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Biomedical subjects

G Jondeau

Publications and source records attributed to G Jondeau.

At least 55 records · Page 3Linked to original sources
PubMed1996

Direct and indirect assessment of skeletal muscle blood flow in patients with congestive heart failure.

Techniques which are currently used to measure skeletal muscle blood flow (SMBF) in patients with congestive heart failure (CHF) are neither convenient nor accurate. They have led to discrepant results in patients with congestive heart failure and are, in part, responsible for the ongoing debate regarding the factors which limit the rise in body oxygen consumption during exercise in these patients. However, direct measurement of SMBF may not be needed during exercise in patients with severe CHF. Their skeletal muscles maximally extract oxygen. Consequently, increase in oxygen consumption by the skeletal muscles is only mediated by a concomitant increase in SMBF. In patients with severe CHF, peak body oxygen consumption attained during maximal exercise closely depends on the rise in SMBF, and thus provides an indirect measurement of SMBF.

Heart Failure↗
PubMed1996

Fibulin-2: genetic mapping and exclusion as a candidate gene in Marfan syndrome type 2.

Fibulin-2 (FBLN2) is a new extracellular matrix protein that has been considered a candidate gene for Marfan syndrome type 2 (locus MFS2) based on chromosomal colocation at 3p24.2-p25 and disease phenotype. In the absence of polymorphic markers reported for FBLN2, direct sequencing of the gene was performed and two intragenic polymorphisms were identified. Linkage was excluded between FBLN2 and the MFS2 gene. Furthermore, two-point lod scores were generated between these markers and anonymous markers arrayed on the genetic map of 3p and closely linked to MFS2. These analyses placed FBLN2 at marker D3S1585.

Calcium-Binding Proteins↗
PubMed1996

[Quality of life: a parameter to be taken into account, but how?].

The treatment of cardiac failure aims to improve the duration and quality of life of patients. This latter parameter is all the more important as the effects of treatment on longevity are relatively weak. However, it is difficult to assess: there is no universally recognised definition and the choice of criteria to take into consideration is very subjective. The different questionnaires of quality of life attempt to be reproducible, sensitive (that is to say capable of determining the effect of a treatment with accuracy), and valid (that is to say measuring that which they are designed to measured). However, the absence of reference values also makes their evaluation difficult. In addition, their use in populations different to that in which they were elaborated raises other problems. Criteria of substitution may be proposed, such as number of hospital admissions, functional tolerance, which are easier to quantify but which only reflect one of the aspects of quality of life. Although the importance of "quality of life" is increasingly recognised and this parameter is increasingly better studied, the quality of its appreciation makes it, as yet, premature for posing therapeutic indications such as circulatory assistance. On the other hand, it is essential to try to recognise the patients most affected by the constraints of their treatment.

Activities of Daily Living↗
PubMed1995

Dynamic cardiomyoplasty: effect of discontinuing latissimus dorsi muscle stimulation on left ventricular systolic and diastolic performance and exercise capacity.

