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Biomedical subjects

T C Gillebert

Publications and source records attributed to T C Gillebert.

At least 19 recordsLinked to original sources
PubMed2007

Poststress left ventricular ejection fraction is an independent predictor of major cardiac events in patients with coronary artery disease and impaired left ventricular function.

AIM: The aim of this study was to investigate the prognostic value of myocardial perfusion and function SPECT imaging in patients with coronary artery disease (CAD) and poor left ventricular (LV) function. METHODS: We studied 261 patients (231 men, age 66+/-10 years) with CAD and a resting LV ejection fraction (LVEF) <or= 40% assessed during myocardial gated SPECT. Perfusion defect extent was calculated using 4D-MSPECT software (Michigan University). Ischemia scoring was performed visually. Considered end points were: 1) major adverse cardiac events (MACE) (cardiac death, non-fatal myocardial infarction or late revascularization), 2) MACE or the need for hospitalization due to heart failure (MACE-HF) and 3) cardiac death or non-fatal myocardial infarction. RESULTS: During a median follow-up of 31 months, 52 patients (20%) died (35 cardiac deaths), 50 (19%) developed a MACE and 69 (26%) a MACE-HF. In a clinical model, diabetes and angina status were the only predictors of MACE (chi-squared=19.3; P<0.001). By multivariate analysis, poststress LVEF (chi-squared-gain of 6.4; P=0.008) and presence of ischemia (chi-squared-gain of 5.8; P=0.018) were predictive of MACE. Similarly, diabetes mellitus (chi-squared=12.1; P<0.001), poststress LVEF (chi-squared-gain of 5.5; P=0.019) and presence of ischemia (chi-squared-gain of 4.3; P=0.044) were independent predictors of MACE-HF. Diabetes mellitus (chi-squared=17.8; P<0.001), presence of angina complaints (chi-squared-gain of 6.8; P=0.028) and poststress LVEF (chi-squared-gain of 6.3; P=0.008) were independent predictors of cardiac death or non-fatal myocardial infarction. CONCLUSION: In patients with impaired LV function and CAD, poststress LVEF is an independent predictor of future cardiac events.

Aged↗
PubMed2006

Aortic reflection coefficients and their association with global indexes of wave reflection in healthy controls and patients with Marfan's syndrome.

Early return of reflected pressure waves increases the load on central arteries and may increase the risk of aortic rupture in patients with Marfan's syndrome (MFS). To assess whether wave reflection is elevated in MFS, we used ultrasound and MRI to measure central pressure and flow waveforms in 26 patients (13-54 yr of age) and 26 age- and gender-matched controls. Aortic systolic and diastolic cross-sectional areas were measured at the ascending and descending aorta (AA and DA), diaphragm (DIA), and lower abdominal aorta (AB). From these measurements, local characteristic impedance (Z(0-xx)) and local reflection coefficients (Gamma(xx-yy)) were calculated. Calculated global wave reflection indexes were the augmentation index (AIx) and the ratio of backward to forward pressure wave (P(b)/P(f)). The aorta was wider in MFS patients at AA (P < 0.01) and DA (P < 0.01). Aortic pulse wave velocity was 42 cm/s higher in MFS patients (P < 0.05). Z(0-xx) was not different between groups, except at DA, where it was lower in MFS patients. In controls, Gamma(AA-DA) was 0.31 +/- 0.08, Gamma(DA-DIA) was 0.00 +/- 0.11, and Gamma(DIA-AB) was 0.31 +/- 0.16. Mean values of Gamma(xx-yy) were not different between MFS patients and controls. In controls, aging diminished Gamma(AA-DA) but increased Gamma(DIA-AB). Clear age-related patterns were absent in MFS patients. AIx or P(b)/P(f) was not higher in MFS patients than in controls. There were indications for enhanced wave reflection in young MFS patients. Our data demonstrated that the major determinants of AIx were pulse wave velocity and the effective length of the arterial system and, to a lesser degree, HR and P(b)/P(f).

Adolescent↗
PubMed2004

The use of Tissue Doppler Imaging for the assessment of changes in myocardial structure and function in inherited cardiomyopathies.

