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Biomedical subjects

D Farge

Publications and source records attributed to D Farge.

At least 91 records · Page 5Linked to original sources
PubMed1990

Effect of systemic hypertension on renal function and left ventricular hypertrophy in heart transplant recipients.

To evaluate the incidence, risk factors and effects of systemic hypertension on renal function and left ventricular hypertrophy after cardiac transplantation, 85 transplant recipients on triple drug, low dosage, immunosuppressive therapy were studied. After a mean follow-up period of 12.5 +/- 8.7 months, a high incidence of hypertension was observed in 57 (67%) of the patients, and 42 (71%) of the 57 had developed new hypertension. None of the pretransplant and posttransplant cardiovascular risk factors were significantly associated with posttransplant hypertension. Faster deterioration of renal function, as assessed by intraindividual variations of serum creatinine values, was demonstrated in hypertensive patients and appeared as an early indicator of cyclosporine nephrotoxicity in patients at risk for hypertension. Serial echocardiographic evaluations demonstrated an early increase in left ventricular mass and fractional shortening in both hypertensive and normotensive heart transplant recipients. Fractional shortening further diminished significantly in normotensive patients but remained elevated in hypertensive patients, demonstrating sustained enhanced contractility in this group. Further studies will help to determine the exact relation between cyclosporine dosages and hypertension and their respective roles in the development of renal insufficiency and left ventricular hypertrophy after cardiac transplantation.

Adult↗
PubMed1990

[Mid-term echographic evaluation of systolic function after cardiac transplantation].

The aim of this study was to analyse variations in left ventricular mass (LVM) and systolic function after cardiac transplantation and to evaluate eventual changes induced by the onset of systemic hypertension (HT). In a retrospective study, we selected the echocardiographic examinations of 42 patients performed at the end of the first month (M1), sixth month (M6), and at the end of follow-up (ME) after cardiac transplantation. The patients were divided into two groups (NT: n = 14; HT: n = 28) depending on whether hypertension occurred during follow-up. The average duration of follow-up was 12.8 +/- 6 months; this was comparable in the two groups. Mild left ventricular hypertrophy was observed from the first postoperative examination: M1 = 193 +/- 50 g; M6 = 199 +/- 62 g; ME = 197 +/- 45 g (NS). The hypertrophy was constant with time and related to wall thickening; it was associated with an increased left ventricular fractional shortening (FS) which decreased with time especially in the NT group (average/42 patients: M1 = 0.38 +/- 0.09; M6 = 0.34 +/- 0.08; ME = 0.35 +/- 0.05; p = 0.03 between M1 and ME). The influence of hypertension on the development of LVH and wall thickening was negligible. The role of transplant rejection should be considered: the repetition of episodes of rejection was less marked than the histological severity of rejection. The role of other factors (ischaemia, persistent haemodynamic abnormalities) is a matter of discussion.

Adult↗
PubMed1990

[Enoximone in the hemodynamic evaluation before heart transplantation. A new test].

A better selection of patients referred for cardiac transplantation should lead to better surgical results. The presence of severe and irreversible pulmonary hypertension is an important factor and its pretransplantation assessment requires pharmacodynamic testing with vasodilators and dobutamine. The aim of this study of 10 patients in congestive cardiac failure referred for cardiac transplantation was to evaluate enoximone in this indication by comparing it with sodium nitroprussiate (3 micrograms/kg/mn). Intravenous enoximone (total dose of 1.5 mg/kg) increased the cardiac index (+49%; p less than 0.01), slightly reduced the mean systemic blood pressure (-8%; p less than 0.05) whilst inducing a greater reduction in systemic arterial resistances (-36%; p less than 0.01); the fall in mean blood pressure was less than with sodium nitroprussiate (-23%; p less than 0.01). Myocardial oxygen consumption (rate-pressure product) did not increase in contrast to the effect of dobutamine (+21%; p less than 0.01). There was a significant reduction in pulmonary arteriolar resistances (p less than 0.01) with all three drugs but the interpretation of this response and its prognostic significance in patients with a low cardiac output and persistent pulmonary hypertension are discutable even when pulmonary arteriolar resistances are less than 6 Wood units. The value of using an inotropic agent such as Dobutamine or Enoximone is to unmask fixed pulmonary hypertension which may be missed in patients with low cardiac output even with vasodilator drugs, and also to mimic the haemodynamic result of transplantation. In this indication Enoximone may be used like Dobutamine but with the advantage of not increasing myocardial oxygen consumption and being probably less arrhythmogenic.

Adult↗
PubMed1990

[Effect of hypertension on the renal and cardiac functions of patients with heart transplantation].

