[Atrial tachycardia after anatomic repair of transposition of the great vessels].
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Publications and source records attributed to S Kacet.
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The presence of a left bundle branch block (LBBB) may hamper the electrocardiographic diagnosis of diseases that involve the QRS complexes. That it may conceal, or even completely erase, major abnormalities of ventricular repolarization induced by certain drugs is not so well known. In this paper, two highly demonstrative examples of such abnormalities observed with bepridil (case 1) or with the amiodarone-aprindine combination (case 2) are reported. In both cases, the intermittent character of the LBBB revealed the phenomenon which deserves to be known as it is not without practical consequences: in patients under treatments likely to modify repolarization and induce severe dysrhythmias (notably torsades de pointes) the presence of a LBBB indicates that the QT and/or QU intervals must be very carefully measured. In case of phase 3 LBBB compression of the carotid sinus or intravenous ATP injection helps the diagnosis since in the presence of even moderately prolonged ventricular cycles such manoeuvres create a refinement of QRS complexes which then demonstrate the major alteration of the underlying repolarization.
At the present time, there is no satisfactory pharmacological treatment for arrhythmia or conduction disorders induced by or aggravated by vagal hypertonia. The limited duration of action of the atropine derivatives currently available justifies the development of new compounds with expected longer acting duration. The aim of this study was to compare the effects of a single blind intravenous injection of ipratropium bromide to those of atropine sulfate in 22 patients. These patients were studied with continuous Holter recordings for three days. During the second and the third nights (patient sleeping), boluses of atropine (0.03 mg/kg) and of ipratropium bromide (0.03 mg/kg), respectively, were added to a continuous saline intravenous infusion. Accurate ECG analysis allowed determination of maximal heart rate peak, timing of maximal heart rate, variations in sinus cycle length, atrioventricular conduction, and durations of drug action. A nonsuggestive questionnaire was presented to patients to detect possible occurrence of side effects. The mean maximal heart rate rose significantly (p less than 0.001) for atropine (+46.2%) and for ipratropium bromide (+57.4%). The effects obtained with ipratropium bromide on the heart rate lasted nearly twice as long as those obtained with atropine (respectively, 120 +/- 38.4 min and 70 +/- 30 min- for the pharmacological half-life). Common minor muscarinic side effects (dryness of the mouth) were noted with the two drugs. In conclusion, this comparative intraindividual study confirmed the prolonged vagolytic effects of intravenous ipratropium bromide, which may be valuable in the treatment of patients with vagally mediated automaticity and conduction disturbances.
Nicaïnoprol, a new class 1 antiarrhythmic drug was given intravenously in a dose of 2 mg kg-1 of body weight (two patients) and 3 mg kg-1 of body weight (nine patients), and the clinical, electrocardiographic and electrophysiological effects were studied. Fifteen minutes after the end of drug administration, the PR interval was prolonged by 24.4% (P less than 0.001), and the QTc by 3.9% (P less than 0.01). The prolongation of QRS duration (+6%) was not significant. There was a slight (-3.9%) but non-significant decrease of the heart rate, with no alteration in sinus node function. Alteration of atrial conduction and atrioventricular (AV) conduction were due to an increase in the PA interval (+57.4%, P less than 0.05), the AH interval (+10.9%, NS) and the HV interval (+43.8%, P less than 0.01). The anterograde Wenckebach cycle length increased by 11% (P less than 0.01). The effective and functional atrial refractory periods increased respectively by 4.5% and 11.4% (P less than 0.05), and the effective refractory period of the AV node increased by 11.2% (P less than 0.05). None of the other electrophysiological variables changed significantly. A non-significant drop in blood pressure was noted between the second minute following injection (-9.4%) and the 15th minute (-3.4%), and two patients complained of dizziness; one of these two patients reported a heat flush with an oral burning. In conclusion, nicaïnoprol seems to possess the electrophysiological properties of some other class I antiarrhythmic drugs, and is clinically well tolerated.
