Echocardiographic Measurements Of Left Ventricular Mass Research Articles

Total arterial compliance, estimated by a novel method, is better related to left ventricular mass compared to aortic pulse wave velocity: The SAFAR study

ABSTRACTAim: The investigation of the association between total arterial compliance (CT)—estimated by a novel technique—with left ventricular mass (LVM) and hypertrophy (LVH). Our hypothesis was that CT may be better related to LVM compared to the gold-standard regional aortic stiffness. Within the frame of the ongoing cross-sectional study “SAFAR,” 226 subjects with established hypertension or with suspected hypertension underwent blood pressure (BP) assessment, carotid-to-femoral pulse wave velocity (cf-PWV), and echocardiographic measurement of LVM. LVM index (LVMI) was calculated by the ratio of LVM to body surface area. CT was estimated by a previously proposed and validated formula: CT = 36.7 /cf-PWV2 [ml/mmHg]. LVMI was related to age (r = 0.207, p = 0.002), systolic BP (r = 0.248, p < 0.001), diastolic BP (r = 0.139, p = 0.04), mean BP (r = 0.212, p = 0.002), pulse pressure (r = 0.212, p = 0.002), heart rate (r = −0.172, p = 0.011), cf-PWV (r = 0.268, p < 0.001), and CT (r = −0.317, p < 0.001). The highest correlation was observed for CT that was significantly stronger than the respective correlation of cf-PWV (p < 0.001). In multivariate analysis, CT was a stronger determinant, compared to cf-PWV, of LVMI and LVH. It remains to be further explored whether CT has also a superior prognostic value beyond and above local or regional (segmental) estimates of pulse wave velocity.

Comparison of Three-Dimensional Echocardiographic Findings to Those of Magnetic Resonance Imaging for Determination of Left Ventricular Mass in Patients With Ischemic and Non-Ischemic Cardiomyopathy

The standard echocardiographic evaluation of left ventricular (LV) mass, particularly in ischemic cardiomyopathy (IC) is challenging because it is based on geometric assumptions. The aim of this study was to assess the accuracy of LV mass calculation using echocardiographic modalities compared with cardiac magnetic resonance (CMR) in IC and in nonischemic cardiomyopathy (non-IC). Echocardiography was performed in 104 patients (mean age 55 ± 15 years) referred for CMR: 63 with IC and 41 with non-IC. CMR, M-mode echocardiography, 2-dimensional echocardiography, and 3-dimensional echocardiography (3DE) were analyzed using standard commercial tools to obtain LV mass. LV mass on 3DE showed a higher correlation with CMR than 2-dimensional echocardiography (r = 0.87 vs r = 0.70, p <0.001). M-mode echocardiography overestimated LV mass (bias +30%) and 2-dimensional echocardiography underestimated LV mass (bias -11%), whereas measurements on 3DE showed only minimal bias (-2%). LV mass on 3DE in non-IC showed a significantly higher correlation with CMR than in IC (r = 0.92 vs r = 0.84, z = 2.3, p <0.05). In non-IC, the mean difference was -2 g (-1% of the mean), with 95% limits of agreement of ±33 g (±19% of the mean). In IC, the mean difference was -7 g (-4% of the mean), with limits of agreement of ±56 g (±31% of the mean). There was a correlation between the absolute LV mass differences (3DE derived and CMR derived) and scar percentage (infarcted mass/total LV mass) using delayed-hyperenhancement images (r = 0.40, p <0.05). The net reclassification index with 3DE was +16% for concentric LV hypertrophy. In conclusion, the most accurate and reliable echocardiographic measurement of LV mass is 3DE, but underestimation and variability remain challenges in IC.

Correlation of Jumping Power with Commonly Used Muscle Function Tests and DXA Appendicular Lean Mass in Older Adults.

