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The Wolff-Parkinson-White syndrome is usually observed in young people and is much rarer in patients over 50 years old. This fact may be explained by the demise of a certain number of patients before the age of 50 and/or a change in the clinical features of the syndrome with age and/or of the electrophysiological properties of the normal and accessory conduction pathways. To test the latter hypothesis, the clinical and electrophysiological data of 15 patients over 50 years old with the Wolff-Parkinson-White syndrome (Group I) were compared with that of 10 patients under 30 years old with the same syndrome (Group II). The same protocol of electrophysiological investigation was used in both groups of patients. The results showed a significant difference (p < 0.001) between the two groups in the incidence of associated cardiac disease. This was more common in Group I (1 4 out of 15 patients) than in Group II (2 out of 10 patients). The cardiothoracic ratio was significantly higher in Group I (p < 0.01). The two groups also differed in the age at which tachycardia first occured. 9 out of 11 patients in Group I only had symptoms after thirty years. On the other hand, there was no significant difference in the types of tachycardia and the frequency of attacks. There was no significant difference in QRS, PR, AH, HV intervals, in the ventriculo-atrial conduction time and the effective refractory periods of the atrium, right ventricle or atrio-ventricular node. There was no significant difference in the anterograde and retrograde refractory periods of the accessory pathways between the two groups. Reciprocating tachycardia, initiated by electrical stimulation in 7 patients in Group I and 6 patients in Group II, was conducted anterogradely to the ventricles through the normal pathway and retrogradely to the atria through the the accessory pathway. This study suggest that age-related changes in the electrophysiological properties of the accessory are not an important prognostic factor in the Wolff-Parkinson-White syndrome.

The left ventricular kinaetics of 29 coronary patients (pure angina and with sequela of myocardial infarction) was studies by biplane angiocardiography. Their contractility was assessed by measurement of the Vmax and VECmax indices derived from the relationship between contractile elements shortening speed-overall wall tension, in isovolumetric phase. An excellent relationship links the hypokinaetic area with decrease of the ejection fraction (SV/LSV): when the hypokinaetic area exceeded 20% of the overall endocardial surface, the ejection fraction deveased below 0.40, and signs of cardiac failure were manifest. Pure anginal patients at rest kept normal kinaetics, late diastolic volume, ejection fraction and myocardial mass. A myocardial hypertrophy develops in the areas adjacent to the fibrous scar. In some cases (group I) it compensates for the ventricular dysfunction; in other cases, it is not sufficient to compensate for the ejection fraction reduction. One must then admit the presence of diminished contractility in the areas adjacent to the fibrous scar, as is suggested by the increase of the late diastolic pressure, the decrease of the externel work of the left ventricle and of the contractility indices. Analysis of both the natural and post-operative courses in these patients shows that Vmax the ejection fraction and the hypokinaetic areas afford excellent criteria for prognosis and operability.

Rat aortic smooth muscle cells isolated by digestion of the vessels by elastase and trypsin and grown in subculture, are examinated by phase, optic and electron microscopy for their ability to synthesize connective tissue components. Large amounts of extracellular material accumulates within the spaces between the cell; it consists of amorphous substance identified histochemically as elastin, of 110 A microfibrils and of periodic fibrils (430-490 A); the chemical nature of these two last components is discussed.

A population of 236 patients with dilated cardiomyopathy (DCM) was studied and followed up for an average of 38.8 +/- 27 months. The most common atrial arrhythmia was atrial fibrillation (AF) which was observed in 27 p. 100 of cases. Patients with AF (n = 43) and without it (n = 193) at the time of diagnosis were compared: the subjects with AF were older (p = 0.036), had a higher left ventricular ejection fraction and lower end diastolic pressures (p = 0.022). AF was associated with mitral valve prolapse (p = 0.007) and with signs of adiastole (p = 0.0015); the most significantly correlated variable was echocardiographic dilatation of the left atrium (p = 0.0012). AF was the presenting symptom of DCM in 13 cases (5.5 p. 100); in 10 cases (4 p. 100) it was the main clinical and therapeutic problem, realizing an arrhythmic form of DCM. Electrical conversion was successful in 7 out of 11 patients with a 2 year follow-up: 3 patients remained in sinus rhythm for over 6 years and have no clinical symptoms, posing the problem of the dominant if not exclusive underlying role of AF in these cases of DCM. An example illustrated by several echocardiographic examinations is presented. Embolic complications were observed in a quarter of the cases with AF and this arrhythmia was present in half the patients with embolic phenomena. However, the prognosis in the groups with and without AF was not significantly different.

