Left ventricular diastolic function in young men with high normal blood pressure

OBJECTIVE: Abnormalities in left ventricular (LV) diastolic filling have been reported in hypertensive patients. This study was designed to compare LV diastolic filling between individuals with high normal blood pressure (HNBP) and optimal blood pressure (OBP). SUBJECTS AND DESIGN: From a survey of 219 young male individuals (age 21 +/- 0.1 years), two groups were selected according to their BP (group A: systolic BP [SBP] 120 mmHg and diastolic BP [DBP] 80 mmHg, n = 23 and group B: SBP 130 to 139 mmHg and/or DBP 85 to 89 mmHg, n = 21). Subjects habits, anthropometric characteristics, LV structure and systolic and diastolic function were compared. RESULTS: No differences were detected between the two groups in habits, systolic function or early diastole. LV mass index (LVMI) was higher in group B (103.6 +/- 4.58 g/m2 versus 90.49 +/- 3.27 g/m2 in group A, P < 0.05), though the values were not high enough to indicate LV hypertrophy. The pattern of LV late filling was different between the two groups. The peak late diastolic flow velocity (A) was 0.45 +/- 0.02 m/s in group B and 0.52 +/- 0.03 m/s in group A (P < 0.05). The early peak velocity (E):A ratio was 1.82 +/- 0.08 in group A and 1.59 +/- 0.08 in group B (P < 0.05). The early filling fraction also demonstrated a significant shift to more prominent late diastolic filling in group B (0.68 +/- 0.01% versus 0.73 +/- 0.01% in group A, P < 0.05). This pattern in LV filling did not correlate to inheritance, age, sex, heart rate, habits or body mass index. CONCLUSIONS: This shift in filling pattern to a late flow in young men with HNBP seemed to be an early indicator of an increased dependence of LV filling on atrial contraction and may reflect an impairment in LV relaxation.     

Evaluation of left atrial contribution to left ventricular filling in aortic stenosis by velocity-encoded cine MRI

Velocity-encoded cine MRI (VEC-MRI) can measure volume flow at specified site in the heart. This study used VEC-MRI to measure flow across the mitral valve to compare the contribution of atrial systole to left atrial filling in normal subjects and patients with left ventricular hypertrophy. The study population consisted of 12 normal subjects (mean age 34.5 years) and nine patients with various degrees of left ventricular hypertrophy resulting from aortic stenosis (mean age 70 years). VEC-MRI was performed in double-oblique planes through the heart to measure both the mitral inflow velocity pattern (E/A ratio) and the volumetric flow across the mitral valve. The left atrial contribution to left ventricular filling (AC%) was calculated. The results were compared with Doppler echocardiographic parameters. The VEC-MRI-derived mitral E/A ratios showed a significant linear correlation with E/A ratios calculated from Doppler echocardiography (r = 0.94), and the VEC-MRI-derived E/A ratios (2.1 +/- 0.5 vs 1.0 +/- 0.4) and AC% values (24.9 +/- 7.2 vs 45.7 +/- 16.4) were significantly different between normal subjects and patients with aortic stenosis (p < 0.01 in both groups). The same differences were seen in the Doppler echocardiographic parameters. The VEC-MRI-derived E/A ratio and AC% showed significant hyperbolic and linear correlations with left ventricular mass indexes (r = 0.95 and 0.86). In addition, the VEC-MRI-determined E/A ratio and the volumetric AC% displayed a highly significant hyperbolic correlation (r = 0.95). Thus VEC-MRI can be used to evaluate left ventricular diastolic filling characteristics in normal subjects and patients with abnormalities of diastolic filling.     

Left ventricular diastolic function--pulsed Doppler echocardiography versus radionuclide angiography

Fifty five consecutive patients diagnosed to have coronary artery disease by coronary angiography had their left ventricular (LV) diastolic functions evaluated by pulsed doppler (PD) methods and radionuclide angiography (RNA). Using PD, the peak velocities of the early filling wave 'E' and the late filling wave 'A' of mitral inflow were measured. LV diastolic dysfunction, defined as E/A ratio less than 1.0, was present in 31 of 38 patients with low RNA peak filling rates (PFR) of 2.3 EDV/sec or less (sensitivity 81.6%). Normal E/A ratios (> 1.0) were seen in 13 of 17 patients with normal RNA PFR of > 2.3 EDV/sec (specificity 76.5%). Both methods were in agreement in 44 of 55 patients (accuracy 80%). There was good direct correlation between RNA PFR and PD E/A ratio (correlation coefficient r = 0.51, P < 0.01). It is concluded that PD echocardiography is a simple and reliable method of identifying diastolic dysfunction in patients with ischaemic heart disease.     

