predictors of LVM in rural areas of Western China. The effects of alcohol consumption on LVM are enhanced among subjects with hypertension.

The impact of obesity on the relationship between epicardial adipose tissue, left ventricular mass and coronary microvascular function.

PurposeEpicardial adipose tissue (EAT) has been linked to coronary artery disease (CAD) and coronary microvascular dysfunction. However, its injurious effect may also impact the underlying myocardium. This study aimed to determine the impact of obesity on the quantitative relationship between left ventricular mass (LVM), EAT and coronary microvascular function.MethodsA total of 208 (94 men, 45 %) patients evaluated for CAD but free of coronary obstructions underwent quantitative [15O]H2O hybrid positron emission tomography (PET)/CT imaging. Coronary microvascular resistance (CMVR) was calculated as the ratio of mean arterial pressure to hyperaemic myocardial blood flow.ResultsObese patients [body mass index (BMI) > 25, n = 133, 64 % of total] had more EAT (125.3 ± 47.6 vs 93.5 ± 42.1 cc, p < 0.001), a higher LVM (130.1 ± 30.4 vs 114.2 ± 29.3 g, p < 0.001) and an increased CMVR (26.6 ± 9.1 vs 22.3 ± 8.6 mmHg×ml−1×min−1×g−1, p < 0.01) as compared to nonobese patients. Male gender (β = 40.7, p < 0.001), BMI (β = 1.61, p < 0.001), smoking (β = 6.29, p = 0.03) and EAT volume (β = 0.10, p < 0.01) were identified as independent predictors of LVM. When grouped according to BMI status, EAT was only independently associated with LVM in nonobese patients. LVM, hypercholesterolaemia and coronary artery calcium score were independent predictors of CMVR.ConclusionEAT volume is associated with LVM independently of BMI and might therefore be a better predictor of cardiovascular risk than BMI. However, EAT volume was not related to coronary microvascular function after adjustments for LVM and traditional risk factors.Electronic supplementary materialThe online version of this article (doi:10.1007/s00259-015-3087-5) contains supplementary material, which is available to authorized users.

Resistive and pulsatile arterial load as predictors of left ventricular mass and geometry: the multi-ethnic study of atherosclerosis.

Arterial load is composed of resistive and various pulsatile components, but their relative contributions to left ventricular (LV) remodeling in the general population are unknown. We studied 4145 participants enrolled in the Multi-Ethnic Study of Atherosclerosis, who underwent cardiac MRI and radial arterial tonometry. We computed systemic vascular resistance (SVR=mean arterial pressure/cardiac output) and indices of pulsatile load including total arterial compliance (TAC, approximated as stroke volume/central pulse pressure), forward wave amplitude (Pf), and reflected wave amplitude (Pb). TAC and SVR were adjusted for body surface area to allow for appropriate sex comparisons. We performed allometric adjustment of LV mass for body size and sex and computed standardized regression coefficients (β) for each measure of arterial load. In multivariable regression models that adjusted for multiple confounders, SVR (β=0.08; P<0.001), TAC (β=0.44; P<0.001), Pb (β=0.73; P<0.001), and Pf (β=-0.23; P=0.001) were significant independent predictors of LV mass. Conversely, TAC (β=-0.43; P<0.001), SVR (β=0.22; P<0.001), and Pf (β=-0.18; P=0.004) were independently associated with the LV wall/LV cavity volume ratio. Women demonstrated greater pulsatile load than men, as evidenced by a lower indexed TAC (0.89 versus 1.04 mL/mm Hg per square meter; P<0.0001), whereas men demonstrated a higher indexed SVR (34.0 versus 32.8 Wood Units×m2; P<0.0001). In conclusion, various components of arterial load differentially associate with LV hypertrophy and concentric remodeling. Women demonstrated greater pulsatile load than men. For both LV mass and the LV wall/LV cavity volume ratio, the loading sequence (ie, early load versus late load) is an important determinant of LV response to arterial load.

