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R Voegtlin

Publications and source records attributed to R Voegtlin.

At least 19 recordsLinked to original sources
PubMed1986

[Spatial ventricular gradient studied by computerized vectorcardiography. Normal and pathological values. Interpretation and clinical evaluation].

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.

Adolescent↗
PubMed1984

[The spatial vectorcardiogram loop. Estimation of its planarity by the calculation of a distortion coefficient. Trial of clinical evaluation].

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.

Adult↗
PubMed1983

[Electrocardiographic criteria of left ventricular hypertrophy and unipolar aVR lead].

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.

Adult↗
PubMed1977

[Systemic lupus erythematosus and congestive heart failure. Heart histological and ultrastructural study (author's transl)].

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.

Aortic Valve↗
PubMed1977

[Concealed permanent ventricular reentry and paroxysmal ventricular tachycardia by circulatory movement].

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.

Anti-Arrhythmia Agents↗
PubMed1976

[Wolff-Parkinson-White syndrome caused by association of atrio-hisian fibers and Mahaim's fibers. Comparison between the electrophysiology and histology].

A child of six who had had several losses of consciousness died suddenly during a spell of tachycardia. The EKG showed at times a type B Wolff-Parkinson-White syndrome, at times a Lown-Ganong-Levine syndrome. Intracavitary electrophysiological explorations had been carried out. The interest of this case lies in the comparison between these electrophysiological explorations and the histological examination of the normal and accessory conduction pathways. The short PR interval, which did not lengthen under the effect of premature atrial stimulation, was accounted for by the presence of atrio-His bundle tracts. The intermittent delta wave was due to Hissio-ventricular Mahaim fibres. These two accessory conduction pathways are considered as abnormal.

Child↗