Relationship between systolic and diastolic function of the left ventricle in patients with impaired relaxation of the left ventricle without symptoms of heart failure. Attempt at quantitative estimation of diastolic function in the impaired relaxation stage

Diastolic dysfunction of left ventricle appears very often in patients with coronary artery disease (CAD) and hypertension (HT) and is a main cause of heart failure in 30-40% of all cases. Relation between systolic and diastolic function of left ventricle (LV) is commonly known but not documented well enough. Moreover, no quantitative classification of diastolic dysfunction is still available. AIM OF THE STUDY: To find out the relations between the parameters of systolic and diastolic function of LV in patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure and to make up the quantitative classification of diastolic dysfunction in the stage of impaired relaxation of LV. METHODS: Investigations were carried out in 57 patients (mean age 55.5 +/- 11.5) with angiographically proven CAD and in 91 patients (mean age 56.3 +/- 10.6) with HT and angiographically excluded CAD, all without regional myocardial contractility abnormalities and valvular heart diseases. Control group consisted of 54 healthy subjects (mean age 55.4 +/- 11.4). During 2D echocardiography examination left ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD) and left atrial dimension (LA) were obtained. Using Doppler method transmitral inflow indices: E velocity (E), A velocity (A), E velocity integral (E-VTI), A velocity integral (A-VTI), total velocity integral (T-VTI), E deceleration time (DT), isovolumic relaxation time (IVRT) and aortic flow velocity integral (Ao-VTI) were measured. Only patients with E/A < or = 1 and--to exclude pseudonormalization of mitral inflow--with DT > or = 140 ms were qualified to the study. We proposed diastolic dysfunction ratio (DDR) calculated from formula: DDR = E/A x E-VTI/T-VTI. Using AFVI, LV outflow diameter, heart rate (HR) and body surface area cardiac index (CI) was calculated. RESULTS: In studied group there were significantly higher values of LA, A, IVRT, DT and lower values of E, E/A, E-VTI and DDR compared to controls. There were no significant differences between these groups in HR, LVEDD, LVESD, T-VTI and CI. No significant differences in any of studied parameters were found between subgroups with CAD and HT. Among healthy subjects in subgroup with abnormal mitral inflow pattern (E/A < or = 1) there were significantly higher values of LA, IVRT, DT and lower values of DDR than in sugroup with normal one. Both subgroups did not differ in LVEDD, LVESD, CI. In the studied group there was positive correlation between DDR and CI (r = 0.69, p < 0.001), DDR and IVRT (r = 0.71, p < 0.001), DDR and DT (r = 0.61, p < 0.001), CI and E (r = 0.34, p < 0.01), CI and IVRT (r = 0.52, p < 0.001), CI and DT (r = 0.42, p < 0.001), CI and E/A (r = 0.54, p < 0.001), CI and E-VTI (r = 0.43, p < 0.001). In the control group significant correlation was found only between DDR and IVRT (r = 0.64, p < 0.02) and between DDR and DT (r = 0.52, p < 0.02) but not between DDR and CI. Using DDR DD was divided into 3 classes: class I with DDR > 0.47, class II with 0.47 > or = 0.30, and class III with DDR < 0.30. Applying of such intervals of values of DDR determined the groups which significantly differed between themselves in CI, IVRT and DT. CONCLUSIONS: (1) In patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure there is relation between parameters of systolic and diastolic function of LV: the more advanced diastolic dysfunction, the more impaired systolic function. (2) In healthy subjects there is no relation between parameters of systolic and diastolic function of LV. (3) DDR is a good indicator of quantitative estimation of diastolic dysfunction in the stage of impaired relaxation of LV.     

