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This case review presents various manifestations of extra long PR intervals, an interesting form of atrioventricular (AV) block first described in 1977. All patients in this study had organic heart diseases and various combinations of multilevel conduction impairment. Perhaps the most common cause of chronic AV conduction impairment is the ill-defined degenerative and/or fibrotic damage to the intraventricular conduction system.

A 46-year-old male without past medical history presented to the emergency department complaining of severe chest pain. Blood pressure was 100/70 mm Hg, heart rate was 66 bpm, and the oxygen saturation was normal. The 12-lead ECG showed ST segment elevation in leads I, avL and throughout the precordial leads (Fig. 1A). Urgent coronary angiography was performed and demonstrated a complete thrombotic occlusion of the mid left anterior descending artery (LAD) as well as a more proximal 70% luminal narrowing of the LAD. Percutaneous transluminal coronary angioplasty and stent implantation of the mid LAD was successfully performed with restoration of grade TIMI 3 flow in the LAD. The patient was admitted to the cardiac intensive care unit after successful stent implantation. ECG performed 1 h after reperfusion (Fig. 1B) showed a wide complex tachyarrhythmia with right bundle branch block (RBBB) morphology and alternating axis deviation. This arrhythmia spontaneously resolved to normal sinus rhythm (Fig. 1C). The patient was discharged with medical therapy including a beta blocker and without any complications. The 12-lead ECG recording demonstrates a bidirectional tachycardia in which all the beats have features of RBBB and the QRS axis in the frontal plane alternates between right and left axis deviations (Fig. 1B). The width of the QRS complex is only 110 ms, thus corresponding to a tachycardia originating within the left bundle branch (LBB) or its fascicles. The illustration (Fig. 2) is based on the assumption that the focus of the tachycardia was situated in the left bundle just above the division into the left posterior fascicle (LPF) and the left anterior fascicle (LAF) with impulses conducting to the myocardium using the LAF and LPF alternately, hence the alternating axis. Even though His bundle potentials were not recorded during the bidirectional tachycardia, the relatively narrow width of the QRS and the alternating axis together with RBB leaves no doubt regarding the location of the automatic focus in the territory of the LBB. This concept was documented by His bundle recordings by Massumi back as 1973 [1] and by clinical observations since 1977 [2]. The QRS morphology and rate of arrhythmia corresponds to the majority of the cases of reperfusion arrhythmias also known as accelerated idioventricular rhythm (AIVR) [3]. However, the unique feature is the alternation of the QRS axis in the frontal plane suggesting functional block in the two fascicles. As is usually the case, the tachycardiawas self-limited and resolved spontaneously. The majority of the AIVR cases have rates under 120/min and do not cause hemodynamic deterioration. However, it is important to distinguish the reperfusion AIVR from the more dangerous type of bidirectional ventricular tachycardia (VT) seen in the course of digitalis intoxication [4] and severe myocardial damage such as myocarditis [5]. This patient had no history of digitalis use and the arrhythmia occurred during the reperfusion period making bidirectional VT very unlikely. Bidirectional VT has not been reported in the setting of acute myocardial infarction. It should also be noted that the early publication of cases of AIVR emphasized the point that the occurrence of AIVR usually indicated restoration of flow to the infarcted region [3]. In recent publications, it has been reported that AIVR also appears in several drug intoxications [3], post-resuscitation [6] and idiopathic dilated cardiomyopathy [7]. There is general agreement that the electrophysiological mechanism of AIVR is enhanced automaticity of the His bundle and/or its divisions. To the best of our knowledge, this is the first report of alternating LAF and LPF block in the setting of the RBBB and fascicular rhythm in a patient with acute anterior myocardial infarction. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [8].

Certain electrocardiographic patterns are well recognized for their propensity to progress to more severe forms of atrioventricular (AV) block, thus requiring pacemaker implantation. This article presents an infrequently recognized and deceptively benign pattern of conduction abnormality with great potential for advancement to severe AV block and necessity for pacemaker therapy. The pattern consists of alternating bundle branch block (BBB) in unison with alternation of the PR interval so that the right BBB beats and left BBB beats appear to be wedded to their own but different PR intervals. It is hoped that the publication of these cases will contribute to the awareness of practicing cardiologists and electrophysiologists to the existence of this potentially serious form of AV conduction abnormality and hasten the implantation of pacemakers in patients who require them.

