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At least 19 recordsLinked to original sources

PubMed2001

Left ventricular early diastolic inflow velocity and atrial ventricular plane downward velocity: useful parameters to test diastolic function in clinical practice? Diastolic parameters tested in a clinical setting.

AIMS: To study the clinical value of the colour-M-mode slope of the early diastolic left ventricular filling phase (Vp) and the early diastolic downward M-mode slope of the left atrioventricular plane displacement (EDS), compared with diastolic function assessed by traditional Doppler evaluation. METHODS AND RESULTS: In 65 consecutive patients EDS and Vp were compared with a four-degree traditional diastolic function classification, based on pulsed Doppler assessment of the early to atrial transmitral flow ratio (E/A), the E-wave deceleration time (Edt), and the systolic to diastolic (S/D) pulmonary venous inflow ratio. Vp (P=0.006) and EDS (P=0.045) were related to traditional diastolic function (Kruskal--Wallis analysis). EDS showed a trend brake between the moderate and severe diastolic dysfunction groups by traditional Doppler evaluation. Vp and EDS correlated weakly in simple linear regression analysis (r=0.33). Vp and EDS discriminated poorly between normal and highly abnormal diastolic function. CONCLUSIONS: Vp and EDS were significantly related to diastolic function by traditional Doppler evaluation. They were, however, not useful as single parameters of left ventricular diastolic function due to a small difference between normal and highly abnormal values, allowing for little between-measurement variability. Consequently, these methods for the evaluation of left ventricular diastolic function do not add significantly to traditional Doppler evaluation.

Adult↗

PubMed2006

Triphasic mitral inflow velocity with mid-diastolic flow: the presence of mid-diastolic mitral annular velocity indicates advanced diastolic dysfunction.

Mitral inflow filling pattern usually consists of 2 forward flow velocities in sinus rhythm: early rapid filling (E) and late filling with atrial contraction (A). However, additional mid-diastolic flow velocity may be present resulting in triphasic mitral inflow filling pattern. When mitral inflow is triphasic, mitral annulus velocity recorded by tissue Doppler imaging (TDI) frequently demonstrates a mid-diastolic component (L'). The significance of L' has not been explored previously. The purpose of this study was to explore possible mechanisms and clinical implications of triphasic mitral inflow with or without L' using TDI and proBNP. Of 9004 patients who underwent transthoracic echocardiography from March to November 2003, 83 (0.9%) patients (33 male, 50 female; mean age, 63+/-10 years) with a triphasic mitral inflow velocity pattern, including mid-diastolic flow velocity of at least 0.2m/s, and sinus rhythm were prospectively identified in our clinical echocardiography laboratory. Peak velocity of E, mid-diastolic (L), and A, and deceleration time (DT) of the E wave velocity were measured. Diastolic mitral annular velocities were measured at the septal corner of the mitral annulus by TDI from the apical 4-chamber view. ProBNP was measured at the time of echocardiogram using a quantitative electrochemiluminescence immunoassay. Mean heart rate was 54+/-6 beats/min (range, 40-67). Mean left ventricular (LV) ejection fraction (EF) was 64+/-13% and LV systolic dysfunction (EF<40%) was present in only 6 (7%). Patients were classified into 2 groups: group 1 (n=47) included those who had L' and group 2 (n=36) included those without L'. Group 1 patients had significantly higher peak velocity (35+/-14 vs 26+/-6 cm/s, p=0.0002) and TVI (35+/-14 vs 26+/-6 cm/s, p=0.0002) of L, E/E' (18+/-8 vs 14+/-6, p=0.02), and left atrial volume index (42+/-14 vs 34+/-10 ml/m(2), p=0.0037). E' (4.7+/-1.3 vs 6.2+/-2.3 cm/s, p=0.001) and A' (6.2+/-2.0 vs 8.6+/-3.4 cm/s, p=0.0006) were significantly lower in group 1 compared with those of group 2. ProBNP was significantly higher in group 1 (847+/-1461 vs 438+/-1039 pmol/l, p=0.0012) and it was above normal in all except in 1 patient of group 1. In conclusion, the presence of L' in subjects with triphasic mitral inflow velocity pattern with mid-diastolic flow is associated with higher E/E', elevated proBNP and enlarged left atrium indicating advanced diastolic dysfunction with elevated filling pressures. This unique mitral annular velocity pattern should be helpful in identifying the patients with advanced diastolic dysfunction and increased LV filling pressures.