OBJECTIVESThe study investigated the relation of age with diabetes, obesity and hypertension on left ventricular mass (LVM).BACKGROUNDEpidemiological studies demonstrate a general rise of LVM with aging, but whether this phenomenon is independent or a function of coexisting diseases that accompany the aging process is unclear. Although obesity, hypertension and diabetes often coexist and increase in prevalence with age, studies of LVM in diabetics have been reported in mostly nonobese populations, and with little regard to the age-hypertension-obesity interactions and effects on LVM.METHODSWe prospectively measured LVM in 875 consecutive, mostly obese individuals (673 men, 202 women). Clinical data were obtained by chart review and clinical history. Echocardiographic measurements of LVM (American Society of Echocardiography criteria) were calculated using the Devereux formula and corrected for height2.7(LVM/Ht).RESULTSMean age was 49.3 ± 12.3 years, body mass index 33.3 ± 8.0 kg/m2, and LVM/Ht2.741.7 ± 13.4 g/m2.7. Of the total cohort, 673 patients were men, 519 obese, 228 hypertensive, and 52 diabetic. Of the 519 obese, 183 were hypertensive and 44 were diabetic (22 of those were hypertensive). Of the 228 hypertensives, 183 were obese and 26 were diabetic. On multivariate analysis, obesity (p = 0.0001), age (p = 0.0001), hypertension (p = 0.0003) and diabetes (p = 0.02) were all independently associated with LVM/Ht2.7. Obesity was the most potent independent predictor of LVM/Ht2.7, associated with an increase of 8.1 g/m2.7in LVM/Ht2.7. In diabetics, obesity had a synergistic effect on LVM/Ht2.7(p = 0.006), which was further amplified by age (p = 0.03).CONCLUSIONSAge, obesity, hypertension and diabetes are all independent determinants of LVM. The magnitude of the effect of diabetes on LVM is mainly consequent to a significant interaction of diabetes with obesity and age.

Associations between cardiac target organ damage and microvascular dysfunction: the role of blood pressure

Microvascular dysfunction may be an early precursor of cardiovascular disease (CVD). Increased left ventricular mass (LVM), concentric left ventricular remodelling and increased left atrial size are the factors that could predict future CVD. We investigated whether microvascular dysfunction was associated with these cardiac measures. Laser Doppler fluximetry of skin vessels was used to study associations with risk factors and echocardiographic measurements of LVM, relative wall thickness (RWT), and left atrial size in 305 people (aged 40-65 years; 117 with type 2 diabetes). Flow in response to a 3-min arterial occlusion was measured. Postischaemic peak flow responses were categorized into three distinct groups: slow rise to peak (normal), nondominant early peak group (mildly abnormal) and a dominant early peak (abnormal). Those with a dominant early peak had higher blood pressure (P = 0.001), weight (P = 0.001), fasting glucose (P = 0.001) and prevalence of diabetes (P = 0.02). LVM (P = 0.01), RWT (P < 0.001) and left atrial size (P < 0.001) were greater with worsening postischaemic peak flow responses. Differences in LVM between postischaemic response groups were accounted for by blood pressure (BP). However, differences in BP and other CVD risk factors did not account for the greater RWT and left atrial size observed in the more adverse peak response groups [geometric mean of RWT [95% confidence interval (CI)] 0.40 (0.38-0.41) vs. 0.41 (0.40-0.42) vs. 0.43 (0.41-0.45), P = 0.007; left atrial size 36.1 (35.4-36.1) vs. 37.4 (36.8-38.0) vs. 38.7 (37.5-40.0), P = 0.002 for normal vs. mildly abnormal vs. abnormal respectively]. An abnormal microcirculatory cutaneous peak flow response following ischaemia is associated with adverse cardiac remodelling, independent of CVD risk factors including blood pressure.