In a study of seven cases of paroxysmal supraventricular tachycardia, it was noted that the fast rate was not caused by the mechanism of rapid firing, reentry, or dual atrioventricular nodal conduction but by an abrupt doubling of the rate by interpolation of junctional extrasystoles between adjacent sinus beats while the sinus mechanism remained undisturbed. Dual ventricular response to a single atrial depolarization was seriously considered in each case. The intervals separating the junctional extrasystoles tended to be quite fixed, thus conforming to the pattern of junctional parasystole with an intrinsic rate very close to the rate of the dominant sinus rhythm. The paroxysms of tachycardia were transient, lasting a few seconds to 3.5 minutes. The onset and termination of the paroxysms were completely unpredictable and appeared unrelated to any change in the basic sinus rate or other identifiable mechanism. In only one case, case 7, the concept of dual ventricular response appeared tenable. However, as will be discussed later, the mechanism of junctional parasystole was found to be physiologically more acceptable.

A case is described of pacemaker pseudomalfunction caused by intermittent displacement of the ventricular lead. The displacement was shown to be caused by critically timed atrial contractions, dislodging the looped ventricular lead, and resulting in intermittent failure to stimulate the heart.

Alterations of cardiac rhythm and conduction occur frequently during exercise stress testing and may provide significant information regarding cardiovascular status. Exertion may induce arrhythmias as a result of sympathetically enhanced phase 4 depolarization of ectopic foci or the induction of myocardial ischemia secondary to increased myocardial oxygen demand. Exercise may abolish arrhythmias present in the resting state, an effect attributed to overdrive suppression and inhibition related to sinus tachycardia. Although a wide spectrum of electro-physiologic changes may be elicited by stress testing, ventricular dysrhythmias are of primary importance. Premature ventricular contractions that are frequent, multifocal, repetitive or associated with light work loads have been particularly indicative of coronary artery disease. Exertional ventricular irritability has been observed more frequently in patients with coronary atherosclerosis involving two or more coronary vessels and accompanied by abnormalities of left ventricular wall motion. Exercise testing may have advantages over portable monitoring in the detection of ventricular arrhythmias. The mere presence of ventricular ectopic beats at rest does not preclude carefully performed graduated stress testing nor does their disappearance during effort exclude the presence of coronary artery disease.

Perhexiline maleate (Pexid), a promising clinical antiarrhythmic and antianginal drug, was evaluated for its electrophysiologic effects on the entire conduction system of the intact canine heart throughout a wide range of therapeutic and potentially toxic doses. Intracardiac conduction times were measured by bipolar intramyocardial and transvenous endocardial electrodes before and following the intravenous administration of each dose of perhexiline maleate, 3 mg/kg every 30 min for a total of 4 doses in 7 open-chest anesthetized dogs. Eight animals served as controls in which similar operative technique and electrophysiologic variables were recorded after infusion of the maleate diluent. In addition, the effects of perhexiline on atrial and ventricular thresholds to electrical stimulation were recorded, as well as the QRS and QT intervals, sinus rate, and rhythm disorders. It was observed that perhexiline did not significantly (p greater than .05) alter sinus rate, QT interval, QRS duration, PR interval, intra-atrial conduction time, atrioventricular nodal conduction time, and His-Purkinje conduction velocity. The drug did not affect the cardiac threshold to electrical stimulation of less than 0.1 ma. No ectopic atrial or ventricular activity emerged during the accumulated influence of the agent. From this study, it is concluded that perhexiline does not exert deleterious actions on the conduction system of the intact canine heart. In view of the negligible toxic effects and its efficacy in treating ventricular tachyarrhythmias in patients, the drug deserves further clinical evaluation.

