Biomedical subjects
Publications and source records attributed to R Jouve.
A new presentation of ECG tracings is presented (contourography) which is suitable for ECG intervals measurements, particularly QT for prolonged periods of time. Possible applications of this method are looked for in the future.
Plasma levels of thromboxane B2, and 6-Keto-PGF1 alpha, stable metabolites of thromboxane and of prostacyclin were determined by radioimmunoassay in 17 patients with arterial disease and 10 control subjects. The production of prostacyclin from incubates of aortic microsomal fractions of patients was also studied. There was a significant elevation of thromboxane B2 in the peripheral venous blood of patients with arterial lesions (142 +/- 152 pg/ml vs 22 +/- 2 pg/ml, p less than 0.005); levels of 6-KetoPGF1 alpha were equally low in controls and patients. Rate of production of prostacyclin, which was 450 +/- 24 pmol/50 mg of proteins in 10 minutes in controls, was reduced to 97 +/- 86 pmol/50 mg prot. 10 min (p less than 0.01) in patients. Co-existence of raised plasma thromboxane levels and a reduced capacity for prostacyclin synthesis in the same patients is supportive evidence of the thrombogenic theory of arterial disease.
Extension of the duration of electric systol in the acute phase of coronary thrombosis can be analysed in satisfying conditions whatever the physiological frequencies by the measurement (formula; see text) represents the average QT measurement of three non-consecutive complexes in five derivations (DI, DIII, aVF, VI and V6). This extension is of prognostic value when the QTc is greater than 44 c/s. Out of 1 255 acute phase thrombosis patients, 18 Out of 20 cases of ventricular fibrillation revealed a QTc greater than 44 c/s in the 24 hours preceding sudden death. Therapeutic intervention with anti-andrenergic drugs such as bretylium tosylate or beta-blocking agents appears to reduce the QTc of these patients and thus prevent sudden death.
The serum content of proteins involved in the inflammatory process was investigated, partly through kinetic immunodiffusion, in 85 men subdivided as follows: 45 men (aged 57 +/- 5 years) with intermittent claudication due to arteriosclerosis obliterans; 20 controls matched for sex and age; 20 sex-matched controls whose mean age was 25 +/- 3 years. Patients with obliterating arteriosclerosis had signs of both subacute and chronic inflammation. Compared to controls, they had a higher sedimentation rate, a lower percentage of serum albumine, higher percentages and absolute serum contents os alpha 1, alpha 2 and beta globulins, and higher serum concentrations of fibrin, orosomucoid, C3 complement fraction and IgA. In addition, the modifications of these proteins were closely correlated. These results are consistent with previous reports concerning patients with coronary heart disease. They point out the relationship between inflammation and atherosclerosis.
Erythrocyte deformability is lower than normal in uncontrolled insulin-dependent diabetics and returns towards normal after 24 h treatment with a feedback-controlled insulin infusion. Deformability of normal erythrocytes is reduced by incubation in plasma from uncontrolled insulin-dependent diabetics but is normal in plasma from insulin-dependent diabetics controlled by 24 h insulin infusion, or in plasma from uncontrolled insulin-dependent diabetics with insulin added in vitro. Therefore, insulin has a direct action on erythrocyte deformability. Platelet aggregation measured in whole blood is raised in uncontrolled insulin-dependent diabetics and returns to normal after 24 h treatment with a feedback-controlled insulin infusion. Aggregation of normal platelets rises in the presence of erythrocytes from uncontrolled insulin-dependent diabetics, but not erythrocytes from the same patients after 24 h treatment with insulin. The effect of insulin on platelet aggregation therefore seems to be at least partly mediated by erythrocytes. The enhanced platelet aggregation seen in uncontrolled insulin-dependent diabetics can be explained either by a direct effect of erythrocyte rigidity or by an increased release of nucleotides (ADP) by the erythrocytes.
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Recent reports have drawn attention to the association between long QT intervals and sudden death in myocardial infarction and certain congenital syndromes. This study was undertaken to determine the relationship between lengthening of the QT interval and primary ventricular fibrillation in acute myocardial infarction. Thirteen cases were chosen out of a total of 21 cases of primary ventricular fibrillation (5.09% of 412 cases of myocardial infarction hospitalised during this period). Ten other cases of myocardial infarction with the same features apart from the arrhythmia were used as controls. Three series of electrocardiogrammes recorded under the same technical and chronological conditions (2 before and 1 after ventricular fibrillation) were analysed. The average QT interval was corrected for heart rate (RR) with Bazett's formula. The average QTc in acute myocardial infarction was longer than the theoretical QTc (p less than 0.05). The graph showing this increase reached a peak at the 48th hour. The average QTc in patients with primary ventricular fibrillation was longer than in the control patients (p less than 0.05) and significantly longer than the theoretical value (p less than 0.001). The average QTc in survivors of ventricular fibrillation was not significantly longer than that of the control group but was longer than the theoretical value (p less than 0.01). These results justify the strict surveillance of the length of electrical systole in the first hours of the acute phase of myocardial infarction. In this series, values greater than 440 ms were associated with a high risk of ventricular fibrillation in the first week after myocardial infarction.
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Electrical systole duration has been studied in two groups of 23 patients (39 M and 7 F) admitted in the coronary care units of two different hospitals for documented acute myocardial infarction (AMI). The mean QT interval duration corrected for heart rate (QTc) was obtained from three measurements of non consecutive complexes in five different leads and compared to the ideal electrical systole duration of a normal population with the same cardiac cycle length. During the evolution of AMI, QT interval increased in both groups of patients (11.5% and 14.8% respectively) and was prolonged (17.6% and 21.5% respectively) at the 48th hour. Prolongation of electrical systole can be best measured using the ratio: QTc (according to Bazett)/normal QT (according to Ashman).
In 81 obese subjects the following studies were performed: --measurement of fat mass and its distribution in the body, --exploration of carbohydrate tolerance and lipid plasma level, --assessment of platelet aggregation and coagulation activity, --investigation of the chemical composition of platelet phospholipids. Platelet hyperactivity was demonstrated in certain patients, as evidenced by the presence of irreversible platelet aggregation with low doses of aggregation agents and by an increase in platelet coagulant activity; the latter phenomenon was not accompanied by a change in the biochemical composition of platelet phospholipids. Results of this work showed that platelet activity was not related to body weight and displayed no correlation or a slightly negative one to fat mass excess. Platelet activity was significantly increased in cases where obesity predominated in the upper body (hyperandroid obesity). The classical association of diabetes and atherosclerosis with hyperandroid obesity did not allow us to distinguish between the relative importance of hyperandroid obesity and diabetes in the observed platelet hyperactivity. Regardless of the causal mechanism involved, the relationship between platelet hyperactivity and upper body fat excess should be kept in mind.
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The authors review the literature on the undesirable side effects of beta blockaders (excluding the cardiovascular system) and report the new therapeutic propects in psychiatry and in various metabolic disorders. The necessity of sufficient follow up made us choose propanolol as reference product without neglecting acebutolol, pindolol and oxprenolol.
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Boy 15. Aspect of delayed puberty with empty scrotum and gynecomastia. Caryotype 46, XX. Presence of H.Y. Antigen. Plasmatic testosterone 1 020 pg/ml. Normal plasmatic FSH and LH. Hypotrophic uterus and tubes. No gonad found. Small right epididymis. Complete virilization by testosterone.
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