Showing papers on "Ventricle published in 1970"

Total Excitation of the Isolated Human Heart

Abstract: To obtain information concerning the time course and instantaneous distribution of the excitatory process of the normal human heart, studies were made on isolated human hearts from seven individuals who died from various cerebral conditions, but who had no history of cardiac disease. Measurements were made from as many as 870 intramural terminals. In the isolated human hearts three endocardial areas were synchronously excited 0 to 5 msec after the start of the left ventricular activity potential. These areas increased rapidly in size during the next 5 to 10 msec and became confluent in 15 to 20 msec. The left ventricular areas first excited were (1) high on the anterior paraseptal wall just below the attachment of the mitral valve; (2) central on the left surface of the interventricular septum and (3) posterior paraseptal about one third of the distance from apex to base. The last part of the left ventricle to be activated usually was the posterobasal area. Endocardial activation of the right ventricle wa...

The shape and movements of the human left ventricle during systole: A study by cineangiography and by cineradiography of epicardial markers☆

Abstract: The shape of the left ventricular cavity and the movements of the mitral valve, aorta and coronary arteries were studied in cineangiograms obtained from normal subjects and patients with coronary arterial disease, mitral stenosis or atrial septal defect. Movements of the left ventricular epicardial surface were studied by postoperative cineradiography of radiopaque markers previously attached during closed mitral valvotomy. The pre-ejection and ejection phases of systole were identified from the simultaneously recorded phonocardiogram, apex cardiogram, indirect carotid pulse pressure tracing and electrocardiogram. The left ventricular epicardial surface contracted in an approximately symmetrical fashion with slight rotational movements about the long axis most marked at the beginning and end of systole, but contraction of the left ventricular cavity appeared less symmetrical because of the systolic increase in wall thickness, approximation of trabeculae and movements of the mitral valve. During pre-ejection, the left ventricular cavity narrowed anteroposteriorly, the descent of the base began and a slight anticlockwise rotation of the epicardial surface was accompanied by a slight thrust of the apex toward the chest wall. During ejection, narrowing of the left ventricular cavity and the descent of the base continued, and a slight clockwise rotation and retraction of the apex occurred in late systole. The symmetry of left ventricular contraction may be due to the similarity of contractility and afterload of individual myocardial fibers, and the slight rotational movements may be a result of sequential activation of the left ventricular myocardium from endocardial to epicardial surface.

Identification of ultrasound echoes from the left ventricle by use of intracardiac injections of indocyanine green.

Abstract: This study was designed to identify the ultrasound echoes originating from the left ventricle. Injections of indocyanine green and saline were made directly in the left ventricular cavity via a cardiac catheter in patients undergoing routine diagnostic cardiac catheterization. The injections produced a cloud of echoes that filled the left ventricular cavity and outlined the left side of the interventricular septum and the endocardial surface of the posterior left ventricular wall. The results of this study verified the origin of echoes that are vital to the ultrasound technics for the detection of pericardial effusion, left ventricular wall size, left ventricular cavity size, and left ventricular stroke volume. This study also provided ways of distinguishing between the true left ventricular wall echoes and intracavitary echoes that often cause confusion.

Quantitative study of infarcted myocardium in cardiogenic shock.

Abstract: A post-mortem study of the heart was performed in 20 patients dying of cardiogenic shock. The extent of infarcted myocardium was defined by using a mitochondrial dehydrogenase stain nitro-BT which allowed macroscopical recognition of tissue death as early as 12 hours. Extensive myocardial injury was found to accompany cardiogenic shock predominantly affecting the left ventricle and the interventricular septum. Severe atheromatous involvement of the coronary arteries was noted.

Experimental myocardial infarction: IV. Reduction of left ventricular compliance in the healing phase

Abstract: Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular end-diastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction.

Systolic and diastolic abnormalities of the left ventricle in coronary artery disease. Studies in patients with little or no enlargement of ventricular volume.