Adult↗

PubMedDate not supplied

Progressive intraventricular drop of early diastolic flow velocity reflects impaired active ventricular diastolic function in hypertensive heart disease: comparative study between early diastolic and atrial contraction phases.

Left ventricular (LV) diastolic function in the early diastolic phase includes both active and passive processes, but in the atrial contraction phase it includes only passive processes. To elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and LV diastolic process, 31 normal volunteers and 12 patients with hypertensive heart disease were studied. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography from the apical long-axis view with the guidance of Doppler color-flow imaging. Although the ratio of regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased from the mitral tip to the apex to the same degree in the normal volunteers and patients with hypertensive heart disease, there was a significant difference in the intraventricular dispersion of the early diastolic flow velocity between the two groups. These results suggest that the progressive intraventricular drop of the flow velocity in the early diastolic phase in patients with hypertensive heart disease may reflect the impairment of active rather than passive LV diastolic function.

Adult↗

PubMed2003

Flow propagation velocity is not a simple index of diastolic function in early filling. A comparative study of early diastolic strain rate and strain rate propagation, flow and flow propagation in normal and reduced diastolic function.

BACKGROUND: Strain Rate Imaging shows the filling phases of the left ventricle to consist of a wave of myocardial stretching, propagating from base to apex. The propagation velocity of the strain rate wave is reduced in delayed relaxation. This study examined the relation between the propagation velocity of strain rate in the myocardium and the propagation velocity of flow during early filling. METHODS: 12 normal subjects and 13 patients with treated hypertension and normal systolic function were studied. Patients and controls differed significantly in diastolic early mitral flow measurements, peak early diastolic tissue velocity and peak early diastolic strain rate, showing delayed relaxation in the patient group. There were no significant differences in EF or diastolic diameter. RESULTS: Strain rate propagation velocity was reduced in the patient group while flow propagation velocity was increased. There was a negative correlation (R = -0.57) between strain rate propagation and deceleration time of the mitral flow E-wave (R = -0.51) and between strain rate propagation and flow propagation velocity and there was a positive correlation (R = 0.67) between the ratio between peak mitral flow velocity / strain rate propagation velocity and flow propagation velocity. CONCLUSION: The present study shows strain rate propagation to be a measure of filling time, but flow propagation to be a function of both flow velocity and strain rate propagation. Thus flow propagation is not a simple index of diastolic function in delayed relaxation.

Blood Flow Velocity↗

PubMed2004

Lack of relationship between Doppler indices of diastolic function and left ventricular pressure transients in patients with definite diastolic heart failure.

OBJECTIVES: The purpose of this study was to compare invasive with noninvasive indices of diastolic function in a well-defined group of patients with diastolic dysfunction and a history of diastolic heart failure. BACKGROUND: Patients with heart failure and a normal left ventricular (LV) ejection fraction comprise a very large portion of the heart failure population and most are thought to have diastolic heart failure. While clinical and Doppler criteria for diastolic dysfunction and diastolic heart failure have been developed, there remains some controversy about the need for invasive cardiac catheterization and/or echo-Doppler evaluation of LV diastolic function. To date, there is no consensus as to the utility of these 2 methods in the diagnosis of diastolic heart failure. METHODS: Forty-seven patients (mean age 58 +/- 11 years) with a history of congestive heart failure and preserved ejection fraction (> or =50%) by echocardiography underwent a combined hemodynamic/echo-Doppler study. Patients with coronary disease were excluded. Invasive parameters of LV diastolic function (tau, LV diastolic pressures) and Doppler parameters (peak E, peak A, E/A ratio, isovolumic relaxation time, and E deceleration time) were measured using standard techniques. RESULTS: There was a close correlation between invasively-determined parameters (tau vs end diastolic pressure: r = 0.62, P <.001). The relationships between standard Doppler parameters and LV diastolic pressures were uniformly poor. However, the relationship between Doppler isovolumic relaxation time and tau improved considerably when patients were subgrouped by hemodynamic load. CONCLUSIONS: Standard echo-Doppler indices of diastolic function correlate poorly with LV diastolic pressure transients. The diagnosis of diastolic heart failure cannot be made on the basis of a single echo-Doppler parameter but, rather, all parameters must be examined in concert and used in combination with clinical observations.

