Higher brachial-ankle pulse wave velocity is associated with more advanced carotid atherosclerosis in end-stage renal disease.

Brachial-ankle pulse wave velocity is a new measure of arterial stiffness. We examined whether higher brachial-ankle pulse wave velocity is associated with more advanced carotid atherosclerosis and left ventricular hypertrophy in patients with end-stage renal disease, and whether this effect would be mediated by the influence of wave reflection on central arterial pressure. In 68 patients with end stage renal disease, we examined blood pressures, brachial-ankle pulse wave velocity and the augmentation index of the left common carotid artery, a measure of the impact of wave reflection on the systolic peak in central arteries. The degree of carotid atherosclerosis was quantified by a plaque score and maximum intimal-medial thickness. Echocardiography was used to determine the left ventricular mass index. In simple regression analysis, brachial-ankle pulse wave velocity was correlated with both plaque score and maximum intimal-medial thickness (r = 0.420, p < 0.001 and r = 0.452, p < 0.0005, respectively) but not with left ventricular mass index. Multiple regression analysis was performed with the plaque score or maximum intimal-medial thickness as the dependent variable and brachial-ankle pulse wave velocity and known clinical risk factors as the independent variables. The brachial-ankle pulse wave velocity was an independent risk factor for both plaque score (beta = 0.006, p = 0.004) and maximum intimal-medial thickness (beta = 0.008, p = 0.04). Independent risk factors for left ventricular mass index were left ventricular diastolic dimension (beta = 3.509, p = 0.000007) and augmentation index (beta = 0.580, p = 0.04). The brachial-ankle pulse wave velocity was unrelated to augmentation index in patients with end stage renal disease. In conclusion, higher brachial-ankle pulse wave velocity was found to be a risk factor for carotid atherosclerosis in patients with end-stage renal disease; this effect was independent of the influence of wave reflection on central arterial pressure. The brachial-ankle pulse wave velocity was unrelated to left ventricular structure.     

Arterial stiffening as a possible risk factor for both atherosclerosis and diastolic heart failure.

While arterial stiffness is known to be related to atherosclerosis, the association between arterial stiffness and cardiac systolic and diastolic function in hypertension has not been fully evaluated. The present study was conducted to simultaneously evaluate the relationship of brachial-ankle pulse wave velocity (PWV) to parameters reflecting atherosclerosis and to those reflecting the risk of congestive heart failure in patients with hypertension. In 147 patients with hypertension, the left ventricular ejection fraction, the ratio of the peak velocity of early rapid filling and the peak velocity of atrial filling (E/A ratio), and left ventricular mass index were obtained from echocardiographs, the intima-media thickness of the common carotid artery was obtained by ultrasonography, the plasma B-type natriuretic peptide (BNP) level was measured by radioimmunoassay, and the brachial-ankle PWV was measured by the volume rendering method. Brachial-ankle PWV correlated positively with the intima-media thickness of the carotid artery, E/A ratio and BNP. Multiple linear regression analysis demonstrated that the relationship between the brachial-ankle PWV and the E/A ratio was significantly independent from other clinical variables. The receiver operator characteristic curve demonstrated that a brachial-ankle PWV of 1,600 cm/s was useful to discriminate mild cardiac diastolic dysfunction (E/A ratio of < or =0.75) (sensitivity=78% and specificity=58%). The present study demonstrated that increased brachial-ankle PWV relates not only to the parameters reflecting atherosclerosis but also to those reflecting cardiac diastolic dysfunction. Therefore, increased arterial stiffness is a possible simultaneous risk for atherosclerotic cardiovascular disease and diastolic heart failure in patients with hypertension.     

Associations of serum salusin-alpha levels with atherosclerosis and left ventricular diastolic dysfunction in essential hypertension

