[Electrocardiogram in pre-excitation].
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Biomedical subjects
Publications and source records attributed to F Saporito.
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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 Drugs were given for a maximum of three days and withdrawn at the restoration of sinus rhythm.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.
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.
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.
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)
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.
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.
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