Assessment Of Left Ventricular Mass Research Articles

Abstract 9529: Effects of Sevelamer Carbonate on Arterial Stiffness and Left Ventricular Mass in Patients with Stage 3 Chronic Kidney Disease: Results of a Randomized Controlled Trial

Introduction: Serum phosphate independently predicts cardiovascular mortality in the general population and in chronic kidney disease (CKD), even when levels are in the normal range. Phosphate has been implicated in the development and progression of vascular calcification and increased arterial stiffness, which is a driver of structural heart disease. We hypothesised that the non-calcium-based phosphate binder sevelamer carbonate would reduce left ventricular (LV) mass, reduce arterial stiffness and improve LV systolic and diastolic function in patients with stage 3 non-diabetic CKD. Methods: This was a single-centre, randomised, double-blind, placebo-controlled trial (figure). All patients received sevelamer carbonate for four weeks before randomisation to sevelamer or placebo for a further 36 weeks. Cardiovascular magnetic resonance imaging and echocardiography were used to assess LV mass and systolic and diastolic function. Arterial stiffness was determined by carotid-femoral pulse wave velocity (PWV). Results: A total of 120 patients were recruited. Mean age was 55 ± 14 years with 55% male and mean glomerular filtration rate 50 ± 13ml/min/1.73m 2 . Mean baseline LV mass, function and volumes were normal. After 40 weeks there were no significant changes in LV mass (-1.0 ± 7.2 vs. -0.2 ± 6.6 grams, P =0.6), LV systolic and diastolic function or PWV between sevelamer and placebo groups (table). Despite regular monitoring only 56% of subjects took ≥80% of prescribed therapy. Conclusion: In patients with stage 3 non-diabetic CKD, 40 weeks of treatment with sevelamer carbonate did not improve LV mass, LV systolic and diastolic function, or arterial stiffness.

Comparative Assessment of 2-Dimensional Echocardiography vs Cardiac Magnetic Resonance Imaging in Measuring Left Ventricular Mass in Patients With and Without End-Stage Renal Disease

While echocardiography (ECHO)-measured left ventricular mass (LVM) predicts adverse cardiovascular events that are common in hemodialysis (HD) recipients, cardiac magnetic resonance imaging (CMR) is now considered the reference standard for determination of LVM. This study aimed to evaluate concordance between LVM measurements across ECHO and CMR among chronic HD recipients and matched controls. A single-centre, cross-sectional study of 41 chronic HD patients and 41 matched controls with normal kidney function was performed to compare LVM measurements and left ventricular hypertrophy (LVH) designation by ECHO and CMR. In both groups, ECHO, compared with CMR, overestimated LVM. Bland-Altman analysis demonstrated wider agreement limits in LVM measurements by ECHO and CMR in the chronic HD group (mean difference, 60.8 g; limits -23 g to 144.6 g) than in the group with normal renal function (mean difference, 51.4 g; limits -10.5 g to 113.3 g). LVH prevalence by ECHO and CMR in the chronic HD group was 37.5% and 22.5%, respectively, while 17.5% and 12.5% had LVH by ECHO and CMR, respectively, in the normal kidney function group. Intermodality agreement in the designation of LVH was modest in the chronic HD patients (κ = 0.42, P = 0.005) but strong (κ = 0.81, P < 0.001) in the patients with preserved kidney function. Agreement was strong in assessing LVH by ECHO and CMR only in those with normal kidney function. Our results suggest that the limitations of LVM measurement by ECHO may be more pronounced in patients receiving HD, and provide additional support for the use of CMR in research and clinical practice when rigourous assessment of LVM is essential.

Abstract 432: Race Differences in the Relationship between Urinary ET-1 and BP-related Target Organ Damage in Youth