Serum salusin-alpha, is decreased in essential hypertension and acute coronary syndrome. The study is aimed to explore whether serum salusin-alpha is associated with atherosclerosis and left ventricular (LV) diastolic dysfunction in essential hypertension. Echocardiography, carotid ultrasonography, brachial-ankle pulse wave velocity (BaPWV) and serum salusin-alpha levels were determined in 60 hypertensive patients (29 with and 31 without carotid plaque) and 30 normotensive controls. Hypertensive patients with plaque, compared with those without plaque or the controls, had the lowest values of salusin-alpha. Then the hypertensive patients were divided into left ventricular hypertrophy (LVH) and non-LVH groups according to the echocardiography. Similarly, hypertensive patients with LVH showed the lowest serum salusin-alpha levels. In all subjects, serum salusin-alpha levels were negatively correlated with carotid mean-intima-media thickness (IMT), BaPWV, left ventricle mass index (LVMI) and E/E' (r=-0.488, P<0.001; r=-0.381, P<0.001; r=-0.294, P=0.006; r=-0.303, P=0.005; respectively). Serum salusin-alpha levels were independent predictors of BaPWV, carotid strain, carotid distensibility, mean-IMT, LVMI and E'/A' (β=-0.399, 0.283, 0.237, -0.346, -0.306, 0.469; P=0.002, 0.031, 0.016, 0.005, 0.012 and 0.001, respectively) in multiple linear regression models. These results suggest that serum salusin-alpha may be associated with atherosclerosis and LV diastolic dysfunction in essential hypertension.     

氨基末端B型脑钠肽前体与非梗阻性肥厚型心肌病患者左心室舒张功能的相关性研究

目的探讨血浆氨基末端B型脑钠肽前体(NT-proBNP)水平与非梗阻性肥厚型心肌病(HNCM)患者左心室舒张功能的关系。方法选择46例HNCM患者,20名健康体检者作为对照组,电化学发光法检测两组血浆NT-proBNP水平,超声心动图、组织多普勒显像(TDI)检测室间隔厚度、射血分数和反映左心室舒张功能的参数。结果HNCM组患者平均NT-proBNP血浆水平明显高于对照组(P<0.001);NT-proBNP血浆水平与以下左心室舒张功能参数均呈正相关:二尖瓣室间隔侧舒张早期最大运动速度e(r=0.74,P<0.001)、e与二尖瓣室间隔侧舒张晚期最大运动速度a比值e/a(r=0.69,P<0.001)、心房收缩开始至左室流出道内心室收缩期前流速开始的间期A-Ar(r=0.63,P=0.029)、Tei指数(r=0.63,P<0.001)、肺静脉频谱收缩期肺静脉血流速度S与舒张期肺静脉血流速度D的比值S/D(r=0.62,P<0.001)、等容舒张时间(IVRT)(r=0.56,P<0.001)、二尖瓣血流频谱舒张早期充盈峰值速度E(r=0.54,P<0.001)、a(r=0.53,P<0.001)、二尖瓣血流频谱舒张晚期充盈峰值流速A(r=0.36,P=0.02)、E/A(r=0.47,P<0.001)。多因素Logistic回归分析显示,e/a、S/D是NT-proBNP血浆水平的独立影响因素。结论NT-proBNP血浆水平与超声心动图左心室舒张功能参数间存在明显的正相关性,可以作为评价HNCM患者左心室舒张功能不全的客观指标。     

Association of arterial wave properties and diastolic dysfunction in patients with type 2 diabetes mellitus

Left ventricular (LV) diastolic dysfunction and increased arterial stiffness are prevalent in patients with type 2 diabetes mellitus (DM). Because the systemic vasculature plays a pivotal role in myocardial loading, this study aimed to determine the effect of arterial characteristics on LV diastolic function in patients with type 2 DM. Conventional echocardiography and tissue Doppler imaging were performed in 155 patients with type 2 DM (88 men; mean age 55 +/- 11 years) with preserved LV ejection fractions (>50%). Patients were stratified into groups on the basis of LV diastolic function (normal, n = 53; delayed relaxation, n = 79; pseudonormal, n = 23). Arterial wave reflection parameters and central blood pressure were determined by radial tonometry. Arterial (brachial and carotid) structure and function were determined by standard ultrasound methods. There were no significant differences among the groups on central pressure or arterial function. LV filling pressure, determined by the ratio of early transmitral inflow velocity to diastolic early tissue velocity (E/E'), was significantly correlated with central pulse pressure (r = 0.21, p <0.05). Late diastolic inflow velocity (A) was significantly associated with central pulse pressure (r = 0.32, p <0.001), total arterial compliance (r = -0.35, p <0.001), and carotid artery stiffness (r = 0.34, p <0.001). Multiple regression analysis found central but not brachial pulse pressure independently predicted E/E' and A. In conclusion, increased central pulse pressure, possibly due to amplified pressure wave reflections, is independently associated with abnormal LV diastolic function in patients with type 2 DM.     