Left ventricular diastolic filling alterations in subjects with mitral valve prolapse: a Doppler echocardiographic study

To assess left ventricular diastolic filling in mitral valve prolapse (MVP), we studied 22 patients with idiopathic MVP and 22 healthy controls matched for sex, age, body surface area and heart rate. A two-dimensional, M-mode and Doppler echocardiographic examination was performed to exclude any cardiac abnormalities. The two groups had similar diastolic and systolic left ventricular volumes, left ventricle mass and ejection fraction. Doppler measurements of mitral inflow were: E and A areas (the components of the total flow velocity-time integral in the early passive period of ventricular filling, E; and the late active period of atrial emptying, A), the peak E and A velocities (cm.s-1), acceleration and deceleration half-times (ms) of early diastolic rapid inflow, acceleration time of early diastolic flow (AT), total diastolic filling time (DFT) (ms), and the deceleration of early diastolic flow (cm.s-2). From these measurements were calculate: peak A/E ratio (A/E), E area/A area, the early filling fraction, the atrial filling fraction, AT/DFT ratio. All the Doppler measurements reported are the average of three cardiac cycles selected at end expiration. The mean peak A velocity, A/E velocity ratio, deceleration half time and atrial filling fraction were each significantly higher for subjects presenting a MVP (60 +/- 12 cm.s-1 vs 49 +/- 14, P < 0.008; 98 +/- 13% vs 64 +/- 12%, P < 0.0001; 120 +/- 36 ms vs 92 +/- 11, P < 0.002; 0.45 +/- 0.14 vs 0.36 +/- 0.08, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of ambulatory blood pressure on left ventricular diastolic dysfunction in uncomplicated arterial systemic hypertension

To determine the relations of 24-hour blood pressure (BP) and its different phases with left ventricular (LV) diastolic filling, 125 subjects (mean age 46 years) not taking cardiac drugs were studied by Doppler echocardiography and ambulatory BP recording. Subjects (excluding those with coronary artery or valvular heart disease, heart failure, or diabetes) were classified into 2 groups according to the level of Doppler-derived ratio of peak early to atrial velocity (E/A ratio): 59 had E/A >1 (normal diastole), 62 had E/A <1 (impaired diastole), and 4 had E/A = 1. Patients with E/A <1 were older and had higher LV mass indexed for height, average 24-hour BP, average nighttime BP, and lower day-night BP decrease, whereas average daytime BP did not differ significantly between the 2 groups. Negative correlations of E/A were found with age, heart rate, office, average 24-hour and average nighttime systolic and diastolic BP, and LV mass index. In a multivariate model that included potentially confounding factors, only age (standardized beta coefficient = -0.52, p<0.00001), nighttime BP (beta = -0.28, p<0.0001), and heart rate (beta = -0.22, p<0.001) were independent predictors of E/A in the pooled population. In conclusion, LV diastolic function is more closely related to ambulatory, rather than to clinic, BP measurements, and high average nocturnal diastolic BP is a powerful marker of LV filling impairment.     

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BACKGROUND: Many factors influence diastolic function indexes obtained by monitoring left ventricular filling. Recent reports suggest that the study of myocardial wall velocity with Doppler tissue imaging (DTI) can give diastolic function parameters that are less affected by the same factors. An altered diastolic function has been demonstrated with invasive methods in patients with left ventricular hypertrophy (LVH). The aims of this study were 1) to compare a group of healthy subjects with a group of patients with LVH and presumably affected by diastolic dysfunction, to try to demonstrate if DTI could give new indexes to discriminate between the two groups; 2) to compare the indexes obtained with DTI against the ones given by Doppler study of left ventricular filling in the two populations. MATERIALS AND METHODS: Forty-two patients with LVH were compared to forty normal subjects. We studied the posterior wall velocity with pulsed DTI from parasternal view, measuring the early diastolic velocity (E'), the late diastolic velocity (A') and the E'/A' ratio. In addition, we estimated the usual ventricular filling parameters and the time interval between R wave of ECG and the peaks of E' and E waves. RESULTS: At left ventricular filling, patients with LVH showed an increase in A-wave peak velocity (mean 75.3 cm/s versus 66.4 cm/s; p < 0.05) and prolonged deceleration time (mean 216 ms versus 181 ms; p < 0.05), as compared to normal reference subjects. E-wave peak velocity and E/A ratio did not differ between the two groups. At DTI, patients with LVH had decreased early diastolic velocity (E') (mean 9 cm/s versus 12 cm/s; p < 0.05) and E'/A' ratio (mean 1.53 versus 1.91; p < 0.05) as compared to the control group. We observed an inverse correlation between E' wave and age in normal subjects. There was no correlation between the early diastolic myocardial velocity (E') and early inflow velocity (E) in both groups. A correlation was found between A and A' waves in normal subjects, but not in hypertrophic ones. The E'-wave peak always preceded the E-wave peak in all the subjects. CONCLUSION: Diastolic function indexes achieved by DTI can offer additional information that is independent of the data derived from left ventricular filling.     

