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Biomedical subjects

R Isnard

Publications and source records attributed to R Isnard.

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

[Right retroauricular hematoma of late manifestation. Contribution of cardiac imaging].

Right intrapericardial retroatrial haematomas are usually discovered in an acute context of tamponade, following cardiac surgery. The original feature of this case was the asymptomatic nature of a right retroatrial haematoma, after surgical closure of an ostium secundum atrial septal defect, with a free interval of more than 20 years between the surgical procedure and the first relatively minor symptoms, consisting of supraventricular arrhythmias. It can be difficult to determine the intra- or extra-atrial topography of a right-sided mass by transthoracic echocardiography. On the other hand, transoesophageal echocardiography and ultrafast CT can provide a precise topographic diagnosis and appear to be complementary to assess the nature of pericardial masses.

Adult↗
PubMed1996

[Epidemiology of cardiac failure and current prognosis of the most seriously ill patients].

The lack of consensus concerning the diagnostic criteria of cardiac failure explains the relative paucity of epidermiological data. Most of the available information comes from American health registers and the Framingham study: in the United States, there are more than 3 million people with cardiac failure (over 1% of the population) and over 400,000 new patients each year. Cardiac failure is the main cause of death in 40,000 deaths and an associated cause in a further 250,000 deaths. In the Framingham study (1948-1988) the mean survival time after diagnosis is 1.7 year in men and 3.2 years in women, corresponding to 1 and 5 year survival rates of 57% and 25% in men and 64% and 38% in women. These figures are worse than those of the large scale therapeutic trials of the last 10 years and represent survival of the most severe cases. Although not strictly epidemiological data, analysis of the large scale trials allows evaluation of the clinical features and survival of patients under optimal medical treatment (ACE inhibitors associated with other treatments): these results are important to bear in mind when considering alternative therapies (transplantation, mechanical assist devices), the accessibility of which may be limited for reasons of availability or cost. In terms of public health, it is important that accurate epidemiological data concerning cardiac failure. In particular severe cardiac failure, is made available in France.

Adolescent↗
PubMed1995

[Reduction of atrial fibrillation. New concepts, new strategies].

Restoring sinus rhythm is patients with non-valvular atrial fibrillation has two objectives: restore haemodynamic performance and reduce the risk of thromboembolism. Whether the cardioversion is spontaneous or induced with drugs or electroshock, the process itself carries the risk of systemic embolism attributed to the transitory inactivity of the left atrium. Current practice of giving anticoagulants at least 4 weeks before electric cardioversion is a compromise between the embolic risk of cardioversion estimated at 0.4 to 0.8% and haemorrhagic complications related to low blood coagulability estimated at about 1% per year. The advent of transoesophageal echography has made it possible to study the atrium in detail in search of thrombi. The result has been a revolution in our concepts and therapeutic approach to atrial fibrillation and cardioversion. Recent studies have shown that "rapid cardioversion" associated with minimal 48-hour anticoagulation with heparin IV and transoesophageal echography to eliminate a thrombus in the atrium and/or the atrial appendage can be proposed without increasing the risk of embolism. Besides simplifying the therapeutic protocols (but at the cost of the semiinvasive nature of the transoesophageal echocardiography), this method also has the merit of restoring atrial function rapidly, particularly in cases of recent onset arrhythmia.

Atrial Fibrillation↗
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↗
PubMed1995

[Clinico-pathological polymorphism of hypertrophic cardiomyopathy in echocardiography].

An echocardiographic Study of 322 adults (age: 40 +/- 16 years), belonging to 20 families with hypertrophic cardiomyopathy (HCM), was undertaken. Affected subjects had a LV diastolic wall thickness > 13 mm. The patients were classified according to the distribution of left ventricular hypertrophy (LVH) and by Maron's classification: 189 subjects were normal, 127 were affected and 6 could not been classified. By Maron's classification: 3% were type I, 33% were type II, 58% were type III and 6% were type IV. LVH was asymmetrical in 95% of cases (septum/posterior wall ratio > 1.3). The familial distribution of LVH of the 4 families in which HCM was genetically related to different loci (chromosome 11, 14 exon 13, 14 exon 8, fifth locus); the LVH was analysed from two short axis LV parasternal views and each plane was divided into 5 segments. The distribution of LVH was said to be identical between two first degree relations when all the same segments were affected, similar when they differed by only 1 or 2 segments and different when they differed by 3 or more segments. In the 26 pairs studied, LVH was identical in 2/26 (8%), similar in 11/26 (42%) and different in 13/26 (50%). Familial HCM usually gives rise to asymmetrical LVH affecting the septum and free wall. An identical distribution in 50% of affected first degree relatives.

