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PubMed2005

[Diastolic dysfunction in diabetic normotensive patients, regardless of the presence of microangiopathy].

OBJECTIVE: To assess the Doppler-echocardiographic changes in normotensive patients with type II diabetes mellitus, in the presence or absence of signs of microangiopathy. METHODS: Patients with type II diabetes mellitus were submitted to funduscopy contrasted with fluorescein and dosage of microalbuminuria for diagnose of microangiopathy and divided into two groups: DMII (patients without microangiopathy, n=19) and DM+A (patients with microangiopathy, n=13). All of them were submitted to a Doppler-echocardiography and the results were compared with normotensive patients of same sex and age (group C, n=20), by using the ANOVA, followed by the test of Tukey. In all comparisons the significance level p<0.05 was adopted. RESULTS: There were no differences among the groups regarding the systolic function indicators or left ventricular mass. Differences compatible with diastolic dysfunction in the two groups of diabetic were observed, regardless of the presence of microangiopathy, which showed significantly higher values of the times of isovolumetric relaxation of the left ventricle (TIRLV, ms): (DMII= 97+/-22.2; DM+A= 107+/-28.2 and C= 80+/-10.7; p<0.05), and lower values of the maximum speeds of the wave of fast ventricular filling (E, cm/s): (DMII= 69+/-17.5; DM+A= 75+/-19.7 and C= 84+/-14.5, p<0.05 between DMII and C). There was no difference among the groups concerning the E/A rate. CONCLUSION: Normotensive patients with type II diabetes mellitus and without clinical signs of cardiovascular compromising showed signs of diastolic dysfunction, non-associated to the presence of microangiopathy.

Adult↗
PubMed1998

Sustained left ventricular diastolic dysfunction after exercise in patients with dilated cardiomyopathy.

OBJECTIVE: To investigate the recovery process of exercise induced diastolic dysfunction in heart failure, using Doppler echocardiographic techniques. DESIGN AND PATIENTS: Transmitral flow velocity profiles and standard noninvasive haemodynamic indices were obtained serially over seven days after symptom limited bicycle exercise tests in 18 patients with dilated cardiomyopathy and eight normal subjects. In three patients with cardiomyopathy we also measured the pulmonary capillary wedge pressure for 24 hours after exercise. RESULTS: The intensity of exercise, as assessed by respiratory gas analysis, was lower in patients with dilated cardiomyopathy than in normal subjects. Despite the higher exercise level, all haemodynamic variables returned to baseline within one hour after exercise in normal subjects. In contrast, patients with dilated cardiomyopathy showed a sustained decrease in the peak early diastolic filling velocity and a sustained increase in the deceleration time of early filling for 24 hours or more after exercise. Because other haemodynamic variables recovered within one hour after exercise even in patients with dilated cardiomyopathy, the postexercise changes in ventricular filling were not explained by changes in loading conditions. CONCLUSIONS: Exercise induced diastolic left ventricular dysfunction of the failing heart persists for 24 hours or more after exercise. The efficacy of exercise training on a daily basis in dilated cardiomyopathy requires further evaluation.

Adult↗
PubMed2000

Transgenic rat hearts expressing a human cardiac troponin T deletion reveal diastolic dysfunction and ventricular arrhythmias.