Dynamic changes in left ventricular mass and in fat-free mass in top-level athletes during the competitive season

Previous cross-sectional studies have demonstrated that fat-free mass (FFM) is an important determinant of left ventricular mass (LVM) in athletes. However, cross-sectional investigations have not the ability to detect the dynamic adaptation occurring with training. We hypothesized that LVM adapts concurrently with the increase of FFM induced by exercise conditioning. We sought to study the relationship between the variations of LVM and of FFM occurring in top-level soccer players during the season. Twenty-three male top-level athletes were recruited. LVM was assessed by echocardiography and FFM by dual-energy X-ray absorptiometry. Serial measurements were performed pre-season, after 1 month, at mid- and end-season, and after 2 months of detraining. LVM significantly increased at mid-season versus pre-season values, reaching the highest value at the end of the season (p < 0.05). While body weight did not vary during the study period, FFM significantly increased (p < 0.05 for mid-/end-season vs. pre-season data). After the detraining, no significant differences were observed between pre-season and detraining echocardiographic data. The only independent predictors of LVM were left ventricular stroke volume and FFM (R = 0.36, p = 0.005; R = 0.35, p = 0.005, respectively). When ΔLVM index was set as dependent variable, the only independent predictor was ΔFFM (R = 0.87, p = 0.002). Changes in LVM occur in close association with changes in FFM, suggesting that the left ventricle adapts concurrently with the increase of the metabolically active tissue induced by training, i.e. the FFM. Therefore, the dynamic changes in FFM and LVM may reflect a physiological adaptation induced by intensive training.

Relationship between serum fibroblast growth factor 23 levels and left ventricular mass measured by three-dimensional echocardiography in patients with end-stage renal disease

Purpose: In patients with chronic renal insufficiency traditional risk factors of left ventricular (LV) hypertrophy include hypertension, overhydration, anemia and impaired calcium-phosphate homeostasis. Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone secreted by osteoblasts and a rising biomarker associated with LV hypertrophy and mortality in patients with end-stage renal disease (ESRD). We sought to determine the relationship between serum FGF-23 levels and left venticular mass measured by three-dimensional (3D) echocardiography in ESRD patients. Methods: This retrospective cohort study included 44 patients (mean age 48±13 years, 54% men) with ESRD on three times per week maintenance hemodialysis. Exclusion criteria were previous history of diabetes and any significant cardiac disease. Beyond conventional transthoracic echocardiographic examination, 3D recordings were obtained using multi-beat reconstruction from 6 consecutive cardiac cycles (GE Vivid E9). After semi-automated tracing of LV endo- and epicardial surface at end-diastolic frame, LV mass was calculated using dedicated software (GE 4D Auto LVQ). Serum FGF-23 levels were measured by enzyme-linked immunosorbent assay (Merck Millipore). Overhydration evaluated by bioimpedance (Fresenius Body Composition Monitor), laboratory test results (including serum calcium, phosphate, parathormone, total iron binding capacity levels) and blood pressure were recorded and averaged in the three previous months. Relationships were calculated by Spearman correlation test and multivariate linear regression. Results: The median value of LV mass measured in ESRD patients was 244 grams (interquartile range 97.5). Serum FGF-23 levels ranged between 34 and 6848 with a median of 687 pg/ml. Serum levels of FGF-23 (ρ=0.52), phosphate (ρ=0.55), parathormone (ρ=0.38), total iron binding capacity (ρ=0.61), systolic blood pressure (ρ=0.38) and pulse pressure (ρ=0.47, all p<0.05) correlated significantly with LV mass. FGF-23 correlated with serum phosphate (ρ=0.83) and parathormone (ρ=0.53, both p<0.001) levels. In a multivariate linear regression model, FGF-23 (β=0.42, p<0.001), total iron binding capacity (β=0.49, p<0.001) and systolic blood pressure (β=0.37, p<0.01) were found to be independent predictors of LV mass. Conclusions: To the best of our knowledge, this is the first study which demonstrates the strong correlation between serum FGF-23 levels and LV mass measured by 3D echocardiography. Beside the chronic volume- and pressure overload, LV hypertrophy is strongly determined by the endocrine effects of FGF-23 in patients with ESRD.

