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PubMed1993

Pitfalls in the echo-Doppler assessment of diastolic dysfunction.

The Doppler echocardiographic assessment of diastolic function is an essential part of the evaluation of heart failure, pericardial diseases, restrictive and infiltrative cardiomyopathies, and many other conditions. However, the echocardiographic evaluation of diastolic function has several limitations. The sonographer and physician must understand the technical factors, the effects of physiological and pathophysiological conditions, and the dynamics of pseudonormalization, all of which affect the evaluation. This article will review the most recent data essential for the proper performance and interpretation of a transthoracic or transesophageal Doppler echocardiographic examination of diastolic function.

Contraindications↗
PubMed2003

Assessment of regional systolic and diastolic dysfunction in familial hypertrophic cardiomyopathy using MR tagging.

Diastolic and systolic left ventricular (LV) dysfunction often significantly contribute to disabling symptoms in familial hypertrophic cardiomyopathy (FHC). This study compares regional LV function (midwall circumferential strain) during systole and diastole in eight FHC patients and six normal volunteers (NVs) using MR tagging. A prospectively-gated fast gradient-echo sequence with an echo-train readout was modified to support complementary spatial modulation of magnetization (CSPAMM) tagging and full cardiac cycle data acquisition using the cardiac phase to order reconstruction (CAPTOR), thus providing tag persistence and data acquisition during the entire cardiac cycle. Total systolic strains in FHC patients were significantly reduced in septal and inferior regions (both P < 0.01). Early-diastolic strain rates were reduced in all regions of the FHC group (all P < 0.03). The combination of CSPAMM and CAPTOR allows regional indices of myocardial function to be quantified throughout the cardiac cycle. This technique reveals regional differences in systolic and diastolic impairment in FHC patients.

Cardiomyopathy, Hypertrophic↗
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↗
PubMed1994

Left ventricular diastolic dysfunction in hypertension.

Abnormalities of left ventricular diastolic function in hypertension are multifactorial in origin. Of importance is the demonstration that abnormalities of left ventricular filling in hypertension may be accompanied by deleterious cardiovascular neurodynamic regulations. However, the left ventricular filling rates can be normalized during medical treatment of hypertension. In particular, regression of left ventricular hypertrophy is almost always associated with or followed by improvement of left ventricular filling. The effects of this normalization on cardiovascular dynamics and the outcome of hypertensive heart disease are yet to be demonstrated.

Antihypertensive Agents↗
PubMed1997

[The mechanisms of diastolic dysfunction and their assessment by a Doppler method].

The Doppler method makes possible to reveal the relaxation disturbances and the increased left ventricular (LV) stiffness-pathophysiologic mechanisms of diastolic myocardial dysfunction (DMD), exerting opposite influence on the correlation of transmitral flow peaks. The decrease of the "diastolic reserve" in the patients with lung congestion is useful to diagnose DMD. But the type of LV filling, when the relative role of early diastole is decreased and of the late diastole-increased, cannot itself be recognized as pathologic. From the other side, the normal transmitral flow graphics doesn't allow to exclude DMD completely. The interpretation of Doppler parameters must take into consideration other factors influencing the LV diastolic filling: preload, systolic dysfunction and mitral regurgitation.

Diastole↗
PubMed1993

[Pharmacotherapy of diastolic dysfunction in heart failure].

Impaired left ventricular diastolic function is an indicator of early stages of heart disease. In cardiac failure it is not necessarily associated with impaired systolic function and correlates more closely with clinical symptoms or load tolerance. Pharmacotherapy leading to improved diastolic parameters improves also the clinical condition of cardiac failure. Based on data in the literature, the authors analyze drugs which exert a favourable effect on left ventricular diastolic function: ACE inhibitors, calcium channel blockers, beta adrenergic agonists, phosphodiesterase inhibitors, diuretic and direct vasodilating agents, from the aspect of clinical administration.

Diastole↗
PubMed1993

[Treatment of diastolic dysfunction of the left ventricle].

Numerous studies have already recognized the importance of diastole in the pathogenesis of congestive heart failure. Non-invasive evaluations are based particularly on echo-Doppler, on radionuclide angiography and on cine-nuclear magnetic resonance: they have enabled an accurate evaluation of diastolic function and dysfunction, although invasive hemodynamic study maintains a gold standard position. All these methods of study have consented the identification of 3 basic components (anatomic and functional): active relaxation, passive elastic relaxation, atrial function. The Authors have identified the causes of diastolic failure with a particular attention to the various components of diastole. They have analyzed the implication of therapy on the basis of a clear understanding of the etiology, pathogenesis and pathophysiology of the underlying cardiac disease.

Diastole↗
PubMed1991

[Diastolic dysfunction in hypertrophic myocardiopathy: evaluation with radioisotopic ventriculography].