Abstract: Left ventricular volume and circumference were calculated from cineangiocardiograms at 60 frames/sec in 15 patients with arteriographically proven coronary artery disease (CAD) and five control subjects. The patients with CAD had no mitral regurgitation and had an average end-diastolic volume equivalent to that reported by others in normal subjects and to that of the control group. The average end-diastolic pressure was higher in CAD and was often abnormal, despite lack of increase in enddiastolic volume. The ejection was lower in the CAD group as was the extent of circumferential fiber shortening. Maximal and mean rates of fiber shortening correlated positively with ejection fraction and were low in some individuals with CAD. We conclude that our patients without significant increase in left ventricular enddiastolic volume had abnormalities of diastolic compliance and contractile performance.

The normal pericardium

Abstract: Under normal conditions the pericardium, with its fluid, lubricates the moving surfaces of the heart, holds the heart in a fixed geometric position and isolates the heart from other structures in the thorax, thus preventing adhesions and spread of infection. It also serves the following functions: (1) prevents dilatation of the heart chambers and insures that the level of transmural cardiac pressures will be low, never exceeding a few mm Hg; (2) prevents hypertrophy of the heart under conditions of strenuous exercise; (3) limits right ventricular stroke work under conditions of increased left ventricular outflow resistance; (4) prevents ventriculo-atrial regurgitation under conditions of increased ventricular end-diastolic pressures; (5) in association with the lungs and tissue surrounding the pericardium it facilitates the filling of the atria by the development of negative pericardial pressure during ventricular systole; (6) responds to nerve stimulation and reflexly affects blood pressure and heart rate; and (7) in association with the pleural fluid constitutes a hydrostatic system that automatically applies compensating hydrostatic pressures on the outside of the heart when gravitational or inertial forces acting on the heart are altered (during acceleration, for example). This automatic hydrostatic compensation insures that end-diastolic transmural pressure is the same at all hydrostatic levels of the ventricle; as a result the stretch of the muscle fibers is uniform, and the Frank-Starling mechanism operates equally at all hydrostatic levels within the ventricles.

Inotropic changes in the left ventricle: the effect of changes in heart rate, aortic pressure and end-diastolic pressure.

Abstract: 1. Under conditions where heart rate, mean aortic pressure and enddiastolic pressure in the left ventricle are held constant, the intravenous infusion of isoprenaline is accompanied by large changes in dP/dt max in the left ventricle. 2. Under similar conditions, during stepwise increments in the rate of infusion of isoprenaline the changes in dP/dt max (measured at a constant paced heart rate) were proportional to changes in the free (intrinsic) heart rate. It is concluded that dP/dt max is a quantitative index of inotropic changes in the left ventricle. 3. In comparison to dP/dt max, three other variables which have been used to indicate inotropic changes in the heart (peak pressure in the left ventricle, duration of systole and stroke work at constant end-diastolic pressure), were shown to be unreliable indices of inotropic changes. 4. Using dP/dt max to indicate inotropic changes, alteration in the heart rate while mean aortic pressure and end-diastolic pressure in the left ventricle were held constant, and in mean aortic pressure while heart rate ane end-diastolic pressure in the left ventricle were held constant, were each shown to be accompanied by small inotropic changes in the heart. 5. Under similar conditions, changes in end-diastolic pressure in the left ventricle alone were not accompanied by inotropic changes as indicated by dP/dt max.

Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction

Abstract: Left ventricular performance in 19 patients with acute myocardial infarction has been evaluated by measuring left ventricular response in terms of cardiac output, stroke volume, work, and power to progressive elevation of filling pressure accomplished by progressive expansion of blood volume with rapid infusion of low molecular weight dextran. Such infusion can elevate the cardiac output, stroke volume, work, and power and thus delineate the function of the left ventricle by Frank-Starling function curves. Left ventricular filling pressure in the range of 20-24 mm Hg was associated with the peak of the curves and when the filling pressure exceeded this range, the curves became flattened or decreased. An increase in cardiac output could be maintained for 4 or more hr. Patients with a flattened function curve had a high mortality in the ensuing 8 wk. The function curve showed improvement in myocardial function during the early convalescence. When left ventricular filling pressure is monitored directly or as pulmonary artery end-diastolic pressure, low molecular weight dextran provides a method for assessment of left ventricular function.

