"Supernormal" phase of atrioventricular conduction with concealed capture beats. Significance of odd numbers of P waves between capture beats.

In 1968 Moe and associates postulated multilevel atrioventricular (A-V) block as a mechanism for some forms of the supernormal phase of A-V conduction. In 1971 Schamroth further postulated that, if this were correct, there would only be odd numbers of sinus P waves between the capturing impulses. This report presents two cases of sinus rhythm dissociated from idionodal escape rhythm as a result of high grade A-V block. The rhythm is complicated by manifest and concealed A-V captures during the so-called supernormal phase. There are only odd numbers of P waves between the capturing impulses.

Modulated ventricular parasystole as a mechanism for concealed bigeminy.

Concealed extrasystolic ventricular bigeminy reflects a distributional pattern of ventricular extrasystoles where intervening sinus beats are always in odd numbers. This has been explained on bigeminal rhythm associated with exit block. This presentation reflects a modification of this concept in that the distributional pattern may be explained on the basis of complex concealed modulation of ventricular parasystole, the concealment being due to impulses falling within the refractory period rather than suffering true exit block.

Supernormal modulation of ventricular parasystole: the triphasic phase-response curve.

Modulation of ventricular parasystole by sinus beats has been shown both in vitro and in vivo to result in a classic biphasic phase-response curve. The first clinical presentation of 3 cases of supernormal modulation of ventricular parasystole resulting in a triphasic phase response curve is reported. Supernormal modulation reflects an unexpected early enhancement expedition of the ectopic ventricular impulses. An alternative explantation for the triphasic phase-response curve is the discharge and resetting of the parasystolic focus by critically timed sinus impulses.

The early signs of right bundle branch block.

Complete right bundle branch block manifests with a rSR' configuration in right orientated leads and a duration of 0.12 sec or longer. Incomplete right bundle branch block is perceived as this classic rSr' configuration and a duration of less than 0.12 sec. This presentation reflects the early development of right bundle branch block which first manifests with a hitherto undescribed sign, namely: a diminution of the S wave amplitude in lead V2. Further progression of the right bundle branch block leads to slurring or notching of the upstroke of the S wave in lead V2 followed by the development of a r' deflection. With further progression, the r' deflection becomes increasingly taller until the advent of complete right bundle branch block which is characterized by a widening of a very tall R' deflection with an apical notch or plateau.

Sinoatrial block with complicating sinoatrial reciprocation.

This presentation reflects an atypical manifestation of sinoatrial block in a patient with chronic renal failure and hyperkalemia (7.8 mEq/L). An allorhythmic distribution of P-P intervals permits the interpretation of sinoatrial block complicated by sinoatrial reciprocation.

Wedensky facilitation. Electrotonic potentiation during complete A-V block.

The electrocardiogram recorded from a patient with third degree A-V block reflected almost regular A-V junctional escape rhythm. Some of the R-R cycles were slightly shorter than the basic escape cycle. A QRS complex ending such a relatively short R-R interval was always preceded by a sinus P wave, and had a QRS configuration which was minimally different from that of the escape complexes. The His bundle recording demonstrated that these minimally premature complexes were associated with an H-V interval which was shorter than that of the escape complexes. This indicates that the premature QRS complex could not be a capture beat. The relationship between the slightly premature QRS complex and the preceding sinus P-waves is explained on the basis of electrotonic potentiation or modulation to due Wedensky facilitation.

Concealed ventricular bigeminy with exceptions due to time-dependent modulation of an ectopic rhythm.

This presentation reflects a case of atypical concealed bigeminy, where some interectopic intervals contain even numbers of sinus beats. Exceptions to the rule of concealed bigeminy only occur during slowing of the sinus node. The pattern is explained on the basis of modulated parasystole, by drawing a phase-response curve which explains all the interectopic intervals on the basis of the modulating effect exerted by the sinus impulses upon a parasystolic focus.

Bigeminal and trigeminal distribution of ventricular extrasystoles as an expression of "atypical" concealed bigeminy.

This report reflects a case of bigeminal and trigeminal ventricular extrasystoles where bigeminal extrasystoles are associated with short coupling intervals, while trigeminal extrasystoles manifest long coupling intervals. The arrhythmia is interpreted as an "atypical" form of concealed bigeminy.

Reciprocating tachycardia with only odd-numbered beats in the Wolff-Parkinson-White syndrome.

A case of Wolff-Parkinson-White syndrome with reciprocating tachycardia from retrograde Kent's bundle conduction is described. The paroxysms of reciprocating tachycardia manifested with the unusual, and hitherto unreported, feature of only odd-numbered beats. The phenomenon is explained on the basis of alternate anterograde conduction through two A-V nodal pathways.

Electrocardiographic differentiation of the causes of left ventricular diastolic overload.

Left ventricular hypertrophy due to diastolic overload is characterized by the following in lead V6: (a) tall R wave; (b) prominent initial Q wave; (c) minimally elevated concave-upward ST segment; and (d) relatively tall symmetrical T wave. Reciprocal deep S waves are seen in lead V1. This study reflects a further evaluation of these parameters in the four main causes of left ventricular diastolic overload: mitral incompetence, aortic incompetence, patent ductus arteriosus, and ventricular septal defect. An S wave in lead V1 which is equal to or greater than the R wave in lead V6 excludes the diagnosis of mitral incompetence.

Atrioventricular junctional parasystole with ventricular fusion beats due to complicating Wolff-Parkinson-White syndrome.

We present a case of atrioventricular (AV) junctional parasystole manifesting with ventricular fusion beats due to the presence of an accessory AV conduction pathway. Ventricular fusion beats are usually impossible in AV junctional parasystole. In the reported case the ventricular fusion occurs because the ectopic AV junctional impulse is conducted through the His bundle, whereas the sinus impulse is conducted to the ventricles through the Kent bundle.

Oral propafenone in the suppression of chronic stable ventricular arrhythmias.

The efficacy of propafenone hydrochloride, a new antiarrhythmic agent, was evaluated in the treatment of chronic stable ventricular arrhythmias. Twenty-five patients who had suffered a myocardial infarction three months or longer before the trial were studied. All exhibited a minimum mean frequency of 30 ventricular ectopic beats per hour over at least two 24-hour Holter monitoring periods with the last recorded tape serving as a control. The mean decrease in ventricular ectopic activity with propafenone was 65.62 percent (p = less than 0.001). Side effects were infrequent, minimal, and of no clinical consequence. Oral propafenone was found to be an effective drug for reducing the level of chronic ventricular ectopy, as reflected by a short-term trial.

QRS normalization by ventricular fusion simulating tachycardia dependent left bundle branch block.

We report an example of ventricular fusion of a sinus impulse conducted with bundle branch block with an ectopic impulse arising on the ipsilateral side of the blocked bundle branch. The manifestation simulates the normalization which occurs during the relatively slow phase of a tachycardia dependent left bundle branch block.

Torsade de pointes due to coxsackie B3 myocarditis.

Viral myocarditis may present with a variety of electrocardiologic aberrations. Torsade de pointes, a potentially malignant ventricular arrhythmia associated with prolongation of the QT interval has not been described in patients with acute viral myocarditis. This report details this finding in a patient with coxsackie B3 myocarditis in whom symptomatic torsade de pointes was documented.

The hyperacute phase of true posterior infarction.

The hyperacute phase of true posterior myocardial infarction is described in detail. This electrocardiographic manifestation, hitherto unnamed as such, presents with slope-depression of the S-T segments with relatively wide and deep T-waves in the right precordial Leads V1 to V4. The condition then progresses to the well-recognized fully evoked phase of acute true posterior wall myocardial infarction.