The overall goal of this study was to determine race/ethnic differences in the associations between renal ET-1 and indices of blood pressure-related target organ damage in healthy adolescents. The subjects ranged in age between 15-19 years, had no history of any disease, and were not on any prescription medications. The 92 subjects consisted of 48 Caucasians (CA) and 44 African-Americans (AA). The two groups were similar with respect to height, weight, body mass index, blood pressure, ET-1), albumin excretion rate (AER), and left ventricular mass). Results: The CA’s were slightly older 17±1 v 16±1 (p=.02). The protocol was preceded by a 3 day self-selected sodium controlled diet of 250 mEq/day day which the subject picked up each day. The test day began with an echocardiogram for the assessment of left ventricular mass. Next, the subjects were seated for 60 minutes of rest during which the subjects consumed 200 ml of water. This was followed by the collection of a urine sample for the measurement of ET-1 and AER. Overall, ET-1 excretion was correlated with AER (r=.278), LV mass/ht 2.7 (r=.341), and systolic blood pressure (SBP; r=.365; p=.01 for each). The significant overall correlations were the result of significant correlations in AAs for AER (r=.344; p=.05), LV mass/ht 2.7 (r=.520; p=.01), and SBP (r=.645; p=.01) which were not apparent in CA’s. These findings suggest urinary ET-1 contributes to the development of BP-related target organ damage in AA youths prior to the development of increases in blood pressure.

Thyroid hormone within the normal range is associated with left ventricular mass in patients with hypertension

Thyroid hormone amplifies hypertrophy of cardiac myocytes. The heart is influenced by the minimal changes of thyroid hormone levels. We hypothesized that thyroid hormone within the normal reference range may be associated with left ventricular (LV) mass in hypertensive subjects. We performed echocardiography to assess LV mass indexed by body surface area (LVMI), and measured thyroid stimulating hormone (TSH), free triiodo-thyronine (fT3), free thyroxine (fT4), and brain natriuretic peptide (BNP) in 318 hypertensive patients without known thyroidal diseases. Glomerular filtration rate (GFR) was estimated using the MDRD formula. Relationship between each thyroid hormone and LVMI in hypertensive patients with euthyroidism were investigated using a multiple linear regression model entering age, gender, height, weight, GFR, log BNP, systolic BP, the use of more than 2 different types of antihypertensive medications, and HbA1c as covariates. Thyroid hormone and TSH levels were within the normal range in 293 patients. In these patients, fT3 (standard β = 0.13) and fT4 (standard β = 0.11) positively, and TSH (standard β = –0.15) inversely correlated with LVMI in the multiple linear regression model. Thyroid hormone may be associated with LV remodeling independent of renal and LV dysfunctions in hypertensive patients with euthyroidism.

Gender specific differences in left ventricular remodelling in obesity may explain differences in obesity related mortality

Summary Across both genders, obesity, in the absence of traditional cardiovascular risk factors, is characterized by concentric LV remodeling. Whereas males show predominantly concentric remodeling, females exhibit eccentric and concentric hypertrophy. This may explain the observed gender difference in obesity related cardiovascular mortality. Background Obesity related cardiovascular mortality, although elevated when compared to normal weight, is lower in females (♀ )t han males ( ♂ )a t every body mass index (BMI) level. Given the fact that males have less fat tissue than females at each BMI level, the reasons behind this trend are unlikely to be attributable to the effects of excess adiposity alone. As different patterns of left ventricular (LV) remodeling have been shown to have varying prognostic value, with concentric hypertrophy being more strongly predictive of cardiovascular mortality than eccentric hypertrophy, our aim was to investigate whether sex-specific differences in LV remodeling could provide an additional explanation for the observed gender difference in obesity related mortality. Methods 703 subjects (♀ n= 390, ♂ n=313) without identifiable cardiovascular risk factors, (BMI range 15.7-59.2 Kg/ M2) underwent cardiovascular magnetic resonance at 1.5 Tesla for the assessment of LV mass (g), enddiastolic volume (EDV; ml) and LV mass/volume ratio (LVM/VR).

Abstract 9196: Assessment of Left Ventricular Mass in Hypertrophic Cardiomyopathy Patients Bb Real-Time 3-Dimensional Echocardiography in Single-Beat Capture Image; Validation with Cardiac Magnetic Resonance Imaging