Adolescent↗
PubMed1994

[Physiopathology of mitral mechanics in hypertrophic cardiomyopathy. Groupe de travail "Cardiomyopathies et insuffisance cardiaque" de la Société Française de Cardiologie].

Ventricular hypertrophy, the only indisputable phenotypical marker of hypertrophic cardiomyopathy, is the basis of the physiopathology and treatment of the disease. Mitral valve abnormalities are usually considered to be secondary to the hypertrophy but the genesis of systolic anterior motion by the Venturi effect has been questioned by many clinical and experimental observations. Abnormalities of the mitral valve apparatus may in themselves (elongation of the valves, antero-internal malposition of the mitral papillary muscles and/or hyperlaxicity of antero-internal corhdae tendinae) create systolic anterior motion or subaortic obstruction in the absence of septal hypertrophy and/or increased subaortic flow velocities. Anatomo-clinical studies have confirmed this hypothesis: a high prevalence of mitral valve disease (increased valvular surface and length) has been found in hypertrophic cardiomyopathy. The recognition of these abnormalities is of value from the therapeutic (mitral valvuloplasty) diagnostic (in borderline cases) and genetic (when the primary nature of the abnormalities is confirmed) points of view.

Animals↗
PubMed1994

[Demonstration of a fifth locus implicated in familial hypertrophic cardiomyopathies].

Hypertrophic cardiomyopathy is familial in about 50% of cases and is transmitted in the autosomal dominant mode. The first morbid gene implicated in the disease was the gene coding the beta myosin heavy chain (beta MHC) on chromosome 14. However, only 30% of families have this genetic abnormality. Recently, three new loci have been identified on chromosomes 1q3, 11p13-q13 and 15q2. In order to determine whether other genes could be implicated in the disease a linkage analysis study was performed in a West Indian family. The method is based on the analysis of the distribution of the disease in the family and the microsatellite markers. The microsatellites used were those which recognised the 4 loci previously mentioned and 4 new markers situated and arranged with respect to known microsatellites. The results show that in the family studied, the disease did not concord with the markers of the beta MHC gene or with those recognising the loci on chromosomes 1q3, 11p13-q13 and 15q2. There is, therefore, a fifth gene implicated in familial HCM. The heterogeneity of the disease seems even greater than originally thought.

Adult↗
PubMed1994

[Pubertal idiopathic gynecomastia].

14 boys with pubertal gynecomastia, aged 9 to 16 years, were presented. Physical assessment, including pubertal maturation, height, weight, bone age, pubic hair stage, testicular and penis calibre and degree of gynecomastia was determined. Sexual steroids, LH-FSH, prolactin, were studied. All patients had psychological stress. 11 patients had been treated surgically by mastectomy with success.

Adolescent↗
PubMed1993

Variations in plasma endothelin concentrations during coronary spasm.

A provocation test using methylergometrine was carried out in patients with a normal coronary angiogram. Patients exhibiting spasm (Group 1, n = 6) were compared with non-spasm patients (Group II, n = 6). The endothelin concentration was determined in all cases at 0800, 1100, 1400, 1600, 1900, 2100, 2300 and 0100 h. The provocation test was carried out at 1700 h and an additional determination was made during spasm if the test was positive. The two groups had similar clinical characteristics and did not differ in terms of risk factors. Apart from the value recorded during spasm, the endothelin plasma level was significantly higher in Group I. A time x measurement interaction was noted in both groups, with a higher endothelin level in the morning. The endothelin level increased significantly during spasm in Group I patients. The plasma concentration of endothelin appeared to be higher in the basal state and during spasm in patients exhibiting spastic angina.

Adult↗
PubMed1993

Glomerular atrial natriuretic factor receptors in experimental congestive heart failure.

