A portrait of a female body: Rubens and Helena's legs.

For a long time the Western world was in a state of denial about the human body. There were conventions governing its representation and it could be regarded as an element of discourse. Between 1636 and 1638, Peter Paul Rubens painted a portrait of his second wife, Helena Fourment, entitled The little fur. This may be a turning-point in the perception of the body. We see in this work that the skin of this 22-year-old woman has lost its elasticity, her breasts are not symmetrical and her ankles are pink, contrasting with the pearly white of the rest of her body. The inside of her left thigh shows signs of a varicose saphenous vein. While today's doctors can suggest the possibility of venous insufficiency and benign familial hyperelasticity, and talk of the consequences of breast-feeding, what this canvas is doing above all is showing the body of a real, named individual, "warts and all". This may be one of the first portraits of a body in the history of European painting.

[Cardiac failure caused by cardiomyopathy disclosing pheochromocytoma. Perioperative treatment]. / Défaillance cardiaque par cardiomyopathie révélatrice d'un phéochromocytome. Traitement péri-opératoire.

A case of cardiomyopathy secondary to an unrecognised pheochromocytoma is reported. It was cured by successful outset with congestive cardiac failure with an ejection fraction of 11%. Following medical treatment including a beta-blocker and converting enzyme inhibitors, the situation remained so disturbing that cardiac transplant was envisaged. It was nevertheless decided to first remove the tumour, with mechanical circulatory assistance cover if necessary. Surgical excision proved to be relatively easy. Cardiac failure disappeared clinically within a few days, though a degree of myocardial impairment revealed by paraclinical investigations persisted after ten months. The pathophysiology, beneficial effect of beta-blockers and the SvO2 usefulness blood during the perioperative period are discussed. The prognosis of the cardiomyopathy, considered up to the present to be uncertain, new seems favourable once it is possible to completely excise the tumour.

[Puerperal thrombosis of the right ovarian vein. Clinical and radiological aspects apropos of a case]. / Thrombose puerpérale de la veine ovarienne droite compliquée d'embolies pulmonaires. Aspects cliniques et radiologiques a propos d'un cas.

The authors report the case of puerperal thrombosis of the right ovarian vein complicated by recurrent small pulmonary emboli in a 32 year old woman. The clinical features of this rare condition are reviewed. The echographic, angiographic and CT scan and magnetic resonance imaging abnormalities are described. The authors underline the value of non-invasive radiological investigations for early diagnosis. The patient was rapidly improved by medical therapy with antibiotics and heparin.

[Demonstration of abnormalities of myocardial mitochondrial oxygenation in cardiac graft rejection]. / Mise en évidence d'anomalies de l'oxydation mitochondriale myocardique au cours du rejet de greffe cardiaque.

Abnormalities of myocardial metabolism during acute rejection may be due to ischemia to primary metabolic changes related to rejection. An experimental study of heterotopic cardiac transplantation in the rat was undertaken to study myocardial mitochondrial oxidation during acute rejection. The receivers were Lewis rats and the donors Fischer (FL: allograft) or Lewis (LL: isograft) rats. The oxygen consumption of the mitochondria (VO2m) isolated from the transplanted and native hearts was measured by oxygraphy six days after transplantation. Using maleate and glutamate substrates, the VO2m of transplanted hearts was significantly lower than that of native hearts in the two groups of rats (FL, p less than 0.01; LL, p less than 0.01). In addition, the VO2m of FL allograft transplanted hearts was significantly lower than in the LL rats (30 +/- 9 vs 100 +/- 15 nanoatoms of oxygen/min.mg/prot, p less than 0.01) as was the VO2m of the native hearts (FL: 106 +/- 23 vs LL: 164 +/- 26, p less than 0.02). The respiratory control ratio (RCR) was significantly lower in the transplanted than in the native hearts in both the FL and LL groups (p less than 0.05 and p less than 0.01 respectively). The comparison of the RCR in the two groups (FL vs LL) showed no significant difference for transplanted or native hearts. Electron microscopy of transplanted (rejected or not) and native hearts showed no morphological abnormality of the mitochondria. The lower VO2m of the allograft group indicates a disturbance in the mitochondrial respiratory pathway during acute rejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence of mitochondrial impairment during cardiac allograft rejection.