OBJECTIVES: This study sought to assess the short-term effect of discontinuing latissimus dorsi muscle stimulation on left ventricular systolic and diastolic performance and exercise tolerance in patients with improved functional status by cardiomyoplasty, in whom latissimus dorsi muscle was fully conditioned. BACKGROUND: Cardiomyoplasty has consistently improved the functional status of patients, but the short-term effect of latissimus dorsi muscle contraction has not been assessed in these patients. METHODS: Right-heart catheterization, Doppler-echocardiography and maximal exercise testing with expired gas analysis were performed in 10 patients with congestive heart failure who had undergone cardiomyoplasty at least 6 months earlier. Data were obtained when the latissimus dorsi muscle was stimulated every other systole and after stimulation was discontinued for 1 h. The power of this study to detect a 10% difference was > 80%. RESULTS: After cardiomyoplasty, left ventricular ejection fraction increased from 0.22 +/- 0.08 (mean +/- SD) to 0.27 +/- 0.07 after 6 months (p < 0.02 vs. before cardiomyoplasty) and to 0.24 +/- 0.09 after 1 year; functional class went from 3.0 +/- 0.0 to 2.0 +/- 0.5 after 6 months and to 2.0 +/- 0.7 after 1 year (both p < 0.001 vs. before cardiomyoplasty). After discontinuation of latissimus dorsi muscle stimulation, cardiac index did not change (2.28 +/- 0.45 vs. 2.30 +/- 0.46 liters/min per m2). Mean systemic arterial and pulmonary capillary wedge pressures were also similar (85.2 +/- 6.0 vs. 88.4 +/- 5.6 mm Hg and 14.9 +/- 7.1 vs. 13.6 +/- 6.8 mm Hg, respectively). Doppler E/A ratio decreased from 1.04 +/- 0.33 to 0.83 +/- 0.25 (p < 0.02), suggesting that left ventricular diastolic function may have been improved by latissimus dorsi muscle stimulation. Peak oxygen consumption was unaltered (1,633 +/- 530 vs. 1,596 +/- 396 ml/min). CONCLUSIONS: Alterations in left ventricular diastolic rather than systolic function may be responsible for the long-term clinical benefits of cardiomyoplasty.

Adult↗
PubMed1995

Doppler echocardiography in familial hypertrophic cardiomyopathy: the French Cooperative Study.

UNLABELLED: Familial hypertrophic cardiomyopathy (HCM) has been poorly studied, although it may represent 50% of all HCM. We studied 346 subjects belonging to 20 unrelated families. Patients were considered affected in view of left ventricular (LV) wall thickness. One hundred twenty-seven adults were considered affected, id est. had a left ventricular wall thickness (LVWT) > 13 mm, whereas 123 had a LVWT > 15 mm, suggesting that the cut-off value is usually not critical. Within affected patients, 95% had an asymmetrical HCM (interventricular septum/left posterior wall thickness > 1.3 mm), whereas 84% had a ratio > 1.5. Distribution of the affected patients according with Maron's classification are in keeping with published studies about sporadic forms. Doppler derived isovolumetric relaxation time was prolonged in HCM (105 +/- 23 vs 88 +/- 16 msec, P < 0.001), and the ratio peak velocity of A wave over peak velocity of E wave was significantly lower in affected individuals (0.99 +/- 0.56 vs 0.83 +/- 0.46, P < 0.05). None of the 24 children studied (10 +/- 3 years) were considered affected according to echocardiographic criteria. CONCLUSION: Echocardiography is the obligatory first step during genetic study for recognizing familial HCM. It allows classification in adults but not in children. Doppler estimate of diastolic function may be helpful in the future to recognize genetically affected subjects with normal or subnormal echocardiographic examination.

Adult↗
PubMed1994

A second locus for Marfan syndrome maps to chromosome 3p24.2-p25.

Marfan syndrome (MFS) is an autosomal dominant connective-tissue disorder characterized by skeletal, ocular and cardiovascular defects of highly variable expressivity. The diagnosis relies solely on clinical criteria requiring anomalies in at least two systems. By excluding the chromosome 15 disease locus, fibrillin 1 (FBN1), in a large French family with typical cardiovascular and skeletal anomalies, we raised the issue of genetic heterogeneity in MFS and the implication of a second locus (MFS2). Linkage analyses, performed in this family, have localized MFS2 to a region of 9 centiMorgans between D3S1293 and D3S1283, at 3p24.2-p25. In this region, the highest lod score was found with D3S2336, of 4.89 (theta = 0.05). By LINKMAP analyses, the most probable position for the second locus in MFS was at D3S2335.

Adult↗
PubMed1994

Oral enoximone as a substitute for intravenous catecholamine support in end-stage congestive heart failure.