Summary In a 67-year-old man with multiple myocardial infarctions in the past, the use of oral verapamil for control of angina pectoris was followed by the appearance of two previously undiagnosed abnormalities, namely, a dual-pathway AV node conduction pattern, and paroxysms of AV nodal reentrant tachycardia precipitated by premature ventricular beats (PVB). It is probable that the differential effects of verapamil on the fast and slow AV node pathways, and the interplay of PVB with its concealment within the AV node, created the necessary circumstances in the AV node to precipitate the tachycardia. Observed off verapamil over several months, the patient remained in normal sinus rhythm but continued to have numerous premature ventricular beats (PVB's). Nevertheless, neither the clinical electrocardiographic features of dual-pathway AV node conduction nor the AV nodal reentrant tachycardia could be found. The proarrhythmic effect of verapamil and its ability to provoke the very arrhythmia against which it is most effective are of particular interest in view of a similar behavior exhibited by the Class I antiarrhythmic agents.

Inhalation of 40 per cent N2O by nine patients who had occlusive disease in two or more coronary arteries with elevation of left ventricular end-diastolic pressures (LVEDP) significantly decreased arterial pressure (average 5 per cent) and myocardial contractility as measured by dP/dt/CPIP (average 14 per cent), and increased LVEDP (average 21 per cent). N2O had no significant effect in four patients who had angina without angiographically demonstrable coronary arterial disease. It is concluded that N2O depresses myocardial function in patients who have occlusion of the coronary arteries and impaired left ventricular function.

The clinical significance of the T wave in representing the electrical recovery process of the ventricular myocardium is well known. This electrical phenomenon, however, has been the subject of much less basic research than other parts of the electrocardiogram. With the development, in recent years, of more reliable recording techniques and the introduction of an incubator in which animal experiments can be performed in a more physiologic medium, this study of the repolarization process of the heart muscle seemed justified. Abundant controversy and confusion have developed over the direction of repolarization through the ventricular wall on the basis of polarity of the T wave. T polarity was studied by means of minute plunge electrodes recording simultaneously at selected depths in the ventricular walls. Moreover, the time course of the electrical recovery process was examined by comparing analogous points of the T wave in simultaneous records from the myocardial surface and the under-lying subendocardium and from different surface points, and these results compared with the polarity of the T waves. Experiments were designed also to study (a) the effect of local thermal changes upon adjacent and remote regions of the heart, (b) the effect of primary T-wave changes upon secondary ones by superimposing thermal changes upon left bundle branch block, and (c) the effect upon the T wave of ischemia due to chronic obstruction of coronary arteries.

The term "reversed pulsus paradoxus" may be used to describe an inspiratory rise of the arterial systolic and diastolic pressures, presumably related to an inspiratory increase in left ventricular stroke output. We have observed a reversed pulsus paradoxus in three unrelated clinical circumstances: idiopathic hypertrophic subaortic stenosis, isorhythmic ventricular rhythms and during intermittent inspiratory positive-pressure breathing in the presence of left ventricular failure. These unusual respiration-related fluctuations of blood pressure must be differentiated from the usual pulsus paradoxus of cardiac tamponade. (N Engl J Med 289:1272–1275, 1973)

Examination of myocardium from 14 patients with idiopathic hypertrophic subaortic stenosis and from 31 patients with non-obstructive cardiomyopathies of various types revealed the consistent presence of plasma membrane processes in intercalated discs. These processes extended for variable distances into the cytoplasm of adjacent cells, contained small nexuses and small knob-like endings, and sometimes terminated in the vicinity of longitudinally oriented T tubules. In three patients (one with polymyositis and congestive cardiomyopathy, one with polymyositis, congestive cardiomyopathy and chronic alcoholism, and one with congestive cardiomyopathy of unknown cause) some of the intercalated discs showed areas of dissociation which involved the undifferentiated regions and myofibrillar insertion sites. Vesicles of various sizes filled many of these areas of dissociation and appeared to be derived from swelling of the plasma membrane processes of intercalated discs.

Results obtained with the technique of Sakakibara and Konno for transvenous biopsy of right ventricular endomyocardium are described. The instrument consists of a metal catheter which bears two 2 × 2.5 mm biopsy spoons at its tip and is introduced into the right ventricle through the use of standard techniques of right-heart catheterization. This simple and safe technique was enployed in 28 patients with a variety of myocardial diseases of known and unknown etiology. Satisfactory specimens, usually multiple, were obtained in all 25 patients in whom the instrument could be introduced into the right ventricular cavity. Complications were minimal and the procedure was acceptable to the patients.