Abnormal Left Ventricular Contraction in Patients with Mitral Stenosis

Abstract: Twenty-five patients with pure mitral stenosis and nine normal subjects were studied by selective left ventricular cineangiocardiography. Left ventricular volumes were measured at end systole, throughout diastole, and at end diastole. Although filling curves showed that the left ventricles filled slowly in patients with mitral stenosis, normal end-diastolic volumes were attained provided diastole lasted 400 msec. Despite normal end-diastolic volumes, end-systolic volumes were significantly larger (P < 0.0005) in the patients with mitral stenosis (av=64.6 ml) than in normal subjects (30.8 ml). Correspondingly, left ventricular ejection fractions were significantly lower (P < 0.0005) in the patients with mitral stenosis (55.7%) than in the normal subjects (76.7%). Qualitative analysis of the cineangiocardiograms demonstrated that 20 patients with mitral stenosis had distortion, immobility, and rigidity of the posterobasal area of the left ventricle. It is hypothesized that a rigid "mitral complex" immobiliz...

The Role of Left Atrial Transport in Aortic and Mitral Stenosis

Abstract: The relationship of left atrial contraction to ventricular filling was studied in 24 patients. Eight patients had aortic stenosis, eight had mitral stenosis, and eight others served as a control group. All had normal sinus rhythm. Cineangiocardiographic volumetric determinations of the left ventricle were done throughout the cardiac cycle, and the rate of left ventricular filling before and during left atrial contraction was calculated. In the group with aortic stenosis 39% of the left ventricular stroke volume entered the ventricle during left atrial contraction; in the group with mitral stenosis 24% was contributed during left atrial contraction, and in the control patients, 26%. The rate of left ventricular filling more than doubled during left atrial contraction in aortic stenosis, while no consistent change in the rate of filling occurred during left atrial contraction in mitral stenosis and in the control group. The character of the resistance to left ventricular filling in aortic stenosis and mitra...

Hemodynamic Evaluation of Intra-Aortic Balloon Pumping in Man

Abstract: Intra-aortic balloon pumping is effective in reducing left ventricular peak systolic pressure and increasing cardiac output in patients with severe cardiogenic shock secondary to acute myocardial infarction. Associated with these effects is a reduction in intravenous catecholamine requirements and increased sensitivity to diuretics. Reduction in left ventricular end-diastolic pressure is implied by improvement in arterial blood gas saturation (reduced arterioalveolar gradient) and was shown directly in one patient. Total myocardial oxygen consumption is probably reduced by counterpulsation. Platelet levels have not fallen significantly with adequate heparinization and the slow infusion of low molecular weight dextran. No complications have occurred related to femoral artery cannulation, nor has there been significant damage to the aorta. The findings suggest that this system is a safe means of assisting the failing left ventricle. The high mortality in this series (seven of eight patients) is related to t...

Relative Contributions of the Atrial Systole-Ventricular Systole Interval and of Patterns of Ventricular Activation to Ventricular Function during Electrical Pacing of the Dog Heart

Abstract: In areflexic canine right heart bypass preparations, little difference in ventricular function was observed as a result of atrial pacing, sequential atrioventricular pacing, or atrial-His bundle pacing at an appropriate atrial systole-ventricular systole (As-Vs) interval. Ventricular function was depressed during ventricular pacing and during atrioventricular pacing with an inappropriate As-Vs interval. In areflexic isovolumic left ventricle preparations, ventricular function was depressed during ventricular pacing compared to atrial pacing, and changes in the As-Vs interval during atrioventricular pacing were accompanied by changes in ventricular function only in association with changing patterns of ventricular activation. In animals with heart block under conditions of right heart bypass, wherein changes in the pattern of ventricular activation were precluded during atrioventricular pacing, ventricular function deteriorated pari passu with shortening of the As-Vs interval. These data indicate that both the temporal relation between atrial and ventricular contraction and the pattern of ventricular activation importantly influence ventricular function during cardiac pacing. The marked changes in ventricular function observed as a function of the As-Vs interval, for any given pattern of electrical activation, suggest that the As-Vs interval is the more important determinant of ventricular function during cardiac pacing.

Interrelationship of architecture and function of the right ventricle.