The recording of late ventricular potentials with high amplification cardiography (HAC) permits to identify patients presenting a risk of sudden death and ventricular tachycardia, especially in the later stage of myocardial infarction. Few authors have studied the prevalence of these potentials in other heart diseases presenting a risk of sudden death. Most series in the literature are too small to specify variations in the prevalence of these potentials according to the severity of the coronary disease. For this purpose, 835 patients including 535 coronary patients were evaluated with HAC compared to data from coronary angiography and Holter test. An automatic quantification method of the late potentials was used on 131 healthy subjects. The prevalence of late potentials is 32 p. cent after infarction, and 75 p. cent when a chronic ventricular tachycardia is present. These potentials retain their significance of tracers of ventricular arrhythmias in primary dilated myocardiopathies, with a prevalence of 25 p. cent reaching 50 p. cent in case of ventricular tachycardia. Their recording in the presence of idiopathic ventricular extrasystoles must be an indication to look for an underlying cardiopathy. It is possible to record them in other diseases especially in advanced valvular cardiopathies, as well as in right ventricular dysplasias with arrhythmia where their presence has a great diagnostic value.
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In vitro and in vivo electrophysiological studies have shown that propafenone could be classified as a class I antiarrhythmic agent. The aim of this study was to investigate the short-term antiarrhythmic efficacy and safety of propafenone in 10 patients compared to disopyramide in a double-blind randomized protocol. Included patients suffered from ventricular arrhythmias with at least 60 ventricular premature beats (VPB) per hour refractory to at least two other antiarrhythmic agents. At the end of the control period and of the two treatment periods during which patients received either propafenone (300 mg three times a day) or disopyramide (200 mg three times a day), clinical examination, Holter recordings, electrocardiogram, and clinical laboratory tests were performed. The PR interval and the QRS interval were significantly increased with propafenone, but not with disopyramide. The cQT interval was not significantly changed by either propafenone or disopyramide. Heart rate was decreased with propafenone (p less than 0.05) with no change in the diurnal/nocturnal circadian ratio variation. Heart rate was significantly decreased with disopyramide only during the day. Five of nine patients in the propafenone group and two of nine patients in the disopyramide group showed a reduction in ventricular premature beats greater than 80%. Total resolution of severe arrhythmias (repetitive events) was seen in 5 of 8 patients with propafenone; 2 of 8 with disopyramide. Adverse events, when they occurred, were mild (visual disturbances, epigastric discomfort, changes in taste perception, transient atrioventricular block with propafenone, and photophobia with disopyramide), and did not require reduction or discontinuation of study drug.(ABSTRACT TRUNCATED AT 250 WORDS)
Bleomycin is sometimes at the origin of a Raynaud's phenomenon (RP). From the literature, there does not seem to exist a dose-dependent relationship. The phenomenon occurs early or late and often is resistant to various medications. The possible physiopathological mechanisms are: direct vascular toxicity, hypersensitivity vascularization, alteration of platelets activity, alteration of Willebrand's factor, and as predisposing factors: association to periwinkle alkaloids or hypomagnesemia.
High amplification electrocardiographic recording of ventricular late potentials was introduced a few years ago and seems to be a simple, reliable and reproducible method to identify patients at a high risk of sudden death and ventricular tachycardia, principally during the chronic phase of myocardial infarction. However, few authors have studied quantitatively the prevalence of late potentials in patients with ventricular tachycardia compared with a sufficiently large sample of healthy subjects. In this study 34 patients with sustained ventricular tachycardia (11 women, 23 men, mean age 58 years) and 131 healthy subjects (29 women, 102 men, mean age 29 years) underwent high amplification time-averaged ECG recording, and an algorithmic analysis of the tracings was conducted, using the Simson method. Three numeric parameters were used in the interpretation of the tracings: HFRMSA = mean RMS amplitude of the last 40 milliseconds of QRS; HFD40 = delay in signal decrease from amplitude 40 mu v to baseline, and delta QRS = difference in QRS duration with 0-250 Hz and 25-250 Hz filterings. Normal values, as determined from measurements in healthy subjects, were: HFRMSA above 27 mu v, HFD40 below 35 ms and delta QRS below 13 ms. Late potentials were present when at least one of these criteria was positive. When these norms were applied to patients with sustained ventricular tachycardia the prevalence of late potentials was 76%, rising to 90.4% in the subgroup of 21 patients with coronary disease. With the method thus defined the specificity for each criterion taken separately is 97.5%. According to the norms, only one control subject (0.8%) gave a false-positive result.(ABSTRACT TRUNCATED AT 250 WORDS)
A case of left intraventricular thrombus, developed from a myxoid mitral valve and revealed by embolic cerebral vascular accidents at the end of a pregnancy, is reported. The links between a mitral valve prolapse and cerebral vascular accidents of embolic origin are studied during pre- and post-partum periods, where coagulation alterations are reviewed. It appears that, in pregnant women with a mitral valve prolapse, there is a maximum risk of developing an intra-cardiac thrombus in the last four weeks of pregnancy or immediately after delivery; this justifies, during that time, a thorough sonocardiographic monitoring.