Cardiac Catheterization↗

PubMed1984

Left ventricular diastolic pressure-segment length relations and end-diastolic distensibility in dogs with coronary stenoses. An angina physiology model.

Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.

Angina Pectoris↗

PubMed2002

Left ventricular long-axis changes in early diastole and systole: impact of systolic function on diastole.

Impaired long-axis motion is a sensitive marker of systolic myocardial dysfunction, but no data are available that relate long-axis changes in systole with those in diastole, particularly in subjects with diastolic dysfunction and a 'normal' left ventricular (LV) ejection fraction. A total of 311 subjects (including 105 normal healthy volunteers) aged 20-89 years with variable degrees of systolic function (LV ejection fraction range 0.15-0.84) and diastolic function were studied using tissue Doppler echocardiography and M-mode echocardiography to determine mean mitral annular amplitude and peak velocity in systole and early and late diastole. The LV systolic mitral annular amplitude (S(LAX), where LAX is long-axis amplitude) and peak velocity (S(m)) correlated well with the respective early diastolic components (E(LAX) and E(m)) and late diastolic (atrial) components (A(LAX) and A(m)). A non-linear equation fitted better than a linear relationship (non-linear model: S(LAX) against E(LAX), r(2)=0.67; S(m) against E(m), r(2)=0.60; S(LAX) against A(LAX) and S(m) against A(m), r(2)=0.42). After adjusting for age, sex and heart rate, linear relationships of early diastolic (E(LAX), r(2)=0.70; E(m), r(2)=0.60) and late diastolic (A(LAX), r(2)=0.61; A(m), r(2)=0.64) long-axis amplitudes and velocities with the respective values for S(LAX) and S(m) were found, even in those subjects with apparently 'isolated' diastolic dysfunction. Long-axis changes in systole or diastole did not correlate with Doppler mitral velocities. We conclude that ventricular long-axis changes in early diastole are closely related to systolic function, even in subjects with diastolic dysfunction. 'Pure' or isolated diastolic dysfunction is uncommon.

Adult↗

PubMed2006

Are left ventricular diastolic function and diastolic asynchrony important determinants of response to cardiac resynchronization therapy?

Cardiac resynchronization therapy (CRT) has been shown to reduce symptoms and reverse left ventricular (LV) remodeling. It is not known, however, whether diastolic function will improve after CRT and diastolic asynchrony will predict LV reverse remodeling. Seventy-six patients (mean age 65 +/- 12 years, 74% men) who received CRT were studied at baseline and after 3 months. Diastolic function was assessed by transmitral Doppler and tissue Doppler imaging. LV systolic and diastolic asynchrony were assessed by the time to peak myocardial contraction (Ts) and early diastolic relaxation (Te) using the 6 basal, 6 mid-segmental model. There were 42 responders (55%) with LV reverse remodeling (defined as a reduction of LV end-systolic volume >or=15%). Parameters of systolic function were significantly improved only in the responders. For diastolic function, there were reductions of transmitral E velocity in the 2 groups, without any change in atrial velocity or the E/A ratio. Tissue Doppler imaging revealed that myocardial early diastolic velocity was unchanged in responders but was significantly worsened in nonresponders. The systolic asynchrony index (the SD of Ts of 12 LV segments) correlated significantly with LV reverse remodeling (r = -0.64, p <0.001) but not the diastolic asynchrony index (the SD of Te of 12 LV segments) (r = -0.10, p = NS). The systolic asynchrony index was the only independent predictor of reverse remodeling (beta = -0.99, 95% confidence interval -1.41 to -0.58, p <0.001). In conclusion, CRT improves systolic function and systolic asynchrony but has a neutral effect on diastolic function and diastolic asynchrony. LV reverse remodeling response is determined by the severity of prepacing systolic asynchrony but not diastolic asynchrony or the diastolic filling pattern.

Aged↗

PubMed1999

Left Ventricular Regional Diastolic Dysfunction in Patients with First Myocardial Infarction Determined by Diastolic Motion of the Atrioventricular Plane.