Impact of the time rate of blood pressure variation on left ventricular mass

Blood pressure (BP) changes are steeper in hypertensive than in normotensive individuals, whereas an increased rate of BP fluctuations is associated with medial hypertrophy of the carotid arteries. We evaluated the association between the rate of BP variation derived from ambulatory blood pressure monitoring (ABPM) data analysis and left ventricular mass (LVM). ABPM and echocardiographic measurements of LVM were performed in 365 normotensive, 185 white-coat hypertensive (WCH) and 448 uncomplicated hypertensive individuals. The daytime and night-time rate of systolic blood pressure (SBP) and diastolic BP variation were significantly higher in hypertensive than in normotensive (P < 0.001) and WCH (P < 0.05) individuals. In the entire study population multiple linear regression models revealed independent determinants of LVM in the following rank order: body mass index (beta + 0.266, P < 0.001), daytime SBP (beta + 0.264, P < 0.001), male sex (beta +0.220, P < 0.001), age (beta + 0.203, P < 0.001), daytime heart rate (HR; beta - 0.191, P < 0.001), daytime rate of SBP variation (beta + 0.167, P < 0.001), and SBP dipping (beta - 0.132, P < 0.001). A 0.1 mmHg/min increase in the daytime rate of SBP variation correlated with an increment of 7.087 g (95% confidence interval 4.775-9.399) in the LVM. The addition of the daytime rate of SBP variation in the multiple regression model for the prediction of LVM significantly increased the adjusted model R [R change 0.024 (2.4%); P for change < 0.001]. Steeper BP variations may produce a greater stress on the left ventricular wall and may have an additive role to body habitus, BP and HR levels in the detection of cardiac hypertrophy. Target-organ damage in hypertensive patients, in addition to BP levels, dipping status and BP variability, may also be related to a steeper rate of BP oscillations.

Computer systems analysis of spaceflight induced changes in left ventricular mass

Circulatory adaptations resulting in postflight orthostasis have frequently been observed in response to space travel. It has been postulated that a decrement in left ventricular mass (LVM) found after microgravity exposure may be the central component in this cardiovascular deconditioning. However, a physiologic mechanism responsible for these changes in the myocardium has not been determined. In this study, we examined the sequential alterations in echocardiographic measured LVM from preflight to landing day and 3 days into the postflight recovery period. In a previous study in returning astronauts we found a comparative 9.1% reduction in postflight LVM that returned to preflight values by the third day of recovery. This data was further evaluated in a systems analysis approach using a well-established advanced computer model of circulatory functioning. The computer model incorporates the physiologic responses to changes in pressures, flows and hydraulics within the circulatory system as affected by gravitational forces. Myocardial muscle progression to atrophy or hypertrophy in reaction to the circulatory load conditions is also included in the model. The integrative computer analysis suggests that these variations in LVM could be explained by simple fluid shifts known to occur during spaceflight and can reverse within a few days after reentry into earth's gravity. According to model predictions, the reductions in LVM found upon exposure to microgravity are a result of a contraction of the myocardial interstitial fluid space secondary to a loss in the plasma volume. This hypothesis was additionally supported by the published ground-based study in which we followed the alterations in LVM and plasma volume in normal subjects in which hypovolemia was induced by simple dehydration. In the hypovolemic state, plasma volume was reduced in these subjects and was significantly correlated with echocardiographic measurements of LVM. Based on these experimental findings and the performance of the computer systems analysis it appears that reductions in LVM observed after spaceflight may be secondary to fluid exchanges produced by common physiologic mechanisms. Reductions in LVM observed after microgravity exposure have been previously postulated to be a central component of spaceflight-induced cardiovascular deconditioning. However, a recent study has demonstrated a return of astronauts’ LVM to preflight values by the third day after landing through uncertain mechanisms. A systems analysis approach using computer simulation techniques allows for a dissection of the complex physiologic control processes and a more detailed examination of the phenomena. From the simulation studies and computer analysis it appears that microgravity induced reductions in LVM may be explained by considering physiologic fluid exchanges rather than cardiac muscle atrophy.

