Torsades de pointes in congenital long QT syndrome following low-dose orphenadrine.

We report the case of a woman, affected by congenital long QT syndrome (LQTS), who experienced three syncopal episodes shortly after the assumption of a low dose of orphenadrine. The ECG revealed a QT interval of 600 ms, and the corrected QT interval (QTc) was 537 ms. No structural cardiac disease was demonstrated by echocardiography. Orphenadrine treatment was discontinued. During the first 12 h of monitoring, three short-lasting, asymptomatic episodes of torsades de pointes occurred. No other sustained ventricular arrhythmia was revealed at Holter monitoring in the following days. During the ensuing 6 months, the patient remained asymptomatic, and the QTc did not change. Orphenadrine is an analogue of diphenhydramine, an antihistaminic drug that produces sodium channel blockade similar to that caused by quinidine and other Class Ia antiarrhythmic drugs. Our case rises the suspicion that orphenadrine could cause life-threatening arrhythmias in LQTS even at a low dose, and independently from concomitant assumption of potentially QT-prolonging drugs.

Acute myocardial infarction and rescue percutaneous transluminal coronary angioplasty in a young HIV-infected patient.

We report a case of acute myocardial infarction in an HIV-infected patient without significant coronary artery disease (CAD) risk factors. The patient underwent rescue percutaneous transluminal coronary angioplasty (PTCA), with a successful outcome. We presume a possible pathogenetic role of anti-retroviral therapy and/or direct viral action on ischaemic heart disease progression. We propose that the current approach to management of AIDS-affected patients needs close monitoring for CAD risk factors and symptoms, to improve prognosis and life expectancy.

QRS complex voltage changes associated with supraventricular tachycardia.

INTRODUCTION: The aim of this study was to evaluate the changes in ventricular complex voltage associated with narrow QRS supraventricular tachycardia (SVT). METHODS AND RESULTS: One hundred forty-five patients undergoing catheter ablation for SVT, 85 with AV nodal reentrant tachycardia (AVNRT) and 60 with AV reentrant tachycardia (AVRT) due to a concealed accessory pathway, were studied. Four consecutive tachycardia beats and four consecutive sinus beats were analyzed, excluding the last tachycardia complex and the first sinus one. For each of the 12 leads, the QRS complex voltage was measured, and the results of four beats were averaged both in SVT and in sinus rhythm (SR). The sum (sigma) of the QRS voltages measured in the 12 leads during SVT (sigmaSVT) and SR (sigmaSR) were calculated, as well as the QRS axis during SVT and SR. QRS complex voltage was significantly increased during SVT, with respect to SR, in leads II, III, aVR, aVF, and V2 to V6. In addition, sigmaSVT was significantly greater than sigmaSR. Only lead V1 showed a significant voltage decrease during SVT. These voltage changes were almost identical in patients with AVNRT and patients with AVRT. No relationship was found between tachycardia rate and QRS voltage variation. The QRS axis showed a significant shift during SVT, from 55.8 degrees to 64.5 degrees. CONCLUSION: QRS voltage increase occurs in reentrant SVT, independent of the underlying reentrant circuit. The phenomenon likely depends on tachycardia-related reduced ventricular filling. This could result in displacement of the heart in such a way that the left ventricle becomes closer to the precordial electrodes (proximity effect). Alternatively, decreased intracavitary blood mass could diminish the intracardiac short-circuiting of potentials, resulting in augmented transmission of cardiac vectors to the body surface.

Myxedema coma of both primary and secondary origin, with non-classic presentation and extremely elevated creatine kinase.