Echocardiographic Study of Cardiac Structure in Cyclists and Runners

We sought to study the cardiac morphology of cyclists and runners in male and female athletes and control subjects and to find association cardiac morphological measurements with body composition measurements. Endurance training is associated with increases in both left ventricular mass (LVM) and left ventricular end-diastolic dimension (LVEDD). Cardiac morphology shows sports specific adaptations which are studied in the two groups, runners involving lower limb and cyclists involving upper limb. 28 runners and 26 cyclists were taken to do a comparison study with 38 control subjects, aged between 18-25 years of age and comprising of males and females both. All participants underwent transthoracic echocardiography and hydrostatic underwater weighing for body composition along with routine measurements. Athletes showed enlarged LV dimensions and mass (p<0.05) as compared to controls. Right ventricular and aortic root dimensions were also found to be significantly higher in athletes (p<0.05). Lean tissue mass was found to be independent predictor of LVM. Increased LV wall thickness in relation to the ventricular dimension appears to be proportionate in runners; it is disproportionate in cyclists, probably because of the isometric training component involved during upper limb training cycling. Hence runners show eccentric hypertrophy and cyclist showed mixed eccentric and concentric hypertrophy. LVM was found to be correlated only to lean tissue mass. The extent of LV remodeling (athletic heart) in trained individuals may reflect a normal physiologic response to increased lean tissue mass induced by training.

Association of left ventricular hypertrophy with high-sensitive C-reactive protein in hemodialysis patients

Micro inflammation and cardiovascular disease such as left ventricular hypertrophy (LVH) are common in hemodialysis (HD) patients. Hence, we have evaluated the relationship between high-sensitive C-reactive protein (hs-CRP), as an inflammation marker, and left ventricular mass index (LVMi) and left ventricular mass (LVM) in HD patients. An analytical cross-sectional study was performed in 104 HD patients. Serum hs-CRP, LVMi, LVM, and blood pressure were evaluated; demographic data and duration of HD were also recorded. Finally, results were analyzed by using Student's t test, Pearson's correlation coefficient, one-way ANOVA and multiple regression to determine the relationship between LVMi and other variables. A total of 66 male patients (63.46 %) and 38 female patients, with a mean age of 51.75 ± 15.98 years-old, participated in this study. Hypertension was the most common underlying disease (65.4 %). The mean LVMi was 366.98 ± 120.89 g/m(2) and the mean hs-CRP was 8.55 mg/l. Eighty-nine percent of patients had LVH. The hs-CRP level was significantly associated with age and with LVM (P = 0.0001, P = 0.039, respectively). On multivariate analysis, hs-CRP and systolic blood pressure were found to be independent predictors of LVM and LVMi. This study shows that hs-CRP and systolic BP are independent predictors of LVH in HD patients.