Heart failure is usually characterized by a relative insensitivity to atrial natriuretic factor (ANF). Downregulation of ANF receptors has been reported but remains controversial. Renal response to ANF infusion, glomerular ANF receptors, and guanosine 3',5'-cyclic monophosphate (cGMP) production have been studied in rabbits with congestive heart failure (CHF) after traumatic aortic regurgitation and abdominal aortic stenosis. Diuresis and natriuresis induced by ANF infusions were significantly decreased in CHF animals. Plasma cGMP was higher in CHF rabbits before ANF administration than in controls (37.6 +/- 7.2 vs. 17.1 +/- 3.9 pmol/ml, P < 0.02) and increased to a same level after ANF in both groups (48.8 +/- 4.2 vs. 52.5 +/- 2.8 pmol/ml, NS). No difference was found in glomerular ANF receptor density (436 +/- 54 vs. 425 +/- 57 fmol/mg protein, NS) nor in affinity between the two groups (dissociation constant; 240 +/- 24 vs. 347 +/- 49 pM, NS). Moreover, in vitro glomerular cGMP production in response to exogenous ANF was preserved. In conclusion, despite a blunted renal response to ANF in vivo, glomerular ANF receptors were unchanged in this model, and no defect in cGMP production in response to ANF was found. This suggests the existence of an intracellular defect beyond the second messenger.

Animals↗
PubMed1993

[Changes in plasma endothelin during coronary spasm].

The role of endothelin, a powerful vasoconstrictor, was studied in coronary spasm. A methylergonovine stress test was performed in patients with normal coronary angiography. Patients who developed spasm (Group I, n = 6) were compared with those who did not (Group II, n = 6). Plasma endothelin was measured at 8, 11 a.m., 2 p.m., 4, 7, 9, 11 p.m. and 1 a.m. The stress test was carried out at 17 hours and an additional endothelin measurement was performed during spasm in positive cases. The clinical characteristics of the two groups were comparable especially with regards to cardiovascular risk factors. Except for the value recorded during coronary spasm, the plasma endothelin levels were significantly higher in the group with coronary spasm. A time-dependent variation was observed in both groups with higher endothelin levels in the morning. In group I the plasma endothelin levels were higher under basal conditions and during spasm in patients with spastic angina.

Adult↗
PubMed1993

[Cardiac and extracardiac abscesses in bacterial endocarditis].

Cardiac abscesses are observed in 20 to 30% of cases of infective endocarditis and in at least 60% of prosthetic valve endocarditis. The aortic valve ring is more frequently affected than the mitral valve ring. A cavity contiguous with a cardiac chamber forming a pseudo-aneurysm or a closed purulent collection, the abscess may extend to the neighbouring cardiac structures or to the ascending aorta. This extension may cause conduction defects, abnormal communications between the cardiac chambers, pericardial disease and, exceptionally, myocardial ischaemia, complications which are clinical signs of abscess formation in patients with infective endocarditis. The presence of a cardiac abscess is a poor prognostic factor in infective endocarditis. The diagnosis must be made at an early stage when surgical treatment is optimal. The most valuable investigation is transoesophageal echocardiography with a sensitivity of over 80% and a specificity of about 95%. This investigation has become practically routine in all patients with endocarditis in order to diagnose abscesses at an early stage, especially in cases of aortic or prosthetic valve endocarditis. Information about the site, size and extension of the abscess may be obtained and existing or potential complications may be envisaged with a view to surgery. Other imaging diagnostic techniques, such as angiography, CT scanning and nuclear magnetic resonance imaging have a number of disadvantages and are not more sensitive than transoesophageal echocardiography. Surgical techniques depend on the site and extension of the abscess. They are sutured or closed with dacron or pericardial patches after having been cleaned and filled with formulated resorcin glue. The valvular prosthesis is inserted either in anatomical position or in a sub or supracoronary dacron tube necessitated by the perivalvular extension of the infectious lesions. These complex procedures may require associated coronary reimplantation or revascularisation when the coronary ostia are affected. The highest operative mortality is observed in prosthetic valve endocarditis with abscess and extra-annular prosthetic implants. The risk of secondary valvular dehiscence, often recurrent, is much higher when there is an abscess at operation. Extracardiac abscesses in cases of infective endocarditis are mainly observed in the cerebral and/or splenic territories. They may become the main problem, especially cerebral abscesses, but they rarely require surgery.

