Aortic calcification and femoral bone density are independently associated with left ventricular mass in patients with chronic kidney disease

Background Vascular calcification and reduced bone density are prevalent in chronic kidney disease and linked to increased cardiovascular risk. The mechanism is unknown. We assessed the relationship between vascular calcification, femoral bone density and left ventricular mass in patients with stage 3 non-diabetic chronic kidney disease in a cross-sectional observational study. Methodology and Principal Findings A total of 120 patients were recruited (54% male, mean age 55±14 years, mean glomerular filtration rate 50±13 ml/min/1.73 m2). Abdominal aortic calcification was assessed using lateral lumbar spine radiography and was present in 48%. Mean femoral Z-score measured using dual energy x-ray absorptiometry was 0.60±1.06. Cardiovascular magnetic resonance imaging was used to determine left ventricular mass. One patient had left ventricular hypertrophy. Subjects with aortic calcification had higher left ventricular mass compared to those without (56±16 vs. 48±12 g/m2, P = 0.002), as did patients with femoral Z-scores below zero (56±15 vs. 49±13 g/m2, P = 0.01). In univariate analysis presence of aortic calcification correlated with left ventricular mass (r = 0.32, P = 0.001); mean femoral Z-score inversely correlated with left ventricular mass (r = −0.28, P = 0.004). In a multivariate regression model that included presence of aortic calcification, mean femoral Z-score, gender and 24-hour systolic blood pressure, 46% of the variability in left ventricular mass was explained (P<0.001). Conclusions In patients with stage 3 non-diabetic chronic kidney disease, lower mean femoral Z-score and presence of aortic calcification are independently associated with increased left ventricular mass. Further research exploring the pathophysiology that underlies these relationships is warranted

Association of increased plasma cardiotrophin-1 with inappropriate left ventricular mass in essential hypertension

Inappropriate left ventricular mass is present when the value of left ventricular mass exceeds individual needs to compensate hemodynamic load imposed by increased blood pressure. The goal of this study was to investigate whether plasma concentration of cardiotrophin-1, a cytokine that induces exaggerated hypertrophy in cardiomyocytes with hypertensive phenotype, is related to inappropriate left ventricular mass in patients with essential hypertension. The study was performed in 118 patients with never-treated hypertension and without prevalent cardiac disease. The left ventricular mass prediction from stroke work (systolic blood pressurexDoppler stroke volume), sex, and height (in meters(2.7)) was derived. An observed left ventricular mass/predicted left ventricular mass value >128% defined inappropriate left ventricular mass. Plasma cardiotrophin-1 was measured by an enzyme-linked immunosorbent assay. The studies were repeated in a group of 45 patients after 1 year of antihypertensive treatment. At baseline 67 and 51 patients presented with appropriate and inappropriate left ventricular mass, respectively. Plasma cardiotrophin-1 was higher (P<0.001) in patients with inappropriate mass than in patients with appropriate mass and normotensive controls. A direct correlation was found between cardiotrophin-1 and observed left ventricular mass/predicted left ventricular mass ratio (r=0.330, P<0.001) in all hypertensive patients. After treatment, plasma cardiotrophin-1 decreased and increased in patients in which inappropriate left ventricular mass regressed and persisted, respectively, despite a similar reduction of blood pressure in the 2 subgroups of patients. Albeit descriptive in nature, these results suggest the hypothesis that an excess of cardiotrophin-1 may contribute to inappropriate left ventricular growth in hypertensive patients

Determinants of left ventricular mass in obesity; a cardiovascular magnetic resonance study

