Early proarrhythmia during intravenous amiodarone treatment.

We present a case of early (within the first 24 hours) development of malignant torsades de pointes (TdP) associated with intravenous amiodarone therapy. After correction of predisposing factors (heart failure, hypokalemia, digoxin) amiodarone again resulted in torsades. This observation suggests that in patients who have experienced amiodarone-induced proarrhythmia, amiodarone administration under different, more stable clinical conditions may still be hazardous.

[Ventricular tachycardia masquerading as supraventricular tachycardia]. / Supraventricularis tachycardiát utánzó kamrai tachycardia.

To distinguish supraventricular tachycardia with aberrancy from ventricular tachycardia is sometimes difficult. It seems to be easy to distinguish the two forms in patients with preexisting bundle branch block: if the QRS morphology during tachycardia is identical to those during at rest the tachycardia is supraventricular, if different, ventricular. We present two cases with preexisting bundle branch block and wide complex tachycardia whose QRS morphologies were almost same to those during normal rest rhythm. The atrioventricular dissociation and the response to adenosine and lidocaine strongly suggests ventricular tachycardia. In these cases ventricular tachycardia masqueraded as supraventricular tachycardia and the identical QRS morphology with the preexisting bundle branch block may suggest a misdiagnosis of supraventricular tachycardia.

A comparison of the effects of mibefradil and atenolol on regression of left ventricular hypertrophy in hypertensive patients.

OBJECTIVE: This study was designed to compare the effect of mibefradil, a selective T-type calcium channel antagonist, with the beta-blocker atenolol on regression of left ventricular (LV) hypertrophy in hypertensive patients. METHODS: In this multicenter, double-blind, active-controlled, randomized, parallel-group comparison, 66 patients with mild-to-moderate hypertension (sitting diastolic blood pressure, SDBP, 95-114 mm Hg) and LV mass index > 102 g/m2 for males and > 88 g/m2 for females were randomized to an initial treatment with 50 mg of either mibefradil or atenolol for 4 weeks. Doses were increased to 100 mg/day if blood pressure was not normalized to < or = 90 mm Hg, and, if needed, 25 mg of hydrochlorothiazide was added. Treatment continued for a total of 24 weeks. LV hypertrophy was assessed by echocardiography, and trough SDBP and adverse events were recorded. RESULTS: Treatment with mibefradil or atenolol resulted in decreases from baseline in LV mass index of 11.1% (p < 0.001) and 9.1% (p < 0.001), respectively. The treatment difference (mibefradil vs. atenolol) was not statistically significant. Reductions in SDBP with mibefradil and atenolol were 14.3 and 10.7 mm Hg, respectively, again not statistically significant. Both drugs were well tolerated; however, overall there were more potentially drug-related adverse events reported with atenolol (48.5%) than with mibefradil (24.2%). CONCLUSIONS: The reductions in LV hypertrophy and blood pressure achieved with mibefradil were larger but statistically equivalent to those with atenolol, but a lower overall incidence of treatment-related adverse events was seen in the mibefradil-treated patients.

Mechanism of endothelin-induced malignant ventricular arrhythmias in dogs.

The development of ventricular tachyarrhythmias caused by low-dose intracoronary infusion of endothelin-1 (ET-1) has recently been observed in dogs. The aim of the present study was to investigate the pathomechanism of ET-1-induced ventricular arrhythmias in 32 anesthetized, open-chest mongrel dogs in group A (n = 14) without, in group B (n = 14), and in group C (n = 4 control) with atrioventricular node ablation. The coronary blood flow (CBF) was measured in the left anterior descending (LAD) coronary artery by an electromagnetic flowmeter. Standard ECG, atrial and ventricular electrograms, and in groups B and C endocardial and epicardial monophasic action potentials (MAPs) were recorded. ET-1 was administered into the LAD at a low dose (30-60 pmol/min). At the time of the appearance of premature beats, CBF was only slightly decreased. The effective ventricular refractory period did not change significantly. Onset of spontaneous polymorphic and monomorphic sustained ventricular tachycardia (sVT) was observed in five dogs without bradycardia and in nine dogs with bradycardia. VTs in dogs with complete AV block were longer and slower. In most of the cases, ventricular fibrillation occurred. ET-1 treatment resulted in a significant increase in MAP 90% duration (255 +/- 9 vs. 290 +/- 8 ms endocardial, 244 +/- 10 vs. 292 +/- 12 epicardial; p < 0.05) at 70 beats/min ventricular pacing. In eight cases (group B), third-phase early afterdepolarization could be recorded. According to our results, the mechanism of ET-1-induced arrhythmias appears to be based on prolongation of MAP duration and development of afterdepolarizations.

