[Follow up of endovascular abdominal aortic anevrysm repair with contrast ultrasound]. / Intérêt de l'échographie de contraste dans la surveillance des endoprothèses aortiques.

Endovascular aortic aneurysm repair (EVAR) is a widely accepted treatment for anatomically fitted abdominal aortic aneurysms. The increasing use of this procedure has prompted the need for close surveillance and reliable post-operative imaging. The current tool for assessing EVAR technical success is to perform computed tomography angiography (CTA) in order to exclude endoleaks and to confirm the exclusion of the aneurysm sac. Contrast enhanced ultrasound with low mechanical index is a promising method for follow-up of patients after EVAR. It seems to allow better identification and characterization of endoleaks than unenhanced ultrasound and even than CTA for very low flow endoleaks.

Modulation of beta1-adrenoceptor activity by domain-specific antibodies and heart failure-associated autoantibodies.

OBJECTIVES: Our study attempted to gain further understanding of the allosteric effects of human autoantibodies on beta1-adrenergic receptor (beta1-AR) function. BACKGROUND: Recently, we reported on the existence of activating anti-beta1-AR antibodies in patients with dilated cardiomyopathy (DCM 26% prevalence) or ischemic cardiomyopathy (ICM, 10% prevalence); however, their functional effects have not yet been thoroughly characterized. METHODS: In this study we detected functionally active receptor-antibodies in 8 out of 30 DCM patients. Their immunological and functional properties were analyzed using both synthetic receptor-peptides and intact recombinant human beta1-AR, and were compared with those of heterologous antibodies to selected beta1-AR domains generated in rabbits and mice. RESULTS: Rabbit, mouse, and human anti-beta1-AR against the second extracellular domain preferentially bound to a native receptor conformation and impaired radioligand binding to the receptor. However, their functional effects differed considerably: Rabbit and mouse antibodies decreased both basal and agonist-stimulated cAMP production, whereas the patient antibodies (n = 8) increased basal, and six of them also increased agonist-stimulated receptor activity (i.e., acted as receptor-sensitizing agents). Two out of eight human anti-beta1-AR increased basal but decreased agonist-stimulated receptor activity (i.e., acted as partial agonists). CONCLUSIONS: Antibodies against the same small beta1-AR domain can have very divergent allosteric effects, ranging from inhibitory to agonist-promoting activities. Activating autoantibodies were associated with severe cardiac dysfunction and thus might be involved in the development and/or course of human cardiomyopathy.

Activating beta-1-adrenoceptor antibodies are not associated with cardiomyopathies secondary to valvular or hypertensive heart disease.

OBJECTIVES: We investigated whether autoantibodies against the human beta-adrenergic receptor (beta-AR) might be involved in cardiomyopathies secondary to valvular heart disease (VHD) or hypertensive heart disease (HHD). BACKGROUND: Autoimmunity to beta-AR has been proposed as a pathogenic principle in human cardiomyopathy. Recently, by the use of intact recombinant human beta-AR, we were able to confirm the existence of functionally active anti-beta-1-AR autoantibodies in patients with dilated cardiomyopathy (26% prevalence) or ischemic cardiomyopathy (10% prevalence); however, their prevalence in other (secondary) cardiomyopathies remained to be determined. METHODS: Immunoglobulin G (IgG) was prepared from the sera of 28 VHD and 19 HHD patients and first screened by a peptide-based enzyme-linked immunosorbent assay (antigens: aminoterminus, second extracellular loop [ECII] and carboxyterminus of human beta-1- and beta-2-AR). IgG from 108 gender- and age-matched healthy subjects served to define the threshold for positive immunoreactions. Positive sera were further screened for their ability to recognize and activate native human beta-AR situated in a cell membrane. RESULTS: Twenty-five percent (VHD) or 11% (HHD) of the patients and 4% of the healthy controls had IgG antibodies randomly directed against all the three domains tested and both beta-AR subtypes. Only one patient with aortic valve and concomitant coronary heart disease and one healthy subject had functionally active anti-b1-AR (targeting beta-1-ECII). Moreover, one HHD patient with concomitant collagenosis had IgG that was cross-reacting with recombinant beta-AR in immunological assays but was unable to affect receptor function. CONCLUSIONS: Autoimmune reactions against the human beta-AR do not appear to be associated with cardiomyopathies secondary to VHD or HHD.

A phylogeny of the genus Nocardia deduced from the analysis of small-subunit ribosomal DNA sequences, including transfer of Nocardia amarae to the genus Gordona as Gordona amarae comb. nov.

According to phylogenetic analyses of nearly complete small-subunit ribosomal DNA sequences, the genus Nocardia should not comprise the two species Nocardia petroleophila and Nocardia amarae. N. amarae should be reassigned to the genus Gordona as Gordona amarae. All of the other Nocardia species form a monophyletic unit, closely related to species of the genus Rhodococcus. It is proposed to revive the name 'CMN' to comprise the genera Corynebacterium, Tsukamurella, Mycobacterium, Gordona, Rhodococcus and Nocardia that form a well identified and monophyletic unit. They are all characterized by a cell wall chemotype IV with mycolic acids.