We performed a double-blind, placebo-controlled study to determine whether oral enoximone would aid weaning dobutamine-dependent patients. Twenty-four patients 64 +/- 10 years, with an echocardiographic ejection fraction of 0.20 +/- 0.06, and receiving maximal therapy were studied. After failure of dobutamine weaning, a dobutamine infusion was set up at 10 micrograms.kg-1.min-1 for 48 h. Oral enoximone (100 mg t.i.d.) or placebo was added from D0 for the next 28 days, while the dobutamine dosage was progressively decreased after D4 and eventually stopped at D7. The patients were then followed-up for 21 days (i.e. until enoximone administration had continued for 28 days). In the placebo group, two patients suffered a relapse of congestive heart failure (CHF) before D4, six patients withdrew during dobutamine tapering (five with a relapse of CHF and one with septic shock) and two during follow-up (one with a relapse of CHF and one with sustained ventricular tachycardia). In the enoximone group, three patients withdrew during dobutamine tapering (two with a relapse of CHF, one with a cutaneous rash). Four patients on placebo and nine receiving enoximone could be weaned from dobutamine, P < 0.05. Echocardiographic LV ejection fraction significantly increased and Doppler-derived indexes of systolic function tended to increase when enoximone but not placebo was associated with dobutamine. Oral enoximone might be helpful in weaning patients with end-stage congestive heart failure from i.v. dobutamine.

Administration, Oral↗
PubMed1994

Enhancement of endothelium-dependent vasodilation by low-dose nitroglycerin in patients with congestive heart failure.

BACKGROUND: Since organic nitroesters and endothelium-derived nitric oxide mediate vasodilation through a final common pathway, that is, by activation of soluble guanylate cyclase in vascular smooth muscle, nitroglycerin (NTG) could specifically enhance the endothelium-dependent vasodilatory response to acetylcholine (Ach) in patients with congestive heart failure (CHF) and endothelial cell dysfunction. Accordingly, the net effects of an intra-arterial infusion of NTG (10(-9) mol/L) on endothelium-dependent and endothelium-independent vasodilation were assessed in the forearm circulation of patients with CHF. METHODS AND RESULTS: The forearm blood flow responses to intra-arterial administration of graded concentrations of Ach (10(-7) to 10(-5) mol/L) were determined by venous occlusion plethysmography (mL/min per 100 mL) in 18 patients with CHF and 5 age-matched normal subjects before and during intra-arterial infusion of NTG (10(-9) mol/L) for 20 minutes. In eight patients, the duration of the infusion of NTG (n = 5) or vehicle control solution (n = 3) was extended to 12 hours with measurement of the forearm blood flow responses to Ach at 20 minutes, 4 hours, and 12 hours. In five additional patients, forearm blood flow response to intra-arterial administration of two doses of phentolamine (0.05 and 0.5 mg) were determined before and during a 20-minute NTG infusion. Regional administration of NTG 10(-9) mol/L did not change resting forearm blood flow in either normal subjects or patients with CHF. Before administration of NTG 10(-9) mol/L, intra-arterial infusions of Ach 10(-7), 10(-5) and 10(-5) mol/L increased forearm blood flow to 14.7 +/- 6.2, 20.2 +/- 4.7, and 38.4 +/- 7.9 mL/min per 100 mL in normal subjects and to 4.1 +/- 0.8, 5.0 +/- 1.1, and 10.6 +/- 2.3 mL/min per 100 mL in patients with CHF. After administration of NTG 10(-9) mol/L for 20 minutes, the vasodilatory response to Ach significantly increased to 5.6 +/- 1.0, 6.9 +/- 1.6, and 17.7 +/- 3.4 mL/min per 100 mL in patients with CHF but did not change in normal subjects. The enhanced forearm blood flow responses to administration of Ach observed after 20 minutes of NTG administration in patients with CHF were sustained throughout a 12-hour NTG infusion. In contrast, regional administration of NTG did not change the vasodilatory responses to phentolamine. CONCLUSIONS: NTG, when administered intra-arterially for 20 minutes at a dose that does not affect resting forearm blood flow, specifically increased the vasodilatory response to intra-arterial administration of Ach in patients with CHF but not in normal subjects. The vasodilatory response to Ach was consistently enhanced by low-dose NTG throughout a 12-hour period. The vasodilating effects of organic nitroesters on the peripheral vasculature of patients with CHF may result in part from an interaction with the vascular endothelium.