[Transient Q-waves in coronary disease]. / Tranziens Q-hullámok coronariabetegségben.

The authors discuss the transient ischemic Q waves in various situations. Five cases are presented. Two patients had exercise-induced Q waves, one patient had right bundle branche block-dependent Q waves, one patient had transient Q waves after thrombolytic therapy and one patient had transient Q waves caused by Prinzmetal angina. Profound ischemia may not result in necrosis but may cause myocardial stunning. Myocardial stunning may be accompanied by deranged electrophysiologic activity with transient loss of electromotive forces.

[The use of adenosine in the diagnosis and treatment of cardiac arrhythmias]. / Adenozin alkalmazása a szívritmuszavarok diagnosztikájában és kezelésében.

The authors investigated the effect of adenosine or ATP on narrow QRS tachycardia in 56 pts, 3 pts with wide QRS tachycardia 9 pts with suspected latent preexcitation and 10 pts with PVC suspected to be ventricular parasystole. After the bolus iv. administration of adenosine or ATP every SVT was stopped related to AV node (44 pts), but in the rest twelve related to atrial origin of SVT only one automatic atrial tachycardia could be stopped. From the 9 patient suspected to have concealed WPW 2 pts had delta wave during the effect of adenosine, and in four pts parasystole was demonstrated among the pts had varying coupling interval PVC. None of the pts who had wide QRS tachycardia was the tachycardia stopped, but in two cases the supraventricular origin--atrial flutter and tachycardia--was discovered. The authors emphasize the favourable effect of adenosine in narrow complex tachycardia and suggest that it can given safely in wide QRS tachycardia of unknown origin either. The diagnostic effect of adenosine can be used in sinus rhythm too if latent preexcitation or ventricular parasystole is suspected.

[Adenosine-sensitive atrial tachycardia]. / Adenozin szenzitív pitvari tachycardia.

The authors describe a case of a 71 year old man who suffered from chronic lung disease and had atrial tachycardias. 18 mg adenosine terminated his paroxysmal supraventricular tachycardia. The Holter monitoring showed that the tachycardia began at the late diastole with normal PQ interval, suggesting that an ectopic atrial tachycardia was terminated. They propose that adenosine is a "new" drug for termination of some form of atrial tachycardia.

[Intermittent Romano-Ward syndrome]. / Intermittáló Romano-Ward-syndroma.

Two cases are described to have intermittent long QT syndrome. This type of long QT syndrome is not easy to recognize and the result could be fatal in case taking I/A type antiarrhythmic drugs. The first patient who was investigated had got "chinidin syncope" two years earlier, the second one had symptoms of syncope and dizziness for 3 months. The long QT syndrome was diagnosed in both cases by Holter monitoring. For these reason this paper underline the value of Holter monitoring as a diagnostic tool to establish the diagnosis of long QT syndrome. The monophasic action potential showed early after depolarisations in both cases.

[Clinical importance of monophasic action potential registration in long QT syndrome]. / Monofázisos akciós potenciál regisztrálás klinikai jelentösége hosszú QT-szindrómában.

For more than 30 years, the monophasic action potential has been used as an experimental tool for the study of myocardial repolarisation. With recent improvements in catheter design, the utility of the tool as a means to identify the bases for ventricular arrhythmias in humans has been greatly improved. Abnormalities of repolarisation leading to ventricular arrhythmia formation can be identified and specific pharmacological therapies may be evaluated. The pathomechanism of major arrhythmias (ventricular tachycardia, ventricular fibrillation) occurring in long QT syndrome (LQTS) is not yet fully elucidated. The authors have recorded the monophasic action potentials (MAP) of the right ventricle in three patients with LQTS and with previous episodes of major ventricular arrhythmias. The changes in MAP duration and after depolarisation in response to spontaneous arrhythmias, programmed electrostimulation, atrial pacing and isoproterenol treatment were studied. In all of the three patients the early afterdepolarisation was present, which in two cases exhibited pause-dependent features. Thus in these patients dual chamber pacemaker implantatious were performed. These were the first permanent recordings of MAP during electrophysiological examination in Hungary and also the first evidences that the early afterdepolarisation does play a pathogenic role in the development of idiopathic LQTS. Further evaluation of the technique by cardiac electro-physiologists may improve both the diagnosis and the treatment of ventricular arrhythmias dependent upon afterdepolarisation formation.