080 Obstructive sleep apnoea and atherosclerosis, vascular dysfunction and cardiac remodelling as assessed by CMR

<h3>Objective</h3> Obstructive sleep apnoea (OSA) is associated with hypertension, coronary artery disease, heart failure and stroke. We investigated whether OSA represents an additional independent risk factor for preclinical atherosclerosis, vascular dysfunction and cardiac remodelling as assessed by CMR. We also examined the effect of OSA severity as expressed by Oxygen Desaturation Index (ODI) on MR derived cardiac and vascular markers. <h3>Methods</h3> In total, 58 patients with OSA and 39 control subjects without sleep apnoea underwent Cardiovascular Magnetic Resonance (CMR) scanning.42 OSA patients were meticulously matched for demographics, body size and cardiovascular risk factors to the 39 controls. CMR protocol: Our assessment included carotid and aortic atheroma burden quantification, central aortic distensibility assessment and left ventricular (LV) as well as right ventricular (RV) diastolic mass and volumes measurements. Multiple weighting, high resolution, imaging of the carotid vessels was used for carotid atheroma composition characterisation. Pulmonary artery (PA) acceleration time, a non invasive pulmonary artery pressure marker, was derived from velocity-encoded pulmonary artery flow imaging. <h3>Results</h3> Carotid (p&lt;0.05 (abstract 080 figure 1a)) and aortic (p&lt;0.001 (abstract 080 figure1b)) wall thickness were increased in OSA patients in comparison with controls. Through multivariate regression analysis, ODI emerged as an independent predictor of both carotid (β=0.41(0.15)(p&lt;0.01)) and aortic wall thickness (β=0.61(0.21)(p&lt;0.01)). Carotid plaques, advanced carotid disease and “high risk” of carotid atheroma were all more prevalent among individuals suffering from OSA (p&lt;0.05)(abstract 080 figure 2). Aortic distensibility was decreased in OSA (p&lt;0.05)(abstract 080 figure 3). Although ODI correlated with aortic distensibility (r=−0.35, p&lt;0.01), this association was not significant after adjustment for age and systolic blood pressure. LV mass (p&lt;0.05) and volume (p&lt;0.01) as well as RV mass (p&lt;0.05) - all indexed to body surface area - were increased in OSA (abstract 080 figure 4). On multivariate regression analysis, ODI emerged as an independent predictor of LV mass (β=0.41(0.17)(p&lt;0.05)), LV volume (β=0.34(0.16)(p&lt;0.05)) and RV mass (β=0.16(0.07)(p&lt;0.05)) in OSA. PA acceleration time was significantly shortened in OSA (p&lt;0.005)(abstract 080 figure5) and significantly correlated with ODI (r=−0.38, p&lt;0.05), RV volume (r=−0.47, p&lt;0.01) and RV mass, even after adjustment for ODI (β=−0.13(0.05)(p&lt;0.05)). <h3>Conclusions</h3> OSA is associated with increased atheroma burden and complicated atheromatic lesions. Increased central aortic stiffening, that appears to be dependent on an increase in systolic blood pressure, is detected in OSA. An independent association between OSA and eccentric LV remodelling and hypertrophy is demonstrated by CMR. CMR reveals for the first time an association between the presence and severity OSA and RV hypertrophy, which may be dependent on an concomitant increase in pulmonary arterial pressure.

Determinants of left ventricular mass and presence of metabolic risk factors in normotensive individuals

Background Insulin resistance and obesity are recognized as left ventricular (LV) mass determinants independent of blood pressure (BP). Prevalence of LV hypertrophy (LVH) and the relationship between LV mass to body composition and metabolic variables were evaluated in normotensive individuals as participants of a population-based study. Methods LV mass was measured using the second harmonic image by M-mode 2D guided echocardiography in 326 normotensive subjects (mean 47 ± 9.4 years). Fasting serum lipids and glucose, BP, body composition and waist circumference (WC) were recorded during a clinic visit. Results Applying a normalization criterion not related to body weight (g/height raised to the power 2.7) and the cut-off points of 47.7 (men) and 46.6 g/m 2.7 (women), LVH was found in 7.9% of the sample. Univariate analysis showed LV mass (g/m 2.7) related to age, body mass index (BMI), WC, fat and lean body mass, systolic and diastolic BP, and metabolic variables (cholesterol, HDL-c, triglycerides and glucose). In multivariate analysis only BMI and age-adjusted systolic BP remained as independent predictors of LV mass, explaining 31% and 5% of its variability. Removing BMI from the model, WC, age-adjusted systolic BP and lean mass remained independent predictors, explaining 25.0%, 4.0% and 1.5% of LV mass variability, respectively. After sex stratification, LV mass predictors were WC (8%) and systolic BP (5%) in men and WC (36%) and systolic BP (3%) in women. Conclusion BMI in general and particularly increased abdominal adiposity (WC as surrogate) seems to account for most of LV mass increase in normotensive individuals, mainly in women.

Corin I555(P568) Allele Is Associated With Enhanced Cardiac Hypertrophic Response to Increased Systemic Afterload

Corin activates pro-A-type naturetic peptide and pro-B-type naturetic peptide into biologically active molecules. We recently identified a minor allele in the corin gene defined by 2 highly linked single nucleotide polymorphisms (T555I and Q568P), which was associated with hypertension in blacks. Because of the direct antihypertrophic effects of the natriuretic peptide system, we hypothesized that the minor corin I555(P568) allele would be associated with an enhanced hypertrophic response to pressure overload. The relationship between systolic blood pressure and indexed left ventricular mass, derived from cardiac MRI, was analyzed in the Dallas Heart Study as a function of corin allele status. The Multi-Ethnic Study of Atherosclerosis was used as a validation cohort. All of the analyses were limited to self-identified blacks without treatment for hypertension. In addition, we genotyped 2114 markers highly informative for African ancestry in the Dallas Heart Study and derived a covariate representing African ancestry for multivariate models. In adjusted analysis, the corin I555(P568) allele was an independent predictor of left-ventricular mass in subjects with elevated systolic blood pressure. Linear spline regression analysis confirmed a significant interaction (P=0.002) between the corin I555(P568) allele and systolic blood pressure as a predictor of left ventricular mass in subjects with systolic blood pressure >120 mm Hg, and this nonlinear interaction was replicated in the Multi-Ethnic Study of Atherosclerosis. In the Dallas Heart Study, the corin I555(P568) allele was also associated with an increased odds for prevalent left ventricular hypertrophy in the presence of untreated hypertension. These data suggest that the corin I555(P568) allele represents a cardiac hypertrophy-sensitizing genetic locus in systemic hypertension.

