During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose ...being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.
Two cases of polymorphic ventricular tachycardia (VT) are reported in siblings: the elder sister (18 years) was admitted to hospital because of syncope and ECG showed incessant attacks of VT. There ...was no obvious cardiac disease on echocardiography or cardiac catheterisation. A second syncopal attack occurred during Holter monitoring: this showed prolonged torsades de pointe which terminated spontaneously after a few minutes. Both syncopal attacks occurred at moments of intense emotional stress. Concomitantly, the duration of ventricular repolarisation was also observed to be increased. The attacks of polymorphic VT disappeared when the atrial rhythm accelerated, for example during exercise of isoprenaline infusion. It was not possible to induce VT by ventricular extrastimulation. The arrhythmia was controlled by nadolol and propafenone or flecainide. A familial investigation revealed that a younger brother had attacks of incessant VT with a long QT interval. The mother had frequent polymorphic ventricular extrasystoles and abnormal ST-T wave changes. The association of familial ventricular arrhythmias and long QT interval is suggestive of the Romano-Ward syndrome, but in this condition the intercritical ECG is normal except for the long QT. Conversely, in benign VT, the arrhythmia disappears during atrial pacing and exercise but there have been a few reports of sudden death. Our two cases could represent an intermediary form between these two pathological entities.
The authors studied 32 patients with ventricular arrhythmias--ventricular tachycardia (VT) or frequent ventricular extrasystoles (VES) and/or runs of extrasystole and cardiomyopathy with dilatation. ...This diagnosis was retained on the following criteria: absence of angina or electrical changes in infarction, normal coronary angiography in patients over the age of 50, diffuse abnormalities of ventricular contraction on 2D echocardiography or angiography, and on the absence of organic valvular heart disease. Thirteen patients had sustained paroxysmal VT, 18 patients had runs of VT and only 8 patients had isolated VES without repetition. The arrhythmia was polymorphic in 25 patients. All possible combinations of morphology of right of left sided delay with variable axes were observed. There were 25 right sided delays and 18 left sided delays; the association of left sided delay and vertical axis was only present in 5 occasions. Twelve patients underwent electrophysiological investigations for sustained VT but the arrhythmia could only be induced by ventricular extrastimulation in 4 cases. Eight patients were investigated during VT; the arrhythmia could only be terminated easily in 2 cases. Three of these 12 patients had biventricular tachycardia. Of the 11 patients with chronic alcoholism, only 2 had sustained VT, 8 had polymorphic VES and 1 monomorphic VES. Conversely, of the 21 patients without alcoholism, 11 had sustained VT, 6 had polymorphic VES, and 4 had monomorphic VES. There was a correlation between the polymorphism of the arrhythmia and the degree of ventricular dysfunction: of the 16 patients in overt cardiac failure (EF less than 30%), only 1 had monomorphic VT; the 15 others all had polymorphic arrhythmias. Only 2 had sustained VT.
To evidence abnormality of cardiac control by the autonomic nervous system in the sudden infant death syndrome (SIDS) we retrospectively analysed the Holter recordings and cardiopneumograms of 19 ...infants (11 boys, 8 girls) of mean +/- SD age 2.3 +/- 1.5 months who had subsequently died of SIDS. Two infants were regarded as normal and the reference diagnoses in the remaining 17 infants were: apparent life threatening event (8), SIDS siblings (8) and prematurity (1). At the time of death the age was 4.2 +/- 2 months. Each of these infants was matched with three control infants in term of postnatal age, gestational age and reference diagnosis, but without SIDS at follow-up of at least one year. Nine hours of Holter recordings (9 p.m. to 6 a.m.) were analysed in term of mean heart rate and sinus oscillations waves. To differentiate between short oscillations of 4 to 6 RR, which are induced by respiration and reflect vagal activity, and long oscillations of 20 to 32 RR, which reflect both neurogenic sympathetic and vagal activity, we used a new method which measures the number and the amplitude in milliseconds of each type of oscillations. The results are expressed as the logarithm of the product of these two variables. Heart rate, correlated to age in both groups, is higher in the deceased infants group (141 +/- 14 mn and 135 +/- 15; p less than 0.05: analysis of covariance with age as an independent variable). Short oscillations, also correlated to age, are lower in the deceased infants group (3.35 +/- 0.59 and 3.65 +/- 0.61; p less than 0.05: analysis of covariance with age).
The authors report their findings in 47 cases of ventricular arrhythmias due to arrhythmogenic dysplasia. The 47 patients were selected on the presence of ventricular tachycardia or fibrillation ...associated with dysplasia affecting selectively (44/47) or predominantly (3/47) the right ventricle at angiography. In this series males were predominant (38/47, 81 p. 100), familial incidence was high (13/47, 28 p. 100) and ECG abnormalities were constant. Most of the dysrhythmias (40/47) consisted of sustained ventricular tachycardia (VT) with left bundle branch block pattern (96 p. 100), occurring at the rate of 1.6 per patient on average and seldom with extreme axial deviation, as seen in post-infarction VT or VT associated with cardiomyopathy. The QRS complex was slightly prolonged (151 +/- 28 ms) and of high amplitude (2.5 +/- 1 mV on a VR, a VL and a VF leads), these values being intermediate between those of mild VT bursts and those of post-infarction or cardiomyopathy-related VT. The tachycardia was easily tippered by EP study, Intercritical Holter recordings showed frequent ventricular extrasystoles in the vast majority of cases; these were usually polymorphous and grouped into short bursts in one-half of the patients. On an 8.3 +/- 7 years' follow-up starting with the first attack of VT, it was found that only during the initial phase the spontaneous onset of VT was mediated by the adrenergic system (triggered by sports). Only 3 patients died during the follow-up period: one of ventricular fibrillation, 2 of right heart failure.
