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Optical microresonator biosensors have proven to be a valid tool to perform affinity analysis of a biological binding event. However, when these microresonators are excited with a single optical mode they can not distinguish between a thin dense layer of biomolecules or a thick sparse layer. This means the sensor is "blind" to changes in shape of bound biomolecules. We succeeded in exciting a Silicon-on-Insulator (SOI) microring with TE and TM polarisations simultaneously by using an asymmetrical directional coupler and as such were able to separately determine the thickness and the density (or refractive index) of a bound biolayer. A proof-of-concept is given by determining both parameters of deposited dielectric layers and by analysing the conformational changes of Bovine Serum Albumin (BSA) proteins due to a change in pH of the buffer.

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We report the case of a Cardiobacterium hominis endocarditis causing an acute mitral insufficiency complicated of left heart failure. The patient has been treated after a few days by surgical valvuloplasty. Cardiobacterium hominis is a bacteria of the HACCEK group, bacille gram-negative, sometimes anaerobic, difficult to isolate. Recently, Polymerase Chain Reaction analysis appears to be effective for the the diagnosis in the identification of fastidious micro-organisms like Cardiobacterium hominis. We have reviewed in the literature 71 cases of Cardiobacterium hominis endocarditis; clinical presentation is often sub-acute, the bacteriological diagnosis is based on hemocultures for which the culture is slow and require enriched environments. Hemodynamic and thrombo-embolic complications are frequent because of the high pathogenicity of the bacteria which provides big and friable vegetations. Despite a high sensibility to antibiotherapy, surgical intervention is often required.

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beta-Adrenergic blocking drugs are effective in reducing sudden cardiac death after acute myocardial infarction but the precise mechanism of this effect is unclear. We investigated the acute and chronic effects of acebutolol, a beta-adrenergic blocker, on electrocardiographic parameters, diastolic excitability threshold (DET), and right ventricular effective refractory period (RVERP) in chronically instrumented conscious dogs. These parameters were determined during spontaneous sinus rhythm and at a fixed pacing rate (200 beats/min). Acebutolol (0.5, 1, and 5 mg/kg i.v.) decreased the heart rate (HR) (by 23, 26, and 24%, respectively) without effects on any electrocardiographic parameters or on the DET. The maximal increases in ERP were 4.7, 7, and 7.8%, respectively, during pacing and 8.5, 13.3, and 10.3%, respectively, during sinus rhythm. Acebutolol, 10 mg/kg/day P.O. for 6 weeks, reduced the HR from the third day onward without altering the PR, QRS, QT, or QTc intervals or the DET. The increase in ERP was significant from the third day (14%) during pacing and from the seventh day (15.5%) during sinus rhythm. The degree of prolongation of the ERP subsequently remained stable during the 6 weeks of treatment. The ERP returned to the baseline value 7 days after acebutolol withdrawal. This increase in ERP, which was more marked during chronic oral treatment, could contribute to the documented protective effect of the beta-blocking drugs against sudden cardiac death after myocardial infarction.

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Circumferential laser thermoexclusion was assessed in the treatment of postinfarction ventricular tachycardia resistant to drug therapy in 11 patients between December 1986 and April 1989. There were 10 men and 1 woman with an average age of 63.7 +/- 5.6 years whose ventricular tachycardia occurred 10.7 +/- 7.5 years after infarction. All had left ventricular aneurysm or an akinetic plaque. Circumferential thermoexclusion was carried out by Mesnildrey's method, systematically associated with resection of the aneurysm or, when this was not feasible, with coronary revascularisation. Programmed ventricular stimulation was performed before and after surgery in 8 patients. Sustained ventricular tachycardia remained inducible in 4 patients after surgery but the prescription of antiarrhythmic drugs in 2 of these cases resulted in tachycardia becoming non-inducible. The increase in the left ventricular ejection fraction after surgery was not statistically significant (36.9 +/- 9.4% to 44.4 +/- 12.8%). After an average follow-up of 16.7 +/- 10.6 months, there were 2 cardiac deaths not related to arrhythmias (18%), 1 early at the 20th postoperative day and 1 late, 10 months after surgery. There were 2 recurrences of tachycardia (18%) controlled by antiarrhythmic therapy. Late ventricular potentials were recorded in 9 out of the 11 patients before surgery but in only 3 of these cases (33%) after surgery. Circumferential laser thermoexclusion guided visually in the border zone of the infarct scar would seem to be a simple, safe, rapid and therefore attractive, surgical antiarrhythmic technique, the efficacy of which should be evaluated by programmed ventricular stimulation. This should be undertaken on a large scale in order to define the indications and results of this method.