Prognostic factors and long-term evolution in a cohort of 133 patients with giant cell arteritis.

OBJECTIVE: Survival in patients with giant cell arteritis (GCA) has generally been found to be similar to that of the general population. The aim of our study was to assess outcome and survival of different subgroups of patients with GCA in relation to clinical, biological data or treatment modalities. METHODS: From 1977 and 1995, 176 patients were treated in the Department of Internal Medicine for GCA. The patient, family or local practitioner were contacted prior to the study (July-October 1995). Treatment modalities and follow-up were obtained for 133 patients. All patients (except 11) had 3 or more 1990 ACR classification criteria for GCA. The 11 patients with 2 criteria had a positive temporal biopsy and were included in the study. RESULTS: Relapse during corticosteroid tapering treatment was observed in 83 patients (62.4%) with a mean 1.57 relapses per patient. No correlation was found in age, sex, initial dose or type of steroid used (i.e. prednisone or prednisolone). Only a slight correlation in the initial erythrocyte sedimentation rate (ESR) was observed (p < 0.01, r = 0.23). In 56 patients free of treatment (mean treatment duration: 40 months), 27 (48%) developed a relapse of the disease 1 to 25 months later. No correlation was found in age, sex, initial dose of steroid, number of relapses during treatment, or initial ESR. Survival analysis was performed using the Kaplan-Meier and Mantel-Menszel methods for comparison of groups. At the time of the study, 41 patients had died (30.7%). A significant reduction of survival was found with the presence of permanent visual loss vs absence (p = 0.04), in patients who required more than 10 mg/d of glucocorticoid (p < 0.001) at 6 months treatment and in patients treated with prednisone (vs prednisolone) (p < 0.01). However, these factors were not independently associated with survival in the multivariate analysis. CONCLUSION: Relapse was observed in 62.4% of the patients during corticosteroid tapering (correlated with initial ESR). A relapse of the disease was also observed in 48% of patients 1 to 25 months after the end of the treatment and was associated with prednisolone use. Long term survival was better in patients with no initial ocular manifestations, in patients who took less than 10 mg/day of corticosteroids at 6 months of the treatment and in patients treated with prednisolone.

[Clinic and morphologic evolution five years after a renal atherosclerotic artery stenosis (RAS): a study of twenty nine hypertensive patients population]. / Evolution clinique et morphologique 5 ans après la revascularisation d'une sténose artérielle rénale (SAR) athéromateuse. Etude d'une population de 29 patients hypertendus.

The indication of renal atherosclerotic artery stenosis revascularisation is always debated in clinical practices when arterial hypertension is stabilized by the treatment, especially if the stenosis is discovered fortuitously. The clinician needs clinical and morphological markers which will indicate or not the revascularisation in the situation of "nephronic protection". The benefits of angioplasty have been studied on the blood pressure, the creatinine clearance, the glomerular function analyzed by scintigraphy, the renal length and more recently on the mean cortical thickness (MCT). The follow-up of these studies is generally inferior to 2 years. In this work, we tried to estimate the clinic and morphologic evolution 5 years after a unilateral artery stenosis angioplasty. From a group of 249 patients who had a renal angioplasty between January 1995 and January 2000 (T0), 29 patients with refractory hypertension and with a unilateral atherosclerotic renal artery stenosis on spiral computed tomographic angiography (TCA) performed at T0 [17 M; 12 W; medium age 68.6 +/- 10 years] were included. The TCA performed at 5 years (T5) eliminated a new renal arterial stenosis or restenosis. We have analyzed 29 revascularized kidneys (kidney S) and 29 controlateral kidneys (kidney C), the blood pressure and renal function. The renal length (mm) was at T0: kidney C=99.4 +/- 13.5; kidney S=93.5 +/- 10.8 and at T5: kidney C=99.4 +/- 12.6; kidney S=94.2 +/- 10.7. MCT (mm) was at T0: kidney C=7 +/- 1.2; kidney S=6.6 +/- 1.1 and at T5: kidney C=6.2 +/- 1.2; kidney S5=6 +/- 1. The cortical atrophy got worse while the renal length and creatinine clearance were stable: only diastolic blood pressure was controlled (78.8 mmHg +/- 11.9). In spite of small strength, this study arguments the fact that the angioplasty isn't sufficient to control the arterial hypertension in an atheromatous context, not allowing to slow the evolution of distal cortical lesions with however a stability of creatinine clearance.

[Psychiatric complications of corticoid therapy in the elderly over 65 years of age treated for Horton disease]. / Complications psychiatriques de la corticothérapie chez le sujet âgé de plus de 65 ans traité pour maladie de Horton.