OBJECTIVE: Familial hypertrophic cardiomyopathy (FHC) due to mutations of cardiac troponin T (cTnT) is associated with a high frequency of sudden death even in the absence of cardiac hypertrophy. To investigate the causal relationship of cTnT mutations and this particular phenotype, we sought to establish a transgenic rat model for the disease. METHODS: Transgenic rats were generated expressing human wild-type cTnT or two truncated cTnT molecules (del ex16, del ex15/16), resulting from an intron 15 splice donor site mutation previously observed in FHC patients. Transgenic rat hearts were characterized by histology, immunohistochemistry and in the 'working heart'. RESULTS: Human wild-type and del ex16 cTnT were stably expressed and incorporated into the sarcomere of transgenic cardiomyocytes. Del ex16 transgenic rats revealed a lower level of expression (4-5%) than human wt cTnT animals (25-40%). In the 'working heart' model del ex16 hearts exhibited significant systolic and diastolic dysfunction without cardiac hypertrophy. In contrast, human wt cTnT hearts showed improved contractile performance and moderate myocardial hypertrophy. After 6 months of daily physical exercise one del ex16 rat died suddenly and three out of five del ex16 hearts revealed ventricular tachycardia/fibrillation. No arrhythmia was observed in human wt cTnT expressors. Myofibrillar disarray was present in del ex16 hearts after training but not in human wild-type cTnT rats or non-transgenic controls. CONCLUSION: A human cTnT deletion overexpressed in transgenic rats exerts a dominant-negative effect and mimics the phenotype of FHC with diastolic dysfunction and arrhythmias. By contrast, human cTnT wild-type animals reveal a gain of function and cardiac hypertrophy without arrhythmias.

Animals↗
PubMed1995

"Accurate" noninvasive detection of diastolic dysfunction by current techniques: fact or fancy?

To evaluate clinically left ventricular (LV) diastolic performance has been recognized in recent years to be an important part in cardiac evaluation, since diastolic abnormalities occur early and are sensitive indicators of diseased myocardium as well as determinants of cardiac output. Data on LV diastolic function are noninvasively acquired in recent years in most laboratories from: 1) radionuclide angiography, 2) echocardiography (M-mode and 2D) and 3) Doppler echocardiography. All these widely accepted and used methods for the detection and quantification of diastolic dysfunction are based on the assessment of indices of either rate of ventricular filling or rate of change of LV diameter and wall thickness during diastole.

Echocardiography↗
PubMed1994

[Preclinical left ventricular diastolic dysfunction in insulin-dependent diabetes].

BACKGROUND: Isolated alterations of the left ventricular diastolic function have been described in diabetic insulin-dependent patients (IDDM), even in the absence of old age, hypertension, ischemic heart disease, left ventricular hypertrophy. Such alterations have been associated with microangiopathy but it is not known whether it is reversible or if there is a relation with the way the therapy is given. METHODS: Fifty-five subjects have been studied, of which 15 were healthy, 30 recently diagnosed IDDM without microangiopathy and 10 IDDM with microangiopathy. All the patients were under 35 years old and did not present risk factors for coronary artery disease, hypertension or autonomic neuropathy. The maximal exercise stress test proved negative. The diastolic function was studied using the results of Doppler echocardiography of the mitral flow and of isovolumetric relaxation time, with continuous and discrete parameters. RESULTS: The velocity of wave A and E, the relationship between them and their integrals are significantly greater in diabetics with microangiopathy than in those without it and in healthy subjects. There are no significant differences between healthy and diabetic subjects without microangiopathy using continuous parameters. Using discrete parameters diastolic damage is absent in the healthy subjects and is present in 48% of diabetics without microangiopathy and in 90% of those with it. CONCLUSIONS: Slight preclinical diastolic dysfunction is present in young recently diagnosed IDDM without microangiopathy. More severe dysfunction is present when there is also microangiopathy.

Adult↗
PubMed2004

Inspiratory muscle weakness in diastolic dysfunction.

OBJECTIVES: To test the hypothesis that patients with well-documented diastolic dysfunction (DD) in the setting of normal systolic function will have inspiratory muscle weakness when compared to normal control subjects, and will experience dyspnea and tachypnea during exercise. BACKGROUND: Respiratory muscle weakness has been described in patients with (systolic) congestive heart failure; however, whether or not patients with DD may present with the findings of congestive heart failure is not known. METHODS: We selected for study 14 patients with DD previously referred for cardiopulmonary evaluation whose diagnosis had been confirmed by data obtained at cardiac catheterization. Seven control subjects matched for age, sex, and weight were recruited from the hospital community. Subjects performed both basic pulmonary function tests and tests of muscle strength: handgrip strength (Hgr), and maximal subatmospheric static inspiratory muscle pressure (Pimax). Subjects then performed a graded exercise test on a bicycle ergometer. Minute ventilation, oxygen consumption, carbon dioxide production, and heart rate were monitored continuously. Echocardiography was performed three times: before exercise, at a selected submaximal exercise level (20% of a predicted maximal workload), and at maximal exercise. Subjects rated their degree of dyspnea using the Borg scale at the same three time intervals. RESULTS: Pimax was - 102 +/- 17 cm H(2)O in control subjects, and - 77 +/- 19 cm H(2)O in patients with DD (p = 0.013) [mean +/- SD]. Hgr was similar between the groups. At the selected submaximal exercise level, patients with DD rated dyspnea to be 2.6 +/- 2.2 Borg scale units (control subjects, 0.5 +/- 0.8 Borg scale units). Hey plots described a rapid, shallow breathing pattern in patients with DD during exercise. Patients with DD and control subjects achieved similar maximal work loads. CONCLUSION: Patients with DD have diminished Pimax, adopt a rapid, shallow breathing pattern during exercise, and experience dyspnea at low work loads when compared to matched control subjects.