Abstract: ARMOUR, J. A., J. B. PACE, AND W. C. RANDALL. kWreZationship of architecture and function uf the right ventricle. Am. J. Physiol. 2N3(1): ,)174-179. 1970.-The sequence of contraction and augmentation patterns in contractile force of the sinus and conus regions of the right ventricle were analyzed under control, vagal, and sympathetic stimulation as well as norepinephrine infusion states. The normal peristaltic contraction wave from sinus to conus was exaggerated during vagal stimulation but made more nearly synchronous or even abolished during stellate ganglion stimulation. The sinus to conus sequence was often reversed as a result of norepinephrine augmentation. Whereas the conus fibers showed greater increase in force of contraction than did the sinus fibers during stellate stimulation and norepinephrine injection, pressures recorded from the sinus portion of the right ventricle greatly exceeded those measured simultaneously from the conus. A marked intraventricular pressure gradient was created from sinus to conus, with a relatively smaller gradient from conus to pulmonary artery. Thus, the functional intervention of the infundibular region of the right ventricle as a pressure regulator protecting the pulmonary vasculature may be hypothesized.

Experimental myocardial infarction: II. Acute depression and subsequent recovery of left ventricular function: serial measurements in intact conscious dogs

Abstract: Acute myocardial infarction causes depression of left ventricular function, but the capacity of the ventricle to recover from such an injury remains unknown. This problem was explored by measuring left ventricular function in eight intact conscious dogs before, 1 hr after, and again 6-8 days after myocardial infarction. Acute myocardial infarction was produced using a technique which entails gradual inflation over an average period of 1 hr of a balloon cuff previously implanted around the left anterior descending coronary artery. Occurrence of anterior wall infarction was detected electrocardiographically and later confirmed by postmortem examination. Left ventricular function was evaluated from the relationship between left ventricular developed pressure (left ventricular peak systolic pressure minus left ventricular end-diastolic pressure) and left ventricular end-diastolic pressure during transient aortic occlusion with a balloon catheter. Left ventricular function curves were obtained by plotting left ventricular-developed pressure at increasing left ventricular end-diastolic pressures up to 50 mm Hg. Acute myocardial infarction caused marked depression of left ventricular function measured 1 hr after onset of infarction, but 1 wk later all eight animals showed improvement with return of function toward the control levels. A small but significant descending limb was noted at left ventricular end-diastolic pressures above 35 mm Hg. Quantitatively, the descending limb was similar before, 1 hr after, and 1 wk after myocardial infarction. Hemodynamic data revealed evidence of left ventricular failure in all animals, but variability in individual hemodynamic parameters was noted. The data indicate that the marked depression of left ventricular function observed immediately after experimental acute myocardial infarction undergoes considerable resolution within 1 wk, but that functional recovery remains incomplete.

Ventriculo-atrial Conduction in Man

Abstract: Transvenous electrodes were placed in the right atrium and ventricle of 50 patients with heart disease and arrhythmias. The ventricles were paced at several rates, each in excess of the sino-atrial rate. An atrial electrogram and surface electrocardiogram were recorded simultaneously in each patient; utilizing strict criteria, the incidence with which 1:1 ventriculo-atrial conduction (VAC) could be elicited in these patients was assessed. These patients were divided into two groups-26 patients with normal A-V conduction comprised group 1, and 24 patients with prolonged A-V conduction, group 2. VAC was demonstrated in 89% of group 1 patients but in only 8% of the group 2 patients. The difference in the incidence of 1:1 VAC between the two groups was statistically significant ( P < 0.01). The presence or absence of 1:1 VAC could not be related to type of heart disease, medication, presence of acute myocardial infarction, or presence of intraventricular conduction defect. Altering the paced ventricular rate or introducing stimulated ventricular premature depolarization in group 1 patients could produce any degree of VAC impairment. During such maneuvers, ventricular reciprocal beats (ventricular echoes) and ventricular reciprocal rhythms were observed.

Alteration of mechanical performance of the ventricle by intraaortic balloon counterpulsation.