Comparison between tissue Doppler imaging and velocity-encoded magnetic resonance imaging for measurement of myocardial velocities, assessment of left ventricular dyssynchrony, and estimation of left ventricular filling pressures in patients with ischemic cardiomyopathy

Velocity-encoded magnetic resonance imaging (VE-MRI), commonly used to perform flow measurements, can be applied for myocardial velocity analysis, similar to tissue Doppler imaging (TDI). In this study, a comparison between VE-MRI and TDI was performed for the assessment of left ventricular dyssynchrony and left ventricular filling pressures. Ten healthy volunteers and 22 patients with heart failure secondary to ischemic cardiomyopathy underwent both VE-MRI and TDI. Longitudinal myocardial peak systolic and diastolic velocities and time to peak systolic velocity (Ts) were measured with both techniques at the level of left ventricular septum and lateral wall. To quantify left ventricular dyssynchrony, the delay in Ts between basal septum and lateral wall was calculated (SLD) and patients were categorized into 3 groups: minimal (SLD <30 ms), intermediate (SLD = 30 to 60 ms) and extensive (SLD >60 ms) left ventricular dyssynchrony. The ratio of transmitral E wave velocity and mitral annulus septal early velocity (E/E' ratio) was also assessed, and patients were divided into 3 groups: normal (E/E' <8), probably abnormal (E/E' = 8 to 15), and elevated (E/E' >15) left ventricular filling pressures. Excellent correlations were observed for peak systolic velocity and peak diastolic velocity (r = 0.95, p <0.001) measured with TDI and VE-MRI. A small bias (p <0.001) of -1.1 +/- 1.1 cm/s for peak systolic velocity and of -0.45 +/- 1.03 cm/s for peak diastolic velocity was noted between the 2 techniques. A strong correlation was also noted between Ts measured with TDI and VE-MRI (r = 0.97, p <0.001) without a significant difference. TDI and VE-MRI showed an excellent agreement for left ventricular dyssynchrony and left ventricular filling pressures classification with a weighted kappa of 0.96 and 0.91, respectively. In conclusion, TDI and VE-MRI are highly concordant and can be used interchangeably for the assessment of left ventricular dyssynchrony and filling pressures.     

Changes in modalities of left ventricular filling associated with aging in normal subjects: secondary to increase in blood pressure and left ventricular mass?

The mechanisms by which aging alters the pattern of left ventricular diastolic filling are still uncertain. To gain more insight into this tissue, the independent contributions of age, sex, heart rate, arterial blood pressure and left ventricular mass (as well as various indexes of left ventricular morphology and function) to left ventricular diastolic filling abnormalities, were investigated by echocardiography in 81 normal subjects (18 to 84 years of age, mean 50), carefully screened to avoid the confounding effects of coronary artery disease and systemic hypertension. With advancing adult age, we found a significant increase in: body mass index (r = 0.25; p less than 0.02), systolic (r = 0.58; p less than 0.0001), pulse (r = 0.61; p less than 0.0001) and mean (r = 0.40; p less than 0.0001) arterial blood pressure; left ventricular wall thickness (r = 0.30; p less than 0.006); left ventricular mass (r = 0.32; p less than 0.004); left ventricular end-diastolic volume (r = 0.24; p less than 0.03); and peak systolic wall stress (r = 0.22; p less than 0.04). Pulsed Doppler analysis of mitral inflow showed a significant age-related decline in the peak early filling velocity (r = -0.51; p less than 0.001), and in the ratio of early and late diastolic filling velocity (r = -0.65; p less than 0.0001). Conversely, duration of isovolumic relaxation (r = 0.77; p less than 0.0001), peak late diastolic flow velocity (r = 0.39; p less than 0.001), and diastolic pressure half time (r = 0.34; p less than 0.01) increased significantly with age. "Stepwise" multivariate linear regression analyses showed that the ratio of early to late diastolic peak filling velocity was independently related only with age (R2 = 0.56; p less than 0.0001) while the isovolumic relaxation time was independently related with age (R2 = 0.48; p less than 0.0001) and duration of cardiac cycle (R2 = 0.06; p less than 0.008). Age-related changes in body mass index, blood pressure, peak meridional wall stress and left ventricular mass index did not show any independent relationship to Doppler parameters of left ventricular filling or duration of isovolumic relaxation. The results of the present study suggest that the effect of age on left ventricular filling modalities and duration of isovolumic relaxation are independent of age-related changes in blood pressure, left ventricular mass, morphology and systolic function.     