We are reporting a case of malignant pheochromocytoma surgically treated initially for an isolated left pararenal localization, and which recurred several years later accompanied with numerous metastases. Despite of a treatment with Iodine 131 MIBG, the evolution was rapidly fatal with a picture of cardiac failure. This cardiac involvement would be linked to a myocarditis directly secondary to the catecholamines and causing a marked increase of the free fatty acids concentration in the heart tissue. In reference to this case, all the data which may tend to suspect the malignant nature of a pheochromocytoma, present in 10 p. cent of the cases, are successively reviewed. There is no clinical specificity. The presence of a mixed secretion with marked urinary dopamine secretion, would not present, for all authors, the same criteria of specificity. Thoraco-abdominal scan and scintigraphy with iodine 131 MIBG are the two tests permitting to demonstrate, with a great sensitivity and specificity, an extra-adrenal localization, which is the best argument in favor of a malignancy since 30 to 40 p. cent of extra-adrenal pheochromocytomas are malignant, more especially as the metastases are located in areas where there are no embryonic remnants of tissues containing chromaffin cells. This permits to appreciate the difference between a non-malignant multicentric pheochromocytoma and a malignant pheochromocytoma. The ideal treatment of a malignant pheochromocytoma rests on surgery under the condition that there are ony one or two metastases. This procedure is preceded by a sodium nitroprusside preparation and followed with an alpha-blockers treatment. In case of multiple metastases, the therapeutic use of iodine 131 MIBG seems to be a tempting alternative.
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The decision of whether or not to treat a ventricular extrasystole depends in the first instance on the benign or severe nature of the disorder, and on whether there is subjacent cardiopathy. The results of 24-hour Holter monitoring, exercise tolerance tests and clinical and echographic examinations will define the pathological character of a ventricular extrasystole and will indicate any subjacent cardiopathy. Electrophysiological exploration with programmed stimulation should be reserved for so-called lethal cases of arrhythmia, such as attacks of sustained ventricular tachycardia. Ischemic cardiopathy is by far the most frequent cause of ventricular extrasystoles. The two major risks of sudden death after myocardial infarction are due to left ventricular dysfunction and repetitive and/or complex ventricular extrasystoles, as well as to attacks of ventricular tachycardia. Heart patients presenting these disorders must receive urgent treatment with antiarrhythmics. Isolated, monomorphic ventricular extrasystoles are also treated in heart patients at risk if their frequency is greater than 10 per hour, measured by 24-hour Holter monitoring. In the absence of subjacent cardiopathies, the therapeutic indications are much less well defined. Approximately five per cent of subjects in a normal population present ventricular extrasystoles, the frequency of which, however, rarely exceeds 100 per 24 hours. Repetitive phenomena are only seen in 10 per cent of cases. Attacks of ventricular tachycardia are almost never seen. Ventricular extrasystoles that develop in apparently normal hearts, but which do not fulfill the above criteria, can be considered abnormal. Nevertheless, there is no categorical proof that these ventricular extrasystoles represent any risk, notably of sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
After having reported the case of a pheochromocytoma associated to Recklinghausen's disease, the authors define the best criteria of detection and localization of the pheochromocytoma and study its association to phacomatoses. Headaches, bouts of tachycardia and excessive inappropriate diuresis are the most evocative clinical signs of a pheochromocytoma. The different hormones and their urinary metabolites must be titrated separately and repeatedly. Two other examinations, scanner and scintigraphy with MIBG, visualize quite reliably the tumor foci. Calcium inhibitors are quite effective in sudden blood pressure rises. The association described here, may be explained by the fact that the two pathologies belong to the group of neurocristopathies.