Distance correction in the electrocardiographic estimation of left ventricular mass

Assessment of the left ventricular mass (LVM) from electrocardiograms may be improved by the addition of clinical variables into a multivariate equation. As the heart-thorax distance may affect the results, its relationships with electrocardiographic and clinical data have been evaluated in a group of 220 subjects (53 ± 15 years, 126 female, 175 without demonstrated heart disease) who were assessed for echocardiographic LVM and heart-thorax distance. Sokolow, Cornell, and total QRS voltage indexes were obtained. Multiple regression equations with LVM as the dependent variable were fit, with an ECG index, body mass index (BMI), age, and gender as the independent predictors. Each of the 3 ECG indexes, BMI, age, and sex was shown to be independent predictors of LVM, with the ECG and BMI contributing with most of the explanatory power. When added to the model, the distance from the interventricular septum to the precordium (septal-LVD) was not a predictor of LVM, but when BMI was withdrawn, septal-LVD became an independent predictor of LVM ( P < .001). This was not observed when septal-LVD was substituted for any other clinical or ECG variable, thus suggesting that septal-LVD accounts for information contained in BMI but not in the remaining variables. In addition, the distance from the center of LV to the precordium (mid-LVD) achieved significance as an independent LVM predictor, although the coefficient of multiple determination ( R) practically did not change. Almost identical results are obtained when LVM is indexed for body surface area. Body mass index supplies virtually all the information contained in the heart-thorax distance.

Ambulatory blood pressure, left ventricular mass, and conduit artery function late after successful repair of coarctation of the aorta

ObjectivesWe sought to evaluate the determinants of hypertension during daily life and left ventricular (LV) hypertrophy in patients with successfully repaired coarctation of the aorta (CoA), as well as their relationship to abnormalities of arterial function. BackgroundArterial hypertension may recur late after repair of CoA, which is related to a more adverse outcome. Furthermore, patients with normal resting blood pressure (BP) may have hypertension during daily life and LV hypertrophy. The determinants of these two adverse prognostic factors have not been investigated. MethodsWe studied 72 patients (9 to 58 years of age) who underwent coarctation repair at age 0.1 to 480 months (42 [60%] at <1 year) and had been followed up for 155 ± 76 months. They underwent ambulatory BP monitoring, echocardiography for LV mass, studies of brachial artery responses to flow (i.e., flow-mediated dilation [FMD]) and glyceryl trinitrate (GTN), and determination of pulse wave velocity (PWV) and measures of arterial reactivity and stiffness. Findings were compared with those of 53 healthy volunteers. ResultsPatients had higher 24-h systolic BP and LV mass than controls. Both endothelium-dependent FMD and the response to the smooth muscle dilator GTN were reduced, and PWV was increased. There was a negative independent correlation between GTN response and 24-h systolic BP in both patients and control subjects. Systolic BP at 24 h was an independent predictor of LV mass, having an accentuated impact in coarctation subjects as compared with controls. ConclusionsIn patients with repaired coarctation, reduced vascular reactivity is associated with hypertension during daily life and with increased LV mass, both of which are important predictors for late morbidity and mortality.