Relative duration of transmitted mitral A wave as a measure of left ventricular end-diastolic pressure and stiffness

BACKGROUND AND OBJECTIVES: The mitral A wave is transmitted to the left ventricular (LV) outflow tract where it is registered as Ar wave. We have related its transit time to the LV late diastolic stiffness. We also observed incidentally that the duration of the transmitted Ar wave exhibited marked variability and hence investigated its hemodynamic correlates. METHODS AND RESULTS: Mitral A wave and the Ar wave in the LV outflow tract were recorded using pulsed wave Doppler technique simultaneous with high fidelity LV pressure recordings in 20 patients undergoing cardiac catheterization. A high-speed contrast left ventriculogram was obtained as well. The duration of both these wave forms were measured and A wave duration minus the Ar wave duration was measured. The A minus Ar wave duration (range 0-95 ms) correlated with LV end-diastolic pressure (r = 0.54, P = 0.014, range 4-32 mmHg), LV late diastolic stiffness (r = 0.62, P = 0.004, range 0.1-1.6 mmHg/ml) and the amount of LV pressure rise with atrial contraction (r = 0.67, P = 0.001, range 2-13 mmHg). CONCLUSION: A minus Ar wave duration is an easily obtainable Doppler parameter that is related to LV late diastolic filling pressures and stiffness and gives insights into aspects of LV diastolic function.     

Relation of arterial stiffness to left ventricular structure and function in adolescents and young adults with pediatric-onset systemic lupus erythematosus

OBJECTIVE: Limited adult data suggested arterial stiffening in systemic lupus erythematosus (SLE). We investigated the hypothesis that arterial stiffening is related to left ventricular (LV) structure and function in adolescents and young adults with pediatric-onset SLE. METHODS: We studied 32 patients with SLE (28 female) aged 17.3 +/- 4.8 years. The arterial stiffness was assessed by the carotid artery stiffness index, while the LV mass and cardiac function were assessed echocardiographically. These indices were compared to those of 15 healthy controls. RESULTS: Compared with controls, patients with SLE had lower LV shortening fraction, ejection fraction and mean velocity of circumferential fiber shortening, reduced mitral early diastolic inflow velocity and early (e(m)) diastolic myocardial tissue velocity, and lower systolic strain and systolic and diastolic strain rates of the LV free wall (all p < or = 0.02). Their global LV function was impaired as reflected by the significantly higher myocardial performance index (MPI; p = 0.02). The carotid arterial stiffness index (p < 0.001) and LV mass (p < 0.001) were significantly greater in patients than controls. Among patients with SLE, the carotid arterial stiffness index correlated with disease activity index (r = 0.46, p = 0.009). Multivariate analysis revealed that carotid arterial stiffness was a significant independent determinant of LV mass (beta = 0.52, p < 0.001), MPI (beta = 0.43, p = 0.002), e(m) velocity (beta = -0.46, p = 0.001), and systolic strain rate of the LV free wall (beta = -0.46, p = 0.001). CONCLUSION: Arterial stiffening occurs in adolescents and young adults with SLE, which may contribute to the development of LV hypertrophy and subclinical myocardial dysfunction.     

Brachial-ankle pulse wave velocity is an independent predictor of carotid artery atherosclerosis in the elderly

Objective Brachial-ankle pulse wave velocity （baPWV） is widely used as a simple noninvasive measure of arterial softness. The aim of this study was to evaluate the usefulness of baPWV as a predictor of the carotid artery atherosclerosis in the elderly. Methods A total of 721 elderly participants （mean ~ SD age, 70.3 -4- 5.6years） were enrolled in the current study. All participant underwent both baPWV measurement and B-mode ultrasound for the intima-media thickness. Carotid atherosclerosis （CAS） was defined as the present of carotid plaque or and/or intima media thickness for at least 1.1 mm. Results A multivariate logistic regression analysis reveals that age, sex, brachial-ankle pulse wave velocity, smoking and LDL-C level showed a significant correlation with the presence of CAS. The odds ratios of CAS associated with a 500cm/s increase of brachial-ankle pulse wave velocity were 2.378 [95% confidence interval, 1.36 to 4.00, P〈0.05], 3.733 [95% confidence interval, 1.729 to 8.058, P〈0.01], 4.438 [95% confidence interval, 1.659 to 11.803, P〈0.01]. The baPWV significantly correlated with IMT by bivariate correlation analysis （r=-0.39; p=0.001）. After adjusting for factors influencing, baPWV all the same correlated with IMT （r=-0.35; p=0.001）.Conclusion These results indicate that brachial-ankle PWV is an independent predictor of CAS in the elderly.It also means that the direct measurement of arterial stiffness by this simple method may be of great help for the evaluation of carotid artherosclerosis, at least in the elderly     