Although there is still a long way to go, our understanding of the genetic basis of cardiomyopathies--dilated or hypertrophic--has significantly improved over the past decade. This new and intriguing era of cardiogenetics has already answered some important questions concerning the pathophysiology of these disorders, but it has also raised some new questions: how do we define "presymptomatic" mutation carriers? Should we treat them? Do we have any diagnostic tools to identify the presymptomatic subjects in those families where the underlying mutation has not been identified yet? To address at least part of these questions, there is a clear need for screening techniques in the early stage of the disease which have to be sensitive and non-invasive. In recent years Tissue Doppler Imaging (TDI) has emerged as a well suited technique for these purposes and several interesting papers on this issue have been published. This paper reviews the findings from TDI in several forms of inherited cardiomyopathy. Although the implementation of this technique in everyday clinical practice still requires some refinement, the results from these studies are encouraging and TDI is likely to be complementary to other established screening tools such as ECG and conventional echocardiography.

Cardiomyopathies↗
PubMed2003

Effects of postural changes on cardiac function in healthy subjects.

AIMS: To analyse the response of Doppler measurements to increased venous return in middle-aged healthy subjects. METHODS AND RESULTS: Left ventricular pulsed Doppler parameters, colour M-mode of early left ventricular filling and septal mitral annulus velocities were measured at baseline and after leg lifting (n=24). Leg lifting resulted in increased stroke volume (69 +/- 14 to 74 +/- 14 ml, P<0.01) and peak systolic annulus velocity (6.8 +/- 1.3 to 7.3 +/- 1.1 cm/s, P<0.01). Leg lifting enhanced peak early (E) mitral flow (74 +/- 13 to 80 +/- 14 cm/s, P<0.01), flow propagation (53 +/- 10 to 59 +/- 13 cm/s, P<0.01) and E' diastolic mitral annulus velocity (10.8 +/- 2.2 to 11.7 +/- 2.0 cm/s, P<0.01). There was a shortening of E wave deceleration time (178 +/- 27 to 163 +/- 27 ms, P<0.01) and isovolumic relaxation time (76 +/- 11 to 68 +/- 10 ms, P<0.01). However, individual changes in Doppler parameters differed among subjects. CONCLUSIONS: Leg lifting improved myocardial function as manifested by increase in stroke volume, systolic annulus motion and acceleration of relaxation. Flow propagation velocity and diastolic mitral annulus velocities were influenced by the induced change in cardiac preload as well.

Adult↗
PubMed2003

Stem cells for the heart, are we there yet?

Although several repair mechanisms have been described in the human heart, all fall too short to prevent clinical heart disease in most acute or chronic pathological cardiac conditions. Moreover, despite many breakthroughs in cardiovascular medicine, the complications of a myocardial infarction such as chronic heart failure remains a serious worldwide problem. Bone marrow stem cells could provide for a promising strategy to restore myocardial infarctions and prevent postinfarct congestive heart failure, because there is growing body of evidence that bone marrow stem cells, such as mesenchymal stem cells, can generate new cardiomyocytes in animals and humans. In this review, we will discuss important issues on stem cell therapy for cardiac regeneration after myocardial infarction, which might be of paramount importance when considering future human trials.

Animals↗
PubMed2000

Load dependent diastolic dysfunction in heart failure.

Congestive heart failure may result from cardiovascular overload, from systolic or from diastolic dysfunction. Diastolic left ventricular dysfunction may result from structural resistance to filling such as induced by pericardial constraint, right ventricular compression, increased chamber stiffness (hypertrophy) and increased myocardial stiffness (fibrosis). A distinct and functional etiology of diastolic dysfunction is slow and incomplete myocardial relaxation. Relaxation may be slowed by pathological processes such as hypertrophy, ischemia and by asynchronous left ventricular function. The present contribution analyses the occurrence of slow and incomplete myocardial relaxation in response to changes in systolic pressure and in response to changes in venous return. The regulation of myocardial relaxation by load is critically dependent on the transition from myocardial contraction to relaxation, which occurs in dogs when 82% of peak isovolumetric pressure has developed or at a relative load of 0.82. This corresponds to early ejection in normal hearts, but is situated even before aortic valve opening in severely diseased hearts. When load is developed beyond this transition, relaxation becomes slow and even incomplete. This is load dependent diastolic dysfunction. Load dependent diastolic dysfunction occurs in normal hearts facing heavy afterload and in severely diseased hearts even with normal hemodynamic parameters. This dysfunction should contribute to elevating filling pressures in most patients with severe congestive heart failure. This dysfunction can be reverted by decreasing systolic pressures or by decreasing venous return. Load dependent diastolic dysfunction gives us an additional reason to aggressively treat CHF patients with diuretics and vasodilators.