Separation by velocity sedimentation at unit gravity according to the STAPUT system of Miller and Phillips was applied to a population of rabbit megakaryocytes previously enriched by density gradient centrifugation. By this means, 80,000 to 100,000 megakaryocytes with 100% purity were collected in eight fractions according to size for a sedimentation velocity of 52 to 30 mm/hr. DNA-Feulgen cytophotometric measurements show significant correlation between megakaryocyte size and ploidy. The study of the eight purified fractions is of particular interest because it reflects megakaryopoiesis evolution. The different stages of megakaryocyte maturation of each fraction were analysed by transmission and scanning electron microscopy and were correlated to ploidy level. Thrombopoietic megakaryocytes with grape-like appearance were found in ploidy fractions 8n to 128n. Cytophotometric determinations of nucleohistones revealed several populations.

Alternate Wenckebach periods have been defined as episodes of 2:1 atrioventricular (AV) block in which conducted P waves exhibit progressive PR prolongation until two or three successively blocked P waves. Ocurrence of this phenomenon during atrial pacing has been established. Thirty-six patients were studied and right atrial pacing was achieved at increasing rates up to 350 beats/min in order to induce alternate Wenckebach periods. His bundle recordings were obtained in every patient. The patients were subdivided into three groups according to the AV nodal conduction time (AH interval): normal AH (75-130 ms) was present in 17 patients, short AH (70 ms) in 13 patients and prolonged AH (130 ms) in eight patients. Alternate Wenckebach periods were observed in 29 patients (80.5%). In every patient alternate Wenckebach periods occurred at the AV node level. Atrial pacing failed to induce alternate Wenckebach periods in seven patients, six of whom belonged to the short AH group. In four patients 3:1 block never appeared because of block at the atrial level. Two patients presented 2:1 and 3:1 infrahissian block without significant AH prolongation. The remaining patient developed atrial fibrillation. Alternate Wenckebach periods were observed in six of nine patients after intravenous atropine. This study suggests: 1. pacing-induced alternate Wenckebach periods at the AV node level are a physiologic phenomenon; and 2. total or partial bypass (or accelerated AV conduction) atrial refractoriness or vulnerability or block at a lower level may prevent its occurrence.

To determinate the part of humoural and parietal factors in atherosclerotic injury genesis, metabolism alteration study is realised on aortic cell wall of rabbits which are submitted to a chronical lathyritic intoxication alone, or simultaneously or alternatively associated with a cholesterolemic diet. Catabolic activity increase of beta-glucuronidase occurs in hypercholesterolemic rabbits. Beta-aminoproprionitrile, lathyrogenic drug used, stimulates biosynthetic pathways: increase of soluble proteins, energetic enzyme activities (lacticodeshydrogenase, malicodeshydrogenase), conjonctival protein metabolism (procollagen lysyl hydroxylase); in the same time, cell wall disturbances and lipidic deposits are facilitate when rabbits are submitted to cholesterolemic diet.

Seventy-two consecutive patients with electrocardiographic evidence of Wolff-Parkinson-White syndrome underwent electrophysiological study (EPS). Fifty-five of these patients (76 p. 100) had episodes of tachycardia, 11 experienced palpitations or syncopes and 6 were asymptomatic. The decision to prescribe an antiarrhythmic agent was reached on the basis of the patients' symptoms and EPS data. One patient was treated by surgery before the medical treatment was tried; 17 patients were discharged without treatment, 4 were discharged with an episodic and 50 with a preventive antiarrhythmic treatment. Among these 50 patients, 46 (92 p. 100) could be followed up for a mean period of 45.7 +/- 28 months. One died of lung cancer; 43 presented with spontaneous episodes of tachycardia, 4 were able to discontinue treatment at the end of the follow-up period since they had very few symptoms and 2 were lost sight of. Among the 37 patients under antiarrhythmic treatment followed up, 29 (78 p. 100) are well controlled, while 8 (22 p. 100) still present with episodes of tachycardia. A tachycardia-reducing pacemaker was implanted in 5 of these 8 patients. It therefore appears that 78 p. 100 of patients presenting with spontaneous episodes of tachycardia associated with WPW syndrome can be controlled with an antiarrhythmic treatment. This result was obtained after trying at least two types of antiarrhythmic agents in 86 p. 100 of the cases.(ABSTRACT TRUNCATED AT 250 WORDS)