Myxedema coma is a rare, often fatal endocrine emergency that concerns elderly patients with long-standing primary hypothyroidism; myxedema coma of central origin is exceedingly rare. Here, we report a 37-year-old woman in whom classical symptoms of hypothyroidism had been absent. Six years earlier, she had severe obstetric hemorrhage and, shortly after, two subsequent episodes of pericardial effusion. On the day of admission, pericardiocentesis was performed for the third episode of pericardial effusion. Because of the subsequent grave arrhythmias and unconsciousness, she was transferred to our ICU. Prior to the endocrine consultation, a silent myocardial infarction had been suspected, based on the extremely high serum levels of creatine kinase (CK) and isoenzyme CK-MB. However, based on thyroid sonography, pituitary computed tomography, elevated titers of antithyroid antibodies and pituitary stimulation tests, the final diagnosis was myxedema coma of dual origin: an atrophic variant of Hashimoto's thyroiditis and post-necrotic pituitary atrophy (Sheehan syndrome). Substitutive therapy caused a prompt clinical amelioration and normalization of CK levels. Our patient is the first case of myxedema coma of double etiology, and illustrates how its presentation deviates markedly from the one endocrinologists and physicians at ICU are prepared to encounter. In addition, cardiac problems as those of our patient should not discourage from substitutive treatment (using L-thyroxine and the gastrointestinal route of absorption), if the age is relatively low.

[A comparison between propafenone and hydroquinidine perorally in the treatment of recent-onset atrial fibrillation]. / Confronto tra propafenone e idrochinidina per via orale nel trattamento della fibrillazione atriale di recente insorgenza.

The aim of this study was to assess the effectiveness of propafenone and quinidine to restore sinus rhythm in patients with paroxysmal atrial fibrillation. Eighty consecutive patients with recent onset atrial fibrillation were randomized to one of the following oral treatments: a) propafenone 450 mg as single dose followed by 300 mg t.i.d.; b) hydroquinidine 900 mg/24 hours + digoxin if necessary. Drugs were given for a maximum of three days and withdrawn at the restoration of sinus rhythm. If atrial fibrillation was persistent, the other drug was administered after two days wash out. The two groups did not differ from each other with respect to left atrial size, age and presence of organic heart disease, and kind of cardiopathies between the two groups. Sinus rhythm was restored in 39 patients of group 1 (93%) and 36 of group 2 (95%). In conclusion, oral propafenone is as effective as quinidine in the treatment of paroxysmal atrial fibrillation.

Triple ventricular parasystole.

This presentation reflects the analysis of an electrocardiographic recording obtained from a patient with hypertensive heart disease. In the initial section of the tracing, fixed coupled monomorphic ectopic ventricular beats occurred in regular trigeminal rhythm. The pattern changed following an atrial extrasystole and several ventricular ectopic beats of various configuration occurred, often in sequence. Analysis demonstrated the presence of three independent parasystolic rhythms, two of which manifested with the character of intermittency, namely they were occasionally reset by extraneous impulses. The interplay of the sinus pacemaker with three parasystolic foci resulted in a very complex arrhythmic pattern. In some periods, however, two out of three ectopic rhythms were inapparent, and the third one manifested with fixed coupled complexes, so that a regular extrasystolic trigeminy ensued, and parasystole was not recognizable.

Atrial parasystole and tachycardia. Modulation and automodulation of a parasystolic focus.

This report deals with a patient reflecting atrial parasystole and episodes of atrial tachycardia. The P' waves during tachycardia were identical to the parasystolic P' waves. Atrial parasystole was at times regular, as revealed by a precise mathematical relationship between the interectopic intervals, and on other occasions irregular. Irregularity was due to modulation, namely electrotonic influence exerted by the sinus impulses upon the parasystolic focus. Atrial tachycardia occurred only during the periods when atrial parasystole was modulated. Atrial tachycardia has been interpreted as due to automodulation, a situation where the propagated parasystolic impulse exerts an electrotonic influence on the ectopic focus itself, leading to a marked unexpected acceleration of the ensuing parasystolic discharge.

[Electrocardiographic diagnosis of ventricular tachycardia in patients with previous myocardial infarct: frequency and significance of diverse diagnostic criteria]. / Diagnosi elettrocardiografica di tachicardia ventricolare in pazienti con pregresso infarto miocardico: frequenza e significato dei diversi criteri diagnostici.