Animals↗
PubMed2000

The physiology of left ventricular pressure fall.

Left ventricular pressure (LVP) fall is the hemodynamic manifestation of myocardial relaxation. This paper reviews the most important aspects of LVP fall and its regulation by load, inactivation and nonuniformity. This regulation is explained in terms of calcium transients and cross-bridge mechanics. Specific effects of systolic pressure on LVP fall and their relation to systolic cardiac function are emphasized. These data constitute a conceptual framework for the analysis of myocardial relaxation in cardiovascular research and in the cardiac patient. Comparison of clinical and experimental data during manipulation of afterload should lead to an improved understanding of relaxation disturbances and to a therapeutic approach which is relevant from the pathophysiological point of view. LVP fall may provide useful and quantitative information on systolic LV function if measurements are performed under different conditions of systolic load.

Blood Pressure↗
PubMed1999

Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction.

BACKGROUND: Diastolic left ventricular (LV) dysfunction manifests as an upward shift of the diastolic pressure-volume relation. One of the possible causes of diastolic LV dysfunction is incomplete myocardial relaxation. It is well known that high afterload slows myocardial relaxation. This contribution investigated to what extent afterload elevation could also affect LV filling pressures including end-diastolic LV pressure (LVP). METHODS: Selective, beat-to-beat elevations of afterload were induced in anaesthetised open-chest rabbits (n = 9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat. This was performed with physiological heart rate and blood pressure. RESULTS: These interventions increased systolic LVP from 90 +/- 3 mm Hg at baseline to 103 +/- 4, 123 +/- 5, 139 +/- 5 and 154 +/- 6 mm Hg. The last intervention was a total aortic occlusion inducing a first beat isovolumetric contraction. Smaller afterload elevations decreased tau (accelerated LVP fall) and did not elevate diastolic pressure-internal diameter relation (P-ID). Larger afterload elevations increased tau (decelerated LVP fall), induced an upward shift of the diastolic P-ID and increased end-diastolic LVP. Effects of afterload on end-diastolic LVP were correlated with effects on tau (r = 0.89; P < 0.01). Incomplete relaxation or load-dependent residual active state appeared to be the mechanism for this diastolic dysfunction. Similar findings were made retrospectively in dogs instrumented with circumferential segment length gauges (n = 16). CONCLUSIONS: Diastolic LV dysfunction was induced by elevated afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.

Analysis of Variance↗
PubMed1999

Load dependence of left ventricular contraction and relaxation. Effects of caffeine.

OBJECTIVE: Load dependence of left ventricular (LV) contraction and relaxation was investigated at baseline and after alteration of intracellular calcium handling by caffeine. METHODS: Afterload was increased by aortic clamp occlusions (n = 281) in anesthetized open-chest dogs (n = 7). Control and first heartbeat after the intervention were considered for analysis. RESULTS: Caffeine (50 mg/kg, iv) had no inotropic effect. The systolic LV pressure (LVP), developed in response to aortic occlusion, decreased as ejection proceeded and this pressure generating capacity was not affected by caffeine. Late-systolic aortic occlusions induced premature onset and accelerated rate of initial LVP fall at baseline and similarly after caffeine. Graded diastolic aortic occlusions induced systolic LVP elevations of various magnitudes. Smaller LVP elevations prolonged ejection and accelerated LVP fall, while larger elevations had opposite effects. The transition from acceleration to deceleration was observed at 83.1 +/- 1.1% of peak isovolumetric LVP at baseline and at lower loads, at 77.6 +/- 1.2%, after caffeine (p < 0.01). Isovolumetric heartbeats prolonged the time constant tau by 238 +/- 70% at baseline and only by 155 +/- 44% after caffeine (p < 0.01). The relaxation-systolic pressure relation, which describes afterload dependence of relaxation, was also modified by caffeine. CONCLUSIONS: Caffeine affected LV relaxation without altering contractility. As a consequence contraction-relaxation coupling was modified by caffeine. These results might help to understand load dependence of relaxation in conditions where intracellular calcium handling is altered.