Comparison of acoustic quantification and Doppler echocardiography in assessment of left ventricular diastolic variables.

OBJECTIVE--To assess the haemodynamic correlations of the waveforms of left ventricular area change obtained by automated boundary detection with newly developed acoustic quantification technology. DESIGN--The timing of events in the cardiac cycle was identified on the wave-form automated boundary detection and was correlated with the corresponding timing derived from pulsed wave Doppler flow velocity traces of the mitral valve and left ventricular outflow tract. The amounts of area change during the rapid filling phase and during atrial contraction were correlated with the time-velocity integrals of early and late diastolic ventricular filling obtained from Doppler tracings of the mitral inflow. SETTING--A university medical school echocardiography laboratory. SUBJECTS--16 healthy volunteers and 19 patients referred for echocardiographic studies. RESULTS--A significant correlation was found between the methods for measurement of the time from the R wave to mitral valve opening (r = 0.72, p < 0.01), isovolumic relaxation time (r = 0.62, p < 0.01), and ejection time (r = 0.54, p < 0.01). The change of total area that occurred during rapid filling and atrial filling phases measured from the acoustic waveform correlated with the time-velocity integrals of the early and late diastolic mitral valve inflow velocity derived from Doppler echocardiography (r = 0.60 and r = 0.80, respectively). CONCLUSION--The waveform of left ventricular area obtained by the automated boundary detection technique identifies the phases of the cardiac cycle and correlates with Doppler values of left ventricular diastolic function. Therefore, this new method of automated boundary detection has potential uses in the assessment of left ventricular diastolic function.     

Right ventricular filling detected by pulsed Doppler echocardiography during the convalescent stage of inferior wall acute myocardial infarction

To evaluate right ventricular (RV) diastolic function in patients with inferior wall acute myocardial infarction (AMI), flow velocity patterns of the RV inflow tract were studied in patients with anterior AMI (n = 32), inferior AMI (n = 32) and angina pectoris without left ventricular asynergy (n = 10) using pulsed Doppler echocardiography. Doppler examinations were performed at least 4 weeks after the attack. Twenty-seven healthy persons served as control subjects. Three Doppler variables were measured at the RV inflow tract: the ratio of the late diastolic peak flow velocity due to atrial contraction to the rapid filling peak flow velocity in early diastole (A/E) and the acceleration time and deceleration time of the RV rapid filling wave. A/E in patients with inferior AMI (1.01 +/- 0.24, mean +/- standard deviation) was significantly greater than in those with anterior AMI (0.80 +/- 0.16, p less than 0.001) and angina pectoris (0.79 +/- 0.17, p less than 0.01) and in normal subjects (0.70 +/- 0.17, p less than 0.001). A/E in patients with inferior AMI correlated with the ratio of left ventricular to RV end-diastolic pressure (r = -0.60, p less than 0.05). A/E in inferior AMI with relatively high RV end-diastolic pressure (more than 8 mm Hg, n = 8) was significantly greater than that in those with normal pressure (8 mm Hg or less, n = 9). A/E in patients with proximal right coronary artery occlusion was significantly greater than that in those with distal occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Change in filling pattern with preload reduction reflects left ventricular relaxation

