Left Ventricular Endocardial Surface Research Articles

Benefit of late coronary reperfusion on ventricular morphology and function after myocardial infarction

Objectives. This study was designed to examine the relation between the timing and adequacy of perfusion of the infarct bed and changes in ventricular size and the extent of abnormal wall motion after acute myocardial infarction.Methods. A validated echocardiographic mapping technique was used to measure the left ventricular endocardial surface area index and the extent of abnormal wall motion over a 3-month period in 91 patients who had either 1) no anterograde or collateral flow to the infarct bed (n = 14), 2) only collateral flow to the infarct bed (n = 18), 3) restoration of anterograde flow to the infarct bed within hours of chest pain (early [n = 43]), or 4) restoration of anterograde flow to the infarct bed within a mean of 5 days after acute myocardial infarction (late [n = 16]).Results. Over the follow-up period, a progressive and significant increase in endocardial surface area index was observed only in the group of patients without anterograde or collateral flow to the infarct bed (entry 64 ± 3.4 cm2/m2vs. 3 months 75.9 ± 6.4 cm2/m2, p < 0.005). In contrast, a progressive reduction in the extent of abnormal wall motion was evident in the group of patients in whom anterograde flow to the infarct bed was restored within hours (entry 26.7 ± 2.5 cm2vs. 3 months 11.8 ± 2.9 cm2, p < 0.001) or days (entry 22.1 ± 3.6 cm2vs. 3 months 11.8 ± 3.3 cm2, p < 0.001) of coronary occlusion. Multiple stepwise linear regression analysis confirmed that by 3 months, 1) ventricular size was independently related to endocardial surface area index and abnormal wall motion at entry (p < 0.0001) and to the change in abnormal wall motion over the follow-up period (p < 0.0001), and 2) the change in abnormal wall motion was related to the presence of anterograde flow to the infarct bed (p < 0.0001) independent of the timing of reperfusion, infarct site or the extent of abnormal wall motion on admission.Conclusions. After myocardial infarction, the process of ventricular remodeling is influenced by changes in the extent of abnormal wall motion, which in turn are related to the adequacy rather than the timing of perfusion of the infarct bed.

Methodology for three-dimensional reconstruction of the left ventricle from transesophageal echocardiograms

A technique is presented for three-dimensional (3-D) reconstruction of the left-ventricular endocardial surface from multiplanar transesophageal echocardiograms, using both commercial software and investigator written Fortran programs for Intel 80286 and 80386 microcomputers. The approach provides quantitative global and regional cardiac performance measures and allows viewing the endocardial surface, at end-diastole and end-systole, from chosen perspectives. Anatomical landmarks are incorporated to aid in orientation. For regional calculation, the surface is divided into equal angular elements with each conceptually connected to the left-ventricular end-diastole centroid, forming a pyramidal volume element. This angular division automatically normalizes for heart size. The fractional change of these elements over the cardiac cycle provides a regional ejection fraction measure which is color-coded on the reconstructed endocardial surface. Composite perspective views, regional ejection fraction histograms and calculations of global end-diastolic, end-systolic, and stroke volumes, are all performed by the method.

The effect of late patency of the infarct-related coronary artery on left ventricular morphology and regional function after thrombolysis

The use of early coronary angiography to assess the benefits of coronary patency on left ventricular size and function fails to account for subsequent reocclusion or spontaneous reperfusion. To investigate the relationship between late vessel patency and changes in left ventricular structure and function after thrombolysis, echocardiography was performed within 48 hours and at 6 to 12 weeks in 30 patients treated with intravenous thrombolysis. Left ventricular endocardial surface area index (ESA i; cm 2/m 2) and extent of abnormal wall motion were quantitated in those with a patent ( n = 20) and those with an occluded ( n = 10) infarct-related artery on coronary angiography performed 8 ± 6 days after thrombolysis. Mean ESA i increased from (53 ± 7 to 61 ± 10 cm 2/m 2; p < 0.02) in the occluded group during the follow-up period but remained unchanged (60 ± 11 to 62 ± 11 cm 2/m 2; p = NS) in the patent group. Mean percentage of abnormal wall motion decreased in the patent group (27 ± 16% to 18 ± 16%; p < 0.01), whereas no significant change was noted in the occluded group (20 ± 13% to 23 ± 17%; p = NS). Thus coronary patency at days after thrombolysis is associated with both improvement in regional left ventricular function and attentuated left ventricular dilatation.