Mechanism of Spaceflight-Induced Changes in Left Ventricular Mass

Decrements in left ventricular (LV) mass observed after microgravity exposure have been previously postulated to be a central component of spaceflight-induced cardiovascular deconditioning. In this study, echocardiographic measurements of LV mass in astronauts demonstrated a comparative 9.1% reduction in postflight LV mass that returned to preflight values by the third day of recovery. A ground-based study in normal subjects determined that these pre- to postflight LV mass changes could be reproduced by simple dehydration. Reductions in LV mass observed immediately after spaceflight may be secondary to simple physiologic fluid exchanges.

1112-149 Does use of harmonic imaging increase the yield of echocardiographic left ventricular mass measurements on a population basis? The strong heart study

1112-149 Does use of harmonic imaging increase the yield of echocardiographic left ventricular mass measurements on a population basis? The strong heart study

Regression of left ventricular hypertrophy after treatment of hypertension: Comparison of directed M-echocardiography with magnetic resonance imaging in quantification of serial mass changes

Background: This study sought to validate the reliability of serial echocardiographic measurements in detecting left ventricular (LV) hypertrophy regression by using magnetic resonance imaging (MRI) as a reference standard. Methods and Results: We studied a small population (n = 20) of patients enrolled in the Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) trial for evaluating LV hypertrophy regression. LV mass was measured by both echocardiography and MRI at baseline and after 1 year. As compared with baseline, systolic and diastolic blood pressures were significantly decreased after 1 year (all P <.05). Echocardiographic technique showed an overestimation of LV mass by 27.6 g at baseline (P =.005) and by 37.1 g after 1 year (P <.001), and there were wide 95% limits of agreement (±36.0 g at baseline; and ±27.6 g after 1 year) when compared with MRI measurement. Significant changes of LV mass from baseline of −20 ± 22 g (P<.01) and −29 ± 19 g (P <.01) were detected by using echocardiography and MRI after 1 year, respectively (P =.02), and there were similarly wide limits of agreement for change in LV mass (±24.2 g). Conclusions: Despite the use of careful methodology, echocardiographic measurement of LV mass at a single time point or for serial studies resulted in significant variation in LV mass estimates from measurement using MRI.

Echo doppler assessment of left ventricular function in rats with hypertensive hypertrophy

Objective: This study attempted to establish echocardiographic measurements of left ventricular (LV) mass and LV systolic and diastolic function, particularly in rats with hypertensive heart. Methods: M-mode LV echograms and Doppler mitral flow were obtained in Dahl salt-sensitive rats placed on 0.3% or 8% sodium chloride diet. Echo Doppler measurements were compared with catheterization and pathologic measurements in 54 rats for LV mass and in 45 rats for LV systolic and diastolic function. Results: Echocardiographic measurement of LV mass correlated well with pathologic measurement (r = 0.94, P <.01, n = 54, SEE = 0.08 mg), independent of LV size, aging, and therapeutic intervention. Endocardial fractional shortening (FS) correlated with LV peak + dP/dt (r = 0.56, n = 45, P <.01), and the correlation was improved to r = 0.71 if 11 rats with marked LV hypertrophy were excluded. Midwall FS correlated well with LV peak + dP/dt (r = 0.72, n = 45, P <.01) even if rats with extremely thickened ventricular wall were included. If midwall FS was lower than 14%, LV systolic dysfunction was very likely (sensitivity 67%, specificity 91%). Association of mitral E/A ratio of 2.0 or greater with deceleration time of shorter than 35 ms was an accurate indicator of elevated LV end-diastolic pressure (sensitivity 82%, specificity 86%) and increased lung weight because of congestive heart failure (sensitivity 89%, specificity 96%) in rats with hypertension. Conclusion: LV mass, LV systolic function, and LV end-diastolic pressure were assessable with echo Doppler in rats with hypertensive heart. (J Am Soc Echocardiogr 2002;15:109-17.)