Background: Left ventricular (LV) mass is an important prognostic factor in hypertrophic cardiomyopathy (HCM). LV mass can be easily accessed by M-mode or 2D echocardiography; however it includes assumption and might be incorrect in LV with asymmetricity. Real time three dimensional echocardiography (RT3DE) has been introduced as an accurate method to assess the LV mass and recently, RT3DE by single beat capture with online analysis program has been introduced. We validated LV mass using new RT3DE technique compared to cardiac magnetic resonance (CMR). Method: Thirty six HCM patients were consecutively enrolled and 3 patients were excluded due to poor RT3DE images. All the patients underwent CMR and RT3DE within the same day. LV mass was derived from the following methods; the ASE formula (M-mode mass), truncated ellipsoid method by 2D echocardiography (2D mass) and RT3DE (RT3DE mass). RT3DE image was acquired using the SC2000 System. The LV mass data were compared with the LV mass analyzed by CMR. Results: Mean frame rate of RT3DE was 13.1±2.3 frame/second. Pearson's interclass coefficient (ICC) showed close correlation of RT3DE mass and CMR mass (r=0.92 and p&lt; 0.0001). However, M-mode mass and 2D mass had smaller ICC when compared with CMR (r=0.50, p=0.01 and r=0.78, p&lt;0.001) Bland-Altman analysis showed reasonable limits of agreement with small positive bias (15.1). Bias was greater in M-mode LV mass and 2D LV mass (-39.1 and 21.2) Conclusions: LV mass measured by single-beat captured RT3DE is a feasible and accurate method in HCM patients. Because LV shape is asymmetrical in many subjects with HCM, LV mass derived from 2D or M-mode is much more inaccurate than symmetrical LVs. Correct assessment of LV mass using single-beat captured RT3DE will be useful in HCM patients in real clinical practice.

Cardiac magnetic resonance assessment of left ventricular mass in autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) is associated with a substantial cardiovascular disease burden including early onset hypertension, intracranial aneurysms, and left ventricular hypertrophy (LVH). A 41% prevalence of LVH has been reported in ADPKD, using echocardiographic assessment of LV mass (LVM). The HALT PKD study was designed to assess the effect of intensive angiotensin blockade on progression of total kidney volume and LVM. Measurements of LVM were performed using cardiac magnetic resonance (MR). Five hundred forty-three hypertensive patients with GFR >60 ml/min per 1.73 m(2) underwent MR assessment of LVM at baseline. LVM was adjusted for body surface area and expressed as LVM index (LVMI; g/m(2)). Baseline BP was 125.1 ± 14.5/79.3 ± 11.6 mmHg. Average duration of hypertension was 5.79 years. Prior use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was present in 59.5% of patients. The prevalence of LVH assessed using nonindexed LVM (g) was 3.9% (n = 21, eight men and 13 women) and 0.93% (n = 5, one man and four women) using LVMI (g/m(2)). In exploratory analyses, the prevalence of LVH using LVM indexed to H(2.7), and the allometric index ppLVmass(HW), ranged from 0.74% to 2.23% (n = 4 to 12). Multivariate regression showed significant direct associations of LVMI with systolic BP, serum creatinine, and albuminuria; significant inverse associations with LVMI were found with age and female gender. The prevalence of LVH in hypertensive ADPKD patients <50 years of age with short duration of hypertension, and prior use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers is low. Early BP intervention in ADPKD may have decreased LVH and may potentially decrease cardiovascular mortality.

Left ventricular hypertrophy

Left ventricular hypertrophy

54 Can microalbuminuria identify silent "pancardiac" target organ damage in a non-diabetic primary prevention population?

Background Microalbuminuria is associated with increased cardiovascular mortality and is a marker of generalised vascular dysfunction. We sought to investigate whether micoalbuminuria identified the presence of silent “pancardiac” target organ damage (TOD) ie, left ventricular hypertrophy (LVH), systolic dysfunction (LVSD), diastolic dysfunction (LVDD), left atrial enlargement (LAE) or silent myocardial ischaemia in a non-diabetic primary prevention population. Methods Two hundred and sixty-three asymptomatic individuals without diabetes or previous cardiovascular disease on primary preventive therapy were prospectively recruited. Each participant underwent a comprehensive echocardiographic examination for the assessment of LV mass, LV systolic and diastolic function, and left atrial volume while the presence of inducible ischaemia was assessed by dobutamine stress echocardiography or dipyridamole myocardial perfusion imaging. A spot urine sample was analysed for microalbuminuria and urinary creatinine by a trained laboratory technician blinded to clinical or echocardiographic data. Microalbuminuria was defined as urinary albumin to creatinine ratio of ≥2.5 mg/mmol in males and ≥3.5 mg/mmol in females. Results Out of 263 participants (Mean age 64±6.3 years, 57% males) 89 (33.8%) had evidence of silent cardiac TOD (29.7% LVH, 16.7% LAE, 17.1% LVDD, 6.8% LVSD and 6.1% Ischaemia). The prevalence of cardiac TOD was significantly higher (53% vs 29%, p=0.002) among those with microalbuminuria than those without. In multivariate analysis adjusted for age, gender, hypertension and dyslipidemia, presence of microalbuminuria was an independent predictor of cardiac TOD with an adjusted HR of 2.54 (95% CI, 1.2 to 4.4, p=0.005). The utility of UACR in discriminating between those with or without cardiac TOD was assessed by receiver operating characteristic analysis but the area under curve was only 0.61±0.04, p=0.003. Conclusion Microalbuminuria is an independent predictor of silent “pancardiac” target organ damage in a non-diabetic primary prevention population. Presence of microalbuminuria may help to identify those primary prevention patients who are at a particularly higher risk.