In contrast to the functional bundle-branch block (BBB) which is frequently rate-related and disappears when heart rate slows, we have encountered seven cases of a paradoxic disappearance of an existing, ischemia-induced BBB in premature beats. Supernormal conduction within the blocked bundle branch was not present in any of the cases. His bundle electrography in three of the cases demonstrated His spikes before each of the narrow-QRS premature beats. The His-Q intervals of the premature beats were considerably shorter than those of the control sinus beats. This finding clearly indicated an ectopic origin midway between the ventricular myocardium and the His bundle, i.e., within the ischemic fascicles of the left bundle, or the ischemic right bundle. From their points of origin such fascicular impulses propagate antegradely toward the respective area of the ventricular myocardium, and retrogradely toward the main His bundle, and at the same time down the remaining two fascicles. The antegrade conduction time in the short pathway down the ischemic fascicle is equaled by the faster conduction through the longer pathways of the remaining, uninjured fascicles, thereby accounting for the almost simultaneous activation of the myocardium of the two ventricles and the resultant narrow-QRS complexes.

Fascicular rhythms are recognizable in electrocardiograms and at first glance resemble junctional beats with aberrancy. Definitive diagnosis is based on His-bundle electrography and demonstration of a short His-Q interval.

SUMMARY 1. The responses of the systemic and pulmonary vascular net pressures to the Valsalva maneuver in patients with emphysema have been studied. 2. In a majority of patients a systemic arterial overshoot after the maneuver was accompanied by an overshoot in right atrial, pulmonary arterial, and pulmonary artery wedge net pressures. 3. In six patients the pulmonary vascular overshoots were reduced or abolished by the ganglionic blocking drug, tetraethyl-ammonium chloride (TEAC). 4. The results support the view that following a Valsalva maneuver a rise in post-arteriolar resistance may contribute to the pressure overshoot in the pulmonary circulation.

A previously unrecognized form of failure of normally functioning noncompetitive R-inhibited or R-triggered pacemakers to sense is described in 30 patients. The failure was produced by the delayed arrival of ventricular depolarization due to intraventricular conduction disturbances at the site of pacemaker sensing electrodes. These patinets with late activation of the right ventricle exhibited right bundle branch block (RBBB) during conducted sinus beats or had ectopic beats arising from the left ventricle. In both these situations, several late occurring QRS complexes were not sensed by the pacemaker electrodes in the right ventricular apex (RVA) and thereby the R-inhibited pacemaker spike discharged into the initial portion of the QRS complex. Activation of the RVA was delayed up to 65 msec in sinus beats with RBBB and even longer in premature beats arising from the left ventricle. The depolarization front of such beats reached the myocardium around the right ventricular pacemaker electrodes late in the QRS and thereby were not sensed up to 65 msec after the QRS onset as seen on the surface electrocardiogram (ECG). It was found in this study that if the inscription of such QRS complexes began up to 65 msec before the next due pacemaker impulse, these complexes were not sensed, allowing discharge of normally functioning R-inhibited pacemakers within the QRS which mimicked pacemaker malfunction. Failure to sense due to this phenomenon was observed in patients with noncompetitive pacemakers, both R-inhibited and R-triggered; temporary and permanent; with unipolar as well as bipolar electrodes. Similarly, patients with left ventricular epicardial electrodes and left bundle branch block in sinus beats also exhibited this phenomenon. Complete evaluation proved that pacemaker function was normal in the entire patient group. Recognition that failure to sense was the result of intraventricular conduction disorder prevented the untimely replacement of the pulse generator. This phenomenon of nonsensing by noncompetitive pacemakers should be considered in the presence of wide QRS complexes before the pacemaker is concluded to be malfunctioning.

A 14-year-old boy, admitted with intractable chest pain, was found to have an enlarged heart and calcification in the apical region, with electrocardiographic features of massive inferolateral myocardial infarction. Left ventricular angiography revealed a large left ventricular aneurysm. He died following resection of the aneurysm and post mortem examination showed changes of a non-specific chronic myocarditis. A vasculitis involving small coronary arterioles was also found in the vicinity of the aneurysm, and the possibility of a rheumatic vasculitis was suggested by a transient episode of an erythema marginatum-like eruption. It is concluded that the association of infarction pattern on the electrocardiogram together with calcification of the heart in children is highly suggestive of a ventricular aneurysm secondary to a myocarditis or a vasculitis involving small, intramyocardial branches of the coronary arteries.

