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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.

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.

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.

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.

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 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.

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.