Early cardiac abnormalities and increased C-reactive protein levels in a cohort of children with sleep disordered breathing

This study aims to evaluate left ventricular (LV) structure and function and inflammation in a paediatric population with sleep disordered breathing (SDB) and in control subjects. Forty-nine children with SDB and 21 healthy, age-matched subjects were enrolled. The diagnosis of obstructive sleep apnoea syndrome (OSAS) was confirmed by the laboratory polysomnography, showing an obstructive apnoea/hypopnoea index of more than one per hour, according to the criteria of the American Academy of Sleep Medicine and modified for paediatric population. Fasting blood samples for the biochemical evaluation (including high-sensitivity C-reactive protein (hsCRP) were drawn in the morning, after the polysomnographic examination in all patients with SDB and in the control group. All children underwent a two-dimensional colour Doppler cardiac examination with LV mass assessment and systolic and diastolic function evaluation. Higher hsCRP levels were observed in subjects with OSAS than in children with primary snoring and in controls (0.8 ± 0.7 vs 0.3 ± 0.1 ng/dl, p = 0.001, and 0.4 ± 0.2 ng/dl, p = 0.01, respectively). The LV diastolic dysfunction was significantly more frequent in patients with severe OSAS and higher hsCRP levels than in control group. This study shows that OSAS in children is associated with higher LV mass, early LV diastolic dysfunction and a pro-inflammatory state (high CRP levels). These findings might help to explain the higher incidence of cardiovascular morbidity in patients with OSAS.

Subclinical organ damage in perimenopausal women with essential hypertension

Hypertension and its complications are more common in postmenopausal women than before menopause. However, whether this is due to the effect of age or menopause is still unknown. The aim of the study was to assess the effect of menopause on blood pressure (BP), left ventricular and vascular structure and function, as well as kidney function in perimenopausal women. The study involved 192 women aged 40 to 60 years (mean age, 51.73 ±1.82 years), including 152 with newly diagnosed essential hypertension and 40 normotensive controls matched for age. In all subjects, 24-hour BP monitoring was performed. Echocardiographic examination with the assessment of left ventricular mass (LVM) and systolic and diastolic function,as well as carotid ultrasound with the measurement of intima-media thickness (IMT) in the common carotid artery were performed. Carotid-femoral pulse wave velocity (PWV) was measured. Glomerular filtration rate (eGFR) was calculated and urinary albumin-creatinine ratio (UACR) was measured. The study group was divided according to hypertension and menopausal status into 4 subgroups: normotensive premenopausal, normotensive postmenopausal, hypertensive premenopausal, and hypertensive postmenopausal women. Menopause did not affect BP or LVM. Differences in LVM between pre- and postmenopausal women were dependent on age and the body mass index. Hypertensive postmenopausal compared with hypertensive premenopausal women had significantly higher IMT (0.72 ±0.34 mm vs. 0.59 ±0.30 mm, P = 0.001) and a lower ratio of early to late mitral inflow velocity (E/A, 1.04 ±0.32 vs. 1.32 ±0.33, P = 0.01). PWV was higher in hypertensives compared to controls (9.7 ±1.6 m/s vs. 8.4 ±1.2 m/s, P = 0.001), without differences between premenopausal and postmenopausal women. Menopause did not affect eGFR and UACR either in the hypertensive or normotensive group. Left ventricular diastolic function and carotid IMT are independently associated with menopausal status in both normo- and hypertensive women. Menopause per se did not affect BP in the examined group.