Acetylcholine↗
PubMed1994

Comparison of treadmill and bicycle exercise in patients with chronic heart failure.

The general opinion that treadmill exercise elicits circulatory reserve more than bicycle exercise derives from studies conducted in normal subjects or subjects with coronary artery disease. To investigate if this also occurs in patients with chronic heart failure (CHF), 40 patients (mean ejection fraction: 26 +/- 9 percent) with normal pulmonary function underwent in random order both treadmill (Naughton modified protocol, holding on handrails permitted) and bicycle (10 W/min) maximal exercise over a 1-week period. Peak oxygen uptake (19.6 +/- 5.3 vs 17.6 +/- 5.1 ml/min/kg, p < 0.0001), ventilatory threshold (14.4 +/- 4.7 vs 12.0 +/- 3.5 ml/min/kg, p < 0.0001), and minute ventilation (59 +/- 18 vs 55 +/- 15 L/min, p < 0.05) were greater on treadmill than on bicycle. Heart rate, systolic blood pressure, breathing rate, respiratory exchange ratio, perceived exertion scale, and lactate were identical. The coefficient of the correlation between oxygen uptake and time was greater with bicycle than with treadmill (r = 0.97 +/- 0.04 vs 0.90 +/- 0.07, p < 0.001). Thus, treadmill exercise is more suitable for determining peak oxygen uptake in patients with CHF. However, the increase in oxygen uptake is more regular with bicycle exercise.

Anaerobic Threshold↗
PubMed1993

Regional specificity of peak hyperemic response in patients with congestive heart failure: correlation with peak aerobic capacity.

OBJECTIVES: The aim of this study was to compare peak reactive hyperemic blood flows in the forearm and calf of patients with congestive heart failure and in age- and gender-matched normal subjects. In addition, we attempted to correlate peak oxygen consumption with forearm and calf peak reactive hyperemic flows in the patients with heart failure. BACKGROUND: Disparate results have been reported regarding forearm peak reactive hyperemia in patients with congestive heart failure. Because training significantly increases peak reactive hyperemic flow in normal subjects, we hypothesized that in patients with congestive heart failure who curtail walking because of exertional symptoms, calf peak reactive hyperemic flow would be preferentially attenuated and that impairment of calf vasculature may correlate with peak oxygen consumption. METHODS: Forearm and calf blood flows were measured by venous occlusive plethysmography at rest and after 5 min of arterial occlusion in 46 patients with congestive heart failure and 7 age- and gender-matched normal subjects. Peak oxygen consumption was measured during graded exercise on a bicycle ergometer. RESULTS: Calf peak reactive hyperemic flow was lower in patients with congestive heart failure than in normal subjects (22 +/- 1 vs. 32.5 +/- 3.5 ml/min per 100 ml, p < 0.001), whereas forearm peak reactive hyperemic flows were similar in the two groups. Calf peak reactive hyperemic flow was linearly related to peak oxygen consumption (r = 0.58, p < 0.0001), but forearm peak reactive hyperemic flow was not. Forearm and calf peak reactive hyperemic flows were not related at rest or after 5 min of arterial occlusion in the patients with heart failure. CONCLUSIONS: Calf peak reactive hyperemic flow is reduced in patients with congestive heart failure, whereas forearm peak reactive hyperemic flow is identical to that of age- and gender-matched normal subjects. Calf peak reactive hyperemic flow is linearly related to peak oxygen consumption in patients with congestive heart failure, but forearm peak reactive hyperemic flow is not.