Aged↗
PubMed1991

Hypertrophy, fibrosis and diastolic dysfunction in early canine experimental hypertension.

To examine the relations among hypertrophy, fibrosis and diastolic performance in early experimental hypertension, 18 control dogs and 12 dogs with experimental left ventricular hypertrophy were studied. Diastolic function was impaired in dogs with left ventricular hypertrophy, with decreased Doppler early to atrial inflow velocity ratio (E/A) (1.35 versus 1.72), increased atrial filling fraction (35% versus 29%), decreased sonomicrometric peak rates of wall thinning (-2.01 versus -3.37 liters/s) and filling (4.33 versus 6.64 liters/s) and prolonged time constant of isovolumetric relaxation (tau; 34.3 versus 28.1 ms). Neither chamber stiffness (k; P = AekV) nor passive elastic stiffness (E; E = k sigma, where sigma = stress) was increased. At postmortem examination, the hypertensive left ventricle weighed significantly more than normal (116 versus 80 g; p less than 0.01) and had greater muscle fiber diameter at endocardial and epicardial sampling sites in the apical free wall, basal free wall and septum (mean diameter 50 +/- 8 microns in hypertensive dogs, 37 +/- 8 microns in normal dogs; p less than 0.01). In contrast, neither percent fibrosis (1.2 +/- 0.8 versus 0.9 +/- 0.6 in normal dogs) nor fibrotic volume (1.21 +/- 0.63 versus 0.72 +/- 0.42%/g in normal dogs) was significantly increased. Peak volumetric filling rate was inversely related to fiber diameter (r = -0.74, p less than 0.001), although no variable of left ventricular function was significantly related to percent or volume fibrosis (all r less than 0.60, all p greater than 0.05). Thus, diastolic dysfunction may exist in the setting of hypertrophy without significant fibrosis. Increased myocyte size was associated with early diastolic filling abnormalities characteristic of the hypertensive left ventricle. Fibrosis appears to be a less important determinant of diastolic performance.

Animals↗
PubMed1990

[The role of Doppler echography in the evaluation of systolic and/or diastolic dysfunction of the left ventricle].

The doppler-echocardiographic assessment of left ventricular systolic and diastolic dysfunction involves numerous indices. Preload is evaluated by measurement of the end-diastolic left ventricular diameter and sometimes by the rapid filling E wave on doppler recordings. The best index of of afterload is the end-systolic stress. Most indices of contractility are load-dependent, including percentage of fibre shortening, FCV, FCVc, EF. This leads to the construction of end-systolic regression slopes by varying the load to determine the myocardial contractile value. In the future, automated analysis of doppler curves will be used to determine the aortic flow maximal acceleration. The diastolic function is easily evaluated through the transmitral flow, but its interpretation must take into account the patient's age, heart rate and filling state. Two aspects are regarded as pathological: the filling disorder aspect with E/A under 1, and the hypernormal assay described by Appleton. In doppler-echocardiographic studies as well as in haemodynamic studies all these indices are interrelated, which shows the complexity of cardiac physiology and the interdependence of its factors.

Diastole↗
PubMed2006

Cardiac diastolic dysfunction in conscious dogs with heart failure induced by chronic coronary microembolization.