Midwall fractional shortening is an independent predictor of left ventricular diastolic dysfunction in asymptomatic patients with systemic hypertension

Conventional measures of left ventricular (LV) systolic performance suggest that diastolic dysfunction precedes the development of systolic dysfunction in hypertension. Midwall fractional shortening is a new measure of systolic function that identifies hypertensive patients who have evidence of target-organ damage, impaired contractile reserve, and increased mortality. We therefore sought to determine whether depressed midwall fiber shortening is associated with abnormal diastolic function. Echocardiograms were obtained in 102 otherwise healthy hypertensive patients without treatment with normal conventional measures of systolic function. Of these, 15 had depressed midwall shortening based on previously described normative relations. Patients with depressed midwall shortening had slightly higher blood pressure. Abnormal diastolic function, defined as late (A) LV inflow velocity greater than early (E) velocity, was observed in 33% of those with normal midwall shortening but in 60% of those with depressed shortening (p <0.05). Patients with A/E >1 had lower absolute midwall fiber shortening (15 +/- 3% vs 18 +/- 3%, p <0.0001) but similar endocardial shortening. Patients with abnormal midwall shortening had higher A/E and longer isovolumic relaxation times (both p <0.05). In multivariate analysis, midwall fractional shortening, age, and heart rate were independent predictors (p <0.01) of A/E in a model including blood pressure, LV mass, and endocardial shortening. We conclude that subnormal midwall shortening predicts LV diastolic abnormalities in this population of hypertensive patients with otherwise normal measures of LV systolic function. Contrary to our previous understanding, depressed LV systolic performance, when identified with this newer method, occurs coincidentally with impaired diastolic function.     

Left ventricular diastolic properties of hypertensive patients measured by pulsed tissue Doppler imaging

Examination of left ventricular (LV) diastolic dysfunction in hypertensive patients has been based on parameters obtained from the transmitral flow velocity during pulsed Doppler echocardiography. However, these parameters are affected by loading conditions. We evaluated LV diastolic function along the longitudinal and transverse axes by pulsed tissue Doppler imaging (TDI) in 50 hypertensive (HT) patients and 36 age-matched healthy volunteers (N). Transmitral flow velocity was recorded by pulsed Doppler echocardiography. LV posterior wall motion velocity along the longitudinal and transverse axes also was recorded by pulsed TDI. In both groups, peak early diastolic velocity of the LV posterior wall (Ew) along the transverse axis (N: 15.8+/-5.2 cm/s, HT: 12.2+/-4.4 cm/s) was higher than that along the longitudinal axis (N: 12.7+/-3.1 cm/s, HT: 9.5+/-3.3 cm/s). Peak atrial systolic velocity of the LV posterior wall (Aw) along the longitudinal axis (N: 9.1+/-1.8 cm/s, HT: 9.7 +/-2.6 cm/s) significantly exceeded that along the transverse axis (N: 8.0+/-2.2 cm/s, HT: 8.4+/-2.4 cm/s) in both groups. The Ews were lower and the Aws were higher along both axes in the patient group than in the control group. The time intervals from the aortic component of the second heart sound to the peak of the early diastolic wave (IIA-Ews) along both the transverse (N: 142+/-18 ms, HT: 154+/-19 ms) and longitudinal (N: 151 16 ms, HT: 162+/-20 ms) axes were longer in the patient group. In 29 patients, Ews along both axes correlated negatively (transverse: r = -0.80, P < .0001; longitudinal: r = -0.71, P < .0001) and IIA-Ews correlated positively (transverse: r = 0.81, P < .0001; longitudinal: r = 0.74, P < .001) with the time constant of the LV pressure decay during isovolumic diastole. The Aws along both axes in the 24 patients without pseudonormalization in transmitral flow velocity correlated positively (transverse: r = 0.60, P < .001; longitudinal: r = 0.74, P < .0001) with the LV end-diastolic pressure. In conclusion, LV relaxation and filling along the longitudinal and transverse axes were impaired in many patients with hypertension. Pulsed TDI was useful for evaluating LV diastolic dynamics in this disease.     