The diagnosis of active pericardial bleeding has traditionally depended on an invasive documentation by needle aspiration, angiography, or direct inspection. Blood pool scintigraphy performed in 2 patients just before and after the development of hemopericardium revealed unique images in which acute pericardial bleeding manifested itself by an additional blood pool adjacent to the cardiac chambers. With appropriate attention to technical factors, such distinctive images should be highly specific for active bleeding into the pericardial sac.

This report describes a patient with pseudo-type II second-degree AV block due to an intermittent parasystolic focus located in the left bundle branch. A paradoxical increase in the fascicular rate was seen following intravenous propranolol, and fascicular extrasystoles were suppressed after intravenous isoproterenol treatment. All propagated fascicular extrasystoles were conducted to the ventricle with incomplete or complete right bundle branch block and a decrease in the H'-V interval compared to the H-V interval during sinus rhythm. Treatment with oral quinidine abolished fascicular extrasystoles without worsening of AV conduction.

The relationship between the resting electrocardiogram and left ventricular contractile pattern, as documented by angiography, was evaluated in 123 patients with coronary artery disease who underwent left ventriculography. Dyssynergy was present in 73/77 (95%) patients with pathologic Q waves on ECG recordings in contrast to 11/46 ( 24%; P < 0.01) without Q waves. The location of Q waves correlated well with the site of abnormal ventricular motion: antero-apical dyssynergy in 40/40 (100%) patients with anterior myocardial infarction (MI) and infero-apical dyssynergy in 25/28 (89%) with inferior MI. Four contraction patterns were defined: 1) normal motion-39 patients (35 without Q waves, four with inferior or posterior Q waves); 2) segmental hypokinesis-37 patients (six without Q, 31 with Q); 3) segmental akinesis-26 patients (four without Q, 22 with Q); and 4) localized dyskinesis-aneurysm in 21 patients (only one without Q, 20 with Q). The presence of ST elevation and T wave inversion (ST↑ - T↓) along with Q waves were associated with dyskinesis or akinesis in 18/19 (95%) patients. The Q wave location reflected the type of dyssynergy: 32/40 (80%) patients with anterior MI had akinesis or dyskinesis, while 18/28 (64%) patients with inferior MI exhibited hypokinesis. Lateral extension of the Q wave in an anterior MI was related to the dyssynergy type (average V lead: 4.9 in dyskinesis and 3.3 in hypokinesis; P < 0.05) and extent (dyssynergy area /LV silhouette: 31% with Q to V 3 and 58% to V 5 or V 6 ; P < 0.05). Dyssynergy area was larger in isolated anterior than inferior MI (42% and 23% of LV perimeter; P < 0.05) and largest in the anterior-inferior MI (68%; P < 0.05). Dyssynergy was more extensive with Q and ST↑-T↓ than with Q alone (48% and 33% LV perimeter; P < 0.05). Thus, specific QRS and ST-T wave alterations, when monitoring coronary disease, accurately predict characteristics of LV dyssynergy: Q identifies its presence and location and Q with ST↑-T↓ estimates its nature and extent.

Thirty cases of congenital stenosis of the branch pulmonary arteries are presented. This defect occurred as an isolated cardiovascular anomaly in 17 of the 30 patients. Clinically the most significant diagnostic feature was the wide distribution of the murmur, which was seldom louder than grade 3 6 . It is suggested that auscultation at the axillas and the back should be included in the routine evaluation of the cardiovascular system. Data are presented which suggest that comparing the rate of rise of the prestenotic with the poststenotic pressure pulse may differentiate organic from functional pressure gradients. Some pitfalls in the interpretation of the hemodynamic data are discussed.

SINCE the statement, "In fact, permanent cessation of the heartbeat or serious ventricular arrhythmias are almost unheard of was made by Lown and Levine1 in 1961, 2 deaths that followed carotid-sin...

Typical cases of ventricular preexcitation by conduction through an accessory pathway are easily recognized on electrocardiograms, but atypical cases require electrophysiologic studies. Recent investigations cast doubt on the long-held assumption that Kent bundles invariably form the accessory pathway.