Diastolic function was evaluated in 13 patients with hypertrophic cardiomyopathy and 10 normal subjects of comparable age. Time-activity curves were used to derive peak filling rate, time to peak filling rate and average filling velocity during the first third of diastole. Left ventricular ejection fraction was significantly higher in patients with hypertrophic cardiomyopathy. Time to peak filling rate and filling velocity during the first third of diastole were significantly lower in patients compared to controls. Thus, radionuclide techniques can be used to evaluate diastolic filling in clinical practice.

Adolescent↗
PubMed2004

Pulse pressure and left ventricular diastolic dysfunction in hypertensive patients.

BACKGROUND: Impaired left ventricular diastolic function is a common finding in essential hypertension. METHODS: In order to investigate possible relationships between flow velocity through the mitral valve (E/A; index of left ventricular diastolic function) and 24-hour blood pressure and heart rate variations, 198 patients with mild to moderate essential hypertension were studied by Doppler echocardiography and ambulatory blood pressure monitoring. They were divided according to age into group 1 (n = 88, age 40-54 years) and group 2 (n = 110, age 55-79 years). Each group was divided into subgroups with (1a, 2a) or without (1b, 2b) left ventricular hypertrophy according to the end-diastolic posterior wall thickness and/or the interventricular septum thickness. RESULTS: In a multivariate stepwise regression analysis, age (beta = -0.25, p < 0.0001), posterior wall thickness (beta = -0.31, p < 0.0057) and mean heart rate during the day (beta = -0.34, p < 0.0284) were the independent predictors of E/A in the pooled population. In group 1a (young subjects with left ventricular hypertrophy), mean systolic blood pressure during the night (beta = -0.33, p < 0.041) was the only independent predictor of E/A. In the elderly group without left ventricular hypertrophy (group 2b), the mean heart rate during the day (beta = -0.44, p < 0.0000) and mean pulse pressure during the night (beta = -0.60, p < 0.0007) were the independent predictors of E/A. CONCLUSIONS: The new finding provided by this study is that in elderly hypertensive patients without left ventricular hypertrophy, a large pulse pressure at night may serve as an independent predictor of abnormal left ventricular diastolic filling.

Adult↗
PubMed1998

Use of pulsed Doppler tissue imaging to assess regional left ventricular diastolic dysfunction in hypertrophic cardiomyopathy.

In this study, regional diastolic patterns and their relations with transmitral Doppler inflow were investigated in hypertrophic cardiomyopathy (HC) by pulsed Doppler tissue imaging (DTI). Doppler echocardiography and DTI of basal septum and lateral wall (apical 4-chamber view) were performed in 20 patients (15 men and 5 women) with HC and in 10 healthy subjects (7 men and 3 women). Diabetes, hypertension, coronary artery and valvular disease, mitral regurgitation, New York Heart Association functional classes III to IV, sinus tachycardia, atrial fibrillation, and inadequate echocardiograms were exclusion criteria. Peak velocity and time-velocity integral of early and late waves and their ratios, and deceleration and isovolumic relaxation times were determined by standard Doppler and by DTI at the septal and lateral wall levels. The 2 groups were comparable for age, heart rate, blood pressure, and ejection fraction. Transmitral peak velocity and time-velocity integral E/A ratios were reduced (both p <0.05) and deceleration and isovolumic relaxation times prolonged (both p <0.00001) in HC. Septal DTI showed lower peak velocity and time-velocity integral e/a ratios (p <0.00001 and p <0.001, respectively) and lengthened regional deceleration (p <0.01) and isovolumic (p <0.001) relaxation times. DTI of the lateral wall showed a prolongation of deceleration and isovolumic relaxation times (both p <0.01). By dividing HC according to transmitral E/A, 8 patients with E/A <1 had lower DTI septal e/a ratio (p <0.01) and prolonged septal deceleration and isovolumic relaxation times (both p <0.01) but no changes in DTI pattern of lateral wall than 12 patients with E/A > 1. In conclusion, DTI is useful and complementary to standard Doppler imaging to characterize diastolic properties in HC, reflecting a typical pattern of intramyocardial impaired relaxation at the level of hypertrophied septum and also providing information about the degree of this regional impairment. The lateral wall presents minor changes in diastolic times, which indicate how diastolic asynchrony is not confined to the hypertrophied segment in HC.

Adult↗
PubMed1994

Doppler echocardiographic evaluation of the spectrum of left ventricular diastolic dysfunction in essential hypertension.

Left ventricular topography and diastolic and systolic functions were studied in 41 patients with essential hypertension (group 1) and 33 age-matched normal adults (group 2) by Doppler echocardiography. In group 1 54% had LV concentric hypertrophy, 19% had combined concentric hypertrophy and eccentric remodeling, and 27% had concentric remodeling. LV systolic function was within the normal range. In concentric LV remodeling, the EDV was significantly decreased (compared with group 2) (84 +/- 15 vs 130 +/- 38 ml, p < 0.05), whereas the NPFR was normal (2.89 +/- 0.65 vs 3.22 +/- 0.83 sec-1, p = NS). In concentric hypertrophy, LV end-diastolic and end-systolic volumes were normal, but the NPFR was decreased (2.04 +/- 0.59 sec-1). Patients with concentric hypertrophy and eccentric remodeling had the largest end-diastolic (140 +/- 48 ml) and end-systolic (62 +/- 32 ml) volumes and the lowest NPFR (1.67 +/- 0.69 sec-1). The LVMI inversely correlated with the NPFR (r = -0.89, p < 0.0001). Thus LV concentric hypertrophy with or without concentric or eccentric remodeling is seen in patients with systemic hypertension. A decrease in peak filling occurs early in the evolution of hypertensive heart disease and is observed even when systolic performance is still normal.

