Benjamin Befeler

Coronary artery aneurysms: Study of their etiology, clinical course and effect on left ventricular function and prognosis

Coronary artery aneurysms were found in 16 men between 37 and 62 years of age, mean 51 years. Aneurysms were of two types: saccular and fusiform. They involved the right coronary artery in 13 (87 per cent), the circumflex artery in eight (50 per cent) and the left anterior descending artery in five (31 per cent). In some patients, more than one vessel was involved. Twelve patients presented with angina pectoris, three with congestive heart failure and one with both. Five were in functional class II, eight were in class III and three were in class IV at the beginning of the study. The electrocardiogram showed evidence of previous myocardial infarction in four patients; four patients had left ventricular hypertrophy, one had left axis deviation, one had left bundle branch block, one had right bundle branch block, two had first degree atrioventricular block and seven had abnormalities in the S-T segment and T wave. Obstructive coronary disease was present in all; the obstruction score was from 1 to 4 in three patients, from 5 to 9 in four patients and from 10 to 14 in the remaining nine. Similar aneurysms were found in the pulmonary artery of one patient and in the abdominal aorta of three patients; in seven of 14 patients with adequate venous angiograms, varicosities of the coronary venous tree were observed. Left ventricular dysfunction and angina pectoris were noted in patients with significant obstructive coronary disease (greater than 70 per cent) and also in patients without obstruction but with coronary aneurysms. Ten patients were treated surgically; nine underwent aortocoronary bypass and one mitral valve replacement. Criteria for bypass was the presence of obstructive disease and medically unresponsive angina pectoris. All but one surgically treated patient showed improvement. The functional class in medically treated patients was unchanged. Fourteen patients were still alive at the completion of the study. The findings of this study suggest that angina pectoris and left ventricular dysfunction can occur with coronary artery aneurysm without coronary artery obstructions. Coronary aneurysms may be a subset of atherosclerosis, and this process may involve other vascular territories. The prognosis in those patients appears to be no worse than in patients with obstructive coronary disease and no aneurysms.

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Factors regulating ventricular rates during atrial flutter and fibrillation in pre-excitation (Wolff-Parkinson-White) syndrome.

known to alternate but the reasons why the ratescould vary so muchhave been a matter of debateandspeculation. Thepresent communicationandaprevious study (Castellanos et al., I973) suggestedthat ventricular rate depended on the duration ofthe effective refractory period of the accessorypathway. When it was longer than that of thenormal AVpathway (and AVnodal block was notpresent) the majority of the impulses were trans-mitted across the normal AVpathwaythrough the

The His-Purkinje electrocardiogram in man: an initial assessment of its uses and limitations.

SUMMARY A metodology is described for noninvasive recording of the electrical activity generated by the His-Purkinje system of man utilizing filtering, high amplification, and signal averaging. A waveform ranging between 1 and 10μ was observed during the P-R segment. In many individuals, there was temporal overlap between the terminal P wave and the initial portion of the His-Purkinje waveform. In ten patients with long P-R intervals there was a strong correlation (r > 0.95) between the H-V time measured by electrode catheter and the duration of the His-Purkinje waveform. In two patients with atrial fibrillation the resultant His-Purkinje waveform was similar in morphology and duration to those observed in the ten patients. In each group H-V time was determined noninvasively and a waveform associated with electrical activation of the major portions of the His- Purkinje system was obtained.

Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations.

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or...

Type I, Type II, and Type III Gaps in Bundle-Branch Conduction

“Gaps” in bundle-branch conduction were observed in three patients using the combined technic of premature atrial stimulation and His bundle recordings.In type I gap a complete LBBB pattern disappeared at shorter coupling intervals because the premature atrial impulses encountered enough delay at the A-V node to reach the left bundle branch after the end of its effective refractory period. When this occurred, the H1-H2 intervals were longer and the H2-V2 intervals shorter than that at which complete LBBB had been present.In type II gap a complete RBBB pattern disappeared at shorter coupling intervals because the premature atrial impulses were so delayed within the proximal His-Purkinje system that they reached the right bundle branch after the end of its effective refractory period. When this occurred the H1-H2 intervals were shorter and the H2-V2 longer than that at which complete RBBB had been present.In the patient with type III gap and complete LBBB, conduction to the ventricles through the right branch failed at long coupling intervals but was resumed at shorter coupling intervals while the H1-H2 intervals were shorter, and the H2-V2 intervals similar, to those at which block had occurred. True supernormal conduction was excluded in the first two cases. Nevertheless, this phenomenon, as well as a longitudinal dissociation, varying pulsatile vagal discharges acting on an area of depressed conductivity, and phase 4 diastolic depolarization in the right branch coexisting with complete block in the left branch, could have been responsible for type III gap.