In the absence of thromboembolic risk factors, signs of thrombosis in situ, or disorders of coagulation, two possible diagnoses must be envisaged when acute recurring ischemia is observed in a peripheral area of tissue: extrinsic compression or rupture of an arterial coat, especially when the subject is young and in good general health. The case of a 35 year old patient presenting with recurring ischemia in the popliteal artery of the right lower limb due to sub-adventitial rupture of the popliteal artery suggests three comments: the period of latency (3 months) between initial trauma to the popliteal artery and the operation of reverse saphenous vein bypass, the necessity for dynamic manipulations together with angiographic and ultrasound examination, the probable underestimation of the traumatic or functional causes of this disorder (popliteal artery), and the surgical prognosis remains excellent.

A fragment of septum was removed for biopsy in 11 patients with obstructive cardiomyopathy who were undergoing surgery. Electron microscopi revealed an increase in the numbers of mitochondria, deposits of glycogen, and deforming fibrosis. As far as the components of muscle fibres are concerned, both lysis and synthesis of neosarcomeres are to be found, together with abnormalities of the Z band and disorientation of the myofibrils. The number and severity of these abnormalities were found to vary from patient to patient and also in different sections. Although these features are virtually constant in cases of obstructive cardiomyopathy, they are not specific for this condition; they are also found in cases of non-obstructive hypertrophic cardiomyopathy.

There is still a place for conservative surgery in valvular disease of the heart to the extent that artificial prostheses have not yet been perfected sufficiently for them to be regarded as the method of choice. While these conservative operations are rarely applicable to the aortic valve, techniques such as Carpentier's ring occupy an important place in the treatment armamentarium for disorders of the mitral valve, and even more so of the tricuspid valve.

The present study intended to investigate the effects of 2-[2-methoxy-4-(methylsulfinyl)phenyl]-3H-imidazo[4,5-b]pyridine (sulmazole, AR-L 115 BS) on mechanical performance of rat myocardial fibers under hypoxia, and subsequent reoxygenation. Because of a possible caffeine-like mechanism of action of sulmazole similar experiments were performed with theophylline and the results compared. 1. Under normoxic conditions, sulmazole and theophylline displayed a positive inotropic action with acceleration of relaxation at small concentrations (sulmazole: 6.4 mumol l-1; theophylline 7.35 mumol l-1). Increasing doses led to a negative inotropic effect with slackened relaxation and loss of its load sensitivity (up to 390 mumol l-1 for sulmazole; up to 350 mumol-1 for theophylline). In agreement with other reports, the dose-effect curve was shifted towards low concentrations. 2. During ischemic crisis, therapeutic doses of sulmazole (6 mumol l-1) and theophylline (7 mumol l-1) induced no additional depression of contractility and protected relaxation. During subsequent reoxygenation, better recovery of contractility was observed without any very significant improvement of relaxation. 3. During reoxygenation beyond 120 mumol l-1, increasing doses of sulmazole depressed contractility. An additional depressive effect on mechanical performance was observed during hypoxia only for the highest dose (390 mumol-1).