Motion of the left ventricular [left ventricle (LV)] atrioventricular (AV) plane has been used to assess systolic LV function. The method has not been used properly to assess diastolic function, especially after a first myocardial infarction (MI). The diastolic function was assessed in 47 previously healthy patients with a first MI assessed by echocardiographic diastolic motion of the LV AV plane. The motion of the AV plane was recorded at four different LV sites, that is, at the septal, anterior, lateral, and inferior walls. Two distinct phases of motion were noticed during diastole at all the sites: one at the early diastole caused by rapid filling of the LV and the other at late diastole during the atrial contraction. The contribution of left atrial contraction to LV filling at different LV sites was calculated by relating the magnitude of the motion caused by atrial contraction to the total diastolic AV plane motion at the respective sites. These left atrial contributions were regarded as the regional diastolic function of the respective LV sites. The global LV diastolic function was determined from the left atrial contribution to total AV plane motion from the above four sites. Patients with anterior MI had a significantly lower ejection fraction than those with inferior MI (41% and 49%, respectively; P < 0.01). Compared with age-matched healthy subjects, the regional atrial contribution to diastolic filling was significantly higher at the anterior wall in anterior MI (38% and 52%, respectively; P < 0.001) and at the inferior wall in inferior MI (43% and 53%, respectively; P < 0.01). The atrial contribution to global LV filling was increased in anterior MI (48% compared with 42% in healthy subjects; P < 0.05) but not in inferior MI. These findings suggest that the diastolic AV plane displacement (AVPD) may be used to assess both the regional and the global diastolic function in patients following an MI.

Journal Article↗

PubMed2006

Role of left ventricular regional diastolic abnormalities for global diastolic dysfunction in patients with hypertrophic cardiomyopathy.

BACKGROUND: The usefulness of Doppler strain rate imaging for assessment of left ventricular regional diastolic function has not been fully determined. OBJECTIVE: We aimed to clarify the relationships between diastolic strain rates and global diastolic function and find a useful index for regional diastolic function in patients with hypertrophic cardiomyopathy (HCM). METHODS: Strain rate curves were obtained using an apical approach at 12 different sites of the left ventricular myocardium in 25 patients with HCM and 20 control subjects, and peak early diastolic strain rate (ESR), peak late diastolic strain rate, and the time from QRS to ESR were measured. The flow propagation velocity was measured using color M-mode Doppler echocardiography as a global diastolic index. RESULTS: Each of the spatially averaged values of ESR and ESR/peak late diastolic strain rate and the coefficients of variation of time from QRS to ESR was significantly correlated with flow propagation velocity, but the best correlation was observed in ESR. Although both ESR and peak late diastolic strain rate of each myocardial segment of patients with HCM tended to decrease as the wall thickness increased, only ESR significantly decreased even in the segments without apparent hypertrophy. CONCLUSIONS: In patients with HCM, the reduction of ESR was more closely associated with global diastolic dysfunction than asynchrony, and ESR may be a useful and sensitive index for regional diastolic function.

Cardiomyopathy, Hypertrophic↗

PubMed2000

Effects of a single dose of oral estrogen on left ventricular diastolic function in hypertensive postmenopausal women with diastolic dysfunction.

OBJECTIVE: To evaluate the acute effects of a single dose of oral estrogen on left ventricular diastolic function in hypertensive postmenopausal women with diastolic dysfunction. DESIGN: Prospective, double-blind, placebo-controlled, clinical study. SETTING: Cardiology and postmenopausal outpatient clinics of a university hospital. PATIENT(S): Thirty postmenopausal women with hypertension (diastolic blood pressure of >90 mm Hg) and left ventricular diastolic dysfunction (mitral E/A ratio [the ratio of peak velocity of early mitral diastolic filling to late diastolic filling] of <1 and isovolumic relaxation time of >100 ms) were included in the study. Thirty normotensive postmenopausal women with normal left ventricular diastolic function served as the control group. INTERVENTION(S): Conjugated equine estrogen (0.625 mg) was given orally. Left ventricular diastolic function was assessed by Doppler echocardiography at baseline and 3 hours after the administration of estrogen. MAIN OUTCOME MEASURE(S): Left ventricular diastolic filling as assessed by Doppler echocardiography. RESULT(S): Estrogen had no effect on heart rate or blood pressure in either study group. The baseline E/A ratios were 0.72 +/- 0.26 and 1.22 +/- 0.30, and the isovolumic relaxation times were 122 +/- 18 ms and 89 +/-14 ms in the hypertensive and normotensive groups, respectively. Estrogen had no significant effect on any of the Doppler parameters in the normotensive group. In the hypertensive group, there was a trend toward normalization of the E/A ratio (from 0.73 +/- 0.11 to 0.84 +/- 20) and a significant improvement in the isovolumic relaxation time (from 124 +/- 20 ms to 105 +/- 13 ms) in response to the administration of estrogen compared with placebo. CONCLUSION(S): A single dose of oral estrogen caused a significant improvement in left ventricular diastolic filling in hypertensive postmenopausal women with diastolic dysfunction.

