[Spatial ventricular gradient studied by computerized vectorcardiography. Normal and pathological values. Interpretation and clinical evaluation]. / Le gradient ventriculaire spatial étudié par vectocardiographie informatisée. Valeurs normales et pathologiques. Essai d'interprétation et d'évaluation clinique.

The ventricular gradient is a reflection of uneven ventricular repolarisation. Until recently is was only appreciated in the frontal plane of the classical electrocardiogramme and expressed as the sum of the vectors representing the surfaces under the QRS complex and T wave. We used computerised vectorcardiography to obtain a more exact evaluation of the size and spatial orientation of the vector gradient. The spatial vector gradient was calculated in a control group and in a number of pathological conditions. The reference values were established in 70 normal subjects with a mean age of 36 +/- 21 years: 0.092 +/- 0.016 m V.s for amplitude: 38.4 degrees +/- 6.1 for thesite and 21.6 degrees +/- 8.7 for the azimuth. The size and spatial orientation of the ventricular gradient can be used to define normal limits and to distinguish subgroups by using the values of the site and azimuth. The spatial ventricular gradient is a new approach to defining the limits of normality in poorly understood abnormalities of ventricular repolarisation. It may also be useful in the comprehension of certain forms of cardiac arrhythmia related to desynchronisation of ventricular repolarisation.

[The spatial vectorcardiogram loop. Estimation of its planarity by the calculation of a distortion coefficient. Trial of clinical evaluation]. / Etude de la boucle du vectorcardiogramme spatial. Appréciation de sa planéité par le calcul d'un coefficient de gauchissement. Essai d'évaluation clinique.

Automatic techniques for interpreting the electrical activity of the heart are based more and more on vectorcardiographic parameters, especially information provided by the spatial vectorcardiographic loop. This data has been shown to be a useful complement to classical electrocardiography. The aim of this study was to define a method of calculation of the planes of the vectorcardiographic loops of depolarisation and repolarisation, and to calculate a coefficient of left-sidedness obtained by the sum of squares of the distances between the points on the loop in the plane. This value is then normalised with respect to the size of the loop. Normal values of this coefficient were first defined in a healthy reference population of 70 subjects: the values are expressed in (MV/10)2 or in mm2, and are 0,28 +/- 0,05 for the QRS and 0,0026 +/- 0,0008 for the ST-T. The coefficient was then calculated in different pathological groups, the diagnosis of which had been formally confirmed: ventricular hypertrophy, valvular heart disease, conduction defects, coronary artery disease. The highest values (four times normal) were obtained in right ventricular hypertrophy, right bundle branch block and infarction associated with conduction defects. The discriminative value of the coefficient of left-sidedness is discussed with the aim of distinguishing the normal from the pathological.

[Electrocardiographic criteria of left ventricular hypertrophy and unipolar aVR lead]. / Critères électrocardiographiques d'hypertrophie ventriculaire gauche et dérivation unipolaire aVR.

The introduction of data processing techniques into the interpretation of electrocardiograms and the rapid progress towards automatization require a multiplication of the criteria of decision and an exact evaluation of their performance. The ECG diagnosis of left ventricular hypertrophy depends on a large number of parameters. Only the aVR lead has not been fully exploited to date. This study proposes a corrected measurement of S in aVR, with an amplitude of S aVRc greater than or equal to 11 mm being the parameter with the best performance and the best predictability.

[Amineptine and depressive symptoms, cardiovascular and ophthalmological acceptabilities (author's transl)]. / Points d'impact de l'amineptine sur les symptômes de la dépression. Acceptabilité cardio-vasculaire et ophtalmologique.

Amineptine is a new compound derived from the tricyclic antidepressants whose mechanism of action is mainly dopaminergic. In a clinical open trial, fifty patients suffering from neurotic, reactive and psychotic depression have been treated by 231 mg/day +/- 7 (mean +/- SEM) during 30 days. Results were assessed from Hamilton Rating Scale for depression before treatment and on D7, D14, D30. Cardiovascular and ophthalmological acceptability is discussed.

Evaluation of myocardial perfusion and left ventricular function by 201T1 scintigraphy after dipyridamole.