The importance of age and obesity on the relation between diabetes and left ventricular mass

OBJECTIVESThe study investigated the relation of age with diabetes, obesity and hypertension on left ventricular mass (LVM).BACKGROUNDEpidemiological studies demonstrate a general rise of LVM with aging, but whether this phenomenon is independent or a function of coexisting diseases that accompany the aging process is unclear. Although obesity, hypertension and diabetes often coexist and increase in prevalence with age, studies of LVM in diabetics have been reported in mostly nonobese populations, and with little regard to the age-hypertension-obesity interactions and effects on LVM.METHODSWe prospectively measured LVM in 875 consecutive, mostly obese individuals (673 men, 202 women). Clinical data were obtained by chart review and clinical history. Echocardiographic measurements of LVM (American Society of Echocardiography criteria) were calculated using the Devereux formula and corrected for height2.7(LVM/Ht).RESULTSMean age was 49.3 ± 12.3 years, body mass index 33.3 ± 8.0 kg/m2, and LVM/Ht2.741.7 ± 13.4 g/m2.7. Of the total cohort, 673 patients were men, 519 obese, 228 hypertensive, and 52 diabetic. Of the 519 obese, 183 were hypertensive and 44 were diabetic (22 of those were hypertensive). Of the 228 hypertensives, 183 were obese and 26 were diabetic. On multivariate analysis, obesity (p = 0.0001), age (p = 0.0001), hypertension (p = 0.0003) and diabetes (p = 0.02) were all independently associated with LVM/Ht2.7. Obesity was the most potent independent predictor of LVM/Ht2.7, associated with an increase of 8.1 g/m2.7in LVM/Ht2.7. In diabetics, obesity had a synergistic effect on LVM/Ht2.7(p = 0.006), which was further amplified by age (p = 0.03).CONCLUSIONSAge, obesity, hypertension and diabetes are all independent determinants of LVM. The magnitude of the effect of diabetes on LVM is mainly consequent to a significant interaction of diabetes with obesity and age.

Two-Dimensional Echocardiography with a 15-MHz Transducer Is a Promising Alternative for In Vivo Measurement of Left Ventricular Mass in Mice

Murine models of left ventricular (LV) hypertrophy recently have been developed. We tested the accuracy of 2-dimensional (2D) echocardiographic measurement of LV mass with high-frequency imaging in mice. Ten anesthetized mice (weight 20 to 31 g, aged 1 to 5 months) were examined with a 15-MHz transthoracic linear-array transducer. End-diastolic myocardial area (A)(epicardial – endocardial) from the parasternal short-axis view at the midpapillary level and LV length (L) from the parasternal long-axis view were measured to calculate LV mass with the area-length method (1.05 [5/6 × A × L]) and data were compared with LV-mass with the 2D guided M-mode method. Within 3 days of echocardiography, the hearts were removed and weighed after potassium-induced cardiac arrest. Two-dimensional echocardiographic measurement with a 15-MHz transducer was performed in all mice. LV chamber dimensions included end-diastolic septal (0.80 ± 0.12 mm) and posterior wall thickness (0.76 ± 0.13 mm), end-diastolic dimension (3.64 ± 0.28 mm), and end-systolic dimension (2.34 ± 0.32 mm). Echocardiographic LV mass with the area-length method, 2D guided M-mode method, and autopsy LV weight were 80.8 ± 16.1 mg, 97.6 ± 17.8 mg, and 78.8 ± 13.2 mg, respectively. A strong correlation existed between LV weight ( x ) and echocardiographic LV mass ( y ) with the area–length method: y = 0.745 x + 18.9, r =0.908, standard error of estimate (SEE) = 5.9 mg, P < .0005. This correlation was stronger than that of LV weight ( x ) and echocardiographic LV mass ( y ) with the 2D guided M-mode method: y = 0.577 x + 22.6, r =0.779, SEE = 8.8 mg, P = .008. These data suggest that serial in vivo measurements of LV mass with the 2D area-length method may be more accurate than M-mode methods in experimental murine models of LV pathology. (J Am Soc Echocardiogr 1999;12:70-5.)

