[Function and dysfunction of the sinus node].
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Biomedical subjects
Publications and source records attributed to C Barnay.
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Direct recording of the sinus node potential in the bipolar mode using two electrodes of a quadripolar recording catheter positioned in the region of the sinus node at the junction of the superior vena cava to the right atrium was performed in 24 patients. Asynchronous overdrive atrial pacing was carried out using Strauss 'technique. Pharmacological denervation was carried out using intravenous propranolol (0,02 mg/kg) and atropine (0,04 mg/kg) using Jose's technique. An intravenous injection of a bolus of 20 mg of ATP was given in 3 cases. The sinus potential was identified by morphological criteria and confirmed after carotid sinus compression and atrial extrastimuli to exclude artefacts, especially the end of ventricular repolarisation of the preceding complex. The sinoatrial conduction time measured directly under basal conditions was considered normal when within 80 to 150 ms. Direct measurement of the sinus potential in the diagnosis of sinus node dysfunction seems to be less useful than the indirect techniques. On the other hand, it does confirm the diagnosis of sinoatrial block: five cases of special interest are described; in four cases the degree of sinoatrial block was variable: a significant increase of sinoatrial conduction time under basal conditions in 1 case; paroxysmal 3rd degree sinoatrial block revealed by programmed atrial stimulation in 2 cases; 2nd degree 2/1 sinoatrial block after injection of ATP in which the direct sinoatrial conduction time and sinus node function had been considered to be normal (1 case).(ABSTRACT TRUNCATED AT 250 WORDS)
The incidence, evolution and prognostic significance of ventricular arrhythmias after myocardial infarctions were studied over a 2 year period in 144 patients (108 men, 36 women: mean age 64 +/- 2 years) by Holter monitoring on the 20th day, 6th month (104 recordings), 12th month (94 recordings), 18th month (76 recordings) and 24th month (82 recordings). A total of 500 recordings was obtained, 471 of which were of good enough quality to be interpreted. On the 20th day, the prevalence of ventricular arrhythmias was independent of the site of myocardial infarction: they were classified as follows (Lown and Wolff grading): no ventricular arrhythmias (34 patients); moderate (Grade I) arrhythmias (73 patients, 50%); severe ventricular arrhythmias (Grades 2, 3, 4, 5) (37 patients, 26%). Fourty-seven patients underwent all 5 Holter recordings, the evolution of the arrhythmias could therefore be followed in detail. Despite considerable individual variation, the overall evolution indicated a clear aggravation at 6 months compared to the recording taken on the 20th day. At the 12th month, there was a higher incidence of arrhythmias but they were of a lower grade in 72% of cases: there was a steady improvement thereafter until the 24th month with the incidences falling to those observed on the 20th day. At the end of 2 years, there were 102 survivors; 41 patients died, and one was lost to follow-up. Over half the deaths (23 cases) occurred during the first 6 months, 4 during the second, 7 during the third and 7 during the fourth 6 months. The cause of death was cardiac in 21 cases, was of other causes in 4 cases and was unknown in 16 cases. The correlation between the death rate and results of Holter monitoring on the 20th day showed: only 4 of the 41 deaths had no recorded ventricular arrhythmia, there was a moderate or severe ventricular arrhythmia in 37 cases; in these patients, the cause of death (cardiac or other) was not related to the degree of arrhythmia. These results confirm previously reported preliminary studies indicating the value of Holter monitoring on the 20th day of myocardial infarction for assessing the 2 year prognosis. Death occurred in I ou of 10 Patients without ventricular arrhythmias, in 1 out of 4 patients with a moderate ventricular arrhythmia, and in 1 out of 2 patients with severe arrhythmias (p less than 0.001). The evolution was characterised by a "critical period", the first year, during which most deaths and aggravation of ventricular arrhythmias (in survivors) were observed; during the second year, there was a progressive improvement.(ABSTRACT TRUNCATED AT 400 WORDS)
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Holter electrocardiographic monitoring and endocavitary electrophysiological investigations are often necessary in order to confirm the diagnosis of sinus dysfunction which may be suggested by the patient's symptoms and/or standard E.C.G. signs. A critical evaluation of these methods can be made on the basis of the experience gained in the course of recent studies. Provided sufficiently rigorous criteria are selected, the Holter monitor has an excellent specificity, about 90%, and a sensitivity of more than 70%. The value of the sinus refractory period reflects both sinus automatism and sino-atrial conduction; it is a sensitive criterion of sinus dysfunction. In contrast, the period of sino-atrial conduction has a much more limited sensitivity. However, analysis of the various parameters which reflect the response of the sino-atrial node to premature atrial stimulation provides important information. The authors also stress the value of the pharmacological tests used to sensitize the manoeuvres of atrial stimulation or to test the effects of the autonomic nervous system on sinus function. Autonomic blocking with a combination of atropine and propranolol can reveal certain disorders which can be masked by sympathetic activity and it can also determine the intrinsic or extrinsic nature of the sinus dysfunction. Thus electrophysiological investigations appear to be often essential in order to confirm a suspected diagnosis and in order to determine the severity and the nature of the sinus dysfunction.