Early effects of coronary artery bypass surgery and cold cardioplegic ischemia on left ventricular diastolic function: evaluation by computer-assisted transesophageal echocardiography

OBJECTIVE: Although left ventricular (LV) systolic function undergoes a temporary decrease after cardiopulmonary bypass (CPB) in patients undergoing coronary artery bypass grafting (CABG), data on the effects of CABG and cardioplegic arrest on LV diastolic function are contradictory. The objective of the present study was to further evaluate the effects of CABG and CPB on LV diastolic function. DESIGN: A prospective study. SETTING: A multi-institutional investigation at a university hospital. PARTICIPANTS: 20 patients on beta-receptor antagonists, scheduled for CABG and with a preoperative ejection fraction over 0.5. INTERVENTIONS: Central hemodynamic measurements, transesophageal LV short-axis images, and mitral Doppler flow profiles were obtained before and after volume loading that in turn was performed both before surgical incision and after weaning from CPB. MEASUREMENTS AND MAIN RESULTS: Heart rate, cardiac output, and peak atrial filling velocity increased; systemic vascular resistance decreased; whereas stroke volume, LV area ejection fraction, deceleration rate and slope of early diastolic filling, time-velocity integral of early diastolic filling, and the ratio between early and atrial peak filling velocity were unchanged post-CPB compared with pre-CPB. LV end-diastolic stiffness that was calculated for each patient pre-CPB and post-CPB using the formula: P = B*eS*A), where P is the LV filling pressure and A is the end-diastolic short-axis area, was unchanged post-CPB compared with pre-CPB. CONCLUSIONS: Both the active and passive components of LV diastolic function are well maintained shortly after CABG and cardioplegic arrest in patients with a good preoperative systolic LV function.     

A new approach for evaluation of left ventricular diastolic function: spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography

OBJECTIVES: To evaluate left ventricular diastolic function and differentiate the pseudonormalized transmitral flow pattern from the normal pattern, the propagation of left ventricular early filling flow was assessed quantitatively using color M-mode Doppler echocardiography. BACKGROUND: Because the propagation of left ventricular early filling flow is disturbed in the left ventricle with impaired relaxation, quantification of such alterations should provide useful indexes for the evaluation of left ventricular diastolic function. METHODS: Study subjects were classified into three groups according to the ratio of early to late transmitral flow velocity (E/A ratio) and left ventricular ejection fraction: 29 subjects with an ejection fraction > or = 60% (control group); 34 with an ejection fraction < 60% and E/A ratio < 1 (group I); and 25 with ejection fraction < 60% and E/A ratio > or = 1 (group II). The propagation of peak early filling flow was visualized by changing the first aliasing limit of the color Doppler signals. The rate of propagation of peak early filling flow velocity was defined as the distance/time ratio between two sampling points: the point of the maximal velocity around the mitral orifice and the point in the mid-left ventricle at which the velocity decreased to 70% of its initial value. High fidelity manometer-tipped measurement was performed in 40 randomly selected subjects. RESULTS: The rate of propagation decreased in groups I and II compared with that in the control group (33.8 +/- 13.8 [mean +/- SD] and 30.0 +/- 8.6 vs. 74.3 +/- 17.4 cm/s, p < 0.001, respectively) and correlated inversely with the time constant of left ventricular isovolumetric relaxation and the minimal first derivative of left ventricular pressure (peak negative dP/dt) (r = 0.82 and r = 0.72, respectively). CONCLUSIONS: Spatial and temporal analysis of filling flow propagation by color M-mode Doppler echocardiography was free of pseudonormalization and correlated well with the invasive variables of left ventricular relaxation.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Clinical application of pulsed Doppler tissue imaging for assessing abnormal left ventricular relaxation