Progressive changes in ventricular structure and function during the year after acute myocardial infarction

To investigate the long-term changes in left ventricular structure and function after myocardial infarction, 51 patients with a first myocardial infarction (17 anterior, 23 inferior, and 11 non-Q wave) were studied by two-dimensional echocardiography at the time of entry into the hospital, at 3 months, and 1 year after infarction. The left ventricular endocardial surface was reconstructed from these echocardiograms, and the endocardial surface area (ESA) index (in cm 2/m 2) and area of abnormal wall motion (AWM in cm 2) were quantitated. Despite different trends in the ESA index between entry and 3-month values in those with and without early infarct expansion, a decrease in the ESA index from 3 months to 1 year was noted in anterior and non-Q wave infarctions (anterior with early expansion: 96.3 ± 8.6 to 81.5 ± 4.2 cm 2/m 2, p < 0.05; anterior without early expansion: 59.7 ± 2.0 to 54.7 ± 2.0 cm 2/m 2, p < 0.01; non-Q wave: 64.1 ± 3.5 to 57.9 ± 4.4 cm 2/m 2, p < 0.01). The mean decline in ESA from 3 months to 1 year of 8.9 ± 2.5 cm 2 was independent of initial infarct size. Regional function, as represented by the area of AWM, was also improved but the timing of the improvement was related to the location and size of the infarction. Although decreases in AWM were noted in both the inferior and non-Q wave groups from entry to 3 months (inferior: 27.1 ± 3.3 to 21.8 ± 3.4 cm 2, p < 0.5; non-Q wave: 18.9 ± 4.5 to 12.1 ± 5.5 cm 2, p < 0.05), decreases in AWM in anterior infarctions were not present until the 3-month to 1-year time period (anterior with expansion: 79.1 ± 18.6 to 59.8 ± 14.9 cm 2, p < 0.05; anterior without expansion: 27.7 ± 6.2 to 16.5 ± 4.9 cm 2, p < 0.05). Even in the absence of intervention, global left ventricular size decreases and regional wall motion improves in both Q wave and non-Q wave infarctions when quantitated 1 year after i infarction.

Left ventricular diastolic and systolic performance during chronic experimental aortic regurgitation

To study the time course of left ventricular structural and functional responses to chronic aortic regurgitation, aortic regurgitation was surgically induced in rabbits, and Doppler echocardiography was performed preoperatively and serially postoperatively for up to 2.5 yr. Twenty-five New Zealand White rabbits underwent surgical induction of aortic regurgitation and 13 control animals underwent sham operation. Left ventricular endocardial and epicardial surfaces were digitized from M-mode echocardiograms to measure the rates of change of cavity dimensions and wall thicknesses during diastolic relaxation and systolic contraction. Aortic regurgitant animals developed left ventricular dilatation and eccentric hypertrophy that remained relatively stable throughout the follow-up period. Compared with baseline values, left ventricular mass increased 120% and left ventricular internal dimension at end diastole increased 40%, whereas posterior wall thickness at end diastole and fractional shortening remained relatively stable. Left ventricular diastolic performance was enhanced at 6 mo after operation, a finding associated with increased volume load and heart rate following induction of aortic regurgitation. Diastolic performance was then reduced at 12 mo after operation and demonstrated no further decline throughout the remainder of the follow-up period. In contrast, left ventricular systolic performance was not altered following operation and remained preserved until the final assessment at up to 2.5 yr. Thus alterations in diastolic performance occurred without impairment of systolic performance during long-term follow-up of chronic experimental aortic regurgitation.

