[Left ventricular filling and left bundle branch block: an echocardiographic and radionuclide study].

Left bundle branch block changes the activation and haemodynamics of the left ventricle. In order to evaluate its consequences on left ventricular filling, the duration of the isovolumic relaxation period, the velocities and the integrals of the rapid and slow filling waves were recorded by Doppler echocardiography and the ejection fraction, the peak filling rate and its time of apparition were measured by gamma angiocardiography in 18 patients aged 55 +/- 9 years and 18 control subjects aged 53 +/- 9 years. Left bundle branch block was associated with a prolonged isovolumic relaxation period (104 +/- 14 vs 88 +/- 11 ms) a delayed and reduced peak filling rate and an increased atrial filling velocity at a heart rate comparable to that of control subjects (69 +/- 9 vs 72 +/- 8 beats/mn).

Oxidized low density lipoproteins exert arrhythmogenic effects in rabbit Purkinje fibers.

The electrophysiological effects of oxidized low density lipoproteins (ox-LDLs) have been studied in rabbit Purkinje fibers using standard microelectrode techniques, in comparison with native LDLs (n-LDLs) and lysophosphatidylcholine (LPC). At the concentration of 100 micrograms protein/ml, ox-LDL but never n-LDL induced the abrupt occurrence of abnormal electrical activities during the basic stimulation of 1 Hz (6/13 fibers) and the development of either early afterdepolarizations (6/13 fibers) or abnormal automaticity (4/13 fibers) at low frequencies (0.1 and 0.

[Contribution of transesophageal echocardiography in the investigation of the atrium in systemic embolism].

Transesophageal echocardiography (TEE) is a semi-invasive examination that provides better images of the atrium than classical transthoracic echocardiography (TTE) due to the anatomical positioning of the captor and the high frequency Doppler apparatus used. We used TEE and TTE to evaluate the incidence of the cardiac origin of emboli in 46 patients with unexplained stroke or transient ischemic attack (TIA): 23 had documented heart disease (mean age 60 years) and 23 had no cardiac disease (mean age 43 years). Among those with existing heart disease, 4% of the anomalies certainly or probably responsible for the emboli in addition to the underlying cardiopathy were detected by TTE versus 37% by TEE (as compared to values reported in the literature: 25% by TTE and 51% by TEE).

Modified low density lipoproteins activate human macrophages to secrete immunoreactive endothelin.

This study attempted to determine if low density lipoproteins (LDL) induce the production of endothelins (ET) by human macrophages. Non-protected LDL from macrophage induced oxidation (n-LDL), copper-oxidized LDL (Ox-LDL), acetylated-LDL (Ac-LDL), butylated hydroxytoluene-LDL (BHT-LDL), BHT-Ac-LDL, polyinosinic acid (PiA, 1.5 micrograms/ml), phorbol myristate acetate (PMA; 0.

Apolipoprotein B polymorphism and altered apolipoprotein B concentrations in Congolese blacks.

The immunoreactivity of apolipoprotein B (apo B) in plasma obtained from 238 unrelated black African male subjects from the People's Republic of Congo was analysed by non-competitive Enzyme Linked-Immunosorbent Assay (ELISA) with monoclonal BIP 45 anti-LDL antibody. The polymorphism detected by BIP 45 monoclonal antibody is identical to the Ag(c,g) polymorphism. Antibody BIP 45 distinguishes three apo B allotypes (immunophenotypes) encoded by the two allelic genes apo B Ag(c) and apo B Ag(g).

Lipoprotein particles in homozygous familial hypercholesterolemic patients treated with portacaval shunt and LDL apheresis.

Lipoprotein particles containing apolipoproteins (Apo) were studied by enzyme-linked-immunosorbent assay in two homozygous familial hypercholesterolemic patients (1 male and 1 female) with portacaval shunts, and in controls. Total Apo B, total cholesterol and LDL cholesterol were increased in both patients while complex Apo B containing particles, Lp CIII: B, were not increased in these FH patients. The dextran-sulfate cellulose columns (Liposorber LA-40) had an excellent adsorption selectivity and adsorption capacity for lipoprotein particles containing Apo B and a minimum adsorption capacity in Apo AI and Apo AII-containing particles.

[Arterial hypertension in Thio (New Caledonia)].

The high blood pressure is one of the main cardiovascular risk factors in New Caledonia as it is every where. A study carried out in THIO from August 1985 to August 1988 displayed a frequency and a seriousness not frequent (17.8 p.

