[Idiopathic ventricular extrasystole : right ventricular parasystole not protected from the sinus rhythm?].
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Biomedical subjects
Publications and source records attributed to R Slama.
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The diastolic (Vd) and systolic volumes, the average free wall diastolic thickness (hd) and left cardiac cavity pressures were determined in 25 subjects using monoplan angiography. Ten subjects presented a normal angiogram (NA), 5 a myocardiopathy with predominant dilatation (MCD), 4 a myocardiopathy with predominant non obstructive hypertrophy (MCH), and 6 a volume overload (VO). All the subjects had a normal coronary-cineangiogram. Myocardial volume (Vw) and systolic thickness were calculated from hd and from end-diastolic and end-systolic internal dimensions. The degree of myocardial hypertrophy was estimated from the value of Vw/Vd. The directional components of the total systolic elemental power due to thickening (average radial power : Pr) and to midwall circumferential shortening (average equatorial power : Pe) were calculated for each subject. Patients with NA, with MCD and with VO presented a positive linear correlation between Pr/Pe and Vw/Vd (r = 0.90). Patients with MCH were clearly below the regression line defined by the other groups. This relationship suggests that the contribution to the total power due to the thickening component is greater with increasing cardiac hypertrophy, except in the case of subjects showing an "inappropriate" hypertrophy.
The authors describe the analysis of a case of atrial flutter with a slow ventricular response, the block being 9:2 with a first RR interval measuring between 3 and 4 PP intervals and a second RR interval between 5 and 6 PP intervals, the second of the 2 RR intervals being exactly 9 PP intervals. The only possible explanation of this sequence is firstly a 3:1 intranodal block (Wenckebach 3:2 in the central zone N of the node and 2:1 block at the nodo-hisian junction) followed by a 3:2 infra- or intra-hisian Wenckebach phenomenon. The His bundle recordings during flutter confirmed this hypothesis with the recording of a 3:2 block after the H potential. When sinus rhythm was restored at atrial level, the intrahisian conduction defect persisted (2:1 or 3:2 Wenckebach block).
The authors report a case of arrhythmogenic right ventricular dysplasia in a 61year old male with a 9 year history of recurrent ventricular tachycardia with a left bundle branch block configuration and without any signs of cardiac failure. A right ventricular angiography showed morphological changes suggestive of Uhl's anomaly and left ventricular angiography showed segmental wall dysfunction. In the absence of coronary artery disease, this case raises the questions of left ventricular extension of right ventricular dysplasia and of the value of left ventricular angiography in adult forms of Uhl's anomaly.
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The authors describe a case of so-called "intra-atrial reentry," associated with sinus node dysfunction. The spontaneous initiation of the tachycardia was always preceded by a sinus pause, and external atrial pacing prevented the appearance of tachycardia. Thus an atrial pacemaker was implanted, and after several months, the atrial dysrhythmias disappeared completely, despite interruption of the antiarrhythmic drugs. When a pacemaker dysfunction occurred, the sinus node dysfunction and the tachycardia reappeared. This is analogous with the "incessant" tachycardias seen in the WPW syndrome, and must be differentiated from the usual forms of the sick sinus syndrome which require both a pacemaker and antiarrhythmic drugs.
22 patients with salvoes of ventricular tachycardia were investigated electrophysiologically and pharmacologically to determine the mechanism of the arrhythmia. The appearance of the ventricular complexes was suggestive of a septal origin. The arrhythmia appeared to occur and regress within precise limits of sinus rhythm. 24 hour ECG recording and endocavitary stimulation techniques showed its essentially variable character, but occasionally a fixed coupling interval with the first extrasystole was observed, suggesting the presence of an unprotected parasystolic focus. The repetition of the extrasystolic activity, which could be triggered and terminated at will, is explained by phenomena of delayed after potentials. The results of the systematic investigation of the effects of quinidine-like drugs, beta-blockers and verapamil do not invalidate these hypotheses and show a difference of degree but not of nature between the two populations A and B of patients classified according to the quantitative character of the extrasystolic activity over 24 hours (more or less than 1000/hour). The observation of intermediate forms with simple extrasystoles and other forms with sustained tachycardia extends the significance of these results to many forms of ventricular arrhythmia.