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.
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The interpretation and significance of postextrasystolic responses obtained in human electrophysiological examinations of patients with sinus node dysfunction has long been a matter of controversy. We carried out programmed atrial stimulation by the method of Strauss et al. in 54 patients with sinoatrial disorder, before and after pharmacologic autonomic blockade (with propranolol 0.2 mg/Kg and atropine sulfate 0.04 mg/Kg intravenously). There were two responses, as follows: computable sinoatrial conduction times and chaotic patterns. Patients were divided into groups on the basis of their intrinsic heart rate (IHR). If the total estimated sinoatrial conduction time over greater than or equal to 200 msec and greater than or equal to 147 msec after autonomic blockade and chaotic pattern were considered to be pathologic, so the ratio of abnormal parameters decreased from 73 to 44% in patients of normal IHR, and increased from 70 to 90% in patients of abnormal IHR. The latter 90% was mostly to the expense of the incalculable chaotic patterns. Interpreting a postextrasystolic curve, the existence of reset zone refers to the functional integrity of the sinoatrial node, to the organisation and synchronism of sinus potentials, which depends on the balance of autonomic nervous system and on the intrinsic electrophysiological integrity of the pacemaker cells.
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The interpretation of post-extrasystolic parameters and their significance is discussed. Programmed extrastimulation according to Strauss was carried out in 49 cases, before and after atropine and propranolol administration. The result was a computable sinoauricular conduction time (SACT), a chaotic picture, or an ascending line without plateau. The patients were selected on basis of their intrinsic heart rates (IHR). If the total SACT exceeded 250 ms, the chaotic post-extrasystolic picture and the ascending 1st phase without plateau were considered pathologic, then after drug testing the ratio of pathologic parameters decreased from 54 to 22% in cases with normal IHR. Including cases with pathologic IHR the ratio increased from 55 to 90%, especially in asynchronous chaotic pictures. After drug testing the chaotic forms were always replaced by a plateau in cases with normal IHR, but in pathologic ones the chaotic picture appeared to be a dominant electrophysiological parameter. It follows that the autonomous nervous system has its part in the development of chaotic post-extrasystolic pictures. A plateau in the post-extrasystolic curve could mean a functional organization and synchronism rather than a conduction disturbance; to the latter a high-level plateau would correspond.
In certain cases because of sinus arrhythmia and/or anarchic return and postreturn cycles caused by premature atrial stimulation, the sinoatrial conduction time cannot be calculated since a chaotic postextrasystolic pattern appears. We examined 49 patients with a history and ECG signs suggesting sinus node dysfunction by programmed extrastimulation method as proposed by Strauss et al. prior to and after pharmacologic autonomic blockade (with propranolol 0.2 mg/kg body weight and atropine sulfate 0.04 mg/kg intravenously). Patients with normal intrinsic heart rate (IHR) (n = 31) showed chaotic postextrasystolic responses in 38%, which in every case could be eliminated by autonomic blockade, resulting in a clear I and II phase with a well estimated intrinsic conduction time. Patients with pathologic IHR (n = 18) gave chaotic responses in 22% which after drug testing increased up to 72%. The chaotic postextrasystolic patterns are to be interpreted as the desynchronization of the sinus potentials, while plateau (phase II) as functional integrity, synchronized activity of the sinus node, dependent on the momentaneous balance of the autonomous tone, and on the integrity of the pacemaker cells. The desynchronized chaotic responses are considered on one hand as a dystonic neurovegetative electrophysiologic characteristic, on the other hand as a primary extrastimulation parameter of the intrinsic sinus node dysfunction.