Conventional assessment of left ventricular (LV) relaxation by calculating the time constant of LV pressure decay during the isovolumic diastole requires an invasive approach. Conversely, noninvasive parameters obtained by measuring isovolumic relaxation time and transmitral flow velocity often give inaccurate information. Using LV pressure curve, pulsed Doppler echocardiography, and pulsed Doppler tissue imaging in 38 patients with heart disease and 12 control subjects, we calculated the time constant and recorded transmitral flow velocity and motion velocities at the endocardial portions of the ventricular septum and LV posterior wall. Compared with the controls, patients exhibited a prolonged time constant, a decreased peak early diastolic velocity of the LV posterior wall, and a prolonged time interval from the second heart sound to the peak of the early diastolic wave. The time constant correlated well with the isovolumic relaxation time and various parameters calculated from the transmitral flow velocity, except in patients with elevated LV end-diastolic pressure. In all subjects, the time constant correlated negatively with the peak early diastolic velocity of the posterior wall and positively with the time from the second heart sound to the peak of the early diastolic wave. Thus, early diastolic parameters derived from the motion velocity of the LV posterior wall by pulsed Doppler tissue imaging were closely related to the time constant. This technique may allow noninvasive evaluation of abnormal LV relaxation in patients with various heart diseases.     

Two-year follow-up study to evaluate the reduction of left ventricular mass and diastolic function in mild to moderate diastolic hypertensive patients

OBJECTIVE: To compare the effects of two antihypertensive agents, amlodipine and lisinopril, on left ventricular mass and diastolic filling in patients from primary care centers with mild to moderate diastolic hypertension. STUDY DESIGN: A second-year, open follow-up of a prospective, double-blind, randomized, parallel group, comparative study. METHODS: Male and female patients between 25 and 75 years-of-age with elevated diastolic blood pressure (four measurements > or = 95 mmHg from multiple measurements taken on three occasions and average diastolic blood pressure < 115 mmHg) were recruited from a population survey. After 4 weeks' placebo run-in, 71 patients were included of whom 60 finished the first study year and 51 finished the second study year. Patients were randomly assigned to receive doses of 5-10 mg amlodipine or 10-20 mg lisinopril, which were titrated on the basis of the effects on blood pressure. Primary endpoints were left ventricular mass index (LVMI) and early to atrial peak filling velocity. Office and ambulatory blood pressure were considered secondary endpoints. RESULTS: The decrease in blood pressure was equal for both treatment regimens in the first year. A statistically significant (P< 0.001) decrease in LVMI in both treatment groups was observed in the first year [-11.0 g/m2 (95% Cl -6.0 to -16.1) in the amlodipine group and -12.6 g/m2 (95% Cl -8.2 to -17.0) in the lisinopril group]. Early to atrial peak filling velocity did not change significantly within the treatment groups in the first year [+0.07 (95% CI -0.01 to +0.15) in the amlodipine group and +0.01 (95%9 Cl -0.06 to +0.08) in the lisinopril group. Blood pressure, LVMI and early to atrial peak filling velocity did not change in the second year of treatment. No significant differences in primary and secondary endpoints between treatment groups were found in the first or second year. Conclusion: The effects of amlodipine and lisinopril on left ventricular mass and early to atrial filling peak velocity after 2 years of treatment were similar and these effects were already observed after 1 year of treatment. Additional studies of longer duration (> or = 4 years) and with a larger sample size are recommended.     