BACKGROUND: The early diastolic mitral valve pressure gradient and the rate of left ventricular filling are determined by the rate of left ventricular relaxation and left atrial pressure at the time of mitral valve opening. Accordingly, we hypothesized that the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved systolic function. METHODS: We evaluated the relationship between the logistic time constant of left ventricular relaxation and left ventricular filling pattern calculated from the time derivative of left ventricular volume using a microtipmanometer and a conductance catheter in 26 consecutive patients with preserved left ventricular ejection fraction (>45%). Left ventricular filling patterns were determined from the maximal rates of early diastolic left ventricular filling (E velocity) and atrial filling (A velocity) before and after preload reduction by inferior venal caval occlusion. RESULTS AND CONCLUSIONS: There was no significant relationship between the logistic time constant of left ventricular relaxation and the E/A velocity ratio at baseline. However, the time constant was correlated with the E/A velocity ratio after venal caval occlusion (r=-0.47, p=0.02). Furthermore, the time constant was correlated with %E/A velocity change, which was defined as the rate of change of E/A before and after caval occlusion divided by E/A after caval occlusion, more significantly (r=-0.67, p<0.01) than with the E/A velocity ratio after caval occlusion. Thus, the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved left ventricular ejection fraction.     

Left ventricular filling in treated essential hypertension. A study using Doppler echocardiography

The first stigmata of left ventricular involvement in hypertension are changes in diastolic filling. Early detection of these abnormalities is important as some antihypertensive agents may have beneficial effects on left ventricular distensibility and filling, in addition to lowering the blood pressure. This study compares parameters of left ventricular filling recorded by pulsed Doppler echocardiography in 44 treated hypertensives (average blood pressure: 157 +/- 20/93 +/- 12 mmHg) without any other coronary risk factors with 33 age-matched (52 +/- 13 years and 48 +/- 13 years) control normotensive subjects (average blood pressure: 130 +/- 11/80 +/- 7 mmHg). The main findings were an increase of the peak. A wave velocity after atrial contraction and of the A/E ratio in the hypertensive group (66 +/- 16 cm/s vs 53 +/- 14 cm/s, p less than 0.05 and 0.99 +/- 0.34 vs 0.78 +/- 0.24, p less than 0.05, respectively). These changes were more pronounced in patients with left ventricular hypertrophy. The rapid filling phase was unchanged (maximum E wave velocity = 68 +/- 18 cm/s vs 70 +/- 14 cm/s). The influence of age on peak A wave velocity and A/E ratio was obvious in control subjects and hypertensives without left ventricular hypertrophy r = 0.80; p less than 0.05). The age factor was not significant in the presence of left ventricular hypertrophy (r = 0.18). A weak linear correlation was observed between the peak A wave velocity, diastolic septal thickness (r = 0.44; p = 0.04) and left ventricular mass (r = 0.44; p = 0.05) in hypertensive patients with left ventricular hypertrophy.     

Aortic Upper Wall Tissue Doppler Image Velocity: Relation to Aortic Elasticity and Left Ventricular Diastolic Function

Background: Aortic stiffening contributes to the left ventricular (LV) afterload, hypertrophy, and substrate for diastolic dysfunction. It is also known that aortic elastic properties could be investigated with color tissue Doppler imaging (TDI) in aortic upper wall. The purpose of this study is to evaluate the relation of aortic upper wall TDI and aortic stiffness and other parameters of LV diastolic function. Methods: We examined aortic upper wall by TDI at the 3 cm above the aortic valves because of patient's chest discomfort or dyspnea. We excluded the patient with arterial hypertension or reduced left ventricular ejection fraction (LVEF) or significant valvular heart disease. So a total of 126 (mean age 53.8 ± 13.9 years, male 49.2%) patients were enrolled in this study and divided normal LV filling group (N = 31) and abnormal LV filling group (N = 95). Results: Aortic upper wall early systolic velocity and late diastolic velocity were not different between the two groups. Only aortic upper wall early diastolic velocity (AWEDV) was related to aortic stiffness index (r =−0.25, P = 0.008), distensibility (r = 0.28, P = 0.003), early diastolic (Em) (r = 0.45, P = 0.001), E/Em (r =−0.26, P = 0.003), and significantly reduced in abnormal LV filling group (6.19 ± 2.50 vs 8.18 ± 2.87, P = 0.001). Conclusions: AWEDV is decreased significantly in abnormal LV filling patients. It is statistically related to aortic stiffness, distensibility and parameters of abnormal LV filling, Em, E/Em. TDI velocity of the aortic upper wall can be a helpful tool for evaluating aortic stiffness, distensibility, and diastolic function.     