Low Cardiovascular Risk Is Associated with Favorable Left Ventricular Mass, Left Ventricular Relative Wall Thickness, and Left Atrial Size: The CARDIA Study

Echocardiographic measures of left ventricular (LV) mass and relative wall thickness and left atrial (LA) size predict future cardiovascular morbidity and mortality. The aim of this study was to compare young adults with low cardiovascular risk (body mass index, 18.5-24.9 kg/m(2); blood pressure < 120/80 mmHg; no tobacco use, no diabetes, and physical fitness) with those without these characteristics with regard to LV mass and relative wall thickness and LA size, to determine the protective effect of a healthy lifestyle on the development of these characteristics. Cross-sectional assessment of 4059 black and white men and women aged 23 to 35 years in the Coronary Artery Risk Development in Young Adults (CARDIA) study at the year 5-examination, when risk factors were measured, and echocardiography to assess LV mass and relative wall thickness were performed. Physical fitness was measured at baseline using a symptom-limited maximal treadmill test. All other covariates were measured concurrently with echocardiography. Gender, body mass index, and systolic blood pressure were associated with LV mass and relative wall thickness and LA size in multivariate models. Additional correlates of LV mass/height(2.7) ratio were tobacco use, resting heart rate (inverse), self-reported physical activity, gender (male higher), and age. Age was associated with LV relative wall thickness but not other measures of LV size. Additional correlates of LA diameter/height ratio were tobacco use, resting heart rate (inverse), serum glucose, and self-reported physical activity. Seven hundred ninety of 4059 subjects (19%) were classified as having low risk; black race was less likely in the low-risk group. Those with low risk had lower LV mass/height(2.7) ratios (32.0 vs 34.6 g/m(2.7), P < .0001), better LV relative wall thickness (0.33 vs 0.35, P < .0001), and lower LA diameter/height ratios (2.02 vs 2.08 cm/m, P < .01). A low cardiovascular risk profile in young adulthood is associated with more favorable LV mass, LV relative wall thickness, and LA size. This may be one mechanism of lifestyle protection against cardiovascular morbidity and mortality.

075 Endothelial function during adolescence predicts left ventricular mass in early adult life

Background Left ventricular mass is a powerful independent predictor of mortality and morbidity in adults. Endothelial function may influence cause cardiac hypertrophy through modification of myocardial biology or arterial stiffness. We sought to determine whether endothelial dysfunction during adolescence and early adult life is independently associated with increased left ventricular mass. Methods Thirty healthy normotensive subjects (43% males) underwent assessment of endothelial function by flow mediated dilatation (FMD) of the brachial artery at the age of 15 years using ultrasound. Subjects were followed up at the age of 23–26 years for assessment of left ventricular mass (LVM) by cardiovascular magnetic resonance imaging (Siemens 1.5 T Sonata scanner), adjusted for body surface area (LVMI), and repeated FMD measurements using the same methods. Cardiovascular risk factors including body size, blood pressure, lipid profile, glucose tolerance and smoking were assessed at both time points. Results FMD in early adulthood was significantly related to LVMI (r −0.55, p 0.002). FMD at the age 15 was similarly inversely associated with LVMI 10 years later (r −0.41, p 0.02) with greater endothelial responses related to reduced left ventricular mass. Those with FMD consistently above the mean at both age 15 and 25 had significantly lower LVMI compared to those with FMD below the mean (58 g/m2 vs 68 g/m2 p Conclusion Endothelial responses during adolescence predict left ventricular mass 10 years later and those with consistently high endothelial responses over this time period have the lowest left ventricular mass. Endothelial function may influence cardiac structure in young people in the absence of classic risk factors such as hypertension and obesity.

Current cardiac imaging techniques for detection of left ventricular mass

Estimation of left ventricular (LV) mass has both prognostic and therapeutic value independent of traditional risk factors. Unfortunately, LV mass evaluation has been underestimated in clinical practice. Assessment of LV mass can be performed by a number of imaging modalities. Despite inherent limitations, conventional echocardiography has fundamentally been established as most widely used diagnostic tool. 3-dimensional echocardiography (3DE) is now feasible, fast and accurate for LV mass evaluation. 3DE is also superior to conventional echocardiography in terms of LV mass assessment, especially in patients with abnormal LV geometry. Cardiovascular magnetic resonance (CMR) and cardiovascular computed tomography (CCT) are currently performed for LV mass assessment and also do not depend on cardiac geometry and display 3-dimensional data, as well. Therefore, CMR is being increasingly employed and is at the present standard of reference in the clinical setting. Although each method demonstrates advantages over another, there are also disadvantages to receive attention. Diagnostic accuracy of methods will also be increased with the introduction of more advanced systems. It is also likely that in the coming years new and more accurate diagnostic tests will become available. In particular, CMR and CCT have been intersecting hot topic between cardiology and radiology clinics. Thus, good communication and collaboration between two specialties is required for selection of an appropriate test.

