Rashid A. Massumi

Electrocardiographic and Cineangiographic Correlations in Assessment of the Location, Nature and Extent of Abnormal Left Ventricular Segmental Contraction in Coronary Artery Disease

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 V3 and 58% to V5 or V6; 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.

Disturbances of cardiac rhythm and conduction induced by exercise. Diagnostic, prognostic and therapeutic implications.

Abstract 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.

Myocardial Performance and N2O Analgesia in Coronary-artery Disease

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.

Phenomenon of Supernormality in the Human Heart

This report documents five cases of supernormal (SN) conductivity in the sense of unexpected normalization of the previously existing bundle-branch block (BBB) and three cases of SN excitability in which impulses delivered to the ventricles propagated to the myocardium only during a well-defined interval in the cardiac cycles corresponding to the U waves of the preceding beat. In none of the patients could SN be abolished by atropine, suggesting absence of an important vagal role. In the five patients with SN conductivity there were three examples of right BBB in which spontaneous, as well as electrically induced premature atrial beats, were followed by normal QRS complexes only if they reached the right bundle during its SN phase. In the other two patients with bilateral BBB, strategically placed sinus P waves and electrically induced atrial impulses were conducted to the ventricles with normal P-His and His-Q intervals. Analysis of the electrocardiograms and His bundle electrograms indicated that SN conductivity resided in the bundle branches, and not in the A-V node. In one of two patients with bilateral BBB and SN conductivity in the right bundle branch, the SN-conducted beats occurred after both left and right ventricular escape beats, but were coupled to the preceding escape beats by longer intervals after left ventricular escape beats than after right ventricular escape beats. The difference was accounted for by the later activation of the right bundle branch when the preceding escape beat originated from the contralateral left ventricle. These observations favor an electrophysiologic explanation for the phenomenon of supernormality which is most probably related to the increased voltage of the transmembrane action potential in the period commonly known as the period of negative afterpotentials. This study provides no support for the hemodynamic or vagal theory of supernormality.

Lack of Sensing by Demand Pacemakers due to Intraventricular Conduction Defects

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.

Paradoxic Phenomenon of Premature Beats with Narrow QRS in the Presence of Bundle-Branch Block

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 Rhythm: Morphologic Features and Protean Manifestations

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.

Electrophysiologic properties of perhexiline

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 > .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 <0.1 mao 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.

The Wolff-Parkinson-White syndrome.

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.