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This paper describes a semi-automated quantitative method to evaluate left ventricular overall and regional wall motion. Left ventricular (LV) outlines are digitized on a frame-by-frame basis using a sonic graf/pen interfaced with a 9845 HP minicomputer. A high fidelity simultaneous LV pressure recording is also digitized. The overall myocardial pump and muscle function are expressed by the projections of the pressure-volume-flow and of the mid-wall equatorial stress-length-velocity relationships. The dynamic regional wall motion is quantitated using a radial coordinate method. The centers of mass of serial frames are superimposed, and the apical anti-clockwise rotation is corrected. The regional wall motion (RWM) and the rate of change of the RWM are calculated with this method, and the results plotted as a single hard copy output. This method permits evaluation of the effect of segmental wall dysfunction on total cardiac performance during different portions of the cardiac cycle. The relationships between the time course of LV pressure and stress and the dynamic RWM can also be studied in subjects with segmental contraction abnormalities.
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An angiographic study, combined with the determination of coronary flow (thermodilution) and of coronary arteriovenous difference was performed in 10 patients with coronary artery disease under basal conditions and following an infusion of trinitroglycerine. The following changes were noted under the influence of trinitroglycerine: significant fall in left ventricular telediastolic pressure (40%), telediastolic volume (18%), telediastolic strain (53%), mean aortic pressure (11%) and mean systolic strain (21%). Significant increase in ejection fraction (8%), mean shortening (Vcf: 22%) and thickening (Vep: 22%) rates. Significant fall in coronary flow (11%) without any change in coronary arteriovenous difference. Decrease in myocardial oxygen consumption parallel to the reduction in mean systolic strain. These results indicate that the essential mechanism of haemodynamic and metabolic action of trinitroglycerine is located at the level of "load", in particular "preload".
The electrocardiograms of 100 patients with rapid and regular PP intervals during atrial arrhythmias (because of atrial tachycardia or flutter, or pacing) were examined for periods of irregular atrioventricular conduction. This irregular conduction corresponds to an alternating Wenckebach phenomenon, of a type that can be determined from simple rules. The different types of conduction encountered in different patients and the changes seen in the same patient suggest that the atrioventricular node functions physiologically with 3 levels of sequential block. The different prevalence of the 2 types of alternating Wenckebach block may reflect functional differences at the level of the atrioventricular node.
The treatment of paroxysmal tachycardia by the use of permanent pacing to prevent or terminate attacks is discussed. The series comprises 18 patients with follow-up periods ranging from 1 to 12 years. In 6 cases the indication for pacing was atrial tachy-arrythmias favourised by bradycardia (5 of whom had vagally- induced atrial arrythmias). The atrial pacemaker successfully prevented attacks in 4 out of 6 cases. Three cases of chronic reciprocating tachycardia were successfully treated by simultaneous atrial and ventricular pacing or using sequential pacing with a very short P-R interval. Eight cases of paroxysmal orthodromic reciprocating tachycardia in the WPW syndrome were paced: in 5 cases pacing was employed to terminate attacks by atrial (3 cases) or ventricular (2 cases) stimulation, in the other 3 cases pacing was used to prevent the bradycardia which favourised the initiation of tachycardia. Good results were obtained in all 8 cases. Ventricular stimulation was used to terminate attacks in one patient with refractory ventricular tachycardia but the patient had a sudden death probably caused by the pacemaker. The place of these different pacing techniques with respect to medical treatment and specialised arrhythmia surgery is discussed.
34 patients aged between 17 and 62 years underwent triple valve replacement, 14 of whom exclusively with Starr-Edwards prosthesis; 25 patients were operated at Stage III and 4 at Stage IV of the NYHA classification; the operative mortality was 14%, the late mortality 21%. The actuarial survival curve shows 66% survival at 5 years; in all, 21 good results were obtained with a follow-up ranging from 3 months to 11 years (average 41 months). A notable late complication specific to these patients was dysfunction of the tricuspid prosthesis; a gradient across the tricuspid prosthesis was observed in 14 postoperative catheter studies; one of these patients had to be reoperated for thrombosis of a Starr-Edwards tricuspid prosthesis. Analysis of the results of this series suggests that surgery is beneficial, especially when the very precarious preoperative state of these patients is taken into consideration.
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