Pervenous atrioventricular sequential demand pacemakers (AVSDPs) were implanted in 18 patients using an atrial electrode positioned in the right atrial appendage and a ventricular electrode positioned at the apex of the right ventricle. The indications included 13 patients with the sick sinus syndrome (72%), five of whom had the tachycardia-bradycardia syndrome, three with paroxysmal supraventricular tachycardia, one with cardiomyopathy and one with carotid sinus syncope. The follow-up ranged from 6 to 38 months, with a mean of 19.4 months (a total of 350 pacing months). Seventeen patients (94%) are asymptomatic. One patient had persistent episodes of paroxysmal supraventricular tachycardia. In the remaining patients with tachyarrhythmia, pacing alone (three patients) or in combination with antiarrhythmic drugs (four patients) controlled the tachyarrhythmia. There was one displacement of the atrial electrode (5.5%). Extrusion of the pacer occurred in three patients. It is concluded from this experience that AV sequential pacing is an effective technique and may be useful in patients with sick sinus syndrome, in patients with tachyarrhythmia and/or patients with poor myocardial function. However, continued research is needed to prolong battery life and to reduce the size of the pacemaker.

The von Willebrand factor (VWF) is a link in the platelet-vessel wall interaction which plays an essential role in the response of the vessel wall to an atherosclerosis-including aggression. However, can von Willebrand's disease really prevent the development of atherosclerosis? The authors report 3 cases of young men aged 36, 40 and 51 years with atherogenic risk factors and von Willebrand's disease (two mild and one severe form). The three patients developed both atherosclerotic lesions and thrombosis. This would suggest that VWF deficiency does not protect humans from atherosclerosis.

Cell cultures of foetal rabbit aorta are cultivated with a lathyric agent (beta-amino-propio-nitrile) or with an hypercholesterolemic serum; if morphological features, in these two cases, correspond with modifications observed, in vivo, when adult rabbits are respectively submitted to the same treatment, enzymatic activities of collagen metabolism vary in opposite way. Therefore, the influence of different parameters to be studied on vascular cell functions become easier.

Various studies have established the increase of sudden death in hypertensive patients with left ventricular hypertrophy (LVH). In order to specify its most important factors, an electrophysiological study consisting of Holter recording (HR) and programmed ventricular stimulation (PVS), was performed in 24 patients with hypertension: 12 with LVH and 12 without LVH, on ultrasonography. In all patients, coronary angiography was normal. The results are the following: 1) LVH increases the ventricular vulnerability, this arrhythmogenic substrate and its stability are explored by PVS; 2) HR and PVS are not correlated, therefore HR does not explore the arrhythmogenic substrate of LVH, but rather the potential triggering factors of severe rhythm disorders; 3) it has not been possible to evaluate the role of the autonomous nervous system in this study; 4) finally, a significant correlation was found between the degree of anatomical hypertrophy of the LV and the duration of the interval AH.

21 chronic anginal patients (AP), 23 patients with an overall number of 37 aorta-to-coronary artery by-passes (ACB) underwent a regular physical training (cycle, quick or uphill walking, gymnastics). The patients were compared to themselves in the course of a calibrated effort test, performed until angina occured or the maximal cardiac rate reached.

Fibrinolytic treatments pose serious problems in subjects at high risk for hemorrhage, such as those requiring chronic dialysis. A 36-year-old patient requiring dialysis for the last 14 years due to chronic kidney failure was hospitalized for unstable angina combined with calcified mitral stricture. Prompt coronary arteriography revealed recent intracoronary thrombi. The failure of drug treatment and the surgical indication in light of unstable angina led the authors to use low-molecular-weight heparin b.i.d. for 12 days with monitoring of laboratory parameters (anti-Xa activity, APTT). No thrombotic or hemorrhagic episode was recorded. Control angiography indicating partial lysis of the left and right intracoronary thrombi led to exact evaluation of the residual underlying stenoses. A double aortocoronary bypass was subsequently performed combined with replacement of the mitral valve. This case gives a glimpse of the potential value of low-molecular-weight heparin as a valid alternative to conventional fibrinolysis in subjects requiring dialysis.

By affinity chromatography on porcine pancreatic elastase bound to Sepharose an anti-elastase antibody was isolated from the serum of rabbits who had been injected with porcine pancreatic elastase and fed a light cholesterol diet. The protein (molecular weight 150,000 daltons) was recovered with both a high degree of purity and intact biological properties. It specifically inhibited elastolysis by a mechanism distinct from that known elastase inhibition by alpha 1 antiprotease and alpha 2 macroglobulin. Results of this study indicate that inhibition is due to an IgG antibody to the porcine elastase. The antigen-antibody reaction appears to involve the active site of elastase. The isolated IgG in turn binds to activated Sepharose and the resulting immunoadsorbent system allows purification of pancreatic elastase by affinity chromatography.