[Isolated stenosis of the popliteal artery after treatment with methysergide. An anatomopathologic study].

One case of isolate stenosis of the popliteal artery in a young woman is reported in this article. Since acid Methysergide maleate had been taken over a longer period, this lesion was placed into the nosological context of toxic arterial fibrodysplasia. Although such lesions usually recede at the end of treatment, the severity and abruptness of ischemia in this case led to operating the patient.

[Wegener's granulomatosis with urethral-penile location. Apropos of a case].

The authors report a case of Wegener granulomatosis presenting as a necrotizing urethral tumor in a 44 year-old man. Involvement of the urethra by Wegener granulomatosis in unusual which explains the delay in diagnosis particularly when the urethral localization is isolated. The prognosis is severe despite urinary diversion and appropriate therapy.

Apolipoprotein B metabolism in homozygous familial hypercholesterolemia.

This report describes the metabolism of apolipoprotein B-containing lipoproteins in seven familial hypercholesterolemic (FH) homozygotes and compares the results to the values obtained from five healthy control subjects. The concentration, composition, and metabolism of large, triglyceride-rich very low density lipoproteins (VLDL1, Sf 60-400) were the same in the control and FH groups, indicating that this component of the VLDL delipidation cascade ws unaffected by the absence of receptors. In contrast, familial hypercholesterolemic small VLDL2 (Sf 20-60) was enriched with cholesterol and depleted in triglyceride.

Apolipoprotein B immunochemical heterogeneity in dialysed patients with chronic renal failure and patients with coronary artery stenosis.

Serum cholesterol, triglyceride, apolipoprotein B (apo B) and the cholesterol and phospholipid content of apo-B-containing particles was determined in 41 male patients on dialysis for chronic renal failure, in 41 male patients with coronary artery disease selected on the basis of a total cholesterol level below 6.72 mmol/l and in 41 male control subjects of similar age. Apo B was assessed as total B protein determined using polyclonal antibodies and also by measuring the expression of epitopes recognized by three different monoclonal antibodies (BL3, BL5 and BL7).

Association between epitopes detected by monoclonal antibody BIP-45 and the XbaI polymorphism of apolipoprotein B.

An epitope of Apolipoprotein B (ApoB), recognised by a monoclonal antibody BIP-45, is associated with the development of ischaemic heart disease (Duriez et al. 1988). We have examined the genetic relationships between this epitope and three Restriction Fragment Length Polymorphisms (RFLPs) of the gene for ApoB detected with the enzymes EcoRI, PvuII and XbaI in a sample of 53 unrelated individuals from France.

Preformed PAF-acether and lyso PAF-acether are bound to blood lipoproteins.

PAF-acether (PAF) is a newly formed mediator not normally present in circulating blood. A compound exhibiting all of its biological characteristics but coeluting with phosphatidylcholine (PC) in high-pressure liquid chromatography (HPLC) was unveiled ('peak X') in normal human plasma. A second HPLC run of peak X HPLC fractions revealed the presence of PAF itself with concomitant disappearance of peak X.

A monoclonal antibody (BIP 45) detects Ag(c,g) polymorphism of human apolipoprotein B.

A monoclonal antibody (BIP 45) against human apolipoprotein B (apo B) was used to study the polymorphism of apo B in families and in unrelated subjects. BIP 45 bound to apo B-containing lipoprotein particles in one of three distinct patterns of immunoreactivity (strong, weak and intermediate). Family studies showed that these binding patterns result from co-dominant transmission of apo B allelic pairs which are temporarily designated allele BIP- and allele BIP+; allele BIP+ would code for the apo B BIP 45 epitope.

Detection of human apolipoprotein B polymorphic species with one monoclonal antibody (BIP 45) against low density lipoprotein. Influence of this polymorphism on lipid levels and coronary artery stenosis.

The immunoreactivity of apolipoprotein B (apo B) in plasma samples obtained from a variety of subjects was analysed by non-competitive ELISA with a polyclonal and a monoclonal (BIP 45) anti-LDL antibody. Three populations were tested: the first, comprising 244 healthy male volunteers, provided reference values; the second consisted of a population undergoing coronary angiography (n = 88) and was divided into a subgroup with (n = 64) and without (n = 24) coronary artery disease (CAD); the third was made up of 56 patients with heterozygous familial hypercholesterolemia. Total apo B (measured with the polyclonal antibody) was increased in the populations with CAD and in the heterozygous familial hypercholesterolemic subjects compared to the reference population.