Diastolic blood pressure as a determinant of Doppler left ventricular filling indexes in normotensive adolescents

Alterations in left ventricular filling can occur with aging and in patients with hypertension, ischemic heart disease, congestive and hypertrophic cardiomyopathy and congenital heart disease. This study examines the effects of blood pressure on left ventricular diastolic filling indexes measured by Doppler ultrasound technique in 47 young normotensive adolescents (mean age 13 years). Left ventricular filling was assessed by Doppler peak early and late diastolic transmitral flow velocities, early and late diastolic flow velocity integrals and early diastolic deceleration. Systolic blood pressure did not correlate with any of the Doppler filling indexes, although it was related to echocardiographic left ventricular mass (r = 0.44, p less than 0.005). Diastolic blood pressure did not correlate with left ventricular mass; however, it was inversely related to peak early diastolic flow velocity (r = -0.44, p less than 0.005), early diastolic flow velocity integral (r = -0.40, p less than 0.01) and early diastolic deceleration (r = -0.32, p less than 0.05). The ratio of late to early peak filling (A/E) was directly related to diastolic blood pressure (r = 0.48, p less than 0.001). Examination of electrocardiograms showed that there was a stronger correlation between A/E ratio and diastolic blood pressure (r = 0.63) in 22 subjects with bimodal P waves in lead V1 than in subjects with unimodal P waves (r = 0.45).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of type 1 diabetes mellitus on cardiac function: a study of monozygotic twins.

OBJECTIVE--To investigate left ventricular size and function in type 1 diabetes and their relation with diabetes duration, glycaemic control, autonomic dysfunction, and complications of diabetes. DESIGN--Cross sectional study using a pulsed wave Doppler echocardiogram to assess left ventricular dimensions, wall thickness, and transmitral blood flow velocity signals. PATIENTS--40 monozygotic twin pairs (23 male, mean age 26 years) discordant for type 1 diabetes and 40 non-diabetic singleton controls with no clinical evidence of cardiac ischaemia. RESULTS--For all Doppler echocardiographic measurements there were strong correlations between monozygotic twins but not between twins and control subjects. Left ventricular dimensions, wall thickness and systolic function, peak E velocity, and the velocity integrals of early left ventricular filling were similar in all three groups. Peak A velocity and the velocity integrals of late ventricular filling (mean (SD)) were greater in diabetic twins (45 (12) v 38 (8) cm/s, P = 0.002; and 32 (11) v 26 (6), P = 0.0002). Diabetic twins had lower E/A ratio (1.59 (0.39) v 1.83 (0.39), P < 0.001), greater atrial filling fraction to total diastolic filling (28 (6) v 25 (5)%, P = 0.002), and prolonged isovolumic relaxation time (72 (12) v 63 (9) ms, P < 0.001). The differences in Doppler findings between diabetic and non-diabetic twins were related to disease duration whereas the prolongation of the isovolumic relaxation time was related to cardiac autonomic dysfunction. CONCLUSIONS--These results show that twins with type 1 diabetes have left ventricular diastolic dysfunction related to diabetes duration and cardiac autonomic dysfunction but not to glycaemic control or microvascular complications. In addition, genetic factors contribute to left ventricular dimension and function.     

Doppler Evaluation of Left Ventricular Diastolic Inflow and Outflow Waveforms in Normal Subjects

The measurements of the left ventricular inflow parameters do not necessarily reflect the measurements of the respective outflow ones. The A wave transit time from the mitral valve to the left ventricular outflow tract has been demonstrated to have a fair correlation with measures of the left ventricular late diastolic stiffness. We performed this study to obtain the normal patterns of the diastolic left ventricular outflow as well as inflow waveforms and to evaluate the roles of aging and other physiological parameters in their evolution. The study population consisted of 60 healthy subjects (aged 22–66 years). They were divided into three groups: group 1 (aged 20–34 years), group 2 (aged 35–49 years), and group 3 (aged 50–70 years). Pulse-wave Doppler echocardiography was performed to get the patterns of diastolic left ventricular inflow and outflow waveforms. With aging, the peak velocity and velocity-time integral of the transmitted transmitral E wave decreased, and those of the transmitted transmitral A wave increased with a progressive decrease in their ratio of transmitted transmitral E to A wave. The diastolic left ventricular inflows followed a similar aging course. There was no obvious aging trend in the A wave transit time from the mitral valve to the left ventricular outflow tract. Multiple linear regression analyses selected age as the most important determinant in the differences in most left ventricular inflow and outflow indices among normal subjects. Besides, heart rate had modest influences on some Doppler indices. This study confirms the age related changes in the left ventricular inflow waveforms and further establishes the concept that the diastolic left ventricular outflow waveforms are also significantly influenced by age and heart rate. Hence, both factors should be taken into account in interpreting the diastolic left ventricular outflow as well as inflow indices.     