The platelet function, fibrinogen level, and the various lipid fractions were studied in 17 coronary patients before, during and after a maximal effort, both before and after a three month period of physical training. Exercise capacity increased by 26%, stickiness went down by 27% at rest (p less than 0.025) and 42% on exercise (p less than 005), and aggregation varied (according to the method used) between 24%, 25% and 2% at rest (p less than 0.001) and 36%, 43% and 32% on exercise (p less than 0.001); the levels of fibrinogen and the lipid fraction remained unchanged. A patient whose exercise capacity was not increased by training had no alteration in platelet aggregation. According to this small series, physical training has an effect similar to that of acetyl salicyclic acid. The possible significance of these results is discussed.

Evaluating the cost of coronary artery disease is difficult because it must take into account not only the cost of the disease process itself, but also that of prevention and research. 1. The cost of the disease process itself may be assessed by: a) an analytical study of the real cost of diagnostic and therapeutic procedures; b) a synthetic study of the procedures according to the clinical forms of the disease. Although this task is simple for a given patient, extrapolation of the results to a whole group of patients is more aleatory; c) an epidemiological study of the different forms of coronary artery disease: although global data is available the absence of a coronary artery disease register makes this a difficult problem; d) an evaluation of the socio-professional repercussions of coronary artery disease with integration of the cost and loss in gross national product. 2 The cost of prevention can be assessed by taking the following factors into consideration: a) cost of individual primary prevention which poses the problems of check-up examinations; b) cost of community primary prevention; c) cost of research including fundamental research on the atheromatous process and myocardial ischemia plus clinical research such as secondary prevention enquiries. In conclusion, it appears that: --it is difficult to determine the cost of coronary artery disease without a specialist register; --the cost of coronary artery disease should be considered from positive (source of economic activity) and negative points of view (socio-professional repercussions); --a reduction in the cost of coronary artery disease requires a deeper understanding of the disease, better prophylaxis and socio-professional rehabilitation, and improved organisation of exciting health structures.

Poor effort tolerance is observed in a small percentage of cases of idiopathic mitral valve prolapse (IMVP). The aim of this study was to assess the possible left ventricular dysfunction in such cases, responsible for poor effort tolerance. Left ventricular function and segmental wall motion were studied retrospectively in a group of 17 patients with IMVP. The patients, average age 53 +/- 12 years, had poor effort tolerance (ST segment depression of 2 to 4 mm in 15 cases, drop in blood pressure in 6 cases) justifying catheter and angiographic studies. All patients had IMVP confirmed on RAO left ventriculography. There was no associated mitral regurgitation or coronary artery disease. Left ventricular function was studied by parameters of global function (systolic and diastolic parameters, volume measurements) and by a quantitative study of segmental wall contraction. The method used for studying regional wall motion was an application of the Stanford method in which segmental shortening is studied over all the endocavitary contour of the LV during an angiographic cycle filmed at 50 frames/second in the RAO projection. The time and velocity amplitudes of wall motion were measured during systole and diastole. The same methodology was applied to 21 normal control subjects. The results showed abnormal volumic compliance and wall motion in the IMVP group. Asynergy was mainly confined to the antero-lateral wall of the LV. The amplitude of contraction was generally normal but the contraction was slower and finished earlier. In the same zone, relaxation was abnormally early and lasted longer.(ABSTRACT TRUNCATED AT 250 WORDS)

Elastase was purified from an acetone-ether powder of porcine pancreas by a one step affinity chromatography procedure on IgG-Sepharose 4B. The IgG was derived from a rabbit immunized with porcine pancreatic elastase and was itself isolated by affinity chromatography on elastase immobilized on the same matrix. The column was calibrated with a known elastase preparation under standardized conditions. Direct isolation of elastase from pancreatic extracts yielded approximately 90 mg from two pancreas. The enzymatic activity and electrophoretic migration in SDS-polyacrylamide gel of the purified elastase were equal to those of the purest commercially available enzymes. Application of this method to aorta of young pigs suggests the presence of active elastase in the aorta.