Abscess↗
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

[Neurohormonal profile in aortic valve stenosis].

The authors studied the responses of the main systems of sympathetic and hormonal regulation in valvular aortic stenosis, a special model of dissociation between arterial pressure and left ventricular function. The series comprised 14 patients with an average age of 70 +/- 9 years without diuretic therapy presenting with pure calcific aortic stenosis without other valvular or coronary disease. All were in sinus rhythm; 5 were taking an angiotensin converting enzyme inhibitor. Plasma concentrations of endothelin 1, atrial natriuretic factor (ANF), arginine vasopressin (AVP), catecholamines, plasma renin activity (PRA), angiotensin II and aldosterone were measured in resting, fasting patients, by blood samplings from a peripheral vein immediately before cardiac catheterisation. The results were compared with the severity of the aortic stenosis (aortic valve area greater or less than 0.7 cm2), the ratio of left ventricular work/myocardial mass (greater or less than 0.6) and treatment (with or without ACE inhibitors). Catecholamine levels were much higher in severe aortic stenosis (noradrenaline: 579 +/- 66 pg/ml when valve surface area > 0.7 cm2 versus 900 +/- 92 pg/ml when valve surface area < 0.7 cm2; p < 0.01). Endothelin -1 and AVP concentrations were normal. Whereas PRA was normal, aldosterone levels were increased in patients without treatment by ACE inhibitors. This treatment did not, however, normalise the noradrenaline levels. The increase in ANF concentration was large when left ventricular work decreased with respect to myocardial mass (190.8 +/- 42.3 pg/ml if W/M was decreased versus 82.7 +/- 15.4 pg/ml when W/M was normal): this could be related to the degree of left ventricular hypertrophy.

Aged↗
PubMed1992

[Atrial natriuretic factor in heart insufficiency].

The atrial natriuretic factor is a peptide with vasodilator and natriuretic properties which is synthesized and released by atrial myocytes. In patients with chronic heart failure the ventricles contribute to the synthesis of this peptide, so that its plasma concentration rises in proportion to the heart filling pressure. The atrial natriuretic factor, therefore, seems to be a good biological marker of functional and haemodynamic severity of heart failure. However, the weight of this factor in the neuro-hormonal balance has not yet been fully evaluated, owing to the usual attenuation of its biological effects. This, and the necessity of continuous parenteral administration limits, for the moment, its therapeutic applications. Inhibitors of the enzyme involved in its metabolism are being tested, but only preliminary results are available in humans.

Atrial Natriuretic Factor↗
PubMed1992

Atrial natriuretic peptide during water deprivation or hemorrhage in rats. Relationship with arginine vasopressin and osmolarity.

The concentrations of atrial natriuretic peptide (ANP) in atria, hypothalami and plasma were investigated in relation to the variations of the plasma endogenous immunoreactive arginine vasopressin (Ir-AVP) during water deprivation or hemorrhage in normal conscious Wistar rats. Furthermore, the in vitro and in vivo effect of extracellular hyperosmolarity on ANP release from right atrium and hypothalamus was examined. Water deprivation elevated circulating immunoreactive ANP (Ir-ANP: pg/ml) to 153 +/- 7 (24 h); 174 +/- 1 (48 h) from the control level (109.6 +/- 7.8). This increase in Ir-ANP concentration which correlated with atrial (r = -0.93) or hypothalamic (r = -0.87) Ir-ANP content decrease, was associated with significantly enhanced levels of plasma Ir-AVP, plasma sodium, osmolarity and hematocrit. An acute volume depletion by hemorrhage significantly reduced plasma Ir-ANP (67 +/- 8.4 pg/ml) from the sham operated level (140 +/- 18 pg/ml). Plasma Ir-AVP was elevated dramatically (207.4 +/- 53.4 pg/ml) compared with the sham operated level (8.8 +/- 2.6 pg/ml). These results, indicating the lack of correlation between plasma Ir-ANP and Ir-AVP in vivo, suggest that the ANP secretion, which is regulated mainly by plasma volume, may be modulated by a change in plasma osmolarity. Extracellular hyperosmolarity stimulated the ANP release from superfused sliced normal rat atria and hypothalami.

Animals↗