Left ventricular (LV) diastolic dysfunction is a fundamental impairment in congestive heart failure (CHF). This study examined LV diastolic function in the canine model of CHF induced by chronic coronary embolization (CCE). Dogs were implanted with coronary catheters (both left anterior descending and circumflex arteries) for CCE and instrumented for measurement of LV pressure and dimension. Heart failure was elicited by daily intracoronary injections of microspheres (1.2 million, 90- to 120-microm diameter) for 24 +/- 4 days, resulting in significant depression of cardiac systolic function. After CCE, LV maximum negative change of pressure with time (dP/dt(min)) decreased by 25 +/- 2% (P < 0.05) and LV isovolumic relaxation constant and duration increased by 19 +/- 5% and 25 +/- 6%, respectively (both P < 0.05), indicating an impairment of LV active relaxation, which was cardiac preload independent. LV passive viscoelastic properties were evaluated from the LV end-diastolic pressure (EDP)-volume (EDV) relationship (EDP = be(alpha*EDV)) during brief inferior vena caval occlusion and acute volume loading, while the chamber stiffness coefficient (alpha) increased by 62 +/- 10% (P < 0.05) and the stiffness constant (k) increased by 66 +/- 13% after CCE. The regional myocardial diastolic stiffness in LV anterior and posterior walls was increased by 70 +/- 25% and 63 +/- 24% (both P < 0.05), respectively, after CCE, associated with marked fibrosis, increase in collagen I and III, and enhancement of plasminogen activator inhibitor-1 (PAI-1) protein expression. Thus along with depressed LV systolic function there is significant impairment of LV diastolic relaxation and increase in chamber stiffness, with development of myocardial fibrosis and activation of PAI-1, in the canine model of CHF induced by CCE.

Animals↗
PubMed1998

Diastolic dysfunction in young patients with insulin-dependent diabetes mellitus as determined by automated border detection.

Diastolic dysfunction is an early harbinger for systolic dysfunction in insulin-dependent diabetes mellitus (IDDM). To determine the role of automated border detection (ABD) in detecting diastolic abnormalities and whether IDDM control correlates with abnormalities, 21 young IDDM patients (22 +/- 4 years old) and 19 control subjects underwent echocardiography. ABD indices included the percent contribution to total left ventricular filling of the three phases of diastole (rapid filling, diastasis, and atrial contraction) and peak filling rate. Doppler indices included E/A ratio and peak filling rate. Rapid filling phase was lower in the IDDM patients compared with control subjects (73% +/- 5% versus 80% +/- 5%, p = 0.0006), and atrial contraction filling was higher (19% +/- 4% versus 14% +/- 3%, p = 0.0003). Doppler indexes showed similar changes. Glycosylated hemoglobin, insulin dosage, and duration of IDDM since puberty were associated with filling abnormalities. Young patients with IDDM have increased atrial contraction and reduced rapid filling phases detected by automatic border detection, and these diastolic abnormalities are related to the diabetic disease process.

Adult↗
PubMed1996

Left ventricular diastolic dysfunction in patients with angina decubitus.

OBJECTIVE: To investigate the relationship between left ventricular diastolic dysfunction and episodes of angina decubitus. METHODS: The study population consisted of three groups, groups I (20 controls) had no cardiovascular diseases. Group II (20 patients) had coronary artery disease (CAD) without angina decubitus. Group III (24 cases with ejection fraction (EF) > 45%) were selected from 26 patients with angina decubitus. RESULTS: Left ventriculography (LVG) showed that left ventricular (LV) first 1/3 filling fraction (1/3FF) was significantly reduced in groups III as compared with groups II and I (P < 0.01). Left ventricular end-diastolic pressure (LVEDP) significantly increased in patients with angina decubitus after LVG as compared with that before LVG (P < 0.01). However, there were no statistically differences in LVEDP, before and after LVG in both groups II and I. CONCLUSIONS: Patients with angina decubitus have abnormalities of LV diastolic filling and decrease in LV compliance.