The authors report the haemodynamic changes observed during isometric stress corresponding to 30% of the maximum isometric effort, sustained for 3 minutes, in 22 normal subjects and 12 patients with cardiomyopathy. Echocardiographic study of the left ventricular diameters of 10 cardiac patients completes the work. The heart rate in normal subjects during effort increases by 45 +/- 30%, and the flow by 30 +/- 24%. The blood pressure is raised by +/- 25 +/- 8 mmHg, without significant change in the left ventricular end-diastolic pressure (less than +4 mmHg), or in peripheral resistance. The external work of the left ventricle increases by 75 +/- 41%, demonstrating an increase in the inotropic state of the myocardium. Max. vec. and the various indices of contractility are increased on average by +8.29 +/- 4.55 28 c/s. Adaptation to the increased pressure brings into play only the contractile reserve of the myocardium.

The antiarrhythmic efficiency of quinidine arabogalactan-sulphate (QAGS) and disopyramide were determined in 38 patients showing chronic, stable frequency premature ventricular beats (PVB). The study which was carried out in 4 medical Centers, used a longitudinal cross-over design. After a baseline evaluation which consisted of two 24 hours electrocardiograms, the patients were randomised to one of the two drugs during a period of 6 or 7 days. The drug sequence were followed by a placebo sequence. A 24 hours electrocardiogram was performed at the end of each sequence. The daily doses were equivalent to 660 mg of quinidine base for QAGS and 600 mg for disopyramide. Among the 38 patients who entered in the study, 32 went through each sequence of the test. The average number of PVB was significantly reduced by QAGS and disopyramide (p less than 0.0001). With QAGS 18 patients had more than 65 p. 100 reduction of PVB and 12 of them more than 80 p. 100. With disopyramide, 14 patients had more than 65 p. 100 reduction of PVB and 12 of them more than 80 p. 100. There was no statistical difference in the overall efficiency of the two drugs. Three patients died, one from myocardial reinfarction, one from ventricular fibrillation; in one other case, the cause of the death remained undetermined. QAGS was better tolerated than disopyramide; adverse effects occurred in 6 patients with QAGS and in 10 with disopyramide. The responsibility of disopyramide in the occurrence of two severe ventricular arrhythmia may be questioned.

The alterations observed in connective tissue of the arterial wall and dermis in atherosclerosis incited us to investigate collagen metabolism in patients with coronary disease. We first studied collagen metabolism in fibroblast cultures, then measured serum levels of type III procollagen aminoterminal peptide. Fibroblast collagen metabolism was investigated in 12 consecutive patients of less than 45 years of age presenting with coronary disease and coronary atherosclerosis was found to be preserved in patients with atherosclerosis, but less type III type I procollagen was synthesized (14.6 +/- 6.6% versus 22.3 +/- 4.3%). This abnormality, found in 83% of our coronary patients, seemed to be unrelated to risk factors or to the severity of atherosclerosis. Serum type III procollagen aminoterminal peptide was assayed comparatively in 36 patients with coronary atherosclerosis confirmed at coronary-ventriculography and in 35 patients free from coronary disease as defined by the W.H.O. criteria. Serum levels of this peptide were significantly higher in patients with coronary atherosclerosis (26.76 +/- 16 ng/ml) than in controls (10.43 +/- 3.18 ng/ml). 61% of coronary patients had a peptide level higher than the normal value (17 ng/ml). No correlation was found between this rise in type III procollagen aminoterminal peptide and the severity of coronary lesions or the importance of risk factors. Thus, collagen metabolism is altered in coronary patients, and this alteration can be detected by a peripheral marker. However, the use of this marker to diagnose the presence or evaluate the course of atherosclerosis requires clarification.