201T1 myocardial imaging was performed at rest and after dipyridamole (0.44 mg/kg) on 50 patients with known or suspected ischemic heart disease. The dipyridamole had no effect in 14 patients (group Dip.0). In 17 patients (group Dip +/-) it significantly modified the contrast of the rest image (by increasing or decreasing a rest perfusion defect). In 19 patients (group Dip - Steal) the drug induced a paradoxical response interpreted as a coronary steal effect (an active region at rest becomes hypoactive after dipyridamole while an underperfused region at rest improves). All patients underwent coronary arteriography and left monoplane ventriculography; results were interpreted in relation to these angiographic data. The mean percentage of stenoses (per patient) was about the same in the three groups but it was found that, despite these stenoses, the patients of the group Dip - Steal had a good left ventricular function (EF = 0.62 +/- 0.12). On the other hand, the ejection fraction was very poor in the two other groups (0.50 +/- 0.17 and 0.48 +/- 0.17). Moreover it was found that: (1) the frequency of high grade or even complete obstruction was notably less in group Dip - Steal (P less than 0.05); (2) the frequency of angiographically visible collaterals was higher in group Dip - Steal (P less than 0.05); (3) the left anterior descending artery was less diseased than the right coronary artery in group Dip - Steal (P less than 0.05). These results have a real prognostic value for the assessment of the preserved cardiac performance in Dip - Steal patients despite severe stenoses, and are discussed in terms of compensatory collateral circulation and preservation of the coronary-flow reserve in the myocardium distal to a critical stenosis.

[Cardiac involvement in a lupus syndrome. Clinical and morphological study apropos of one case necessiting a double valve replacement]. / Atteinte cardiaque au cours d'un syndrome lupique. Etude clinique et morphologique à propos d'un cas ayant nécessité un double remplacement valvulaire.

A patient with disseminated lupus erythematosus developed mitral and aortic valve disease, requiring double valve replacement. The ultra-structure of the lesions of the endo- and myocardium are described, and their significance discussed.

[Systemic lupus erythematosus and congestive heart failure. Heart histological and ultrastructural study (author's transl)]. / Lupus érythémateux disséminé et insuffisance cardiaque. Etude histologique et ultrastructurale du myocarde.

Histological and ultrastructural studies were performed on myocardial biopsies and aortic and mitral valve leaflets obtained during an operation on a patient with Systemic Lupus Erythematosus (S.L.E.). Congestive heart failure and valvular dysfunction appeared five years after the diagnosis of S.L.E. was made. On histological study, aortic and mitral valve leaflets are uniformly thickened by fibrous tissue with a nodular appearance. No active endocarditis was associated with the fibrous scarring. Atrial myocardium and papillary muscle countain a fibrous net-work discret in the former, extensive in the latter. The scattered foci of fibrosis in the papillary muscle surround vessels without obliteration or parietal necrosis. Ultrastructurally their lumina appears narrowed by prominent endothelial cells with cytoplasmic aggregates of tubuloreticular structures (T.R.S.). These tubules are also present in some endocardial endothelial cells but are rare in the normal intrapapillary or atrial vessels that are not associated with a scar. Myocardial fibrous foci enclose atrophic and severely degenerated cardiac muscle cells; other cells situated at the periphery of the foci are normal in size or hypertrophic and moderately degenerated. The most altered muscle cells show an important loss of myofibrils, a proliferation of sarcoplasmic reticulum in myofibril free spaces, or necrosis with macrophagic resorption. Focal changes with loss of myofilaments, Z material streaming and concentric lamellar bodies are found in moderately degenerate cardiac muscle cells. The remaining papillary muscle cells and the atrial cells are all hypertrophied without degeneration. These changes suggest that focal myocardial fibrosis and associated cardiac muscle cell degeneration may be responsible for impaired cardiac performance in some patients with S.L.E. According to the constant topographic relation between the narrowed vessels whose endothelial cells contain T.R.S. and the surrounding fibrous foci, we believe that the myocardial fibrous patches may correspond to scarring of microinfarcts related to active S.L.E. vascularitis.

[Concealed permanent ventricular reentry and paroxysmal ventricular tachycardia by circulatory movement]. / Réentrée ventriculaire permanente cachée et tachycardie ventriculaire paroxystique par mouvement circulaire

Endocavitary recording in a patient with attacks of ventricular tachycardia demonstrated a late potential which activated the bundle of His in a retrograde fashion, and the right bundle branch in a forwards direction. This late potential is evidence of a persistant ventricular microeentry which cannot be seen on the peripheral leads. In certain conditions which have been studied, this localised microreentry leads to ventricular tachycardia by macroreentry using the branches of the bundle of His. Tanks to this unusual case, we were able to study the effects of certain anti-arrhythmic drugs on the micro- and macroreentry circuits. By these means a therapeutic solution has been found for paroxysms of ventricular tachycardia.