NADH laser fluorimetry and mitochondrial oxigraphy were used to study myocardial oxidative energy metabolism during cardiac allograft rejection. Heterotopic cardiac transplantation was performed on Lewis rats; allografts (with Fischer rat donors) were compared with isografts (with Lewis rat donors). In vivo and in vitro assays were performed six days after transplantation. Myocardial NADH fluorescence was recorded in vivo from grafted hearts, at baseline; during brief, complete ischemia; and during reperfusion. Oxygen consumption of mitochondria isolated from both native and grafted hearts was determined. Neither baseline levels nor maximum ischemic levels of NADH fluorescence (F0 = k[NADH]) were found to be significantly different between allografts (0.45 +/- 0.05 to 0.87 +/- 0.10) and isografts (0.45 +/- 0.04 to 1.11 +/- 0.05). During recovery, the rate of fluorescence decrease was significantly lower in allografts than in isografts (0.024 +/- 0.001 vs. 0.038 +/- 0.002 delta F0.s-1, P less than 10(-3], indicating a lower rate of NADH reoxidation. In the presence of malate and glutamate substrates, mitochondrial O2 consumption was significantly lower in allografts than in isografts (30 +/- 9 vs. 100 +/- 15 nanoatoms O2. min-1.mg prot-1, P less than 10(-2]. These results indicate that mitochondrial oxidative metabolism was impaired during the rejection process. Such energy production disturbances may contribute to the dysfunction of rejecting hearts.

[Dynamic left ventricular obstruction increased by nitroglycerin in elderly patients with hypertension and concentric left ventricular hypertrophy]. / Obstruction dynamique intraventriculaire gauche aggravée par la nitroglycérine chez les patients hypertendus âgés avec une hypertrophie ventriculaire gauche concentrique.

Left ventricular outflow tract (LVOT) obstruction has been observed in elderly patients with concentric hypertrophic hypertensive cardiomyopathy (HHCM) and no significant valvular disease or regional wall motion abnormalities. In order to determine whether nitroglycerin (NTG) can increase the intraventricular obstruction, we performed echocardiographic (echo) and doppler studies, before and during administration of sublingual NTG (0.8 mg). Twenty patients (n = 20) with long-standing hypertension (19 women and 1 man, mean age 78 +/- 8 yr, mean duration of hypertension 13 +/- 10 yrs were examined. The clinical findings in 17 patients were: angina 5 (29%), dyspnea 9 (53%), syncope or malaise 4 (23%). Electrocardiographic criteria of left ventricular hypertrophy was present in 4 patients and an increased cardio-thoracic ratio (greater than 0.5) in 9 cases. The following echo parameters were determined using M-mode echocardiograms: LV end-diastolic (LVID) and systolic diameter (LVIS), fractional shortening (FS), ventricular septum thickness (IVST), posterior wall thickness (PWT) and the ratio ISVT/PWT (less than 1.3 in all patients). LVM could be calculated in 15 patients and was corrected for body surface area (LVMI). Pulsed and continuous wave Doppler study showed a characteristic late-peaking velocity waveform. We localized the elevated velocities in the LVOT and determined before and during administration of NTG: LVOT peak velocities (V) and peak intraventricular gradients (G) using simplified Bernoulli equation. Results were as follows: [table: see text] Mild mitral regurgitation was observed in 14 patients (70%) and mitral annular calcifications in 11 (55%). Systolic function, as assessed by FS, was normal in all patients. NTG induced a significant acceleration of the LVOT velocities in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular outflow obstruction after mitral valve repair (Carpentier's technique). Proposed mechanisms of disease.

Left ventricular outflow tract obstruction (LVOTO) after mitral valve repair by Carpentier's technique has been recently reported in the literature. To assess the mechanisms of this phenomenon, we investigated 307 mitral valve repairs performed between July 1985 and December 1986. Incidence of LVOTO related to the mechanism of the mitral insufficiency and to the etiology demonstrates a direct relation to preoperative mitral valve prolapse (posterior leaflet +/- anterior leaflet) of degenerative origin. No LVOTO occurred after rheumatic mitral insufficiency repair regardless of size of the left heart cavities or of the prosthetic ring. Intraoperative and surficial two-dimensional echocardiography, color Doppler methods, and cardiac catheterization were used to investigate the mechanisms leading to LVOTO. Nonspecific modifications induced by reduction in size of the mitral annulus by the prosthetic ring (anterior displacement of the posterior ventricular wall and of the posterior mitral leaflet and narrowing of the mitroaortic angle) are not sufficient to explain the LVOTO. The association of mitral leaflets (composed of excess tissue and opposed to flow by a perpendicular position attributable to a narrow mitroaortic angle) and geometric left ventricular modifications (responsible for the superposition of mitral inflow to ventricular outflow) also qualifies as a mechanism for the induction of LVOTO after mitral surgical repair.