Restrictive Left Ventricular Filling Patterns Are Predictive of Diastolic Ventricular Interaction in Chronic Heart Failure

Objectives. The purpose of this study was to determine whether restrictive left ventricular (LV) filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure.Background. We recently demonstrated a diastolic ventricular interaction in ∼50% of a series of patients with chronic heart failure, as evidenced by paradoxic increases in LV end-diastolic volume despite reductions in right ventricular end-diastolic volume during volume unloading achieved by lower body negative pressure (LBNP). We reasoned that such an interaction would impede LV filling in mid and late diastole, but would be minimal in early diastole, resulting in a restrictive LV filling pattern.Methods. Transmitral flow was assessed using pulsed wave Doppler echocardiography in 30 patients with chronic heart failure and an LV ejection fraction ≤35%. Peak early (E) and atrial (A) filling velocities and E wave deceleration time were measured. Left ventricular end-diastolic volume was measured using radionuclide ventriculography before and during −30-mm Hg LBNP.Results. Nine of the 11 patients with and 2 of the 16 patients without restrictive LV filling patterns (E/A >2 or E/A 1 to 2 and E wave deceleration time ≤140 ms) increased LV end-diastolic volume during LBNP (p = 0.001). The change in LV end-diastolic volume during LBNP was correlated with the baseline A wave velocity (r = −0.52, p = 0.005) and E/A ratio (r = 0.50, p = 0.01).Conclusions. Restrictive LV filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. Volume unloading in the setting of diastolic ventricular interaction allows for increased LV filling. Identifying patients with chronic heart failure and restrictive filling patterns may therefore indicate a group likely to benefit from additional vasodilator therapy.     

Origin and significance of diastolic Doppler flow signals in the left ventricular outflow tract

Diastolic Doppler flow signals (greater than or equal to 0.2 m/s) in the left ventricular outflow tract have not been well characterized, and their origin and significance remain controversial. Fifty-nine patients (55 +/- 16 years of age) with technically good Doppler echocardiographic studies were studied prospectively. There were 14 normal subjects, 21 patients with left ventricular hypertrophy, 10 with dilated cardiomyopathy and 14 with other cardiac disease. The rhythm was sinus in 55 and atrial fibrillation in 4. Two distinct Doppler flow signals were detected in the left ventricular outflow tract during diastole. These were termed E' (early) and A' (active) because they occurred 40 to 100 ms after higher velocity mitral inflow E (passive filling) and A (atrial contraction) signals. Among 59 patients, E' signals were present in 48 (81%) and had a mean velocity of 0.41 +/- 0.23 m/s. In 55 patients with normal sinus rhythm, A' signals were present in 52 (95%) and had a mean velocity of 0.52 +/- 0.24 m/s. No A' signals were present in the four patients with atrial fibrillation. The E' and A' velocities by pulsed wave Doppler ultrasound were low at the left ventricular apex and increased along the basal septum in the left ventricular outflow tract. Prominent A' velocities (greater than or equal to 0.45 m/s) were seen in 62% of patients with left ventricular hypertrophy, 50% of normal subjects and 10% of patients with dilated cardiomyopathy. The A' velocity was higher in patients with left ventricular hypertrophy (0.63 +/- 0.26 m/s) than in those with a normal heart (0.45 +/- 0.16 m/s; p less than 0.05) or dilated cardiomyopathy (0.25 +/- 0.13 m/s; p less than 0.01). The major determinants of diastolic outflow tract velocity were the mitral inflow E and A velocities and left end-diastolic dimension, particularly when combined (r = 0.64, p less than 0.0001 for E'; r = 0.72, p less than 0.0001 for A'). Distinctive E' and A' Doppler outflow tract signals result from mitral inflow and may be detected in most patients with normal heart size. These E' and A' velocities increase from apex to base and are more prominent in patients with a small, normally contracting heart or left ventricular hypertrophy.