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We conducted a randomized, double-blind, double-placebo study in two groups of elderly hypertensive patients aged over 60 years to compare nitrendipine to enalapril, given once daily over 4 months, as monotherapy with 20 mg tablets. Clinic blood pressure was measured monthly and 24 h ambulatory monitoring was obtained at day 0 and day 120. Fifty-two patients entered the study (22 in the nitrendipine group, 30 in the enalapril group); 4 patients in both groups were dropped from the study because they withdrew their consent to participate. Three patients under nitrendipine and five patients under enalapril were not included in the analysis of data because of insufficient follow-up. The two groups were comparable on final analysis. The clinical blood pressure was similarly reduced in both groups at 24 h postdose (172/97 to 157/85 mm Hg on nitrendipine vs. 177/98 to 154/86 mm Hg on enalapril). Seventy percent of the patients had their blood pressure normalized at the end of the study in the two groups. With ambulatory blood pressure recording, no 24 h blood pressure significant differences were found on day 120 when we calculated the mean of systolic blood pressure (SBP) or diastolic blood pressure (DBP) (137 +/- 12/82 +/- 9 mm Hg on nitrendipine vs. 136 +/- 16/82 +/- 11 mm Hg on enalapril), or for daytime or nighttime periods. The pulse pressure or the mean of the five highest SBP values was also similar in nitrendipine and enalapril patients.(ABSTRACT TRUNCATED AT 250 WORDS)

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Protein C, a physiological inhibitor of coagulation, acts by inactivating coagulation factors V and VIII. It was identified 20 years ago and purified 10 years later. Its anticoagulant properties have been confirmed by the demonstration of thromboembolic diseases associated with constitutional protein C deficiency. Deficiency is defined as a less than 65 p. 100 level of the protein. There is no correlation between protein C level and clinical severity. Constitutional protein C deficiency is transmitted as an autosomal dominant trait. The protein C level observed in homozygous deficiency is about 50 p. 100, more often quantitative (type I) than qualitative (type II), the other coagulation factors being present at normal levels. Protein C deficiency is responsible for recurrent and familial thromboembolic necrosis and for cutaneous necrosis during treatment with antivitamin K drugs. Protein C assays must now be part of the aetiological evaluation of thromboembolic disease. Physiological variations in protein C levels have been encountered in neonates and pregnant women as well as in some pathological conditions, after surgery or under certain treatments. Familial inquiries are essential to detect asymptomatic protein C deficient subjects. Treatment rests on anticoagulants: antivitamin K drugs after effective heparinization in thromboembolic accidents, prevention of accidents by heparin in protein C deficient subjects and when a risk of thromboembolic disease is present. We report here one case of venous thrombosis and one case of arterial thrombosis, both being characterized by the finding of protein C deficiency during full evaluation of haemostasis factors.