Electrocardiographic tracings of ventricular tachycardia were recorded from 34 patients with old myocardial infarction. The diagnostic criteria of ventricular tachycardia were carefully assessed in each tracing. The most commonly observed signs were: 1) QRS duration greater than 140 msec; 2) a prevalent negative deflection in Lead V6; 3) an interval from the beginning of the QRS complex to the S wave nadir greater than 100 msec in at least one precordial lead. The cases were subdivided into two groups on the basis of a predominant positive or negative deflection in Lead V1 (Group 1 and 2, respectively). The most common signs in Group 1 were a monophasic R wave configuration of the QRS complex in Lead V1, and a QS configuration in Lead V6. On the other hand, the most frequent criteria in Group 2 were an interval between the beginning of the QRS complex and the S wave nadir greater than 60 msec in Lead V1, and a QS configuration in Lead V6. Furthermore, none of the cases reflected a normal frontal plane QRS axis, but an axis deviation was evident in all 29 cases where axis could be calculated.

[A-V conduction in atrial fibrillation and flutter]. / La conduzione A-V nella fibrillazione e nel flutter atriale.

The assessment of A-V conduction in the presence of atrial fibrillation is based upon analysis of the R-R intervals. This is because in atrial fibrillation it is impossible both to identify the impulse that has been conducted to the ventricles, and to measure the A-V conduction time. The first step is, therefore, to evaluate whether the QRS complexes are the expression of conducted atrial impulses, or they are A-V junctional or ventricular in origin. In other words, it is necessary to distinguish between A-V conduction and A-V dissociation. Conduction in atrial fibrillation commonly results in irregular R-R cycles, whereas in the presence of dissociation the R-R cycles are mainly regular. This differentiation can be difficult in the presence of: aberrant conduction; A-V conduction disturbances; or A-V junctional tachycardia with anterograde 2nd degree exit block. The problem occurs both with tachycardia-dependent (or phase 3), and with bradycardia-dependent (or phase 4) aberrant conduction. Distinction between aberration and ectopy is helped by: the sequence long cycle-short cycle; the pause that follows the wide QRS complex; the configuration of the wide QRS complex. Since aberrant conduction may be sustained, due to the linking phenomenon, the pattern may mimick ventricular tachycardia. In atrial flutter the atrial electrical activity is far less chaotic than in atrial fibrillation, so that assessment of A-V conduction is less difficult. Nevertheless, it is impossible to determine exactly which out of the atrial impulses has been conducted, due to the extremely fast atrial rate: the conducted impulse, indeed, is not always the one that immediately precedes the QRS complex. Furthermore, it is also difficult to measure the A-V conduction time, because the F waves follow to each other without any interruption, so that it is impossible to define exactly the beginning of atrial activation. In atrial flutter, thus, as well as in atrial fibrillation, A-V conduction may be assessed by analysis of the R-R intervals, apart from measurement of F-R intervals. In the absence of drugs, atrial flutter is usually associated with 2:1 (or, less frequently, 4:1) conduction ratio, being the odd ratios (3:1, 5:1) far more rare. Due to concealed penetration of non-conducted impulses, A-V conduction intervals are often variable, so that the R-R cycles are irregular even in the presence of a constant A-V conduction ratio. The most common mechanisms leading to irregularity are the alternation of A-V conduction times, and the alternating Wenckebach phenomenon.(ABSTRACT TRUNCATED AT 400 WORDS)

Concealed ventricular hexageminy.

The authors report a case of concealed ventricular hexageminy in which, with a few exceptions, extrasystoles were separated by sinus beats conforming to the formula 6n - 1. Whenever an exception to this formula occurs, the intervening beats are not all of sinus origin, but include also a ventricular extrasystole that is different from those occurring in hexageminal distribution. The pattern is explained by a parasystolic rhythm modulated by sinus impulses, assuming a 3:1 ratio between the parasystolic cycle and the sinus cycle. Such a ratio would have to be associated with a trigeminal or concealed trigeminal distribution. There is, however, a 2:1 ectopic-ventricular block, leading to a change of the ectopic distributional pattern from the expected concealed trigeminy to that of the concealed hesageminy.