Case-Control Studies↗
PubMed1993

High flow coronary fistula closure by percutaneous coil packing.

Few cases of transcatheter coronary fistula closure have been reported. High flow coronary fistulae are usually treated by surgery. This case report presents a 5.4 liters/min flow coronary fistula percutaneously closed by steel coils. This large flow needed the packing of 25 coils, 10-15 cm long, for its total occlusion.

Arteriovenous Fistula↗
PubMed1993

Low incidence of stroke in ambulatory patients with heart failure: a prospective study.

The current study was undertaken to determine prospectively the risk of cerebral thromboembolism and the prognostic significance of left ventricular thrombus in ambulatory patients with chronic congestive heart failure. A total of 264 ambulatory patients (mean age 62 years, mean left ventricular ejection fraction 27%) were followed prospectively for 24 +/- 9 months to determine the incidence of nonhemorrhagic stroke, transient ischemic attack, and mortality. Two-dimensional echocardiographic studies, performed for clinical indications other than previous systemic thromboembolism in 109 patients, were analyzed to relate the presence of left ventricular thrombus to subsequent outcome. Nine cerebral thromboembolic events occurred in 264 patients during the two-year mean follow-up period, yielding a rate of 1.7 thromboembolic events per 100 patient-years of follow-up. Known risk factors for stroke (hypertension, diabetes mellitus, and/or atrial fibrillation) were present in all nine patients with cerebral thromboembolic events. The 109 patients with echocardiographic studies had more severe heart failure than patients without echocardiographic studies (functional class 2.6 vs 2.1, p < 0.01), greater risk of a thromboembolic event (2.4 vs 1.4 events/100 patient-years of follow-up, p < 0.01), and higher mortality (21.3 vs 5.5 deaths/100 patient-years, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Doppler-derived aortic maximal acceleration. A reliable index of left ventricular systolic function.

We compared maximal acceleration of aortic blood flow (aortic Amax), calculated from maximal aortic velocity obtained with a conventional echo-Doppler machine with the invasive inotropic index left ventricular end-systolic pressure/left ventricular end-systolic volume (LVESP/LVESV) ratio and left ventricular ejection fraction (LVEF). Continuous wave (CW) and pulsed wave (PW) Doppler aortic blood flows were recorded from the apical view in 16 patients (age, 62.3 +/- 6.4 years) within 24 h of left-sided catheterization. The theoretical exponential relationship between LVEF and LVESP/LVESV was confirmed in our study population (r = 0.92; p < 0.0001). The relationship between aortic Amax determined either by CW or PW and LVESP/LVESV was linear (r = 0.92 and 0.93, respectively, p < 0.001), whereas the relationship between aortic Amax and angiographic LVEF was exponential (PW: r = 84; CW: r = 0.85; both p < 0.001). We conclude that (1) aortic Amax, derived from maximal velocity obtained with a conventional machine, can be used as an index of left ventricular systolic function, and (2) PW as well as CW Doppler signals can be used for this calculation.

Aged↗
PubMed1993

[Simultaneous measurement of systolic pulmonary artery pressure by catheterization and contrast enhancement doppler echocardiography].