High-density lipoprotein cholesterol and left ventricular hypertrophy in essential hypertension

The proportion of left ventricular (LV) mass variability explained by blood pressure in essential hypertension is small, and several non-haemodynamic determinants of LV mass have been identified or hypothesized. This study examines the possible relation between blood lipids and LV mass in hypertension. Never-treated non-diabetic hypertensive patients. Hospital hypertension outpatient clinics in Umbria, Italy. We investigated the association between high-density lipoprotein (HDL)-cholesterol and echocardiographic LV mass in 1306 never-treated subjects with essential hypertension. Subjects with previous cardiovascular events, diabetes and current or previous antihypertensive or lipid-lowering therapy were excluded. HDL-cholesterol showed an inverse association with LV mass (r = -0.30, P < 0.001). No association was found between LV mass and total or low-density lipoprotein cholesterol. With multiple linear regression analysis we tested the independent contribution of several potential determinants of LV mass in women and in men. Average 24 h blood pressure (both pulse and mean), body mass index, height, stroke volume, age (all P < 0.01) and low HDL-cholesterol (P < 0.0001 in women, P < 0.001 in men) were associated with a greater LV mass in both sexes. Triglycerides showed a weak univariate association with LV mass in women (r = 0.11, P < 0.02), which did not hold in a multivariate analysis. Low HDL-cholesterol is an independent predictor of LV mass in untreated hypertensive subjects. Common hormonal and metabolic mechanisms, including insulin resistance, could explain this association, which may contribute to the adverse prognostic significance of low HDL-cholesterol levels.

Differing Roles of Body Mass and the Renin-Angiotensin System in Mediating the Hypertension Syndrome

Background: Hypertension is characterized not only by a metabolic syndrome that includes obesity and insulin resistance, but also by increases in left-ventricular mass (LVM), reduced arterial compliance and altered renal function. This investigation has examined a possible role for the renin-angiotensin system as well as body mass and insulin values in mediating these cardiovascular and renal aspects of the hypertension syndrome. Methods: This was a cross-sectional study of 142 patients identified by community screening. Mean (±SE) age was 46 ± 1 years and patients had stage I–II hypertension (blood pressure: 145 ± 1/98 ± 0.5 mm Hg). For analysis, patients were divided into 2 groups: those with body mass index (BMI) <27 kg/m² (lean, n = 72) or BMI >27 kg/m² (overweight, n = 70). Results: By univariate analysis, LVM in lean patients correlated significantly with plasma renin activity (PRA), plasma aldosterone, BMI and systolic BP; but with multivariate regression, only PRA (p < 0.01) and BMI (p < 0.04) remained in the model as independent predictors of LVM. For LVM in overweight patients, only BMI (p < 0.02) remained in the model. For total arterial compliance (stroke volume/pulse pressure) only fasting plasma insulin (in the overweight group) was significantly related (p < 0.01). For urinary protein excretion, the only predictor in lean patients was PRA (p < 0.02), whereas in overweight patients it was BMI (p < 0.03). For creatinine clearance, BMI (p < 0.01 in overweight patients) remained in the model, though by univariate regression PRA had an age-dependent dichotomous relationship to clearance: r = +0.25 (p < 0.01) in patients <55 years, but r = –0.54 (p < 0.01) in patients ≥55 years. Conclusion: These findings suggest that in overweight patients cardiovascular and renal values depend chiefly on body weight and insulin, but that in normal weight hypertensives the renin-angiotensin system may play the major role.

Factors Influencing Left Ventricular Mass in Salt Sensitive and Salt Resistant Essential Hypertensive Patients

To investigate whether salt sensitivity is associated with differences in left ventricular mass or geometry, salt sensitivity testing and Doppler echocardiography was performed in 30 essential hypertensive patients (7 women and 23 men) with mean age 43+/-9 years. Salt sensitivity was defined as a 10% increase or more in 24-h blood pressure (24hBP) when going from low to high dietary sodium intake based on a single test. Eight patients were characterized as salt sensitive and 22 as salt resistant. At baseline, there was no difference in casual blood pressure (156/103+/-17/9 vs 158/100+/-18/11 mmHg) or 24hBP (152/ 90+/-25/15 vs 159/89+/-19/8 mmHg), in duration of hypertension (5+/-4 vs 4+/-3 years), daily sodium excretion (144+/-68 vs 171+/-68 mmol), left ventricular mass (LVM) (212+/-45 vs 246+/-52 g) or left ventricular relative wall thickness (RWT) between the salt sensitive and salt resistant groups of patients. In the total study population, increased RWT was found in 17 patients, and increased LVM in 10 patients. In only 10 patients were both these variables normal. Left ventricular geometric pattern did not differ between the salt sensitive and salt resistant groups. LVM and RWT were significantly correlated with 24hBP (r = 0.57 and 0.51, respectively; both p < 0.01). Significant correlation was also found between LVM and casual blood pressure, blood volume, body surface area, serum creatinine and albuminuria (r = 0.53, 0.60, 0.54, 0.54 and 0.43, respectively; all p < 0.01). In multiple regression analysis, 24hBP and blood volume were identified as independent predictors of LVM (R = 0.51, p < 0.001). increased RWT or LVM is common in both salt sensitive and salt resistant essential hypertensive patients. Salt sensitivity status based on a single test does not influence left ventricular hypertrophy or geometry. Twenty-four-hour blood pressure is related to increased RWT and LVM.