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At the present time, there is no satisfactory pharmacological treatment for arrhythmia or conduction disorders induced by or aggravated by vagal hypertonia. The limited duration of action of the atropine derivatives currently available justifies the development of new compounds with expected longer acting duration. The aim of this study was to compare the effects of a single blind intravenous injection of ipratropium bromide to those of atropine sulfate in 22 patients. These patients were studied with continuous Holter recordings for three days. During the second and the third nights (patient sleeping), boluses of atropine (0.03 mg/kg) and of ipratropium bromide (0.03 mg/kg), respectively, were added to a continuous saline intravenous infusion. Accurate ECG analysis allowed determination of maximal heart rate peak, timing of maximal heart rate, variations in sinus cycle length, atrioventricular conduction, and durations of drug action. A nonsuggestive questionnaire was presented to patients to detect possible occurrence of side effects. The mean maximal heart rate rose significantly (p less than 0.001) for atropine (+46.2%) and for ipratropium bromide (+57.4%). The effects obtained with ipratropium bromide on the heart rate lasted nearly twice as long as those obtained with atropine (respectively, 120 +/- 38.4 min and 70 +/- 30 min- for the pharmacological half-life). Common minor muscarinic side effects (dryness of the mouth) were noted with the two drugs. In conclusion, this comparative intraindividual study confirmed the prolonged vagolytic effects of intravenous ipratropium bromide, which may be valuable in the treatment of patients with vagally mediated automaticity and conduction disturbances.

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The recording of late ventricular potentials with high amplification cardiography (HAC) permits to identify patients presenting a risk of sudden death and ventricular tachycardia, especially in the later stage of myocardial infarction. Few authors have studied the prevalence of these potentials in other heart diseases presenting a risk of sudden death. Most series in the literature are too small to specify variations in the prevalence of these potentials according to the severity of the coronary disease. For this purpose, 835 patients including 535 coronary patients were evaluated with HAC compared to data from coronary angiography and Holter test. An automatic quantification method of the late potentials was used on 131 healthy subjects. The prevalence of late potentials is 32 p. cent after infarction, and 75 p. cent when a chronic ventricular tachycardia is present. These potentials retain their significance of tracers of ventricular arrhythmias in primary dilated myocardiopathies, with a prevalence of 25 p. cent reaching 50 p. cent in case of ventricular tachycardia. Their recording in the presence of idiopathic ventricular extrasystoles must be an indication to look for an underlying cardiopathy. It is possible to record them in other diseases especially in advanced valvular cardiopathies, as well as in right ventricular dysplasias with arrhythmia where their presence has a great diagnostic value.

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Bleomycin is sometimes at the origin of a Raynaud's phenomenon (RP). From the literature, there does not seem to exist a dose-dependent relationship. The phenomenon occurs early or late and often is resistant to various medications. The possible physiopathological mechanisms are: direct vascular toxicity, hypersensitivity vascularization, alteration of platelets activity, alteration of Willebrand's factor, and as predisposing factors: association to periwinkle alkaloids or hypomagnesemia.

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High amplification electrocardiographic recording of ventricular late potentials was introduced a few years ago and seems to be a simple, reliable and reproducible method to identify patients at a high risk of sudden death and ventricular tachycardia, principally during the chronic phase of myocardial infarction. However, few authors have studied quantitatively the prevalence of late potentials in patients with ventricular tachycardia compared with a sufficiently large sample of healthy subjects. In this study 34 patients with sustained ventricular tachycardia (11 women, 23 men, mean age 58 years) and 131 healthy subjects (29 women, 102 men, mean age 29 years) underwent high amplification time-averaged ECG recording, and an algorithmic analysis of the tracings was conducted, using the Simson method. Three numeric parameters were used in the interpretation of the tracings: HFRMSA = mean RMS amplitude of the last 40 milliseconds of QRS; HFD40 = delay in signal decrease from amplitude 40 mu v to baseline, and delta QRS = difference in QRS duration with 0-250 Hz and 25-250 Hz filterings. Normal values, as determined from measurements in healthy subjects, were: HFRMSA above 27 mu v, HFD40 below 35 ms and delta QRS below 13 ms. Late potentials were present when at least one of these criteria was positive. When these norms were applied to patients with sustained ventricular tachycardia the prevalence of late potentials was 76%, rising to 90.4% in the subgroup of 21 patients with coronary disease. With the method thus defined the specificity for each criterion taken separately is 97.5%. According to the norms, only one control subject (0.8%) gave a false-positive result.(ABSTRACT TRUNCATED AT 250 WORDS)

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