The aim of this study was to assess the value of echocardiographic contrast in measuring systolic pulmonary artery pressures. Thirty-four patients with an average age of 61 +/- 15 years undergoing right heart catheterisation had a simultaneous measurement of systolic pulmonary artery pressures by catheter and colour-coded Doppler echocardiography under basal conditions and after injection of 5% dextrose agitated with 1 cm3 of air to form microcavitations. The Doppler echocardiographic measurements were performed after withdrawal of the catheter into the inferior vena cava before and after injection of contrast. Patients were divided into two groups according to the pulmonary artery pressures at catheterisation: Group I, comprising 11 patients with systolic pulmonary artery pressures of less than 35 mmHg; Group II, comprising 23 patients with systolic pulmonary artery pressures of over 35 mmHg; The injection of contrast significantly increased the number of patients in whom systolic pulmonary artery pressures could be calculated from the Doppler signal of tricuspid regurgitation (TR) in Group I (control: 18%; contrast: 100%, p < 0.01) and Group II (control: 65%; contrast: 96%, p < 0.05). There was a close correlation between the catheter and Doppler measurements of the trans-tricuspid valve pressure gradients before and after injection of contrast in Group I (n = 11, r = 0.85, p = 0.001, with an estimated standard error (ESE) = 3.8 mmHg) and in Group II (control: n = 15, r = 0.89, p = 0.001, ESE = 10.5 mmHg, and after contrast: n = 22, .r = 0.90, p = 0.001, ESE = 7.95 mmHg) with the catheter in the right ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[French familial multicenter survey of hypertrophic cardiomyopathy. Initial Doppler echocardiographic results].

A French multicentre study of hypertrophic cardiomyopathy has recruited 260 subjects belonging to 18 families. At least 3 persons from each family included had a hypertrophic cardiomyopathy. A Doppler echocardiographic examination was performed in all members of these 18 families. The diagnosis of hypertrophic cardiomyopathy was based on M mode and/or 2D observations of parietal hypertrophy: wall thickness over 13 mm. Asymmetrical forms were distinguished from symmetrical forms by a septum/posterior wall ratio of over 1.3 in M mode or 2D study. The patients had an average age of 40 +/- 18 years, 127 were men and 133 women. One hundred and sixty eight were considered to be normal, 87 had hypertrophic cardiomyopathy and 5 were border line. The maximal diastolic wall thickness on M mode recording of pathological cases was 19.2 +/- 4.8 mm compared with 9.5 +/- 1.9 mm in healthy subjects (p < 0.001). The septum/posterior wall ratio was 1.8 +/- 0.62 in pathological cases and 1.1 +/- 0.8 in normal ones (p < 0.001). Eighty five per cent of the cardiomyopathic cases were asymmetrical (74/87) and only 15% were considered to be symmetrical (13/87) on M mode study whereas 5% were concentric on 2D echocardiography. By Maron's classification, type I hypertrophy was observed in 6% of cases (4/64), type II in 30% (19/64), type III in 58% (37/64), and type IV in 6% (4/64). Signs of obstruction were looked for and systolic anterior motion of the mitral valve was observed in 52% of pathological cases (45/86) and mid-systolic aortic valve closure in 30% (25/83).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Hypertrophic↗
PubMed1993

Autosomal dominant Marfan-like connective-tissue disorder with aortic dilation and skeletal anomalies not linked to the fibrillin genes.

We describe a large family with a connective-tissue disorder that exhibits some of the skeletal and cardiovascular features seen in Marfan syndrome. However, none of the 19 affected individuals displayed ocular abnormalities and therefore did not comply with recognized criteria for this disease. These patients could alternatively be diagnosed as MASS (mitral valve, aorta, skeleton, and skin) phenotype patients or represent a distinct clinical entity, i.e., a new autosomal dominant connective-tissue disorder. The fibrillin genes located on chromosomes 15 and 5 are clearly involved in the classic form of Marfan syndrome and a clinically related disorder (congenital contractural arachnodactyly), respectively. To test whether one of these genes was also implicated in this French family, we performed genetic analyses. Blood samples were obtained for 56 family members, and four polymorphic fibrillin gene markers, located on chromosomes 15 (Fib15) and 5 (Fib5), respectively, were tested. Linkage between the disease allele and the markers of these two genes was excluded with lod scores of -11.39 (for Fib15) and -13.34 (for Fib5), at theta = .001, indicating that the mutation is at a different locus. This phenotype thus represents a new connective-tissue disorder, overlapping but different from classic Marfan syndrome.

Adult↗