Relation of Hemodynamic Volume Load to Arterial and Cardiac Size

Objectives. This study sought to assess the relation of Doppler stroke volume (SV) to cardiac and carotid artery size and to determine whether volume load accounts for the parallelism between the two.Background. It has been suggested that altered hemodynamic volume load can modify the degree and pattern of left ventricular (LV) hypertrophy from that predicted from blood pressure (BP) alone.Methods. We related Doppler echocardiographic SV in 342 normotensive or unmedicated asymptomatic hypertensive adults to echocardiographic LV mass, LV internal dimension (LVID), wall thickness, carotid ultrasound arterial lumen diameter, intimal–medial thickness (IMT) and cross-sectional area (CSA).Results. SV was positively related to LV mass (r = 0.42), LVID (r = 0.45), ventricular wall thickness (r = 0.20 to 0.29) and carotid diameter (r = 0.23, all p < 0.0001); CSA (r = 0.17, p < 0.002); and IMT (r = 0.12, p = 0.03). In multivariate analyses controlling for awake ambulatory BP and the circumferential end-systolic stress/end-systolic volume index ratio, SV remained an independent predictor of LV mass and chamber size (both p < 0.0001) but not LV wall thickness. SV also predicted carotid diameter (p < 0.0002), CSA (p = 0.001) and, to a lesser degree, IMT (p = 0.02) after controlling for mean awake BP and age. In additional analyses, LV and carotid dimensions were significantly interrelated independent of SV.Conclusions. SV measured by invasively validated Doppler echocardiography is associated with LV and carotid artery enlargement and eccentric hypertrophy, independent of arterial pressure, LV contractility, age and body size; however, SV and other variables do not account for the previously documented parallelism between cardiac and arterial structure.(J Am Coll Cardiol 1997;29:1303–10)

Factors Influencing LVM in Hypertensive Type-1 Diabetic Patients

Gerdts E, Myking OL, Lund–Johansen P, Omvik P. Factors influencing LVM in hypertensive type-l diabetic patients.Diabetes mellitus is associated with a high prevalence of hypertension and left ventricular hypertrophy (LVH), and a causative relationship with abnormal sodium metabolism in diabetic patients has been suggested. Factors influencing left ventricular mass (LVM) were assessed in 30 hypertensive type–1 diabetic patients, mean age 46 ± 9 (range 24–67) years, with a mean duration of diabetes and hypertension of 19 ± 10 and 6 ± 5 years, respectively. In the total study population, casual blood pressure was 163/94 ± 24/10 mmHg and 24 h blood pressure was 155/87 ± 17/8 mmHg. Twenty-four-hour urine samples were obtained to measure daily albumin excretion (0.77 ± 1.06 g) and dietary sodium intake was assessed as 24 h sodium excretion (173 ± 77 mmol). Creatinine clearance averaged 1.41 ± 0.53 ml/s. LVM determined by echocardiography was 221 ± 74 g (range 104-408 g) and 33% of the patients had LVH. Multiple regression analysis identified dietary sodium intake and plasma atrial natriuretic peptide as independent predictors of LVM (R2 = 0.52, p < 0.001). No significant association was found between LVM and blood pressure or albuminuria. The results propose dietary sodium intake as an important factor in the development of LVH in hypertensive type-l diabetic patients.