Controversies in the Assessment of Left Ventricular Mass

With the recognition that left ventricular (LV) mass (LVM) contributed to the prediction of cardiovascular morbidity and mortality, independent of conventional risk factors, including those that partially determined LVM (body size, blood pressure, and tobacco), interest in better understanding the clinical and epidemiological roles of LVM measurement accelerated.1 Over the last 2 decades, substantial progress has been made in this regard. For example, clinical trials have been designed to demonstrate the independent contribution of pharmacological LVM reduction, beyond blood pressure reduction in hypertensive patients, to improvement in cardiovascular outcomes.2 The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents incorporates LVM measurement in its evaluation algorithm with intensification of antihypertensive management recommended in the presence of LV hypertrophy.3 Despite this success, the role of LVM in clinical practice has not been firmly established. There are a number of controversies surrounding the measurement of LVM. These include the fact that LVM is principally determined by body size so that some component of LVM is adaptive rather than pathological, that LVM can be increased by healthful behaviors (eg, physical training) and cardiovascular risk factors, that there are significant problems in standardizing echocardiographic measurement of LVM by echocardiography across laboratories, that MRI provides more accurate measurement of LVM than echocardiography, and that a firm definition of LV hypertrophy based on the calculation of heart weight has not been established by consensus. Historically, one method for overcoming these several limitations has been indexing LVM to body size. Most commonly this is done by dividing LVM by body surface area or height elevated to some power, usually height2 or height2.7.1,4,5⇓⇓ Driving these analyses has been a concern for accommodating the strong relationship of LVM to lean body mass (and …

Left ventricular mass assessment by CMR; how to define the optimal index

Cardiac magnetic resonance imaging (CMR) is an accurate and reliable means of evaluating cardiac morphology, and therefore very well suited for identifying and characterizing patients with various manifestations of left ventricular hypertrophy (LVH) [1, 2]. For instance, CMR can resolve the question whether training-induced LVH in athletes is a physiological rather than a pathophysiological phenomenon [3–5]. A meta-analysis, involving 59 studies and 1451 athletes (both endurance-trained and strength-trained athletes), showed that the athlete’s heart demonstrated normal systolic and diastolic cardiac function, implying that training-induced LVH in athletes is predominantly a physiological phenomenon [6–10]. However, in pathophysiological LVH, such as in patients with hypertension and hypertrophic cardiomyopathy, the presence of LVH portends a poor prognosis whereby there is a negative relation between prognosis and the stage of LVH [11–21]. On the other side of the spectrum, a significant decrease in LV mass, such as in patients following myocardial infarction, may also be associated with a poor prognosis as these patients are prone to the development of heart failure [22–39]. Within the latest 10 years, research in LVH as cardiac target organ damage has uncovered its prognostic importance. Several studies have indicated that adequate pharmacological treatment, such as beta-blocking agents, ACE-inhibition, and angiotensin II receptor blockade, is very effective in reducing LVH [40–47]. In addition, reduction of LV mass is associated with substantial and significant reduction of cardiovascular morbidity and mortality [46]. Hypertension is strongly associated with increased risk of subsequent heart failure, and meta-analysis data have suggested that reduction in blood pressure and LV mass is associated with very substantial reductions in incident heart failure [47, 48]. Consequently, LV mass should be accurately calculated as mass size may have important clinical implications [49–53]. Generally, LV mass divided by body surface area (BSA) has been used clinically to account for body size, but its validity is not fully clear. Methods to index LV mass for body size have not been investigated using CMR. In the current issue of the International Journal of Cardiovascular Imaging, Brumback et al. [54] sought for new accurate indices of LV mass. The main purpose of the study was to develop allometric indices for LV mass measured by CMR and to compare estimates of the prevalence and predictive value of LVH defined new allometric indices. Two indices were derived from linear regression models fit to CMR data from the reference sample of the Multi-Ethnic Study of Atherosclerosis (MESA) participants. The indices are called allometric as they are proportional to LV mass divided by a body size variable raised to a scalar exponent. The authors evaluated 5,004 participants from the MESA trial with CMR measurements of LV mass without signs of clinical cardiovascular disease at baseline who were followed for a median of 4.1 years. The new indices and limits for hypertrophy (95th percentile) were finally derived from 822 normal-weight, normotensive, non-diabetic subjects. There were 107 events consisting of coronary heart disease or stroke. The estimated prevalence of LVH at baseline and hazard ratio for events associated with LVH were 8% and 2.4 with the new allometric height-weight index, 11% and 2.2 with LV mass/BSA, 23–24% and 2.0–2.1 with height indices, and 20% and 1.7 with un-indexed LV mass. A statistically significant difference was detected between the hazard ratios based on the new height-weight index and un-indexed LV mass. It was concluded that the prevalence of hypertrophy is higher for indices that do not account for weight. The predictive value of hypertrophy was significantly better with the new allometric height-weight index than with un-indexed LV mass and may be better than indices without weight. The current study is clinically important since an evaluation of the most suitable indices for LV mass has not previously been performed using CMR. An indexed LV mass should be more predictive of a cardiovascular event than un-indexed LV mass. Therefore, the authors should be complimented for developing new allometric indices for CMR-derived LV mass with potential major implications in clinical practice.