Erythrocyte filterability has been studied in 80 patients (44 men and 36 women) with recent stroke (mean age of patients was 68). 200 adults were studied as reference. The filtration time is significantly higher in patients than in normal subjects (p less than 0,001). High individual variations are found in patients, in relation with the presence of cardiovascular risk factors. In conclusion, the role of erythrocyte deformability in cerebrovascular disease is discussed.

Aortic tissues consisting of all three tunics were removed from normal adult rabbits and cultured in a semisynthetic gelosed medium supplemented by 10% serum obtained either from normal or hypercholesterolemic rabbits. Fibrillar cross-striated aggregates appeared with a high frequency (50%) in the extracellular space of explants cultured from four to eight days in medium supplemented by serum from hypercholesterolemic rabbits, but did not appear in explants cultured in serum from control animals (3%). The electron-dense segment was ruthenium red positive and digested by testicular hyaluronidase. The electron-lucent segment, composed of ruthenium red negative thin filaments, was not modified after hyaluronidase treatment but was strongly digested after collagenase treatment. It is believed that this material was fibrous long spacing collagen synthetized under culture conditions, as shown after tritiated proline incorporation.

10 control subjects and 27 patients with prosthetic valves (15 with Björk aortic valves, 6 with mitral prostheses, 4 with aortic and mitral valves, 1 with a Björk mitral and a Starr aortic valve, and 1 with a Beall mitral valve) underwent, at intervals of 24 hours, two maximal exercise tests, initially without (day J) and subsequently with (day J + 2) propranolol in a dose of 80 mg/24 h, haemolysis and platelet function being assessed immediately before and immediately after each test. Exercise tolerance was not altered by propranolol in this dose, provided the heart size was not more than 1500 ml. Haemolysis, as assessed by the level of lactic dehydrogenase (LDH1) was increased by exercise, especially in the aortic prosthesis cases in which the LDH1 was increased by 21.6% (p less than 0.025). The increase was less marked under propranolol treatment, when it was 12.3% (p less than 0.05). Propranolol did not correct the platelet clumping caused by the prosthetic mitral valves, but did decrease platelet stickiness on exercise in the patients with prostheses (delta = -11.7%; p less than 0.05). Propranolol can not therefore be recommended for increased haemolysis if there is no demonstrable dysfunction of the prosthetic valve. Neither would we advise its use at present with the aim of reducing thrombotic accidents.

Low (LDL) and high (HDL) density lipoproteins stimulate prostacyclin (PGI2) synthesis in cultured rabbit and human aortic smooth muscle cells. In this respect, the efficacy of HDL exceeded that of LDL, HDL3 being the most effective. HDL3 obtained from hypoalphacholesterolemic patients' serum had a lesser stimulative effect on PGI2 synthesis as compared with HDL3 of normolipidemic subjects. Partially purified apoprotein A-1 stimulates the metabolism of 14C-arachidonic acid accompanied with enhanced formation of prostaglandins, especially 6-keto-PGII alpha. Within a 24 h incubation in the fetal calf serum-free medium, prostaglandins I2 and E1 (1 x 10(-7) M) reduce the intracellular cholesterol level in human aortic smooth muscle cells by 30%. Total HDL fraction as well as HDL3 and HDL2b applied in combination with prostaglandins have a synergistic effect resulting in a 50% fall in intracellular cholesterol. Hypothetically, the uptake of cholesterol by HDL may include the following stages: (1) HDL interacts with the cell and activates the intracellular PGI2 synthesis probably via apo A-1 modulatory action on arachidonic acid metabolism; (2) newly synthesized PGI2 activates cholesteryl ester hydrolase leading to the formation of free cholesterol; (3) HDL takes up free cholesterol.

The present paper deals with the particular behavior of the complexes formed between pancreatic elastase and seric inhibitors in the Pig, when they were set in contact with homologous elastin. The previously known values of dissociation constants of alpha 1-antiprotease-elastase and alpha 2-macroglobulin-elastase complexes indicated they were very stable and almost irreversible. Nevertheless, our results suggest that, when the overall complexes between porcine pancreatic elastase and seric inhibitors were isolated in non drastic conditions, they might develop an elastolytic activity against elastin fibers. This result is important as regards atherosclerosis--in Human--where a destruction of elastin is involved at a early stage of the disease.