To evaluate the incidence, risk factors and effects of systemic hypertension on renal function and left ventricular hypertrophy after heart transplantation, 85 recipients under triple drug low low dosage immunosuppressive therapy were studied. After a mean follow-up of 12.5 +/- 8.7 months, high incidence of hypertension was observed in 67% of the patient and 71% had developed de novo hypertension. None of the pre-transplant nor post-transplant cardiovascular risk factors were significantly associated with post-transplant hypertension. Faster deterioration of renal function, as assessed by intraindividual variations of serum creatinine values, was demonstrated in hypertensive patients and appeared as an early indicator of cyclosporine nephrotoxicity in patients at risk for hypertension. [table: see text] Serial (early, intermediate, late) echocardiographic evaluations demonstrated early increase in left ventricular mass and in fractional shortening in both hypertensive and normotensive heart transplant recipients with sustained enhanced contractility in hypertensive patients. [table: see text] Further studies will help to determine the exact relationship between cyclosporine dosages and hypertension, and their respective roles in the development of renal insufficiency and left ventricular hypertrophy after heart transplantation.

Adult↗
PubMed1989

[Glomerulonephritis by glomerular anti-basement membrane antibodies after renal transplantation].

Glomerulonephritis (GN) due to antiglomerular basement membrane (GBM) antibodies after kidney transplantation may be classified into two groups: 1. Recurrent GN are very rare provided circulating anti-GBM antibodies are absent at grafting. If present, linear fixation along the GBM occurs but does not lead to GN in some cases. 2. De novo anti-GBM diseases have been rarely reported. They developed in 8 patients with Alport's syndrome and in at least 3 additional patients in whom hereditary nephritis was not the original disease. A prospective and retrospective study was performed in 54 transplanted patients with hereditary nephritis: circulating anti-GBM antibodies were detected in only one case; linear fixation along the GBM was found but no evidence of GN. The risk of anti-GBM disease after kidney transplantation is low in patients with hereditary nephritis but this complication must be rapidly identified. Its occurrence is probably related to the defect in GBM antigenicity involving the Goodpasture antigen, found in some patients with Alport's syndrome or related hereditary nephritis.

Antibodies↗
PubMed1988

[Acute response to calcium inhibitors in secondary arterial hypertension: does renin play a role?].

Calcium channel blocking agents are considered to be particularly effective in reducing blood pressure (BP) in low renin essential hypertension and in primary aldosteronism. The aim of this study was to compare the acute BP response to nicardipine in 2 opposite situations of stimulation of the renin angiotensin system: eight patients (49 +/- 13 years, mean arterial BP (MAP) 123 +/- 8 mmHg) with primary aldosteronism (active renin less than 5 pg/ml, group 1) and nine patients (38 +/- 17 years, MAP: 107 +/- 13 mmHg) with renovascular hypertension and high level of active renin (greater than 25 pg/ml, group 2). They had not taken any antihypertensive treatment since at least one week. After 60 minutes in the supine position (T0) nicardipine was infused at a rate of 7.5 mg/h during 10 minutes (T10), 15 mg/h from the 10th to 20th minute (T20) and 30 mg/h during the last ten minutes (T30). Thus, a total cumulative dose of 8.75 mg was administrated in 30 minutes. BP was recorded by an indirect oscillometric method (Sentrom) every 2 minutes and renin was assayed through an immuno-radiometric procedure (IRMA). There was an important and similar BP fall in the 2 groups (Gr 1: T10-6 p. 100, T20-17 p. 100, T30-25 p. 100; Gr 2: T10-7 p. 100, T20-13 p. 100, T30-18 p. 100) with a very significant dose-effect relation (r = 0.67, p less than 0.001). There was also an important increase in heart rate similar in the 2 groups (+35 p. 100, +25 p. 100, ns).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Malignant adrenal cortex carcinoma revealed by an isolated picture of primary hyperaldosteronism].

Adrenocortical carcinoma (ACC) is a rare disorder with an estimated incidence of only 0.023 percent of all malignancies. In most cases, Cushing's syndrome and virilization or feminization due to abnormal steroid production by the tumor rapidly lead to the diagnosis. Occasionally, the tumor produces an excessive amount of mineralocorticoids only and ACC can be revealed by an isolated syndrome of primary aldosteronism. Out of 100 cases of tumoral primary aldosteronism studied from 1977 to 1987, we observed 4 ACC and 96 Conn's adenomas (CONN). When primary aldosteronism was diagnosed, ACC and CONN had same clinical features, although hypokalemia in ACC was more profound: 2.2 +/- 0.76 mmol/l (1.4 to 3.2) compared to 2.9 +/- 0.5 (1.6 to 4.2) in CONN. Mean supine plasma aldosterone levels, plasma renin and aldosterone responses to the upright posture or to serum saline infusion, cortisol at 8 a.m. were not different in patients with ACC from those observed in patients with CONN. 24 hours urinary cortisol excretion and 17-ketosteroids excretion were highly increased in three out four patients with ACC. Clinical, biological and hormonal investigations were therefore not sufficient to diagnose malignant tumoral primary aldosteronism. Systematic computed tomographic scanning allowed to differentiate carcinomas from adenomas on the following criteria: ACC showed enlarged tumor size that was always above 30 mm in diameter, whereas the largest CONN measured 20 mm.ACC appeared as an heterogeneous tumor with the presence of internal calcifications in each case of ACC, that were diagnosed both on ultrasound and CT scan, whereas none of the CONN showed any calcification, using the same screening procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