Blood Pressure↗

PubMedDate not supplied

Left ventricular diastolic function assessment by tissue Doppler echocardiography in relation to hormonal replacement therapy in postmenopausal women with diastolic dysfunction.

The objective of this study was to evaluate the effect of hormone replacement therapy (HRT) regimens on left ventricular diastolic function by using mitral pulsed wave Doppler (MPWD) and tissue Doppler velocities (TDE). Seventy-eight postmenopausal women with normotensive and impaired diastolic left ventricular filling were included in the study. All the patients began a six-cycle HRT course. This formulation consisted of E2 valerate plus Medroxy progesterone acetate (MPA). Left ventricular diastolic function at rest was evaluated by M-mode, two-dimensional, MPWD and TDE in 78 postmenopausal women with normal blood pressure before the treatment for 6 months of HRT. The M-mode, two-dimensional, and MPWD parameters assessed were heart rate, systolic blood pressure, diastolic blood pressure, left ventricular mass index, ejection fraction of the left ventricle (EF), septal (IVS) and posterior wall (PW) thickness, left ventricular end-systolic (LVESD) and end-diastolic (LVEDD) diameter, left atrial diameter, peak early diastolic velocity (E), peak atrial velocity (A), E/A ratio, E acceleration time, E deceleration time, diastolic filling period, and isovolumic relaxation time (IVRT). The TDE parameters assessed were peak early diastolic velocity (E'), peak late diastolic velocity (A'), peak systolic velocity, E'/A' ratio, E' acceleration time, E' deceleration time, IVRT', and E/E' ratio. Quantitative data were analyzed using Student t test. Among the MPWD parameters, peak A velocity, E deceleration time, and IVRT significantly decreased, while peak E velocity and E/A ratio increased after a 6-month treatment. From the point of TDE parameters, E' velocity and E'/A' ratio increased, while A' velocity, E' deceleration time, E/E' ratio and IVRT' decreased. Some MPWD and TDE parameters were partially reversed after HRT. TDE velocities and especially E/E' ratio may provide better and true information of the diastolic function. TDE parameters were independent from the preload and did not produce pseudonormal pattern. HRT may cause increase in the blood volume and produce pseudonormal pattern in transmitral flow. In that case, TDE may be a beneficial method for evaluation of diastolic function.

Diastole↗

PubMed2001

Heart failure with a normal ejection fraction: is measurement of diastolic function necessary to make the diagnosis of diastolic heart failure?

BACKGROUND: The diagnosis of diastolic heart failure is generally made in patients who have the signs and symptoms of heart failure and a normal left ventricular (LV) ejection fraction. Whether the diagnosis also requires an objective measurement of parameters that reflect the diastolic properties of the ventricle has not been established. METHODS AND RESULTS: We hypothesized that the vast majority of patients with heart failure and a normal ejection fraction exhibit abnormal LV diastolic function. We tested this hypothesis by prospectively identifying 63 patients with a history of heart failure and an echocardiogram suggesting LV hypertrophy and a normal ejection fraction; we then assessed LV diastolic function during cardiac catheterization. All 63 patients had standard hemodynamic measurements; 47 underwent detailed micromanometer and echocardiographic-Doppler studies. The LV end-diastolic pressure was >16 mm Hg in 58 of the 63 patients; thus, 92% had elevated end-diastolic pressure (average, 24+/-8 mm Hg). The time constant of LV relaxation (average, 51+/-15 ms) was abnormal in 79% of the patients. The E/A ratio was abnormal in 48% of the patients. The E-wave deceleration time (average, 349+/-140 ms) was abnormal in 64% of the patients. One or more of the indexes of diastolic function were abnormal in every patient. CONCLUSIONS: Objective measurement of LV diastolic function serves to confirm rather than establish the diagnosis of diastolic heart failure. The diagnosis of diastolic heart failure can be made without the measurement of parameters that reflect LV diastolic function.