OBJECTIVES: To analyse steroid psychiatric related complications in aged (> 65 years old) with temporal arteritis (TA). METHODS: Retrospective cohort study. PATIENTS: In a cohort of 126 elderly patients with a diagnosis of TA and followed with a mean period of 64 months, clinical and biological presentations, outcome and corticoid adverse effects were recorded throughout the follow-up period. RESULTS: Twenty patients (16%), (mean age: 73 +/- 7.9 years, male n = 6) exhibited corticosteroid related psychiatric complications. Symptoms appear to be dose dependent and generally begin during the first month of treatment. Psychiatric disorders were as follow: mood disturbances (n = 8), depression (n = 6), mania (n = 3), anxiety neurosis (n = 2) and dementia (n = 1). Three patients were hospitalized in psychiatric units and 2 in nursing home. Psychiatric adverse affects appears to be more frequent with prednisone than prednisolone (P < 0.05).

[Value of sonographic contrast agents in the evaluation of the cerebral arteries]. / Apport des agents de contraste dans l'exploration ultrasonographique des artères cérébrales.

Stroke is a frequent and severe disorder. Most strokes are ischemic in nature and 20% are due to atherosclerosis of the cerebral arteries. Sonographic examination plays a key role in the diagnosis and management of patients with cerebrovascular disease. However, shortcomings can be encountered in the ultrasound evaluation of cervical and intracranial arteries. Contrast agents are known to improve the signal / noise ratio and they can therefore compensate for these shortcomings in most cases. They have proved to be helpful in unfavorable examinations in daily practice. Moreover, their use increases the accuracy and the potential of the technique especially in the intra-cranial examination, increasing the role of ultrasound techniques.

Autoantibodies activating human beta1-adrenergic receptors are associated with reduced cardiac function in chronic heart failure.

BACKGROUND: Autoantibodies against synthetic peptides of beta-adrenergic receptors have been observed in human cardiomyopathy. However, it has never been shown that such antibodies really interact with native human beta-adrenergic receptors, nor has the clinical impact of such an interaction been investigated in larger groups of patients. METHODS AND RESULTS: We screened 104 patients with dilated or ischemic cardiomyopathy (NYHA functional classes II to IV) and 108 healthy subjects for IgG antibodies reacting with beta-receptor peptides. Such IgGs were further analyzed for binding and functional interactions with native recombinant human beta-adrenergic receptors. Antibodies reacting with synthetic receptor peptides were present in 51% of the patients. However, only a subgroup directed against the second extracellular receptor domain also recognized native human beta-adrenergic receptors situated in a cell membrane. All antibodies of this subgroup impaired receptor ligand binding and enhanced receptor-mediated signaling, which could be blocked by 5 micromol/L bisoprolol in vitro. Their prevalence was 1% in healthy subjects and 10% in ischemic cardiomyopathy, whereas it amounted to 26% in dilated cardiomyopathy and was associated with a significantly poorer left ventricular function. CONCLUSIONS: Our data show that activating autoantibodies against human beta-adrenergic receptors exist in approximately 25% of patients with dilated cardiomyopathy. Counteraction of such autoantibodies might contribute to the beneficial effects of beta-adrenergic receptor blockade in chronic heart failure.

Immunofluorescent imaging of beta 1- and beta 2-adrenergic receptors in rat kidney.

BACKGROUND: beta-Adrenergic receptors (beta-ARs) are known to participate in the regulation of glomerular filtration, NaCl reabsorption, acid-base balance, and renin secretion; however, the precise histologic localization of beta-AR at putative signaling sites involved in these processes remains an open issue. METHODS: We used a set of subtype-specific rabbit antibodies to visualize beta(1)- and beta(2)-AR in rat kidney by immunohistochemistry and specified cells and segments of the nephron thought to be regulated by catecholamines. In addition, the relative proportion of beta-AR subtypes in cortical and medullary portions of rat kidney was determined by Western blotting and by competing [(125)I]-cyanopindolol binding with the beta(1)- or beta(2)-selective antagonists bisoprolol or ICI 118,551, respectively. RESULTS: Immunoreactivity for beta(1)-AR was found in mesangial cells, juxtaglomerular granular cells, the macula densa epithelium, proximal and distal tubular segments, and acid-secreting type A intercalated cells of the cortical and medullary collecting ducts. Immunoreactivity for beta(2)-AR was predominantly localized in the apical and subapical compartment of proximal and, to a lesser extent, distal tubular epithelia (suggesting interactions with luminal fluid catecholamines). Both subtypes were dense in the membranes of smooth muscle cells from renal arteries. Concordant data were obtained by radioligand binding and immunoblotting of membranes prepared from cortical and medullary portions of the kidney. CONCLUSION: Our data provide an immunohistochemical basis for the cellular targets of beta-adrenergic regulation of renal function. Moreover, they could help to devise therapeutic strategies directed at renal beta-ARs.