Assessing the effect of uncertainty in intracavitary electrode position on endocardial potential estimates.

The aim of this simulation study is to determine the effect of uncertainty in intracavitary probe electrode position on the accuracy of estimated endocardial potentials. Intracavitary probe position uncertainty is simulated by randomly moving an idealized probe surface about the center of an idealized left ventricular endocardial surface. These random deviations represent possible probe locations that are incorporated as correlated noise. An optimum inverse transfer coefficient matrix, relating intracavitary potentials to endocardial potentials, is computed and subsequently used to calculate the best linear estimate of the true endocardial potentials. For uncorrelated endocardial potentials and probe position uncertainty within 1.5 mm of the coordinates of the exact probe electrode locations, a root-mean-square (rms) error of 34.0% is obtained. Increasing probe position uncertainties to 3.0 and 6.0 mm results in rms errors of 60.8 and 88.3%, respectively. For endocardial potentials that are 90% dipolar, the rms errors for probe position uncertainties of 1.5, 3.0, and 6.0 mm are 11.3, 19.6, and 28.5%, respectively. These simulation results imply that position uncertainty of a multielectrode, intracavitary probe can be a major source of error in estimating endocardial potentials from intracavitary potentials.

Geometrically accurate transaortic mapping of left ventricular endocardial activation during surgery

A device was developed for mapping left ventricular endocardial activation through the aortic valve during surgery. It uses an exploring electrode at the tip of a hand-held probe that is mounted on a mechanical arm with six joints whose movements are digitized by a computer while the position of the probe tip is calculated continuously. The probe is inserted by the surgeon into the left ventricle retrogradely through the aortic valve after the patient is on total cardiopulmonary bypass, the aorta has been opened and the coronary arteries cannulated.The electrode position relative to the aortic valve and left ventricular apex is displayed continuously on a computer screen. When electrograms are recorded fron the probe, their positions are displayed on the screen relative to a stylized grid of the left ventricular endocardial surface and are color-coded to indicate the activation sequence. In a patient with nonischemic ventricular tachycardia, the arrhythmia was successfully mapped and cryoablated with use of the device. The device will be developed so that a cryoprobe can be substituted for the exploring electrode and positioned at the source of activation determined by the map.

Spatial and temporal registration of cardiac SPECT and MR images: methods and evaluation.

Image registration may assist in the integration of information from multiple sources by allowing direct point-for-point comparisons of studies. To determine the usefulness of such a technique, a method for the spatial and temporal registration of four-dimensional single photon emission computed tomographic (SPECT) and magnetic resonance (MR) cardiac images was developed. Automatically detected left ventricular endocardial surfaces were used to determine the best transform between the two sets of surface points, and that transform was applied to the original SPECT image. A fused image created from the MR and the transformed SPECT images combined the information in both. The authors tested the method with seven patient studies. Registration reduced the distance between the MR and SPECT left ventricular endocardial surfaces by 30%, to an average of 2.7 mm. The authors found that, by using the fused images, perfusion abnormalities could be easily localized and correlated to high-resolution endocardial wall motion and systolic wall thickening.

Role of cardiac ATP-regulated potassium channels in differential responses of endocardial and epicardial cells to ischemia.