Diastolic function parameters and atrial arrhythmias in patients with arterial hypertension

OBJECTIVE: To investigate in patients with arterial hypertension (HT) the extent of left ventricular (LV) hypertrophy and diastolic function in relation to atrial arrhythmias. PATIENTS AND METHODS: In 112 hypertensive patients (40 women, 72 men; mean age 50 +/- 6.6 years) with a mean systolic blood pressure for the cohort of 170 +/- 5 mmHg, their first invasive coronary angiography was performed between July 1995 and October 1997 because of angina pectoris and/or an abnormal stress electrocardiogram. After excluding coronary heart disease LV dimensions and diastolic function were measured by echocardiography; in 59 of the 112 patients LV hypertrophy was demonstrated. In addition, long-term blood pressure monitoring, exercise and long-term electrocardiography, late-potential analysis and measurement of heart rate variability were undertaken. The control group consisted of 51 patients without arterial hypertension after exclusion of coronary heart disease. RESULTS: Even in the hypertensive patients without LV hypertrophy diastolic LV function and ergometric exercise capacity were reduced. The risk of LV arrhythmias was significantly higher in patients with LV hypertrophy than those without and in the control group, as measured by the complexity of atrial arrhythmias (P < 0.001), the incidence of abnormal late potentials (P < 0.001) and reduction in heart rate variability (29.3 +/- 5.3 ms vs 47.8 +/- 12.1 ms vs 60.7 +/- 6.6 ms; P < 0.001). There were similar results regarding severe complex atrial arrhythmias (38.5 vs 15.0 vs 0%; P < 0.001). The incidence of atrial arrhythmias correlated with the LV diameter (r = 0.68, P < 0.001), LV morphological dimensions and diastolic function (isovolumetric relaxation time r = 0.44, P < 0.001) and the ratio of early to late diastolic inflow (r = 0.46; P < 0.001). CONCLUSIONS: Hypertensive patients have a higher risk of atrial and ventricular arrhythmias, depending on the degree of LV hypertrophy. But atrial arrhythmias, in contrary to ventricular arrhythmias, are also closely related to abnormalities in LV diastolic function.     

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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 approximately 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 < or = 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 < or = 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.     

Prognostic importance of left ventricular diastolic filling velocity profiles in dilated cardiomyopathy

To determine the prognostic importance of pulsed Doppler-derived left ventricular diastolic filling velocity profiles and the relationship between Doppler variables and clinical functional status, the follow-up outcome of 58 patients with dilated cardiomyopathy and symptoms of left ventricular dysfunction was analysed. During a mean follow-up period of 31.2 +/- 12.8 months, 23 died of either progressive pump failure or sudden death. Peak early filling velocity (E) was higher and late atrial filling velocity (A) lower in nonsurvivors than in survivors. The E/A ratio was higher and the deceleration time (DT) of early diastole shorter in nonsurvivors. The mortality was significantly higher in patients with an E/A ratio > 2 or a DT < 150 ms than in those without. Repeated Doppler echocardiographic examinations in 31 of 35 survivors after intense treatment showed decreased E, increased A, reduced E/A ratio and prolonged DT in 18 patients with clinical functional improvement, whereas these measurements were unaltered in the remaining 13 patients whose functional status was unchanged or deteriorated. This study suggests that pulsed Doppler-derived left ventricular diastolic filling variables may be important predictors of outcome in dilated cardiomyopathy and provide useful measures in observing the effects of therapy during long-term follow-up of the patients.     

Evaluation of transmitral flow velocity profile in supine and sitting positions by pulsed Doppler echocardiography in elderly hypertensives

To evaluate left ventricular diastolic filling properties in elderly hypertensive case with left ventricular hypertrophy (LVH), we investigated the influence of postural change from a supine to sitting position on transmitral flow velocity profile as assessed by pulsed Doppler echocardiography in 12 normotensives (N group) and 24 hypertensives, aged 65 to 80 years. Hypertensive subjects were divided into two groups on the basis of left ventricular mass index (LVMI): 12 hypertensives without LVH (H1 group; LVMI < 130 g/m2); 12 hypertensives with LVH (H2 group; LVMI > 130 g/m2). Peak early filling velocity (E), peak atrial filling velocity (A) and the E/A ratio were similar in the three groups in the supine position. The postural change decreased E and A in N and H1 groups. On the other hand, the change decreased E, but not A in the H2 group. The E/A ratio was decreased in the H2 group compared with both the N and H1 group in the sitting position. As a result, the sitting position increased atrial contribution to diastolic filling in the H2 group. These observations indicate that a reduction in preload changes the transmitral flow velocity profile in elderly hypertensives with left ventricular hypertrophy. The Doppler alterations may be related to impaired left ventricular diastolic function.     