Adult↗
PubMed1992

Left ventricular hypertrophy and diastolic dysfunction.

The hypertrophied heart generally preserves systolic function, but it pays a price in diastolic dysfunction. Coronary reserve is impaired and susceptibility to myocardial ischemia increased. The pathophysiology is managed by addressing causes of pressure overload, preventing tachycardia, or, of course, by specific strategies to reduce or eliminate ischemia.

Adaptation, Physiological↗
PubMedDate not supplied

Clinical correlates of isolated left ventricular diastolic dysfunction among hospitalized older heart failure patients.

Heart failure due to isolated left ventricular diastolic dysfunction (LVDD) is common among older adults. The purpose of this study was to develop a model based on admission clinical features to predict isolated LVDD in older adults hospitalized with heart failure. The authors studied 394 Alabama Medicare beneficiaries discharged with a primary discharge diagnosis of heart failure. All patients had data on LV function determined by echocardiography performed during the index hospitalization. Isolated LVDD was defined by LV ejection fraction >/=45% or LV function described as normal. The authors used all subsets multiple logistic regression analyses to examine various models predicting isolated LVDD. Patients had a mean (+/-SD) age of 78 (+/-7) years and 58% were women. One hundred thirty nine (35%) patients had isolated LVDD. More women (47%) than men (21%) had isolated LVDD (p<0.001). Variables independently associated with isolated LVDD in the selected 12-predictor model were female sex (odds ratio [OR]=3.10; 95% confidence interval [CI]=1.86-5.15), pulse 100 beats/min or greater (OR=0.43; 95% CI=0.25-0.72), systolic blood pressure (OR=1.01; 95% CI=1.00-1.02), diastolic blood pressure (OR=0.98; 95% CI=0.96-0.99), pulmonary vascular congestion by chest x-ray (OR=0.51; 95% CI=0.30-0.88), coronary artery disease (OR=0.54; 95% CI=0.32-0.92), cardiomyopathy (OR=0.21; 95% CI=0.10-0.47), and admission to a teaching hospital (OR=0.36; 95% CI=0.15-0.88). The authors concluded that the proportion of patients with isolated LVDD among this cohort of elderly hospitalized heart failure patients was low and was associated with few clinical characteristics. Except for female sex and systolic blood pressure, all model variables were negatively associated with isolated LVDD.

Aged↗
PubMed1989

Left ventricular diastolic dysfunction and cardiovascular regulation in hypertension.

The determinants and physiologic consequences of altered left ventricular diastolic filling rate in hypertension has not yet been fully assessed. Data suggesting that left ventricular diastolic dysfunction in hypertension is associated with impaired peripheral vascular regulation by cardiopulmonary reflexes has been reported recently. Other functional correlates of alteration of left ventricular diastolic function are reviewed, as well as the effects of antihypertensive therapy on the rate of left ventricular filling.

Diastole↗
PubMedDate not supplied

[Diastolic dysfunction of the myocardium: the mechanisms of its development, its diagnosis and treatment characteristics].

Diastolic dysfunction of the myocardium (DDM) is a very common abnormality having an important part in the origination of cardiac insufficiency. The main factors of DDM pathogenesis include greater rigidity of the myocardium, its hypertrophy and failure to relax normally. Findings from echocardiography and invasive techniques allow the DDM diagnosis to be made and hemodynamic patterns to be ascertained. Treatment options are to be chosen with regard to the underlying condition, with the beta-blockers and calcium antagonists being given the preference over other medicinal substances.

Diastole↗
PubMed1997

Angiotensin receptor antagonism and angiotensin converting enzyme inhibition improve diastolic dysfunction and Ca(2+)-ATPase expression in the sarcoplasmic reticulum in hypertensive cardiomyopathy.