Abstract: Intraaortic balloon counterpulsation has been shown to reduce the immediate mortality due to acute myocardial infarction in dogs. Previous studies have emphasized the importance of the absolute or relative increases in coronary blood flow that result from augmentation of diastolic aortic pressure. This study was designed to clarify the role of the decreased systolic pressure characteristic of counterpulsation in increasing the cardiac output. Eleven dogs were studied without intervention except for counterpulsation. A decrease in peak left ventricular pressure from 138 ± 7 to 116 ± 6 mm Hg ( P Hg . As a result of the decreased impedance to ejection, peak aortic flow, stroke volume and cardiac output increased by 15 percent. In 6 dogs studied after acute myocardial infarction secondary to ligation of the left anterior descending coronary artery, there were parallel but less marked changes in the hemodynamic measurements. The external performance of the ventricle when evaluated in terms of peak flow, stroke volume and output was an inverse function of the impedance to ejection. Since effective assistance to the failing heart must result in increased external performance, the importance of adequate reduction of systolic impedance must not be underestimated.

Left ventricular abnormality with late mitral insufficiency and abnormal electrocardiogram

Abstract: An abnormal contraction that alters the contour of the left ventricle only during systole but not in diastole and results in mild mitral insufficiency has been demonstrated in 6 girls with apical systolic click, late systolic murmur and T wave inversion. They have remained asymptomatic during a period of follow-up studies ranging from 3 to 17 years. Their young age and the absence of myocarditis, pericarditis and coronary arterial abnormality suggest that they have a congenital anomaly in a localized area of the left ventricular myocardium which results in late systolic dysfunction of the mitral apparatus. We believe that the findings in this group constitute a distinctive syndrome among the heterogeneous causes of mitral insufficiency late in systole.

Hemodynamic effects of ventricular defibrillation

Abstract: Hemodynamic responses to ventricular defibrillation were studied in anesthetized dogs. Observations were made on arterial, right atrial and left ventricular end-diastolic pressures, on cardiac output (dye dilution), heart rate, and right atrial electrocardiogram. Ventricular fibrillation was induced electrically with a bipolar electrode catheter placed in the right ventricle. Fibrillation was maintained for 15 or 30 sec and terminated with a 400 w sec capacitor discharge across the thoracic cage. Responses lasted 1-10 min after conversion and included a cholinergic and an adrenergic component. The cholinergic component was characterized by sinus bradycardia, periods of sinus arrest, atrioventricular block, and ventricular premature beats. The adrenergic component included increases in arterial pressure, in cardiac output, and in left ventricular stroke work at a time when left ventricular end-diastolic pressure was normal; there was no change in total peripheral resistance. The pH of arterial blood decreased slightly and pCO2 increased but pO2 and the concentration of lactate were unchanged. Bilateral vagotomy and intravenous administration of atropine blocked the cholinergic component, unmasked a sinus tachycardia, and accentuated the adrenergic component of the response. The latter was blocked by intravenous administration of propranolol and phenoxybenzamine. These responses were related primarily to conversion of ventricular fibrillation rather than to the electrical discharge of countershock because countershock without ventricular fibrillation caused more transient and smaller responses than those observed with defibrillation: furthermore, the hemodynamic effects of defibrillation were augmented by prolongation of the duration of fibrillation. The results suggest that the cholinergic component of the response may be detrimental in that it favors spontaneous recurrence of fibrillation; on the other hand, the adrenergic component may be essential for conversion since only one of six dogs depleted of endogenous catecholamines with reserpine survived ventricular defibrillation.

Effects of diphenylhydantoin on excitability and automaticity in the canine heart.

Abstract: Studies were performed on the dog heart in situ to determine the effects of diphenylhydantoin (DPH) on excitability and automaticity. DPH decreased automaticity in the His-Purkinje system, evidenced by an increase in the ventricular escape time both during vagal stimulation in intact dogs and after ventricular overdrive in dogs with heart block. The spontaneous ventricular rate of dogs with heart block was unaffected by doses up to 20 mg/kg. DPH had no significant effect on either atrial or ventricular diastolic threshold when this variable was tested with bipolar stimuli or with stigmatic anodal or cathodal stimuli. The effective refractory period of atrial and particularly of ventricular muscle was shortened by DPH (10 mg/kg); a leftward shift in the strength-interval curve occurred consistently. Multiple response threshold and fibrillation thresholds were elevated by DPH in both the ventricle and atrium (20 of 24 experiments). In anesthetized dogs, intraventricular conduction velocity increased minimally after DPH administration. DPH increased transmembrane threshold voltage and reduced the current required to stimulate isolated Purkinje fibers. The commercial solvent used clinically as a diluent for DPH was found to increase diastolic threshold and prolong the effective refractory period.