Cardiac Catheterization↗

PubMed1997

[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].

UNLABELLED: 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.

Adult↗

PubMed1983

Diastolic function in hypertrophic cardiomyopathy: effects of propranolol and verapamil on diastolic stiffness.

In patients with hypertrophic cardiomyopathy (HCM), impaired left ventricular (LV) relaxation and diastolic filling have been reported. Therefore, we determined LV diastolic stiffness in nine patients with HCM before and 10 to 15 min after 0.15 mg/kg propranolol i.v. (group 1) and in six patients with HCM before and 10 to 15 min after 0.1 mg/kg verapamil i.v. (group 2). Simultaneous LV cineangiography and high-fidelity pressure measurements were performed in group 1 and simultaneous M-mode echocardiography and high-fidelity pressure measurements in group 2. Passive LV chamber stiffness was determined in group 1 from the diastolic pressure-volume data using an exponential three-parameter model: P = ae beta V + C, where P = pressure, alpha = intercept, beta = constant of chamber stiffness, V = volume and C = baseline pressure. Passive LV myocardial stiffness was estimated in group 2 from the diastolic stress-strain data using a viscoelastic model: sigma = alpha' (e beta' epsilon -1) + eta epsilon, where sigma = meridional wall stress, alpha = intercept, beta' = constant of myocardial stiffness, epsilon = midwall strain, eta = constant of myocardial viscosity and epsilon = strain rate. LV relaxation was assessed from the time constant of LV pressure decay (T) by plotting LV pressure versus negative dP/dt. LV diastolic filling was evaluated from peak and mean LV filling rate in group 1 and from peak and mean midwall lengthening rate in group 2. LV chamber and myocardial stiffness, respectively, remained unchanged before and after administration of propranolol (beta = 0.054 and 0.047) and verapamil (beta' = 14.8 and 12.6); however, the time constant of LV pressure decay T increased significantly in group 1 from 45 to 66 ms (P less than 0.05) and decreased significantly in group 2 from 53 to 43 ms (P less than 0.05). Parallel to the changes in LV isovolumic relaxation, mean LV diastolic filling rate decreased significantly in group 1 from 257 to 196 ml m-2 s-1 (P less than 0.025) and mean LV midwall lengthening rate increased significantly in group 2 from 2.37 to 4.31 cm/sec (P less than 0.05). It is concluded that LV diastolic stiffness remains unchanged in patients with HCM after propranolol and verapamil. LV relaxation and mean diastolic filling, however, are impaired in patients with HCM following propranolol but are improved after verapamil. Thus, the beneficial effect of verapamil on diastolic mechanics is related to improved relaxation and diastolic filling rather than to changes in LV diastolic stiffness.

Cardiomyopathy, Hypertrophic↗

PubMed1995

Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction.

Mitral flow velocity patterns are frequently "normalized" by the alteration in the loading condition even in the presence of left ventricular (LV) diastolic dysfunction. In addition, a simple index, the ratio of mitral peak early diastolic flow velocity to mitral peak flow velocity at atrial contraction, is not obtainable in patients with atrial fibrillation (Af). Thus these limitations hamper the value of analyzing the mitral flow velocity pattern in the assessment of abnormal LV diastolic characteristics. This study was designed to elucidate the hypothesis that peak early diastolic flow velocity decreases progressively from the base to the apex in patients with LV diastolic dysfunction. Regional diastolic flow velocity patterns at 1, 2, or 3 cm from the mitral tip toward the apex were simultaneously recorded with the mitral flow velocity pattern by using multigate pulsed Doppler echocardiography in 42 subjects with normal LV function (31 normal volunteers and 11 patients with Af only), 17 patients with hypertensive heart disease, and 22 patients with dilated cardiomyopathy. In the normal subjects early diastolic flow velocity at the mitral tip was maintained at the positions 1 to 3 cm away from the tip into the LV cavity. In contrast, regional peak early diastolic flow velocity progressively decreased toward the apex in patients with hypertensive heart disease and dilated cardiomyopathy. These findings were observed even in patients with a normalized mitral flow velocity pattern or those with Af. Thus the assessment of the intraventricular decrease in peak early diastolic flow velocity may be useful in detecting LV diastolic dysfunction, particularly in patients with Af or a "normalized" mitral flow velocity pattern.