A 9 year old child was investigated for attacks of wide QRS complex tachycardia occurring exclusively during the daytime and favoured by exercise or stress, with ventricular extrasystoles of the same ...form occurring between attacks. Endocavitary investigation showed a concealed atrioventricular accessory pathway during sinus rhythm with anterograde 1/1 conduction up to 270/min; retrograde conduction was not so good with block occurring at 175/min. The spontaneous tachycardia was reproduced by catecholamine infusion: it was an antidromic reciprocating rhythm triggered by a ventricular extrasystole of identical form to that of a pure preexcitation complex and to that of the tachycardia complexes. Spontaneous termination of attacks always occurred when conduction from the ventricle to the atria stopped. The attacks could be induced by ventricular extrastimuli when they caused an increment in retrograde conduction time resulting from retrograde conduction up the nodohisian pathway and not the Kent bundle. The tachycardia could also be initiated by atrial extrastimuli providing pure pre-excitation could be obtained. In both cases, retrograde conduction of the nodohisian pathway had to be improved by catecholamines. When the patient was given betablocker therapy the attacks of tachycardia completely disappeared. The association of ventricular extrasystoles and antidromic reciprocating rhythm and their morphological identity suggest that these extrasystoles were in fact automatic activity of the Kent bundle. Escape phenomena as signs of passive automatism have been described in this conditions but, to our knowledge, extrasystoles suggesting an active automatic process have not been previously reported.
The frequency components of heart-rate variability (HRV) as evaluated by spectral analysis are now widely used as an index of the autonomic nervous system. Other parameters, such as quantification of ...asymmetric ascending and descending trends and continuous evaluation of their amplitude, could also be of value. To make these parameters available, the authors describe two new methods: (1) an algorithm to detect the sites of inversion between successive accelerations and decelerations, and to store their wavelengths, numbers and amplitudes; and (2) an adaptive demodulating method based on a sinusoidal function sampled by the RR series. Instantaneous phase and amplitude deviations between the predicted model and the real value give access to the modulation of each frequency studied. For comparison with classical spectral analysis, data were averaged over buffers. Correlations were good for fast and slow variations, but higher for fast ones.< >
For a period of 20 months, 50 consecutive infants (mean age: 11 months) were given Diphemanil (atropine like synthetic drug) for reflex symptomatic bradycardia of probable vagal origin. Treatment's ...results were evaluated with the study of oculo-cardiac reflex (OCR) and Holter monitoring performed before and 3 months after the beginning of Diphemanil. If tolerance was generally good, it was not possible to demonstrate the clinical efficacy of the treatment on the whole group. However, assertive success was seen on individual cases. Holter and OCR data improved statistically. The other therapeutical means aiming at warning possible complications of the hypertonic vagal reflex were reviewed: inserting a cardiac pace-maker does not always prevent sudden death; a nodal sinus surgical selective denervation might be justified in certain exceptional cases, because of the severity of the spontaneous evolution or of the resistance to medical treatment.
Beta-blockers were used to treat 20 patients (mean age 55 +/- 12 years) presenting with severe ventricular arrhythmia on chronic heart failure (NYHA stages II to IV; mean ejection fraction 29.7 +/- ...7.8%) due to coronary disease (18 cases) or to cardiomyopathy (2 cases). Ventricular tachycardia sustained (7.6 +/- 6.3 attacks/patient) in 19 patients, unsustained in 18, monomorphous in 8 and polymorphous in 12, had been present for 12.4 +/- 18 months. In all but one hitherto untreated patient, the condition had failed to respond to amiodarone combined with a type Ia (19 patients) and type Ic (16 patients) antiarrhythmic drug. Short-term results were: 17 successes, 2 failures and 1 death due to cardiogenic shock. Fifteen patients were followed up for 14 +/- 6.7 months. Thirteen of them benefited from smaller doses of a formerly ineffective treatment; there was one failure, and one patient in whom the attacks of tachycardia, but not the numerous and polymorphous extrasystoles, were controlled by the beta-blockers suddenly died at night. The actuarial mortality rate was 11.4% as against an expected figure of 30% in such a high risk group. Although no significant changes in ejection fraction were observed, heart failure became worse in 8 patients, but it was compensated by diuretics and/or vasodilators. The effects of beta-blockers in resistant ventricular arrhythmia on heart failure suggest that an adrenergic factor is involved in the mechanism of arrhythmia. Provided treatment is progressive and its haemodynamic consequences carefully monitored, beta-blockade is well tolerated. Its effectiveness on severe arrhythmia and on mortality rate seems to confirm that it prevents sudden death by an anti-arrhythmic mechanism.