Effect of adenosine on ventricular parasystole.

The cases of two patients with ventricular parasystole revealed a new depressive effect of adenosine on ventricular parasystolic activity. To the authors' knowledge, this is the first report that clearly demonstrates the disappearance of "true" parasystole.

[Experience with a transvenous pacemaker-cardioconverter-defibrillator without subcutaneous patch]. / Transzvénás, subcutan patch nélküli pacemaker-cardioverter-defibrillátorokkal szerzett tapasztalataink.

Sudden cardiac death caused by malignant ventricular arrhythmias is one of the main causes of cardiovascular mortality. Implantation of cardioverter-defibrillators has resulted in the reduction of the incidence of sudden cardiac death caused by malignant ventricular arrhythmias from the yearly 10-30% to 1%. For the very first time in Hungary, the authors applied only transvenous lead configuration for automatic cardioverter defibrillators in three patients. The indications of the implantation were ventricular fibrillation in one case, ventricular tachycardias refractory to drug treatment in two cases. Ventricular arrhythmias were secondary to coronary heart disease in two patients, dilatative cardiomyopathy in one patient. Preoperative, intraoperative and postoperative electrophysiological studies were regularly taken. Using Biotronik Phylax 03 device with a right ventricular electrode and a superior vena cava electrode and without subcutaneous patch the intraoperative defibrillation thresholds were 6, 11 and 12 J respectively. The fractally iridium coating increases the surface of the electrodes that has a very good effect on defibrillation threshold. During a mean follow-up of six months the occurring spontaneous ventricular arrhythmias (1 ventricular fibrillation and 5 ventricular tachycardias) were terminated by Phylax 03 with cardioversion-defibrillation or overdrive stimulation. The authors' results of intraoperative testing and clinical experiences show that the Phylax 03 biphasic system due to low defibrillation thresholds without subcutaneous patch can safely be applied with only transvenous implant technique in patients with major ventricular arrhythmias to prevent sudden cardiac death and to terminate ventricular tachycardia.

Scope and limitations of a general unknown screening by gas chromatography-mass spectrometry in acute poisoning.

The gold standard for the diagnosis of acute poisoning is toxicological analysis. Because information on the incorporated toxic substance provided by the patient or his relatives is known from experience to be unreliable in about 40% of all intoxications, a screening procedure that covers most relevant drugs and toxicants is required rather than an analytical procedure optimized for the identification of a single class of substances. The special task for a general unknown screening procedure is to identify a toxic substance among endogenous or food-derived substances as well as environmental toxicants in a biological matrix on an emergency basis. Because the unknown toxic substance may vary considerably in its physicochemical properties and its concentration range, a universally applicable screening procedure is required. Although gas chromatography-mass spectrometry has been used for three decades, it still offers many unique advantages in terms of sensitivity, specificity, reliability, and coverage of a large number of toxic substances. Because the procedure has to be kept as simple and as short as possible, compromises have to be made with respect to extraction, derivatization, and mass-spectral techniques. The specimen of choice for a general unknown screening is-if available-urine. The standard mode of ionization is electron impact. The identification of unknown substances is highly challenging because, in our experience, previously unknown metabolites may be detected rather frequently in acute poisoning. Although an automated mass spectra library search considerably facilitates the identification process, expert knowledge on the identification of substances not included in the library as well as knowledge in clinical toxicology and metabolism is indispensable.

Fatal poisoning with detajmium: identification of detajmium and its metabolites and artifacts by gas chromatography-mass spectrometry and quantification by high-performance liquid chromatography.

After ingestion of an unknown dose of detajmium, a 14-year-old female collapsed with asystolia. Resuscitation efforts were not successful. A medicolegal autopsy was carried out, and blood, liver and gastric content were extracted and analyzed by gas chromatography-mass spectrometry (GC-MS). After derivatization with acetic anhydride, detajmium and twelve of its derivatives and metabolites were identified. The main metabolic pathways include hydroxylation and subsequent O-methylation of the indol ring, and oxidation as well as reduction of the C-21 hydroxyl function. Cleavage of the N-alkyl side-chain is a further, possibly non-enzymatic degradation pathway. Artifact formation induced by acetylation included dehydratation of the hydroxyl function of C-21 and the N-alkyl side-chain. The detajmium concentration in blood of the decreased was determined by high-performance liquid chromatography with fluorimetric detection (12 micrograms/ml).