Adult↗

PubMed2006

Diastolic and systolic asynchrony in patients with diastolic heart failure: a common but ignored condition.

OBJECTIVES: The present study aimed to examine whether diastolic and systolic asynchrony exist in diastolic heart failure (DHF) and their prevalence and relationship to systolic heart failure (SHF) patients. BACKGROUND: Few data exist on mechanical asynchrony in DHF. METHODS: Tissue Doppler echocardiography was performed in 373 heart failure patients (281 with SHF and 92 with DHF) and 100 normal subjects. Diastolic and systolic asynchrony was determined by measuring the standard deviation of time to peak myocardial systolic (Ts-SD) and peak early diastolic (Te-SD) velocity using a 6-basal, 6-mid-segmental model, respectively. RESULTS: Both heart failure groups had prolonged Te-SD (DHF vs. SHF vs. controls subjects: 32.2 +/- 18.0 ms vs. 38.0 +/- 25.2 ms vs. 19.5 +/- 7.1 ms) and Ts-SD (31.8 +/- 17.0 ms vs. 36.7 +/- 15.2 ms vs. 17.6 +/- 7.9 ms) compared with the control group (all p < 0.001 vs. control subjects). Based on normal values, the DHF group had comparable diastolic (35.9% vs. 43.1%; chi-square = 1.48, p = NS), but less systolic asynchrony than the SHF group (39.1% vs. 56.9%; chi-square = 8.82, p = 0.003). Normal synchrony, isolated systolic, isolated diastolic, and combined asynchrony were observed in 39.1%, 25.0%, 21.7%, and 14.1% of DHF patients, respectively, and these were 25.6%, 31.3%, 17.4%, and 25.6%, correspondingly, in SHF (chi-square = 10.01, p = 0.019). The correlation between systolic and diastolic asynchrony, and between the myocardial velocities and corresponding mechanical asynchrony appeared weak. A wide QRS duration (>120 ms) was rare in DHF (10.9% vs. 37.7% in SHF) (chi-square = 16.69, p < 0.001). CONCLUSIONS: Diastolic and/or systolic asynchrony was common in 61% of DHF patients despite narrow QRS complex. The presence of asynchrony was not related to myocardial systolic or diastolic function. Systolic and diastolic asynchrony were not tightly coupled, implying distinct mechanisms.

Aged↗

PubMed2006

Systolic and diastolic dyssynchrony in patients with diastolic heart failure and the effect of medical therapy.

OBJECTIVES: The purpose of this study was to determine the prevalence of systolic and diastolic dyssynchrony in diastolic heart failure (DHF) patients and identify the effects of medical therapy. BACKGROUND: The prevalence of systolic and diastolic dyssynchrony in DHF patients is unknown with no data on the effects of medical therapy on dyssynchrony. METHODS: Patients presenting with DHF (n = 60; 61 +/- 9 years old, 35 women) underwent echocardiographic imaging simultaneous with invasive measurements. An age-matched control group of 35 subjects and 60 patients with systolic heart failure (SHF) were included for comparison. Systolic and diastolic dyssynchrony were assessed by tissue Doppler and defined using mean and SD values in the control group. RESULTS: Systolic dyssynchrony was present in 20 patients (33%) with DHF and 24 patients (40%) with SHF and was associated in both groups with significantly worse left ventricular (LV) systolic and diastolic properties (p < 0.05 vs. control group and patients without systolic dyssynchrony). Diastolic dyssynchrony was present in 35 patients (58%) with DHF and 36 patients (60%) with SHF and had significant inverse correlations with mean wedge pressure and time constant of LV relaxation. In DHF patients, medical therapy resulted in significant shortening of diastolic time delay (39 +/- 23 ms to 28 +/- 20 ms; p = 0.02) but no significant change in systolic interval (p = 0.15). Shortening of diastolic time delay correlated well with tau shortening after therapy (r = 0.85; p < 0.001). CONCLUSIONS: Systolic dyssynchrony occurs in 33% of DHF patients, and diastolic dyssynchrony occurs in 58%. Medical therapy results in significant shortening of the diastolic intraventricular time delay which is closely related to improvement in LV relaxation.

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