<p>Abstract</p> <p>Background</p> <p>Obesity is linked to increased left ventricular mass, an independent predictor of mortality. As a result of this, understanding the determinants of left ventricular mass in the setting of obesity has both therapeutic and prognostic implications. Using cardiovascular magnetic resonance our goal was to elucidate the main predictors of left ventricular mass in severely obese subjects free of additional cardiovascular risk factors.</p> <p>Methods</p> <p>38 obese (BMI 37.8 ± 6.9 kg/m²) and 16 normal weight controls subjects, (BMI 21.7 ± 1.8 kg/m²), all without cardiovascular risk factors, underwent cardiovascular magnetic resonance imaging to assess left ventricular mass, left ventricular volumes and visceral fat mass. Left ventricular mass was then compared to serum and anthropometric markers of obesity linked to left ventricular mass, i.e. height, age, blood pressure, total fat mass, visceral fat mass, lean mass, serum leptin and fasting insulin level.</p> <p>Results</p> <p>As expected, obesity was associated with significantly increased left ventricular mass (126 ± 27 vs 90 ± 20 g; p < 0.001). Stepwise multiple regression analysis showed that over 75% of the cross sectional variation in left ventricular mass can be explained by lean body mass (β = 0.51, p < 0.001), LV stroke volume (β = 0.31 p = 0.001) and abdominal visceral fat mass (β = 0.20, p = 0.02), all of which showed highly significant independent associations with left ventricular mass (overall R²= 0.77).</p> <p>Conclusion</p> <p>The left ventricular hypertrophic response to obesity in the absence of additional cardiovascular risk factors is mainly attributable to increases in lean body mass, LV stroke volume and visceral fat mass. In view of the well documented link between obesity, left ventricular hypertrophy and mortality, these findings have potentially important prognostic and therapeutic implications for primary and secondary prevention.</p

In vivo measurement of myocardial mass using nuclear magnetic resonance imaging

To examine the accuracy of nuclear magnetic resonance imaging in measuring left ventricular mass, measurements of left ventricular mass made using this technique were compared with left ventricular weight in 10 mongrel dogs. Left ventricular myocardial volume was measured from five short-axis ehd-diastolic images that spanned the left ventricle. Left ventricular mass was calculated from left ventricular myocardial volume and compared with the left ventricular weight determined after formalin immersion-fixation.Linear regression analysis yielded the following relation in grams: left ventricular mass determined using nuclear magnetic resonance imaging = (0.94) (left ventricular weight) + 9.1 (r = 0.98, SEE = 6.1 g). The small overestimation of left ventricular weight by nuclear magnetic resonance imaging was judged to be secondary to both difficulty with proper border definition and partial volume effects. Hence, this imaging technique can be used to obtain accurate measurements of left ventricular mass in dogs in vivo

Progressive regression of left ventricular hypertrophy two years after bariatric surgery.

BACKGROUND: Obesity is a systemic disorder associated with an increase in left ventricular mass and premature death and disability from cardiovascular disease. Although bariatric surgery reverses many of the hormonal and hemodynamic derangements, the long-term collective effects on body composition and left ventricular mass have not been considered before. We hypothesized that the decrease in fat mass and lean mass after weight loss surgery is associated with a decrease in left ventricular mass. METHODS: Fifteen severely obese women (mean body mass index [BMI]: 46.7+/-1.7 kg/m(2)) with medically controlled hypertension underwent bariatric surgery. Left ventricular mass and plasma markers of systemic metabolism, together with body mass index (BMI), waist and hip circumferences, body composition (fat mass and lean mass), and resting energy expenditure were measured at 0, 3, 9, 12, and 24 months. RESULTS: Left ventricular mass continued to decrease linearly over the entire period of observation, while rates of weight loss, loss of lean mass, loss of fat mass, and resting energy expenditure all plateaued at 9 [corrected] months (P \u3c.001 for all). Parameters of systemic metabolism normalized by 9 months, and showed no further change at 24 months after surgery. CONCLUSIONS: Even though parameters of obesity, including BMI and body composition, plateau, the benefits of bariatric surgery on systemic metabolism and left ventricular mass are sustained. We propose that the progressive decrease of left ventricular mass after weight loss surgery is regulated by neurohumoral factors, and may contribute to improved long-term survival

Reproducibility of left ventricular mass measurements by two-dimensional and M-mode echocardiography