Animals↗
PubMed1999

Effects of nicardipine and urapidil on length-dependent regulation of myocardial function in coronary artery surgery patients.

OBJECTIVE: To assess effects of a decrease in left ventricular (LV) afterload (pharmacologically induced by nicardipine and urapidil) on myocardial contraction and relaxation, with emphasis on the effects on load dependence of myocardial function. DESIGN: Prospective, blinded study. SETTING: University hospital. PARTICIPANTS: Coronary artery surgery patients. INTERVENTIONS: Alterations of systolic load were effected by leg elevation in control conditions and after administration of either nicardipine or urapidil before and after cardiopulmonary bypass. MEASUREMENTS AND MAIN RESULTS: High-fidelity LV pressure tracings were obtained at end-expiration while hearts were paced at a fixed rate of 90 beats/min. Hemodynamic effects of leg elevation were compared before and after nicardipine, 7 microg/kg (n = 15), and before and after urapidil, 0.4 mg/kg (n = 15). The effects of leg elevation on parameters of contraction and relaxation were coupled. Both nicardipine and urapidil similarly decreased systolic pressures and peripheral resistance. Nicardipine decreased rate of pressure development (dP/dtmax) and slowed LV pressure fall, whereas load dependence of LV relaxation was not altered. Urapidil did not alter dP/dtmax, rate of LV pressure fall, or load dependence of relaxation. Similar results were observed after cardiopulmonary bypass. CONCLUSIONS: The results of the present study indicate that a pharmacologically induced moderate reduction in LV afterload with nicardipine or urapidil did not alter the length-dependent regulation of myocardial function.

Adrenergic alpha-Antagonists↗
PubMed1999

The effects of beta-adrenergic stimulation on the length-dependent regulation of myocardial function in coronary surgery patients.

UNLABELLED: Increasing cardiac load by leg elevation identifies patients with load-dependent impairment of left ventricular (LV) function. This impairment is related to a deficient length-dependent regulation of LV function. We investigated the effects of dobutamine on length-dependent regulation of LV function in coronary surgery patients (n = 25). High-fidelity LV pressure tracings were obtained at end-expiration, while hearts were paced at a fixed rate of 90 bpm. Effects of leg elevation on contraction and relaxation were compared before and during dobutamine 5 microg x kg(-1) x min(-1). Effects on contraction were evaluated by analysis of changes in dP/dtmax. Effects on relaxation were assessed by analysis of R (slope of the relation between the time constant of isovolumic relaxation and end-systolic pressure). Correlations were calculated with linear regression analysis using Pearson's coefficient r. The effects of leg elevation on variables of contraction and relaxation were coupled. We found a close relationship between changes in dP/dtmax and individual values of R (r = 0.84; P < 0.001). Dobutamine improved myocardial function and accelerated LV pressure decrease. Under dobutamine, the increase in dP/dtmax with leg elevation was larger (P < 0.001) and load dependence of LV relaxation was reduced (P = 0.001). Dobutamine improved the effects of leg elevation on LV function, reflecting improved length-dependent regulation of LV function. IMPLICATIONS: This study demonstrated that beta-adrenoreceptor stimulation with dobutamine improved length-dependent regulation of myocardial function assessed during leg elevation in cardiac surgical patients.

Adrenergic beta-Agonists↗
PubMed1999

Contraction-relaxation coupling and impaired left ventricular performance in coronary surgery patients.

BACKGROUND: Dependence of left ventricular (LV) relaxation on cardiac systolic load is a function of myocardial contractility. The authors hypothesized that, if a tight coupling would exist between LV contraction and relaxation, the changes in relaxation rate with an increase in cardiac systolic load would be related to the changes in LV contraction. METHODS: Coronary surgery patients (n = 120) with preoperative ejection fraction >40% were included. High-fidelity LV pressure tracings (n = 120) and transgastric transesophageal echocardiographic data (n = 40) were obtained. Hearts were paced at a fixed rate of 90 beats/min. Effects on contraction were evaluated by analysis of changes in dP/dt(max) and stroke area. Effects on relaxation were assessed by analysis of R (slope of the relation between tau and end-systolic pressure). Correlations were calculated with linear regression analysis using Pearson's coefficient r. RESULTS: Baseline LV end-diastolic pressure was 10+/-3 mm Hg (mean +/- SD). During leg raising, systolic LV pressure increased from 93+/-9 to 107+/-11 mm Hg. The change in dP/dt(max) was variable and ranged from -181 to +254 mm Hg/s. A similar variability was observed with the changes in stroke area, which ranged from -2.0 to +5.5 cm2. Changes in dP/dt(max) and in stroke area were closely related to individual R values (r = 0.87, P<0.001; and r = 0.81, P<0.001, respectively) and to corresponding changes in LV end-diastolic pressure (r = 0.81, P< 0.001; and r = 0.74, P<0.001, respectively). CONCLUSIONS: A tight coupling was observed between contraction and relaxation. Leg raising identified patients who developed a load-dependent impairment of LV performance and increased load dependence of LV relaxation.