Reversibility of changes in left and right ventricular geometry and hemodynamics in pulmonary hypertension. Echocardiographic characteristics before and after pulmonary thromboendarterectomy

Pulmonary thromboendarterectomy (PTE) leads to an acute decrease of right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension. We investigated the changes in right and left ventricular (LV) geometry and hemodynamics by means of transthoracic echocardiography. The prospective study was performed in 14 patients (8 female, 6 male; age 55 +/- 20 years) before and 18 +/- 12 days after PTE. Total pulmonary vascular resistance and systolic pulmonary artery pressure were significantly decreased (PVR: preoperative 986 +/- 318, postoperative 323 +/- 280 dyn x s/cm5, p < 0.05; PAP preoperative 71 +/- 40, postoperative 41 +/- 40 mm Hg + right atrial pressure, p < 0.05). End diastolic and end systolic RV area decreased from 33 +/- 12 to 23 +/- 8 cm2, respectively, from 26 +/- 10 to 16 +/- 6 cm2, p < 0.05. There was an increase in systolic RV fractional area change from 20 +/- 12 to 30 +/- 16%, p < 0.05. RV systolic pressure rise remained unchanged (516 +/- 166 vs. 556 +/- 128 mm Hg/sec). LV ejection fraction remained within normal ranges (64 +/- 16 vs. 62 +/- 12%). Echocardiographically determined cardiac index increased from 2.8 +/- 0.74 to 4.1 +/- 1.74 l/min/m2. A decrease in LV excentricity indices (end diastolic: 1.9 +/- 1 vs. 1.1 +/- 0.3, end systolic: 1.7 +/- 0.6 vs. 1.1 +/- 0.4, p < 0.05) proved a normalization of preoperatively altered septum motion. LV diastolic filling returned to normal limits: (E/A ratio: 0.62 +/- 0.34 vs. 1.3 +/- 0.8; p < 0.05); Peak E velocity: 0.51 +/- 0.34 vs. 0.88 +/- 0.28 m/sec, p < 0.05; Peak A velocity: 0.81 +/- 0.36 vs. 0.72 +/- 0.42 m/sec, ns; E deceleration velocity: 299 +/- 328 vs. 582 +/- 294 cm/sec2, p < 0.05; Isovolumic relaxation time: 134 +/- 40 vs. 83 +/- 38 m/sec, p < 0.05). We could show a marked decrease in RV afterload shortly after PTE with a profound recovery of right ventricular systolic function--even in case of severe pulmonary hypertension. A decrease in paradoxic motion of the interventricular septum and normalization of LV diastolic filling pattern resulted in a significant increase of cardiac index.     

Reduced left ventricular hypertrophy in type 1 diabetic patients with end-stage renal failure. A comparison between groups investigated 1977-80 and 1991-93

BACKGROUND: During the last decade, control of hypertension, oedema, anaemia, uraemia, and blood glucose has improved in patients with diabetic nephropathy. We have investigated whether this has influenced cardiac function at the time of end-stage renal failure. STUDY DESIGN: Echocardiographic investigations were performed in 26 type 1 diabetic patients evaluated for kidney transplantation and the results compared with those obtained in healthy controls and in a similar group of patients investigated in 1977-1980. RESULTS: Blood pressure was 153 +/- 21/85 +/- 12 mmHg versus 174 +/- 17/91 +/- 9 (recent group versus early group). The left ventricular (LV) diameter index, a measure of volaemia, was increased in systole and diastole in the early but not in the recent group. Both groups had LV hypertrophy, but this was much less pronounced in the recent group; posterior wall thickness was 1.1 +/- 0.16 cm versus 1.3 +/- 0.26 cm (P = 0.0001) and LV mass index 132 +/- 43 g/m2 versus 166 +/- 44 g/m2 (P = 0.009). Blood pressure correlated significantly with indices of LV hypertrophy in the recent group. Systolic function was normal in both groups but diastolic function was disturbed in both and to the same extent, atrial systole contributing by 27 +/- 14% to ventricular filling. CONCLUSION: Better treatment of hypertension, fluid overload, and uraemia has led to less pronounced LV hypertrophy. The remaining correlation with blood pressure suggests that more could be gained by intensified antihypertensive treatment.