There are relatively few reported studies of continuous electrocardiographic recordings by the Holter method in children. We report our experience of 296 24-hour recordings in 160 patients (average age 10.5 years), investigated for suspected or known cardiac arrhythmias. One hundred and ten patients (68.75%) had no organic heart disease and 6 patients (3.75%) had acquired lesions. Eighty-three patients (52%) were symptomatic. Sixty-three patients (39%) had normal recordings; 97 patients (61%) had a total of 126 arrhythmias. There were 45 cases of atrioventricular block, 24 cases of sinus node dysfunction, 39 cases of supraventricular arrhythmias and 18 cases of ventricular arrhythmias. Overall, 47.6% of these rhythm disturbances were diagnosed by Holter monitoring. This technique was particularly valuable in the diagnosis of arrhythmias in symptomatic patients, patients with arrhythmogenic cardiac lesions and in the detection and surveillance of postoperative arrhythmias in congenital heart disease, of pacemakers, of congenital atrioventricular block and of the chronic arrhythmias of childhood.
Ten patients suffering from chronic premature ventricular complexes (greater than 60/h) were treated orally in a double-blind crossover study with encainide (50 mg three times a day) and disopyramide (200 mg three times a day), with five 7 day study periods: survey, placebo, encainide or disopyramide, washout placebo and disopyramide or encainide. At the end of each 7 day period, a 12 lead electrocardiogram, a 48 hour ambulatory electrocardiogram and a treadmill exercise test were performed. Blood levels of encainide and its metabolites and of disopyramide were measured at the end of each treatment (steady state). Drug efficacy was assessed by: 1) more than 80% reduction in the number of premature ventricular complexes per 24 hours, and 2) absence of ventricular tachycardia. Encainide was effective in four patients (complete suppression of premature ventricular complexes) and ineffective in five. One patient who showed a 92% reduction in the number of premature ventricular complexes developed sustained ventricular tachycardia after 24 hours of treatment. Disopyramide was effective in three patients (greater than 80% reduction in the number of premature ventricular complexes) and ineffective in seven patients. With encainide, the percent increase in PR, QRS and QT interval duration was, respectively: 32.7 (p less than 0.001), 30.8 (p less than 0.001) and 10.6% (p less than 0.01). With disopyramide this increase was not significant. Despite the variability of drug blood levels, a relation between blood levels and suppression of premature ventricular complexes on the 48 hour ambulatory electrocardiogram was found with encainide, but not with disopyramide.(ABSTRACT TRUNCATED AT 250 WORDS)
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Encainide is a new antiarrhythmic class IC agent. Eleven patients were given 1 mg/kg of encainide i.v. over a 15-min period. Electrophysiological studies were done before and l h after drug administration. Blood levels of encainide and its principle metabolites O-demethyl-encainide, 3 metoxy-O-demetyl-encainide and N-demethyl-encainide were measured serially after drug administration. Heart rate, blood pressure, and conduction intervals were monitored. Sixty minutes after drug administration there was a marked increase of the QRS, PA, AH, and HV intervals of 28.1% (p less than 0.01), 17.2% (p less than 0.01), 22.4% (p less than 0.01), and 32.2% (p less than 0.01), respectively, and a slight increase of the Wenckebach cycle length of 8% (p less than 0.05). BP, RR, QT, CSNRT, ESACT, ERP, and FRP did not vary significantly. The HV interval already was increased significantly 2 min after drug administration, while AH was not increased until 15 min after drug administration. The average blood levels of encainide and ODE 60 min after drug administration were 0.410 +/- 0.12 and 0.176 +/- 0.09 microgram/ml, respectively (mean +/- SE of the mean). There was a positive correlation between the increase of the AH and the blood level of ODE, which points out the importance of prolonged electrophysiological studies when testing drug with possibly active metabolites.