Epicardial cells are more susceptible to the electrophysiological effects of ischemia than are endocardial cells. To explore the ionic basis for the differential electrophysiological responses to ischemia at the two sites, we used patch-clamp techniques to study the effects of ATP depletion on action potential duration and the ability of ATP-regulated K+ channels in single cells isolated from feline left ventricular endocardial and epicardial surfaces. During ATP depletion by treatment with 1 mM cyanide (CN-), shortening of action potential durations was significantly greater in epicardial cells than in endocardial cells. Thirty minutes after initiating exposure to 1 mM CN-, action potential duration at 90% repolarization was reduced to 0.70 +/- 0.12 of the control value for endocardial cells versus 0.39 +/- 0.18 for epicardial cells (p less than 0.01), and action potential duration at 20% repolarization was reduced to 0.72 +/- 0.13 for endocardial cells versus 0.12 +/- 0.09 for epicardial cells (p less than 0.01). In both endocardial and epicardial cells, the shortening of action potential by CN- treatment was partially reversed by 0.3 microM glibenclamide; the magnitude of reversal, however, was much greater in epicardial cells. After exposure to 1 mM CN-, the activity of ATP-regulated K+ channels in cell-attached membrane patches was significantly greater in epicardial cells than in endocardial cells. To study the dose-response relation between ATP concentration and open-state probability of the channels, intracellular surfaces of inside-out membrane patches containing ATP-regulated K+ channels were exposed to various concentrations of ATP (10-1,000 microM). The concentration of ATP that produced half-maximal inhibition of the channel was 23.6 +/- 21.9 microM in endocardial cells and 97.6 +/- 48.1 microM in epicardial cells (p less than 0.01). These data indicate that ATP-regulated K+ channels are activated by a smaller reduction in intracellular ATP in epicardial cells than in endocardial cells. The differential ATP sensitivity of ATP-regulated K+ channels in endocardial and epicardial cells may be responsible for the differential shortening in action potentials during ischemia at the two sites.

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

To investigate the natural history of regional dyssynergy and left ventricular size after myocardial infarction, 57 patients with a first Q wave myocardial infarction (18 anterior, 35 inferior, and four apical by echocardiography) were studied by two-dimensional echocardiography and compared with 30 control patients. Measurements from the echocardiograms were used to construct maps of the left ventricular endocardial surface from which the endocardial surface area index (ESAi) and the percent of the endocardial surface area involved by abnormal wall motion (%AWM) were calculated. The maps from entry and 3-month echocardiograms were used to classify patients based on changes in ESAi and abnormal wall motion. Two subgroups of patients were identified at entry--those with a normal ESAi (group 1, n = 50) and those with an increased ESAi (group 2, n = 7). Group 1 patients was subdivided at 3 months by changes occurring in ESAi (1A, 5% increase [n = 19]; 1B, no change [n = 23]; 1C, 5% decrease [n = 8]). The increase in ESAi (64.9 +/- 5.2 to 75.4 +/- 7.5 cm2/m2, p less than 0.0001) in group 1A was associated with global ventricular dilatation (n = 11) and clinically silent infarct extension (n = 8). Groups 1B and 1C were composed predominantly of patients with inferior infarctions, and all exhibited either no change or a significant decrease in infarct size (infarct regression). Group 2 patients demonstrated a continued increase in ESAi by 3 months (88.2 +/- 10.0 to 101.4 +/- 15.5 cm2/m2, p less than 0.007). This group comprised only patients with anterior infarctions, and all exhibited infarct expansion at the left ventricular apex. The changes in left ventricular size and functional infarct size are heterogeneous after acute myocardial infarction and relate to the initial endocardial surface area, infarct location, and functional infarct size.

Relation of left ventricular hemodynamic load and contractile performance to left ventricular mass in hypertension.