Lack of independent relationships between left ventricular mass and cardiovascular reactivity to physical and psychological stress in the Coronary Artery Risk Development in Young Adults (CARDIA) study

The objective of this study was to determine whether exaggerated blood pressure (BP) reactivity to stress and psychosocial characteristics are related to left ventricular mass (LVM) in a large cohort of young adults. Analyses were conducted with 3,742 participants of the CARDIA study (945 white men, 1,024 white women, 781 black men, and 922 black women), evaluated in 1990 to 1091 with echocardiographic measurement of LVM. Analyses were stratified by gender and race. The relationships of LVM/height 2.7 and cardiovascular reactivity to physical and psychological stressors (treadmill exercise, cold pressor, video game, and star-tracing tasks), were examined in both univariate and multivariate analyses adjusting for baseline BP, weight, and other relevant biobehavioral variables. The relationships between LVM and several psychosocial characteristics (hostility, anger suppression, anxiety, depressive symptoms, and education) were also assessed. Systolic blood pressure (SBP) reactivity to exercise was significantly related to LVM in black and white men; LVM was 10% greater among white men with exaggerated (upper quintile) peak exercise SBP than among other white men. SBP reactivity to the cold pressor test was related to LVM in all race/gender groups, although the relationship remained significant only among white men and women in the multivariate analysis. Diastolic blood pressure (DBP) reactivity to the video game was related to LVM only among black men in adjusted analyses. After adjusting for resting BP, weight, and other covariates in linear multiple regression models, SBP reactivity to exercise explained only 3% of the variance in LVM among white men. Otherwise, reactivity to other stressors or psychosocial variables accounted for no more than 1% of the variance in LVM. It was concluded that among a cohort of young adults, blood pressure reactivity to physical and mental stressors did not add substantially to the prediction of LVM when resting BP, weight, and other covariates were taken into account.

Hypertensive heart disease: Relationship of silent ischemia to coronary artery disease and left ventricular hypertrophy

ECG evidence of silent ischemia occurs commonly in patients with systemic hypertension, but its relationship to left ventricular hypertrophy (LVH), large-vessel coronary artery disease (CAD), and neurohumoral factors remains unclear. Accordingly we validated the results of the echocardiographic method used to measure left ventricular (LV) mass in the Soviet Union by comparison with necropsy measurements in 30 patients, and we examined the relationships in 46 men with essential hypertension among ST segment depression during ambulatory monitoring, exercise stress and transesophageal pacing (n = 38), and LV mass, catheterization evidence of CAD (n = 25), and neurohumoral factors (plasma catecholamines and platelet aggregability). Echocardiographic measurements of LV mass by both the Soviet and Penn methods were closely correlated with necropsy values ( r = 0.78 and 90, respectively; both p < 0.001). During ambulatory monitoring from 1 to 17 episodes of ≥ 1 mm ST depression occurred in 26 of 46 (65%) patients with hypertension; ischemia was also provoked by exercise or pacing stress in most but not all of these patients (65% and 80%, respectively). Neither ST depression nor the occurrence of additional episodes of symptomatic angina was related to the presence of coronary obstruction at catheterization; patients with and without ST depression did not differ in age, blood pressure, or LV mass. No systematic differences between patients with and without CAD or ST depression were noted in catecholamine levels or platelet aggregability, but the subset in whom ischemia developed at a lower heart rate (×) blood pressure product during pacing stress than during exercise stress had significantly lower norepinephrine levels at rest and during pacing stress (68 ± 34 versus 157 ± 47 ng/L, p < 0.02; and 86 ± 39 versus 254 ± 86 ng/L, p < 0.01). Thus asymptomatic ST depression occurs commonly during normal activity and induced stress in patients with systemic hypertension but is not consistently related to the presence of large-vessel CAD, LVH, or neurohumoral abnormalities.