17-Ketosteroids↗
PubMed1987

Isolated clinical syndrome of primary aldosteronism in four patients with adrenocortical carcinoma.

Adrenocortical carcinoma is a rare disorder that can be revealed by an isolated syndrome of mineralocorticoid excess. In a retrospective study of 137 patients referred to our hypertension clinic in the past 10 years for primary aldosteronism, four cases of adrenocortical carcinoma were identified. The clinical presentation of these patients was similar to that of patients with Conn's adenoma, but preoperatively, malignant tumoral primary aldosteronism was suspected because of profound hypokalemia, marked elevation in plasma aldosterone levels, and enlarged size and weight of an heterogenous adrenal tumor with internal calcifications. Malignancy was confirmed by the histologic features. No prognostic criteria could be established and two patients died despite specific surgery, which was performed in all cases. More recent developments in the use of mitotane led to the addition of adrenocorticolytic therapy in the remaining two patients, who are still alive at the time of this report.

Adolescent↗
PubMed1987

Synthesis and antisecretory and antiulcer activities of derivatives and analogues of 2-(2-pyridyl)tetrahydrothiophene-2-carbothioamide.

New thioamide derivatives of 2-(2-pyridyl)tetrahydrothiophene-2-carbothioamide (29) and related compounds (in which the tetrahydrothiophene ring was replaced by tetrahydrothiopyran, tetrahydrofuran, 1,3-dithiane, or 1,3-oxathiane and where the pyridine ring was replaced by other nitrogen heterocycles) were synthesized and tested for their antisecretory and antiulcer activities. These thioamides were prepared according to one of the following methods: reaction of an isothiocyanate with the carbanion of the corresponding cyclic precursor (for secondary thioamides); reaction of ammonia or an amine with the dithio ester prepared from the same precursor (for primary, secondary, and tertiary thioamides). These thioamides were evaluated by the Shay method to measure their antisecretory activity and by the stress-induced-ulcer method to test their antiulcer activity. Structure-activity relationships are discussed. N-Methyl-2-(2-pyridyl)tetrahydrothiophene-2-carbothioamide (R.P. 40749, 30) exhibited activities that were at least 10 times higher than those reported for cimetidine.

Animals↗
PubMed1987

No involvement of antidiuretic hormone in acute antidiuresis during PEEP ventilation in humans.

Decreased urinary output (Vu ml/min) after institution of PEEP is attributed to a variety of mechanisms including decreased cardiac output and renal blood flow (RBF), activation of neurohormonal reflexes, increased catecholamines, plasma renin activity (PRA), and antidiuretic hormone (ADH) release. To evaluate these factors, seven normovolemic patients (36 yr +/- 13 SD), free of preexisting lung, cardiac, or renal disease, requiring continuous mandatory ventilation for neurologic reasons were studied. The authors measured or calculated: total blood volume (TBV) (51Cr); right atrial, pulmonary arterial, pulmonary wedge, and systemic pressures, cardiac index (CI); renal plasma flow (RPF) (iodohippurate sodium 131I [131I PAH] clearance); glomerular filtration rate (GFR) (creatinine clearance), free water clearance (CH2O), osmolal clearance (Cosm), fractional excretion of sodium (FENa+) and potassium (FEK+); and plasma renin activity (PRA) (ng X ml-1 X h-1), plasma ADH (pg/ml; radioimmunoassay), epinephrine (E in pg/ml), and norepinephrine (NE in pg/ml) (double-isotope radioenzymatic assay). Two conditions were studied after 90-min steady state: 1) zero PEEP (ZEEP); and 2) 15 cmH2O PEEP. PEEP caused a significant decrease in CI (-21%; P less than 0.01) and RPF (-19%; P less than 0.05) without significant decrease in GFR. A significant decrease in Vu (-55%; P less than 0.05), FENa+ (-39%; P less than 0.05) and Cosm (-36%; P less than 0.25) occurred without modification in CH2O. Plasma ADH remained in the normal range and did not increase when PEEP was applied.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Analysis↗