Effects of the pacing site on A-H conduction and refractoriness in patients with short P-R intervals.

His bundle recordings were studied in four patients with short P-R and A-H intervals, and narrow QRS complexes, who had experienced several episodes of supraventricular tachyarrhythmias. The heart was paced from the high right atrium (HRA) and the coronary sinus (CS). In three patients the A-H Wenckebach phenomenon occurred at higher rates (greater than 200 pacing beats/min) when the CS was paced than when pacing was performed from the HRA. Moreover, CS stimulation produced smaller increments in the A-H interval than did pacing from HRA. The extrastimulus method of testing was done. In cases 1 and 2 the functional refractory period of the A-H tissues was 15 to 25 msec shorter during CS pacing than when pacing from the HRA. In case 3, the low right atrium (LRA) as well as the other two sites were paced. A type I gap was seen from HRA, a type 2 gap from CS, and both types appeared when the LRA was paced. Case 4, in which the mid-right atrium (MRA) was also stimulated, had a double pathway from HRA and CS with conduction through the accessory pathway late in the cycle and through the A-V node earlier in the cycle. However, the A-V node could not be penetrated during MRA stimulation. It appeared that the pacing site influenced the A-H conduction pattern and refractoriness, possibly by changing the site and/or mode of entry of the stimulus into the pathways that are responsible for this syndrome.

Transverse Spread and Longitudinal Dissociation in the Distal A-V Conducting System

Isolated preparations of portions of the canine intraventricular conducting system were studied by microelectrode techniques in order to determine the nature of transverse spread and longitudinal dissociation of impulses in bundle branches and false tendons. Driving stimuli were delivered to an eccentric location on normal conducting tissue, and the arrival times of the propagating impulses were mapped along the length and width of the bundle branch, or along the false tendon ipsilateral and contralateral to the site of stimulation. The difference between the arrival times on the two sides was found to decrease progressively as a function of distance from the site of stimulation, the data suggesting that transverse spread of impulses involves propagation through transverse crossover points between the longitudinally oriented conducting elements. Impulses originating eccentrically became uniformly conducted across the transverse axis of bundle branches 8-15 mm from the level of the stimulating electrode, and of false tendons 2-4 mm from the stimulus site. True longitudinal dissociation, producing conduction maps different from those representing normal transverse propagation, was seen occasionally in tissue having longitudinally oriented strips of abnormal tissue. However, early premature stimulation commonly resulted in longitudinal temporal dissociation of the premature responses, possibly due to functional block in the transverse crossover fibers.

Double accessory pathways in Wolff Parkinson White syndrome

Intracardiac electrophysiological studies were performed in two patients with Wolff-Parkinson-White (WPW) syndrome. Atrial pacing at increasing rates or shorter coupling intervals produced inscription of the forward His bundle deflection at progressively longer intervals after the onset of ventricular depolarization. There was an associated increase in QRS duration without any change in the P-R (or St-V) interval. This response was consistent with a Kent bundle. Case 1 also had a short A-H interval which did not show the expected prolongation with stimulation at progressively faster rates. This suggested the presence of a James bundle in addition to the Kent bundle. In case 2 beats conducted exclusively through the atrioventricular (A-V) node had a short H-V interval but a delta wave was not inscribed. Absence of an initial slurring was attributed to the existence of an infra-His bundle bypass of the Mahaim type causing only slight pre-excitation, which was not of sufficient magnitude to be recorded by body surface leads. However, the existence of a congenitally short anterosuperior division of the left bundle could nt be excluded.

Cardiovascular dynamics during coronary sinus, right atrial, and right ventricular pacing

Abstract Permanent pervenous right atrial pacing has not been widely used to date. The coronary sinus may provide a site from where reliable permanent pacing can be performed so as to preserve atrial contribution in patients with intact A-V conduction who require pacing, as in sinus bradycardia, sinus arrest, and recurrent tachyarrhythmias. To test this hypothesis, 15 individuals, 37 to 70 years old (average 56.6 years), with a variety of heart diseases, but with normal A-V conduction, were studied. After control cardiac index had been obtained, coronary sinus, right atrial pacing, and right ventricular pacing were performed at two levels above the control sinus rate. Mean cardiac index was virtually identical for coronary sinus and right atrial pacing at the first level, 2.38 and 2.37 L./min./M. 2 , respectively, and at the second level, 2.45 and 2.42 L./min./M. 2 , respectively. During the first level of right ventricular pacing mean cardiac index was 1.87 L./min./M. 2 , 21.8 per cent lower than during coronary sinus pacing (p 2 , 23.3 per cent lower than during coronary sinus pacing (p The coronary sinus provides an area from which the heart can be paced with the hemodynamic advantages of atrial pacing if intact A-V conduction exists.