Quantitative determination of human plasma apolipoprotein A-II by a non competitive enzyme-linked immunosorbent assay.

A noncompetitive enzyme-linked immunosorbent assay (ELISA) for apolipoprotein A-II (ApoA-II) was developed. Microtiter plates were coated with affinity purified antibodies to ApoA-II. After incubation with human plasma, the amount of ApoA-II bound to the coated plate was determined with peroxidase-labeled antibodies to ApoA-II.

Quantification of apolipoprotein C-III in serum by a noncompetitive immunoenzymometric assay.

We used a noncompetitive immunoenzymometric assay to measure the concentration of total apolipoprotein C-III in human sera. Affinity-purified antibodies to apolipoprotein C-III were adsorbed to the surface of microtiter plates. After washing, this solid-phase antibody was incubated with antigen (serum from fasting subjects), washed, and then incubated with peroxidase-labeled purified antibodies to apolipoprotein C-III.

[Effects of nicardipine on electrophysiologic alterations and enzyme leakage induced in vitro in the guinea pig].

Ventricular strips of guinea-pig left myocardium were placed in a special tissue bath bisected by a thin membrane latex. One of the two compartments was flowed during 2 hours with modified Tyrode's solution in order to mimic the in vivo ischemia-induced effects. Replacement in standard conditions during 30 minutes was considered as representative of ischemic heart reperfusion.

[The effects of propranolol and sotalol on the electrophysiologic and enzymatic impact of myocardial ischemia induced in vitro in the guinea pig heart].

Antiarrhythmic and cardioprotective effects of propranolol and sotalol were examined by studying their action on cellular electrical activity (recorded using standard microelectrode techniques) and creatine-kinase leakage (measured in the effluent from the experimental bath chamber) in the in vitro guinea-pig left ventricular myocardium exposed to conditions mimicking severe or moderate ischemia. Returning the tissue to the normal conditions was considered as equivalent to ischemic-heart reperfusion. Propranolol (2 X 4 mg/kg) was intraperitoneally administered to guinea-pigs, daily for 21 days.

[Electrophysiological study of the arrhythmogenic effects of digoxin in ventricular myocardial fragments of guinea pigs stimulated at low frequency. Inhibitory action of caffeine].

Arrhythmogenic effects of digoxin were studied in guinea pig ventricular myocardium driven at a low frequency, using microelectrode technique. Prolonged exposure to digoxin made two distinct phases of arrhythmias to appear: the first phase early occurred without apparent alteration in membrane diastolic potential of the impaled ventricular cells, the second phase was later initiated from oscillatory afterpotentials in diastolic potential. It is proposed that phase 1 of arrhythmias is initiated from oscillatory afterpotentials generated in Purkinje fibers more sensitive to digoxin-induced arrhythmogenic effects than myocardial cells.

Digoxin-induced toxicity and experimental atrioventricular block in dogs. Relation between ventricular arrhythmias and oscillatory afterpotentials.

In anesthetized dogs, digoxin intoxication was performed after and before production of a definitive complete atrioventricular (A-V) block induced by formaldehyde injection in A-V node area, compared to intoxication in dogs in sinus or junctional rhythm. The results showed that digoxin toxicity was decreased in dogs with previous A-V block. This A-V block protective effect was abolished by resetting initial sinus-like frequency with ventricular pacing before digoxin administration.

High extracellular sodium and digoxin-induced arrhythmias in guinea-pig ventricular myocardium.

Oscillatory fluctuations in diastolic potential [4, 10] and triggered rhythmical activity [4] are well known manifestations of digitalis intoxication and are attributed to intracellular Ca2+ overload consecutive to an elevated intracellular Na+ [7]. In the present paper we report the electrophysiological effects of elevated extracellular Na+ on the spontaneous rhythmical activity and oscillatory fluctuations in digoxin-intoxicated ventricular cells. Our results show that by increasing extracellular Na+ from 135 mM to 175 mM, we were able to abolish spontaneous rhythmical activity but were not able to suppress the damped sinusoidal oscillations in the resting membrane potential.

[Electrophysiological effects of subtherapeutic levels of procainamide on hypoxic myocardial cells (author's transl)].

1. The electrophysiological effects of hypoxia alone or combined with subtherapeutic concentrations of procainamide superfusion were investigated in guinea-pig ventricular muscle fibres in order to elucidate the procainamide activity on suffering myocardial cells. 2.