The weak relation of systolic blood pressure to left ventricular mass in hypertensive patients is often interpreted as evidence of nonhemodynamic stimuli to muscle growth. To test the hypothesis that left ventricular chamber size, reflecting hemodynamic volume load and myocardial contractility, influences the development of left ventricular hypertrophy in hypertension, we studied actual and theoretic relations of left ventricular mass to left ventricular diastolic chamber volume, pressure and volume load, and an index of contractility. Data were obtained from independently measured M-mode and two-dimensional echocardiograms in 50 normal subjects and 50 untreated patients with essential hypertension. Two indices of overall left ventricular load were assessed: total load (systolic blood pressure x left ventricular endocardial surface area) and peak meridional force (systolic blood pressure x left ventricular cross sectional area). A theoretically optimal left ventricular mass, allowing each subject to achieve mean normal peak stress, was calculated as a function of systolic blood pressure and M-mode left ventricular end-diastolic diameter. Left ventricular mass measured by M-mode echo correlated better with two-dimensional echocardiogram derived left ventricular end-diastolic volume (r = 0.56, p less than 0.001) than with systolic blood pressure (r = 0.45, p less than 0.001) and best with total load or peak meridional force (r = 0.68 and 0.70, p less than 0.001). In multivariate analysis both end-diastolic volume and blood pressure were independent predictors of systolic mass (p less than 0.001) and explained most of its variability (R = 0.75, p less than 0.001). Theoretically optimal left ventricular mass was more closely related to end-diastolic volume (r = 0.72, p less than 0.001) than to systolic blood pressure (r = 0.46, p less than 0.001); thus, the relatively weak correlation between blood pressure and optimal mass reflected the influence of left ventricular cavity size, rather than a lack of proportionality between load and hypertrophy. Actual and theoretically optimal left ventricular mass were closely related (r = 0.76, p less than 0.001), indicating that left ventricular hypertrophy in most cases paralleled hemodynamic load. Left ventricular mass was positively related to stroke index and inversely to contractility (as estimated by the end-systolic stress/volume index ratio), the main determinants of left ventricular chamber volume. In multivariate analysis, systolic blood pressure, stroke index, and the end-systolic stress/volume index ratio were each independently related to left ventricular mass index (all p less than 0.001, multiple R = 0.81) and accounted for 66% of its overall variability.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of electrophysiologic studies resulting in electrical countershock or burst pacing on left ventricular systolic and diastolic function

To determine the acute effects of electrophysiologic study on left ventricular systolic and diastolic function in patients requiring termination of induced tachyarrhythmias by either electrical countershock or burst pacing, we examined 16 patients (11 men and five women), aged 43 to 78 years (mean 58 ± 13), undergoing programmed electrical stimulation. Indices of systolic and diastolic left ventricular function were measured by M-mode echocardiography before and within 1 minute after termination of 22 episodes of induced tachyarrhythmias by defibrillation (n = 16) and burst pacing (n = 6). The left ventricular septal and posterior endocardial surfaces were digitized immediately below the mitral valve leaflets, and indices of systolic and diastolic function were calculated. The results showed a significant impairment in both systolic and diastolic function after termination of tachyarrhythmias by defibrillation, as seen by a decrease in the shortening fraction (23.7 ± 7.6% to 19.8 ± 7.8%; p < 0.005) and a decline in the peak rate of increase in left ventricular diameter during diastole called dD dt max (87.4 ± 36.1 mm/sec to 71.5 ± 28.9 mm/sec; p < 0.01), respectively. In addition, indices of systolic and diastolic function measured at baseline were predictive of impairment in diastolic function, as seen by modest but highly significant correlations between the absolute change in dD dt max after defibrillation versus the peak velocity of fiber shortening ( r = −0.69; p < 0.005) and dD dt max ( r = −0.60; p < 0.02) measured at baseline. Left ventricular function after termination of tachyarrhythmias by burst pacing was not significantly altered. Although electrophysiologic study with the induction of sustained ventricular tachyarrhythmias has been performed safely, the potential for left ventricular dysfunction from hemodynamic instability and electrical countershock exists. Burst pacing termination of ventricular tachycardia appears to be devoid of deleterious effects on left ventricular function and should be employed whenever hemodynamic stability permits.

An analytical descriptor of three-dimensional geometry: application to the analysis of the left ventricle shape and contraction.

A novel method to describe the instantaneous three-dimensional (3-D) geometry of the left ventricular (LV) endocardial surface by an analytical time-varying scalar function of Fourier spectrum coefficients is suggested. The method utilizes experimental echocardiographic data and uses a helical coordinate system to transform the 3-D data into a unidimensional numerical function. The instantaneous numerical function is then represented by its Fourier sine series which serves as an analytical shape descriptor from which the 3-D shape is reconstructed. The procedure can also be applied to data compression (spatial low-pass filtering), spectral analysis, and the evaluation of geometric similarity of 3-D shapes. When applied to the endocardial surface of the LV at end-diastole (ED) and end-systole (ES) this technique gives a quantitative analysis of the global LV contraction of the real heart.