Nocturnal blood pressure and progression to end-stage renal disease or death in nondiabetic chronic kidney disease stages 3 and 4

The objective was to assess the role of office and ambulatory blood pressure (BP) on the development of end-stage renal disease (ESRD) in nondiabetic chronic renal failure. Seventy-nine patients [mean age 57 (standard deviation 11) years, 47 men, BMI 28 (4), office BP 151 (25)/92 (14) mmHg, estimated glomerular filtration rate 28 (14) ml/min per 1.73 m3] were included. The causes of renal disease were nephrosclerosis (n = 33), glomerulonephritis (n = 19), interstitial (n = 12) and others (n = 15). The average follow-up was 44 months (range 9-72 months). The primary outcome was a composite of death, from any cause, or the development of ESRD that require initiation of renal replacement therapy. In all patients, 24-h ambulatory BP monitoring and left ventricular mass assessment were performed at the beginning of the study. During the follow-up period, 41 (52%) patients progressed to ESRD. In addition, nine (11%) patients died, four before reaching ESRD. Then the combined endpoint rate, 45 patients, was 6.3/100 patients per year. In a multivariate Cox proportional hazard model, which includes age, sex, angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker status and the estimated glomerular filtration rate, office BP still provided no further prognostic information on risk of the primary outcome. In addition, daytime ambulatory BP and the no-dipper status did not further discriminate in terms of predicting endpoint. Nocturnal SBP more than 130 mmHg was associated with a doubling of risk [heart rate 2.07 (95% confidence interval 1.01-4.25)] on top of the other significant factors. Glomerular filtration rate and nocturnal SBP values, but not nondipper pattern, were associated with risk to develop ESRD.

Hypertensive Heart Disease – Diagnosis, Prognostic Value and Changes During Antihypertensive Treatment, Left Ventricular Structure and Function

Hypertensive heart disease is prevalent and during the last decade it has been determined that patients with left ventricular (LV) hypertrophy have increased cardiovascular morbidity and mortality. However, many have doubted the effectiveness of LV mass assessment because it is difficult to measure, and there were no data showing a relation between reduced LV mass and improvement in LV systolic and diastolic function and improved cardiovascular outcome. However, improvements to echocardiographic equipment have made it possible to measure LV mass with the same precision as for aortic valve replacement. Reduction of LV hypertrophy, independent of the simultaneous blood pressure reduction, is associated with large improvements in cardiovascular morbidity and mortality. A reduction in LV mass by 25g/m² leads to a 34% reduction in cardiovascular mortality. Time-varying analyses showed 66% associated risk reduction in cardiovascular mortality if patients with LV hypertrophy were treated to limits of LV mass. Hypertension causes impaired LV systolic function by increased afterload and LV hypertrophy. Normal estimations of LV ejection fraction tend to overestimate LV systolic function; however, improvement of LV systolic function by antihypertensive treatment leads to an improvement of cardiovascular morbidity and mortality. Furthermore, even though there is significant improvement in LV diastolic function during antihypertensive treatment, this occurs more slowly compared with the treatment effects on LV systolic function, and diastolic function does not, compared with LV systolic function, translate into improvement in cardiovascular morbidity and mortality. The perspective of finding cardiac target organ damage is used not only to classify the cardiovascular risk of patients, but also to indicate to the treating physician that specific treatment is needed.

Relation of left ventricular mass and concentric remodeling to extent of coronary artery disease by computed tomography in patients without left ventricular hypertrophy: ROMICAT study.