AbstractBoth two-dimensional and M-mode echocardiography provide accurate estimates of left ventricular mass. However, their reproducibility in serial studies has not been compared, although this issue is critical to evaluation of regression of hypertrophy. To determine which technique provides more reproducible estimates of left ventricular mass, three serial studies were performed prospectively in each of eight normal adults over 5 months. Both two-dimensional and M-mode echocardiograms were obtained at each of these 24 studies. Measurements were performed by two independent observers who did not know patient identity. For the two-dimensional method, left ventricular mass was determined with use of a computer light-pen system and the truncated ellipsoid formula. For the M-mode method, mass was calculated from Penn convention measurements with use of the cube formula.At study 1 the group mean left ventricular mass by two-dimensional echocardiography (115 ± 20 g) did not differ from that by M-mode study (127± 37 g, p = NS). However, serial estimates of left ventricular mass were more reproducible by two-dimensional echocardiography. The mean difference among the three serial two-dimensional studies in each individual was 4.8 ± 4 g (4.2 ± 3%) by the two-dimensional method, but was 18.5 ± 13 g (14.9 ± 10%) by the M-mode method (p = 0.01). Interobserver results for left ventricular mass by two-dimensional echocardiography correlated closely (r = 0.95, n = 24, p < 0.001).The superior reproducibility of two-dimensional echocardiographic estimates of left ventricular mass in normal adults supports the use of two-dimensional echocardiography when serial studies are to be performed

Aortic Calcification and Femoral Bone Density Are Independently Associated with Left Ventricular Mass in Patients with Chronic Kidney Disease

Background Vascular calcification and reduced bone density are prevalent in chronic kidney disease and linked to increased cardiovascular risk. The mechanism is unknown. We assessed the relationship between vascular calcification, femoral bone density and left ventricular mass in patients with stage 3 non-diabetic chronic kidney disease in a cross-sectional observational study. Methodology and Principal Findings A total of 120 patients were recruited (54% male, mean age 55±14 years, mean glomerular filtration rate 50±13 ml/min/1.73 m2). Abdominal aortic calcification was assessed using lateral lumbar spine radiography and was present in 48%. Mean femoral Z-score measured using dual energy x-ray absorptiometry was 0.60±1.06. Cardiovascular magnetic resonance imaging was used to determine left ventricular mass. One patient had left ventricular hypertrophy. Subjects with aortic calcification had higher left ventricular mass compared to those without (56±16 vs. 48±12 g/m2, P = 0.002), as did patients with femoral Z-scores below zero (56±15 vs. 49±13 g/m2, P = 0.01). In univariate analysis presence of aortic calcification correlated with left ventricular mass (r = 0.32, P = 0.001); mean femoral Z-score inversely correlated with left ventricular mass (r = −0.28, P = 0.004). In a multivariate regression model that included presence of aortic calcification, mean femoral Z-score, gender and 24-hour systolic blood pressure, 46% of the variability in left ventricular mass was explained (P<0.001). Conclusions In patients with stage 3 non-diabetic chronic kidney disease, lower mean femoral Z-score and presence of aortic calcification are independently associated with increased left ventricular mass. Further research exploring the pathophysiology that underlies these relationships is warranted

Importance of obesity, race and age to the cardiac structural and functional effects of hypertension