Clinical comparisons of methods of myocardial protection

Currently, numerous methods are in use for myocardial hypothermia as a myocardial preservation modality for cardiac operations. During cardiac ischemia we have compared myocardial surface cooling with topical cold saline (Group I, N = 9), crystalloid cardioplegia plus topical cold saline (Group II, N = 8) and cardioplegia with a specially designed cooling jacket (Group III, N = 8) in patients undergoing aortic or mitral valve replacement, or both. Temperatures were assessed and recorded continuously in standardized locations for the right and left ventricular epicardium and endocardium. In Group I the rate of cooling was significantly slower than in the other two groups. Also, excessive gradients were developed across the left and right ventricular walls. In Group II the rate and depth of cooling were adequate and initial temperature gradients were eliminated. However, over the period of ischemia, significant rewarming occurred. In Group III temperatures were reduced rapidly and uniformly and maintained at or below 10 degrees C for the duration of the ischemic period. These differences are statistically significant (p less than 0.05). For optimal myocardial hypothermia, we recommend the following: separate cannulation of the superior and inferior venae cavae with caval snares; venting of the pulmonary artery (if inadequate, pulmonary vein occlusion or direct left atrial venting); induction of myocardial hypothermia with crystalloid or cold blood cardioplegia; and maintenance of hypothermia by the cooling jacket described herein. It is also desirable to continuously monitor temperatures of the right and left ventricular endocardial and epicardial surfaces.

A Method for Quantitative Display of Three-Dimensional Regional Myocardial Function

The DSR (dynamic spatial reconstructor), a multiple X-ray source scanner that generates stop action three-dimensional (3-D) images of a cylindrical volume, was used for quantitative imaging of left ventricular 3-D wall geometry and function in experimentally induced canine left ventricular myocardial infarction. Impaired regional myocardial function was induced by myocardial ischemia or infarction in four mongrel dogs by closed-chest occlusion of the proximal left anterior descending (LAD) coronary artery. At intervals of 6-14 weeks post occlusion, the dogs were scanned with the DSR during biatrial contrast injection. The 3-D shape, extent, and function of hypokinetic myocardium was measured from the DSR images utilizing measurement of the rate of local systolic wall thickening to detect regions of normal, ischemic, or scarred myocardium. The results were compared to scar size and anatomic distribution measured at postmortem examination. The anatomic extent and relationship of hypocontractile to normally contracting muscle was visualized by computer generated, pseudo 3-D shaded surface displays of the left ventricular chamber and by topographic projections of regional wall thickening rates onto a map of the left ventricular endocardial surface. The location of myocardial infarction and the surrounding zone of impaired function is clearly defined by this 3-D CT scanning procedure. The display method presented here provides both localization and quantification of the volume of ischemic and infarcted myocardium.

Response of the heart to nonpenetrating cardiac trauma.

The purpose of this investigation was to study the acute effects of blunt cardiac trauma upon left ventricular (LV) function. In 34 open-chest anesthetized dogs, direct impact to the anterior surface of the heart was produced by an air-pressurized impactor at 12 m/sec in 15 dogs and at 18 m/sec in 19 dogs. Impact displacement was limited to 2 cm. Seventeen dogs (50%) died of arrhythmias within a few minutes of impact. In nine surviving dogs impacted at 12 m/sec, there was an immediate reduction of LV function following impact. At 5 minutes following impact this reduction of LV function was characterized by a 19% reduction of cardiac output, 35% reduction of maximal isovolumic LV rate of change of pressure (dp/dt), a 12% reduction of peak aortic flow, and a 23% reduction of peak rate of change of flow. These indices of ventricular performance returned nearly to control levels 60 to 90 minutes following impact. In eight surviving dogs that experienced impact at 18 m/sec, impairment of LV function was greater in the immediate impact period following impact and impaired function remained throughout the 90-minute duration of observation. Autopsy of all dogs showed cardiac contusion. Following the more severe impact, contusions were more extensive and involved the left ventricular endocardial surface and intraventricular septum as well as the epicardial surface. Parallel changes, therefore, of the extent of pathologic changes and the extent of functional impairment were observed. Animals that survived the potentially fatal arrhythmias immediately after impact showed functional impairment of the heart that was only moderate and compatible with life.