Diastole↗
PubMed1992

Biological basis of diastolic dysfunction of the hypertensive heart.

To study the diastolic properties of the heart includes examining active relaxation, passive ventricular stiffness and atrial contraction. (i) The main determinant of active relaxation is the adenosine triphosphate (ATP) concentration. Relaxation needs to occur so that the ATP content of the cell can be decreased by activation of the myosin ATPase, which in turn depends upon an intracellular messenger, elevation of the calcium transient. In a model of cardiac hypertrophy active relaxation is always slower. This slowing accompanies a slowing of the calcium transient, a diminution in the activity of the Na+/Ca2+ exchanger, a change in the properties of Na+, K+ ATPase and a decreased concentration of Ca2+ ATPase in the sarcoplasmic reticulum. (ii) Chamber stiffness is likely to be increased only in relation to the degree of ventricular hypertrophy. The main, if not unique, determinant of ventricular diastolic tissue stiffness is the structure and concentration of the collagen. Consequently tissue stiffness is augmented in cardiac hypertrophy in which the ventricular collagen concentration is elevated. It is important that both clinically and experimentally cases of cardiac hypertrophy, even those resulting from pressure overload in which myocardial stiffness and cardiac collagen concentration remain unchanged, have been documented. A good example of this is the DOCA-salt model of arterial hypertension. (iii) Atrial contraction is normally more rapid than ventricular contraction, the biological basis for which is the difference in isomyosin content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Diastolic dysfunction during acute cardiac allograft rejection.

Left ventricular diastolic function was evaluated in 41 heart transplant patients during acute rejection by an analysis of echocardiograms and surgically implanted intramyocardial tantalum markers. In 35 patients, isovolumic relaxation time was calculated from M-mode tracings selected from two-dimensional echocardiographic recordings. A total of 84 biopsy findings of no rejection, moderate rejection, and severe acute rejection after treatment were correlated with measurements of isovolumic relaxation time. In six patients, end-diastolic volume, end-systolic volume, stroke volume, ejection fraction, and peak filling rate were obtained from biplanar cineradiographic images of intramyocardial markers. Data from 11 prerejection periods were compared with those of moderate acute rejection. All echocardiograms and marker images were analyzed without previous knowledge of biopsy findings. At times of acute rejection, isovolumic relaxation time decreased from 107 to 65 msec (p less than 0.01) and returned to 98 msec after immunosuppressive therapy. Ejection fraction and end-systolic volume did not change significantly with acute rejection, whereas stroke volume decreased from 76 to 67 ml (p less than 0.05). In contrast to the effects on systolic function, episodes of acute rejection were accompanied by a decrease in end-diastolic volume from 166 to 153 ml (p less than 0.01) and a reduction in peak filling rate from 514 to 460 ml/sec (p less than 0.05). These data suggest that acute cardiac rejection is associated with relative preservation of left ventricular systolic performance but with alterations in diastolic dynamics similar to those seen in "restrictive" cardiomyopathy.

Acute Disease↗
PubMed2005

Young MLP deficient mice show diastolic dysfunction before the onset of dilated cardiomyopathy.

Targeted deletion of cytoskeletal muscle LIM protein (MLP) in mice consistently leads to dilated cardiomyopathy (DCM) after one or more months. However, next to nothing is known at present about the mechanisms of this process. We investigated whether diastolic performance including passive mechanics and systolic behavior are altered in 2-week-old MLP knockout (MLPKO) mice, in which heart size, fractional shortening and ejection fraction are still normal. Right ventricular trabeculae were isolated from 2-week-old MLPKO and wildtype mice and placed in an apparatus that allowed force measurements and sarcomere length measurements using laser diffraction. During a twitch from the unloaded state at 1 Hz, MLPKO muscles relengthened to slack length more slowly than controls, although the corresponding force relaxation time was unchanged. Active developed stress at a diastolic sarcomere length of 2.00 microm was preserved in MLPKO trabeculae over a wide range of pacing frequencies. Force relaxation under the same conditions was consistently prolonged compared with wildtype controls, whereas time to peak and maximum rate of force generation were not significantly altered. Ca2+ content of the sarcoplasmic reticulum (SR) and the quantities of Ca2+ handling proteins were similar in both genotypes. In summary, young MLPKO mice revealed substantial alterations in passive myocardial properties and relaxation time, but not in most systolic characteristics. These results indicate that the progression to heart failure in the MLPKO model may be driven by diastolic myocardial dysfunction and abnormal passive properties rather than systolic dysfunction.

Animals↗