Cardiac computed tomography allows for simultaneous assessment of left ventricular mass (LVM) and coronary artery disease (CAD). We aimed to determine whether LVM, LVM index (LVMi), and the left ventricular geometric pattern of concentric remodeling are associated with the extent of CAD in patients without left ventricular hypertrophy. In 348 patients from the Rule Out Myocardial Infarction Using Computer Assisted Tomography trial, 64-slice computed tomography was performed and LVM measured at end-diastole. We used three LVM indexation criteria to obtain three cohorts: LVM indexed to body surface area by echocardiography (n = 337) and computed tomography criteria (n = 325), and by height (n = 326). The cohorts were subdivided into concentric remodeling and normal geometry. Extent of coronary plaque was classified based on a 17-segment model, treated as a continuous variable, and stratified into three groups: zero segment, one to four segments, and more than four segments. Patients with more than four segments of coronary plaque had higher LVM (Delta12.8-15.1 g) and LVMi (Delta4.0-5.5 g/m and Delta2.2 g/m) than those without CAD (all P < or = 0.03). After multivariable adjustment, LVM and LVMi remained independent predictors of extent of coronary plaque, with 0.27-0.29 segments more plaque per 20 g increase of LVM (all P = 0.02), 0.32-0.34 segments more plaque per 10 g/m increase of LVMi (both P = 0.02), and 0.80 segments more plaque per 10 g/m increase of LVMi (P = 0.008). Concentric remodeling patients had 1.1-1.3 segments more plaque than those with normal geometry (all P < or = 0.05). Patients with more than four segments of plaque had two-fold increase in odds (all P < or = 0.05) of having concentric remodeling as compared with those without CAD. Increased LVM, LVMi, and concentric remodeling are associated with a greater degree of coronary plaque burden in patients without left ventricular hypertrophy. These findings could provide an indication to intensify medical therapy in patients with subclinical CAD and hypertension.

Effect of the Direct Renin Inhibitor Aliskiren, the Angiotensin Receptor Blocker Losartan, or Both on Left Ventricular Mass in Patients With Hypertension and Left Ventricular Hypertrophy

Left ventricular (LV) hypertrophy, a marker of cardiac end-organ damage, is associated with an increased risk of cardiovascular morbidity and mortality. Inhibitors of the renin-angiotensin-aldosterone system may reduce LV mass to a greater extent than other antihypertensive agents. We compared the effect of aliskiren, the first orally active direct renin inhibitor, the angiotensin-receptor blocker losartan, and their combination on the reduction of LV mass in hypertensive patients. We randomized 465 patients with hypertension, increased ventricular wall thickness, and body mass index >25 kg/m(2) to receive aliskiren 300 mg, losartan 100 mg, or their combination daily for 9 months. Patients were treated to standard blood pressure targets with add-on therapy, excluding other inhibitors of the renin-angiotensin-aldosterone system and beta-blockers. Patients underwent cardiovascular magnetic resonance imaging for assessment of LV mass at baseline and at study completion. The primary objective was to compare change in LV mass index from baseline to follow-up in the combination and losartan arms; the secondary objective was to determine whether aliskiren was noninferior to losartan in reducing LV mass index from baseline to follow-up. Systolic and diastolic blood pressures were reduced similarly in all treatment groups (6.5+/-14.9/3.8+/-10.1 mm Hg in the aliskiren group; 5.5+/-15.6/3.7+/-10.7 mm Hg in the losartan group; 6.6+/-16.6/4.6+/-10.5 mm Hg in the combination arm; P<0.0001 within groups, P=0.81 between groups). LV mass index was reduced significantly from baseline in all treatment groups (4.9-, 4.8-, and 5.8 g/m(2) reductions in the aliskiren, losartan, and combination arms, respectively; P<0.0001 for all treatment groups). The reduction in LV mass index in the combination group was not significantly different from that with losartan alone (P=0.52). Aliskiren was as effective as losartan in reducing LV mass index (P<0.0001 for noninferiority). Safety and tolerability were similar across all treatment groups. Aliskiren was as effective as losartan in promoting LV mass regression. Reduction in LV mass with the combination of aliskiren plus losartan was not significantly different from that with losartan monotherapy, independent of blood pressure lowering. These findings suggest that aliskiren was as effective as an angiotensin receptor blocker in attenuating this measure of myocardial end-organ damage in hypertensive patients with LV hypertrophy.