Direct electrical stimulation of the left atrium in intact human subjects was performed in 11 patients. The resultant P waves did not conform to the strict left to right direction suggested by previously published studies. Marked variability was observed in the P waves resulting from electrical stimulation of the same area of the left atrium in different subjects. The existing criteria for diagnosis of left atrial P waves based on preconceived notions could not be corroborated. No new criteria could be established, and none is proposed. Recording of an esophageal or intracavitary atrial lead simultaneously with surface leads should be regarded as the first, indispensable prerequisite in any future study of left atrial P waves. It is suggested that stimulation of a given point on the walls of the left atrium may give rise to varying P waves probably because of the interplay of slow, wave-like intramyocardial conduction with the more rapid, non-wave-like spread via the specialized interatrial pathways. P waves resulting from electrical stimulation of the right lower aspect of the interatrial septum at or near the coronary sinus were virtually indistinguishable from left atrial P waves.

The differential diagnosis of anterior chest pain has always been an important problem in clinical medicine. In the past few decades, it has grown steadily in importance and clinicians have become increasingly aware of the manifestations of coronary artery disease and its potentially malignant nature. This disease is so common and its recognition so essential that the clinician may feel safe in considering it as a possibility in any patient complaining of pain in the anterior chest wall. This is particularly true if the patient has an authenticated history of myocardial infarction or is in the so-called coronary age group. On the other hand, there are innumerable noncardiac conditions, visceral as well as somatic, that give rise to anterior chest pain and are to be suspected if one is to avoid an unwarranted diagnosis of coronary artery disease and the resultant unwise restrictions and their psychological consequences. It is well

Comparative hemodynamic and electrocardiographic investigation of antiarrhythmic doses of procainamide and lidocaine was carried out in 19 patients with acute myocardial infarction or with severe left ventricular failure of other etiologies. In 12 patients in whom the standard recommended dosage of these agents was equally effective in abating ventricular tachyarrhythmias, there were no significant adverse hemodynamic and electrical effects or differences (p > 0.05) between relatively small salutary doses of lidocaine and procainamide after their intravenous administration in similar quantity and manner (100 mg in 3 min followed by 2 mg/min for 20 min). Furthermore, larger doses of procainamide (500 mg given 20 mg/min intravenously), which were also therapeutically beneficial in seven additional patients with acute myocardial infarction, caused no significant alteration (p > 0.05) in hemodynamic function. With the 500 mg dose, there was a small difference (p

Out of a large series of patients with coronary artery disease 6 were selected with high anterior myocardial infarction. These cases are presented in detail and their special electrocardiographic characteristics are described. The difficulty in making the diagnosis of infarction by the usual leads and the need for special leads are pointed out.

A case of angina pectoris manifested by S–T segment elevation (Prinzmetal's variant form or angina pectoris inversa) is described, and the electrocardiographic changes are shown to be reproducible by ingestion of iced water.

Excerpt The ECG has not been fully evaluated for its relation to ventricular function and clinical status. One-hundred and four patients with angina pectoris and documented coronary artery disease ...

pectoris (38.7 Y0 ) , and in both VPB and control patients with ECG evidence of left ventricular hypertrophy (32 and 56%) respectively). These data help to define the high-risk patient who may profit from prophylactic therapy. Spontaneous Closure of Small Ventricular Defects. Probability Rates in the First 5 Years of Life BRUCE ALPERT, BA*; RICHARD DESMOND ROWE, MD, Balti

• Undue reliance on the electrocardiogram has created many problems in the diagnosis and management of heart disease. Subjective cardiac symptoms are frequently occasioned or intensified by the physician's unwarranted diagnosis of heart disease on the basis of some poorly understood or misinterpreted electrocardiographic aberrations. It is estimated that an average physician caring for cardiac patients sees from 10 to 25, and perhaps more, such cases of heart disease of electrocardiographic origin per year. The two most important symptoms of this disease are anxiety and chest pain. Departure from the assumed normal, especially of the S-T segment and the T wave, does not always mean abnormality of the myocardium. Severe myocardial abnormality is sometimes present without significant electrocardiographic abnormality. Diffuse changes in the deeper layers of the myocardium sometimes fail to alter the electrocardiogram, while relatively insignificant lesions in the superficial layer sometimes alter it markedly. The most reliable guide in the diagnosis and management of heart disease is the patient's clinical state.