BACKGROUND: Hypertensive cardiomyopathy is a major risk factor for the development of chronic heart failure. OBJECTIVE: To investigate whether treatment with an angiotensin converting enzyme inhibitor (ACEI) or with an angiotensin type 1 receptor antagonist (AT1-RA) is sufficient to prevent the development of hypertensive cardiomyopathy and cardiac contractile dysfunction. Special emphasis was placed on the effects of both treatments on sarcoplasmic reticulum Ca(2+)-ATPase (SERCA 2a) gene expression as a major cause of impaired diastolic cardiac relaxation. METHODS AND RESULTS: Eight-week-old rats harboring the mouse renin 2d gene [TG(mREN2)27] were treated for 8 weeks with 100 mg/kg captopril (Cap) in their food and 100 mg/kg of the AT1-RA Bay 10-6734 (Bay) in their food. Untreated TG(mREN2)27 and Sprague-Dawley rats (SDR) were used as controls. Both treatment regimens normalized the left ventricular weight, which was increased significantly (P < 0.001) in TG(mREN2)27. Both treatments normalized the left ventricular end-systolic and end-diastolic pressures, which were significantly (P < 0.001) higher in TG(mREN2)27 than they were in SDR, and they improved the velocity of the decrease in pressure [P < 0.05, Bay and Cap versus TG(mREN2)27]. Decreased left ventricular SERCA 2a mRNA and protein levels and increased atrial natriuretic peptide messenger RNA levels were normalized by Bay and Cap treatments (P < 0.05, Bay and Cap versus TG(mREN2)27, by Northern and Western blotting). According to radioimmunoassay and an enzyme assay, respectively, Bay, but not Cap, increased plasma angiotensin I concentrations and the renin activity above normal levels (P < 0.05), whereas myocardial angiotensin II concentrations (determined by radioimmunoassay), which were significantly (P < 0.05) increased in TG(mREN2)27, were normalized equally by Bay and Cap. CONCLUSIONS: In renin-induced hypertensive cardiomyopathy, left ventricular diastolic dysfunction occurs at the stage of compensated myocardial hypertrophy. The decreased left ventricular relaxation velocity might be due to reduced SERCA 2a gene expression. In this model of hypertensive cardiomyopathy, AT1-RA and ACEI treatments are similarly effective at reducing the arterial pressure, preventing myocardial hypertrophy and diastolic contractile dysfunction. Normalization of SERCA 2a gene expression, either by AT1-RA or by ACEI treatment, might contribute to the improvement in diastolic function.

Angiotensin I↗
PubMed2004

Left ventricular diastolic dysfunction in Ebstein's anomaly.

This study was performed to evaluate left ventricular (LV) diastolic function in patients with Ebstein's anomaly using Doppler echocardiography. We found that LV abnormal relaxation in this anomaly cannot be explained by right ventricular volume overload alone. Furthermore, LV diastolic dysfunction persists even after intracardiac repair.

Cardiac Catheterization↗
PubMed2002

Left ventricular diastolic dysfunction as an early manifestation of diabetic cardiomyopathy.

AIMS/HYPOTHESIS: Early determination of myocardial manifestations of diabetes mellitus is of major importance, since myocardial involvement considerably influences the prognosis of diabetic patients. The aim of this study was to investigate whether young patients with insulin-dependent diabetes mellitus and normal systolic left ventricular (LV) function already show a diastolic LV dysfunction and an increased risk of arrhythmias. METHODS: Echocardiography was performed in 87 patients suffering from type I diabetes mellitus, without known cardiac disease and in 87 controls. Patients with a known manifest cardiac disease or a long-term diabetic syndrome were excluded. Morphological parameters were determined using M-mode echocardiography. Doppler echocardiography was used to evaluate parameters of LV diastolic function. The risk of arrhythmia was assessed by means of electrocardiography, heart rate variability, and late potential analysis. RESULTS: The left atrial and ventricular dimensions and systolic functional parameters of all patients were normal. A diastolic dysfunction with a reduction in early diastolic filling, an increase in atrial filling, an extension of isovolumetric relaxation and deceleration time was documented in diabetic patients, as well as an increased number of supraventricular and ventricular premature beats. CONCLUSION: Even young patients with diabetes mellitus suffer from a diastolic dysfunction while systolic ventricular function is normal. Therefore, echocardiography with measurements of diastolic functional parameters appears to be a sensitive method for evaluating the manifestation and course of early diabetic cardiomyopathy.

Adult↗