Double-Outlet Left Ventricle with an Intact Ventricular Septum: Clinical and Autopsy Diagnosis and Developmental Implications

Abstract: Clinical, laboratory, and anatomic findings were presented concerning the first clinically diagnosed and autopsy proved case of origin of both great arteries from the morphologically left ventricle. The salient pathologic findings were: normally interrelated chambers (noninverted) in situs solitus; no ventricular septal defect; infundibular atresia; infundibulum related only to the right ventricle; absence of infundibular musculature beneath the great arteries, with aortic-mitral and pulmonary-mitral fibrous continuity; semilunar valves side by side, aortic to the right and pulmonary to the left, and at approximately the same height; thick-walled and small-chambered right ventricle with endocardial fibroelastosis of the apical half of the ventricle; hypertrophy and enlargement of both atria and of the left ventricle; absence of the left coronary ostium; and a fistula between the right ventricular apex and the anterior descending coronary artery. The main developmental implications of this rare case appear to be as follows: (1) strong support is given for the differential conal growth hypothesis concerning the morphogenesis of great arterial interrelationships; (2) truncus arteriosus communis would appear to have atresia, not absence, of the subpulmonary infundibulum; (3) the truncal septum does extend a short distance below the semilunar valves; and (4) the conus arteriosus appears to be a separate cardiac segment, not part of the right ventricle and not part of the great artelies.

Left Ventricular Chamber Volume, Mass, and Function in Severe Coronary Artery Disease

Abstract: Twenty-three patients, 15 of whom had clinical and electrocardiographic evidence of previous myocardial infarction, were studied by coronary arteriography and biplane angiocardiography. End-diastolic volume ranged from 55 to 317 ml/m2, left ventricular mass from 83 to 294 g/m2 and ejection fraction from 0.13 to 0.75. An increased enddiastolic volume was associated with an increased left ventricular mass (r = 0.77, P < 0.01). In 15 of the 23 patients mitral regurgitant volume ranged from 0.7 to 4.7 L/min/m2 and an end-diastolic volume greater than 154 ml/m2 was associated with mitral regurgitation. The ejection fraction was significantly reduced in the absence as well as the presence of mitral regurgitation. These observations on coronary artery disease in 23 patients with refractory angina pectoris or persistent congestive heart failure, or both, reveal that in this group of patients (1) a dilated left ventricle was hypertrophied and the extent of hypertrophy was proportional to the dilatation; (2) an enl...

Significance of His and Left Bundle Recordings from the Left Heart in Man

Abstract: Eight patients were studied by simultaneous intracardiac recordings of the specialized conduction system from left and right heart. Five patients had normal A-V conduction, one had left axis deviation (LAD), and two had bundle-branch block. Bundle of His (BH) and right bundle (RB) recordings from the right heart were obtained and validated as previously described. In addition a bipolar electrode catheter was introduced into the root of the aorta and left ventricle via the right brachial artery. BH and left bundle (LB) electrograms were recorded at the level of the aortic cusps and just below the aortic valve, respectively. BH recordings from both sides could be temporally superimposed and were similar in onset and duration. In patients with normal A-V conduction the duration of these deflections was BH 15 to 20, LB 15, and RB 10 msec. The conduction time from the proximal LB to ventricular (V) activation (LB-V) ranged from 20 to 25 msec. The LB-V and RB-V conduction times from comparable points were similar and support the previous observations that interventricular septal activation occurs almost simultaneously on both sides. In the patient with right bundle-branch block (RBBB) and LAD with a slightly prolonged H-V time (50 msec), the delay was localized distal to the main LB (LB-V = 30 msec). During ectopic "ventricular," probably left bundle rhythm, retrograde activation of the BH was demonstrated. Aberration (RBBB) of the supraventricular impulse resulting from invasion of the RB by the preceding interpolated premature "ventricular" beat is suggested.