Biomedical subjects
Publications and source records attributed to N Saoudi.
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Aortic valvular dilatation with a balloon catheter was performed in 44 patients, 20 men and 24 women, most of whom were very elderly (average age 77 years). The indication for valvular replacement had not been retained in these cases because of surgical contra-indications or a very high operative risk and in 3 cases because of patient refusal. Twenty-nine patients were in functional classes III or IV of the NYHA classification; 12 had syncopal episodes and 18 had invalidating angina. The dilatation was performed by a femoral arterial approach in 34 cases, and by a brachial arterial approach in 10 cases. MEDI-TECH catheters with 15, 18 or 20 mm diameters when inflated were used in the majority of cases. Several inflations lasting 10 to 240 seconds were performed in each case with balloons of increasing size. This was well tolerated in all but one patients who had a sharp syncope. The immediate results confirmed valvular dilatation. The average transvalvular pressure gradient fell from 76 +/- 25 mmHg to 30 +/- 13 mmHg (p less than 0.001). The aortic valve surface area calculated by the Gorlin formula increased from 0.5 +/- 0.18 cm2 to 1 +/- 0.42 cm2 (p less than 0.01). After dilatation the gradient was less than or equal to 40 mmHg in 37 cases; aortic valve surface area was greater than or equal to 1 cm2 in 14 cases and less than or equal to 0.7 cm2 in only 5 cases. The left ventricular ejection fraction increased immediately after valvuloplasty from 44 +/- 16 p. 100 to 49 +/- 15 p. 100 (p less than 0.01). In the 18 cases in which it was less than 40 p. 100 before valvuloplasty, it increased from 30 +/- 6 p. 100 to 36 +/- 9 p. 100 (p less than 0.02). Residual aortic regurgitation was only observed in one case. Two patients died in the hospital period (4.6 p. 100). There were no other serious complications. During an average follow-up period of 60 days (3 weeks to 6 months) there was a big improvement in symptoms in the great majority of cases and, in particular, syncopal and anginal attacks disappeared. Only 4 patients remained in functional classes III or IV after valvuloplasty. Percutaneous aortic valvuloplasty is a new, relatively simple, low risk, economic and very effective therapeutic procedure in all cases in which aortic valve replacement is contra-indicated or refused by the patient.(ABSTRACT TRUNCATED AT 400 WORDS)
Few studies have dealt with the effects of isoproterenol on ventricular parasystole. Intravenous isoproterenol (2 to 4 micrograms/min) was administered to 11 nonmedicated patients with ventricular parasystole. At the onset of the drip infusion, 8 patients had continuous parasystole, 2 had intermittent parasystole, and 1 patient (in whom intermittent parasystole was documented 2 to 5 days earlier) showed no manifest parasystolic activity. In all patients, whose control parasystolic cycle length varied between 960 and 2,530 ms, isoproterenol caused a decrease of the parasystolic cycle lengths ranging from 12 to 36%. Therefore, isoproterenol produced a consistent increase of the parasystolic rate. In 4 patients, parasystolic activity ceased to be manifest when the concomitantly enhanced (by isoproterenol) sinus cycle lengths became shorter than 430 ms. This phenomenon reflected a tachycardia-dependent parasystolic concealment, presumably as a result of interference in the parasystolic-ventricular junction. In every case, the arrhythmia reappeared at its initial rate upon stopping the drip infusion. In no patient did parasystolic ventricular tachycardia develop. In the patient without manifest parasystolic beats, isoproterenol unmasked the intermittent parasystole that previously had been intrinsically manifest. The latter effect reflected a true exposure, or unmasking of a latent, rate-independent concealed, parasystolic focus.(ABSTRACT TRUNCATED AT 250 WORDS)
There seems to be a high risk of reobstruction after local fibrinolytic therapy in myocardial infarction because the severity of the residual stenosis. However, it is quite common to observe a significant improvement of these stenoses at follow-up coronary angiography. Also, one may demonstrate a patent coronary artery after initial failure of the recanalisation procedure. The aim of this research was to study objectively the outcome of the residual coronary stenosis after intracoronary fibrinolytic therapy during myocardial infarction. The degree of stenosis expressed as a percentage reduction of the average diameter of the vessel measured in two perpendicular incidences was assessed immediately after initial fibrinolytic therapy, and at 15 days and 3 months' follow-up. The study group of 31 patients was divided into two subgroups: group I (16 patients) with successful revascularisation and a patent vessel at the first control; and group II (15 patients): unsuccessful revascularisation or with reobstruction at the first control angiography (2 cases). The coronary angiographies were interpreted by an observer who had no knowledge of the patients or of the order of the investigations. In group I, the degree of stenosis decreased from 74 +/- 18 p. 100 to 64 +/- 16 p. 100 (p less than 0.05) at the first control, and then to 47 +/- 24 p. 100 (p less than 0.001) at the second control (less than 50 p. 100 in 7 cases).(ABSTRACT TRUNCATED AT 250 WORDS)
Using a three part model of canine false tendon in which an inexcitable gap intervenes between the proximal and distal region of Purkinje fibers, Jalife and Moe recently individualized a biological model of parasystole and showed how the electrotonic depolarization can modulate, entrain or annihilate pacemaker activity. We report the ECG of 9 patients with parasystole (as assessed by the direct recording of ectopic cycle length) in which the early nonparasystolic beats delayed whereas the late shortened the parasystolic cycle length. The phase response curve is specific for a given patient. In two cases a nonparasystolic impulse falling at a critical point in the ectopic cycle length was followed by the suppression of any parasystolic activity on the surface EKG. The recently described phenomenon called pace maker annihilation is thus discussed.
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We studied the electrophysiological effects of clonidine in 10 patients (mean age, 69 years) without sinus dysfunction or atrioventricular block. An endocavitary study was performed with two multipolar catheters, one to record and stimulate the right atrium, the other to record the His bundle potential. The stimulations were delivered by an orthorhythmic stimulator. Clonidine, 150 micrograms, was injected intravenously over 10 min. The usual electrophysiological parameters for studying atrioventricular conduction and sinus function were measured under basal conditions, between the 10th and 25th min, and between the 25th and 40th min following the onset of the injection of clonidine. Sinus cycle length, maximum corrected sinus node recovery time, estimated atrio-sinoatrial conduction time, and premature atrial stimulation-response curve were not influenced by clonidine. There were also no changes in conduction interval, anterograde conduction point, effective refractory period of the atrioventricular node, and intraventricular conduction time. We conclude that intravenous clonidine does not change the electrophysiological parameters in man.
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