Aged↗
PubMed1999

Length-dependent regulation of left ventricular function in coronary surgery patients.

BACKGROUND: Load-dependent impairment of left ventricular (LV) function was observed after leg elevation in a subgroup of coronary surgery patients. The present study investigated underlying mechanisms by comparing hemodynamic effects of an increase in LV systolic pressures with leg elevation to effects of a similar increase in systolic pressures with phenylephrine. METHODS: The study was performed in patients undergoing elective coronary surgery prior to cardiopulmonary bypass. High-fidelity LV pressure tracings (n = 25) and conductance LV volume data (n = 10) were obtained consecutively during leg elevation and after phenylephrine administration (5 microg/kg). RESULTS: Leg elevation resulted in a homogeneous increase in end-diastolic volume. The change in stroke volume (SV), stroke work (SW) and dP/dtmax was variable, with an increase in some patients but no change or a decrease in other patients. For a matched increase in systolic pressures, phenylephrine increased SW and dP/dtmax in all patients with no change in SV. Load dependence of relaxation (slope R of the tau-end-systolic pressure relation) was inversely related for changes in SV, SW, and dP/dtmax with leg elevation but not with phenylephrine. CONCLUSIONS: The different effects of leg elevation and phenylephrine suggest that the observed decrease in SV, SW, and dP/dtmax with leg elevation in some patients could not be attributed to an impaired contractile response to increased systolic LV pressures. Instead, load-dependent impairment of LV function after leg elevation appeared related to a deficient length-dependent regulation of myocardial function.

Aged↗
PubMed1998

Sodium nitroprusside enhances in vivo left ventricular function in beta-adrenergically stimulated rabbit hearts.

OBJECTIVE: Sodium nitroprusside (SNP) is an activator of soluble guanylate cyclase, which depresses myocardial contractility. These exclusively negative inotropic effects of SNP were recently challenged by in vitro data.. In isolated rat ventricular myocytes, a moderate increase of cGMP improved the contractile response at baseline and in isoprenaline-stimulated conditions. The present study evaluated in vivo the inotropic effects of SNP at baseline and during administration of low dose dobutamine. METHODS: Anesthetized open-chest rabbits (n = 18) were instrumented with micromanometers, ultrasound crystals and atrial pacing wires. Measurements were obtained during caval occlusion with ventilation suspended at end-expiration. Systolic function was assessed with dP/dtmax and the slope Ees of the end-systolic pressure-volume relation. Diastolic function was assessed with the time constant tau and the stiffness constant Kc of the diastolic pressure-volume relation. SNP (0.02, 0.08, 0.32 microgram x kg-1) was administered at baseline and during low dose dobutamine. RESULTS: At baseline, SNP reduced dP/dtmax from 3750 +/- 88 to 3470+/- 88 mmHg/s (mean +/- s.e.m.) and Ees from 148 +/- 16 to 103 +/- 13 mmHg/ml (P < 0.01) . During dobutamine infusion, SNP increased dP/dtmax from 4340 +/- 125 to 4681 +/- 230 mmHg/s and Ees from 148 +/- 19 to 190 +/- 30 mmHg/ml (P < 0.01). Effects of SNP on dP/dtmax and Ees were different at baseline and during dobutamine (interaction P < 0.01). SNP did not alter Kc at baseline nor during dobutamine. CONCLUSIONS: SNP enhances in vivo systolic function in beta-adrenergically stimulated rabbits.

Adrenergic beta-Agonists↗