To study the diagnostic possibility and the mechanisms involved in sinus node dysfunction, 23 patients with sick sinus syndrome were evaluated by the basic electrophysiological method (recovery times, secondary postpacing phases, sinoatrial conduction times) before and after pharmacologic autonomic blockade with i.v. propranolol 0.2 mg/kg and atropine 0.04 mg/kg, and by continuous rhythm monitoring. Patient groups of normal (I) and pathological (II) intrinsic heart rate (IHR) were compared. In group I (no. 15) prolonged recovery time (2/15), postpacing sinoatrial-block (1/15) and chaotic postextrasystolic patterns (5/15) ceased after autonomic blockade; we obtained normal intrinsic recovery time, gradual return to the stable intrinsic sinus cycle length in the secondary phase, and a normal intrinsic sinoatrial conduction time. In group II (no. 8) during the control study only 50% of patients had pathological electrophysiological parameters before, and 100% after the drug test (no gradual postpacing return to the intrinsic heart rate, abnormal recovery times, abnormal sinoatrial conduction times or chaotic postextrasystolic patterns). Holter monitoring revealed significant differences between the minimal heart rate during sleeping (group I: 48 +/- 10 bpm, mean +/- SD group II: 32 +/- 4 bpm, probability less than 0.001) as well as in the average sinus cycle length for 24 hours (group I: 848 +/- 88 ms, group II: 1254 +/- 136 ms, P less than 0.001) with a very characteristic histogram. In the patients with pharmacologically and electrophysiologically documented abnormal intrinsic rhythmicity (group II), the first 24 hour Holter monitoring revealed positive ECGs for sinus node dysfunction. In patients with normal intrinsic electrophysiological sinus node properties (group I) repeated continuous rhythm recordings revealed severe sinus bradycardia (1 patient), sinoatrial-block (1 patient), tachybrady syndrome (1 patient) and sinus-arrest (2 patients, up to 29 120 ms in waking period). These findings suggest that 1) IHR is the best and simplest diagnostic method of intrinsic sinus node dysfunction (in patients of abnormal low IHR we found positive electrophysiological and Holter parameters), and 2) in autonomic sinus node dysfunction electrophysiological parameters are essentially negative showing normal intrinsic sinus node function; in these patients systematically repeated Holter monitoring is the most valuable diagnostic method.
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The sympathetic and parasympathetic neurological cardiac effects were blocked with atropine and propranolol. The intrinsic heart rate (IHR) was determined and rapid atrial pacing (RAP) was carried out before and after administration of the drugs. The primary and secondary postpacing parameters were examined in both circumstances. Normal (n = 31) and pathological (n = 20) cases were differentiated on the basis of the IHR. In the secondary phase (PPC 2-10) after autonomic blockade returned to the basic frequency was of exponential character in the great majority of normal IHR cases. Anomalies may appear in both the primary and secondary phases. They are of different types: one of them concerns the recovery time; another electrophysiological anomaly occurs when there is no return to the predrive normal cycle length after pharmacological neurotomy. In the secondary phase there may appear sinoauricular blocks. They may depend on or appear independently of the effect of the vegetative nervous system. The new test allows a physiopathological classification of normal and pathological sinus node function.
The concept of sinus node disease is defined by a group of clinical and electrocardiographic features related to sinus node dysfunction whatever its mechanism; the organicity of the disease can be proven if total or subtotal histological alterations of the sinus node are demonstrated. The most typical symptoms are neurological (syncopes and dizziness). Sinoatrial block, sinus arrest, sinus bradycardia or bradyarrhythmia, and the bradycardia-tachycardia syndrome are the most usual electrocardiographic aspects. The diagnosis is often rendered difficult by the usually intermittent and frequently nonspecific character of the symptoms and of the ECG signs. Holter monitoring is often essential to resolve these difficulties. If the diagnosis remains dubious, the use of electrophysiological methods is necessary: direct recording of the sinus nodal intracardiac potential can now be added to the classical rapid and premature atrial stimulation, possibly complemented by pharmacological tests. Finally, therapeutic indications can be considered after a correct clinical, electrocardiographical and electrophysiological evaluation of the patient. Medical treatment alone is usually ineffective in controlling the attacks of arrhythmia and the neurological episodes. If the sinus nodal dysfunction is obvious and symptomatic, permanent pacing is the treatment of choice. Its short and medium term results are generally excellent, while the long term results, especially with regard to survival of the patients, could be improved by the most recent pacing techniques.
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Forty-five patients with Wolff-Parkinson-White syndrome (WPW) were reviewed. The preexcitation using Boineau's classification was: right anterior (six patients), left lateral (nine patients), right posterior (15 patients) and left posterior (15 patients). Normal pathway conduction was observed to occur either spontaneously or after administration of ajmaline, procainamide, or by eye-ball pressure. Disappearance of preexcitation was associated with T wave abnormalities in 39 patients (86.6%). The orientation of the T spatial vector (SAT), after suppression of the WPW aspect, varied according to the site of ventricular preexcitation. In eight patients with left lateral ventricular preexcitation (LLVP), the frontal T wave axis was between +70 degrees and +120 degrees (mean +92 degrees) and the horizontal T wave axis was located in the left anterior quadrant. In the five patients with right anterior ventricular preexcitation (RAVP), the frontal axis was between + 40 degrees and - 10 degrees (mean + 26 degrees) and the horizontal axis was in the left posterior quadrant. The 26 cases with right posterior ventricular preexcitation (RPVP) and left posterior ventricular preexcitation (LPVP) had a frontal axis between - 10 degrees and - 70 degrees (mean -39 degrees) and the horizontal T wave axis in the left anterior quadrant. This study suggests that the T wave anomalies observed after suppression of the WPW aspect are in direct relation to the localization of the preexcitation according to Boineau's classification. The analogy between the abnormalities of the T wave and those which are observed after right ventricular pacing (VP) or after disappearance of left bundle branch block (LBBB) is discussed.
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