AbstractObjectives. The purpose of this study was to determine the effects of obesity and its interaction with age, race and the magnitude of blood pressure elevation in a large cohort of patients with mild to moderate hypertension and a high prevalence of left ventricular hypertrophy.Background. Obesity, race and age each have important effects on the incidence and severity of hypertension and may contribute to the effects of blood pressure elevation on the cardiac manifestations of hypertension.Methods. Left ventricular structure and function were assessed with two-dimensional targeted M-mode echocardiography in 692 men with mild to moderate hypertension (average blood pressure 153/100 mm Hg), and the data were compared in relation to obesity (determined from body mass index), age, race, blood pressure, physical activity, plasma renin activity, urinary sodium excretion, hematocrit, heart rate and serum lipids.Results. Left ventricular hypertrophy was common (630% with increased left ventricular mass, 22% with left ventricular hypertrophy on the electrocardiogram [ECG]). On multivariable regression analysis, body mass index was the strongest predictor of left ventricular mass and magnified the slope relation of blood pressure to left ventricular mass. Despite a greater prevalence of ECG left ventricular hypertrophy in blacks (31%) than in whites (10%), left ventricular mass and echocardiographic prevalence of left ventricular hypertrophy did not differ by race. However, septal, posterior left ventricular and relative wall thickness were greater in black than in white men.Conclusions. Obesity is the strongest clinical predictor of left ventricular mass and left ventricular hypertrophy la men, even in those with mild to moderate hypertension of sufficient severity to be associated with a high prevalence of left ventricular hypertrophy. Moreover, independent effects of systolic blood pressure on left ventricular mass an amplified by obesity. Although race does not affect left ventricular mass or the prevalence of left ventricular hypertrophy, black race is associated with greater relative wall thickness, itself a predictor of unfavorable cardiovascular outcome

Leptin, blood pressure, and left ventricular mass in obese adolescents

Background Obesity is characterized by an excessive accumulation of body fat and has become a major health problem in industrialized societies especially with regards to heart disease. Adipose tissue derived hormone (leptin) can cause obesity. Leptin acts to reduce food consumption and enhance energy expenditure. Objective To assess for a relationship between leptin, blood pressure, and left ventricular mass in obese adolescents. Methods This was a cross-sectional study conducted from November 2011 to April 2012 in Prof. Dr. RD. Kandou Hospital. This study included obese and healthy adolescents aged 13-18 years who attended school in Tuminting District ofManado. Each subject underwent measurements of body mass index (BMI), boold pressure, and plasma leptin level. Correlation regression test was used for data analysis. Results were considered to be statistically significant if P values < 0.05. Results There was a significant relationship between leptin and left ventricular mass (r=-0.467; P=0.006), as well as leptin and systolic blood pressure (r=-0.366; P=0.028), but not between leptin and diastolic blood pressure (r=-0.261; P=0.09). We also found significant relationships between systolic blood pressure and left ventricular mass (r=0.724; P<0.001), and between diastolic blood pressure and left ventricular mass ( r=0.615; P< 0.001) in obese adolescents. Conclusion Higher leptin levels are associated with lower left ventricular mass and lower systolic blood pressure, but are not associated with diastolic blood pressure

Pulmonary Hyperinflation and Left Ventricular Mass

Background—Left ventricular (LV) mass is an important predictor of heart failure and cardiovascular mortality, yet determinants of LV mass are incompletely understood. Pulmonary hyperinflation in chronic obstructive pulmonary disease (COPD) may contribute to changes in intrathoracic pressure that increase LV wall stress. We therefore hypothesized that residual lung volume in COPD would be associated with greater LV mass. Methods and Results—The Multi-Ethnic Study of Atherosclerosis (MESA) COPD Study recruited smokers 50 to 79 years of age who were free of clinical cardiovascular disease. LV mass was measured by cardiac magnetic resonance. Pulmonary function testing was performed according to guidelines. Regression models were used to adjust for age, sex, body size, blood pressure, and other cardiac risk factors. Among 119 MESA COPD Study participants, the mean age was 69±6 years, 55% were male, and 65% had COPD, mostly of mild or moderate severity. Mean LV mass was 128±34 g. Residual lung volume was independently associated with greater LV mass (7.2 g per 1-SD increase in residual volume; 95% confidence interval, 2.2–12; P=0.004) and was similar in magnitude to that of systolic blood pressure (7.6 g per 1-SD increase in systolic blood pressure; 95% confidence interval, 4.3–11; P<0.001). Similar results were observed for the ratio of LV mass to end-diastolic volume (P=0.02) and with hyperinflation measured as residual volume to total lung capacity ratio (P=0.009). Conclusions—Pulmonary hyperinflation, as measured by residual lung volume or residual lung volume to total lung capacity ratio, is associated with greater LV mass