Left Ventricular Approach for Recording His Bundle Potential in Man

The electrical potentials of the His bundle (HB) were recorded from the left ventricular endocardial surface in 28 patients ranging from 16 to 63 years of age. In 14 of the patients the left bundle branch (LB) potentials were also obtained. Placement of a bipolar electrode catheter tip toward the interventricular septum, right at and also 1 to 2 cm below the aortic valve, resulted in stable recordings of both potentials in successive cardiac cycles even at performing atrial or HB pacing from the right heart. The following intervals were measured in milliseconds (msec): P-A, A-H, H, H-V, LB, and LB-V. The average values in 12 patients (average age 26 plus or minus 7 years and average heart rate 90 plus or minus 16 beats per minute) with normal A-V conduction were as follows: P-A 28 plus or minus 7, A-H 76 plus or minus 16, H 19 plus or minus 3 and H-V 45 plus or minus 6 msec. The average values for LB and LB-V in 10 of these 12 patients were 15 plus or minus 3 and 25 plus or minus 3 msec respectively. Validation of the His bundle electrogram (HBE) from the left ventricular endocardial surface was based on simultaneous recordings of the intracardiac electrograms from both left and right sides of the heart in 18 patients. The individual average values for the intervals obtained from both sides of the heart in these patients were statistically not different, except that the H potential was slightly longer in duration fr m the left heart (P equals 0.05). Among these, 16 showed simultaneous onset of the H potentials, and the LB-V and RB-V conduction times from comparable points were almost the same. Indications for the left sided electro-physiologic studies include the following situations: (a) inability to record H from the right of the heart; (b) giant right atrium; and (c) possibly during atrial fibrillation.

HIS bundle electrogram in rheumatic mitral valve disease with special reference to Bachmann's bundle block in P mitrale.

HBEs were recorded from either the right or left ventricle or simultaneously from both in 26 patients with chronic rheumatic mitral stenosis alone or in association with other mild valvular lesions during the diagnostic cardiac catheterization. Eleven of the patients had auricular fibrillation. Of the remaining 15 patients with sinus mechanism and P mitrale in the surface electrocardiogram, 12 were noted to have H potential preceded the termination of P wave and gave P2H interval of negative value- so-called "Bachmann's bundle block". Among these, double atrial activities (A and A' waves) could be identified on the HBE recorded from the left ventricular endocardial surface with catheter electrodes positioned at the subarotic region in 7 patients studied. Interatrial conduction time (P1A' interval) measured in these patients was prolonged in all and ranged from 47 to 82 with an average of 66 msec. Prolongation of intraatrial (or internodal) conduction time was noted in only one patient who also had first degree A-V block and prolonged A-H interval. There was no correlation of either P1P2 or P2H interval to the degree of left atrial enlargement. The P1P2 or P2H interval also had no correlation with hemodynamic parameters. In patients with auricular fibrillation, all impulses unable to conduct to the ventricle were blocked proximal to the His bundle and concealed conduction was not observed distal to it.

Functional anatomy of the canine left bundle branch

To elucidate the architecture of the left bundle branch, activation of Purkinje (P) and myocardial (M) cells of the canine left ventricular endocardial surface was mapped in vitro before and after lesions were placed in the proximal left bundle branch. Close bipolar electrodes or microelectrodes were employed to record P and M potentials by standard techniques. The left bundle branch has conspicuous and straight border fibers that continue as bridging strands to the papillary muscles. In addition, there is a less conspicuous network of serpentine interwoven fibers in the interior of the septal portion of the bundle that has interconnections with the border fibers. Below the mid-septum and over the free wall the P fibers form a densely interwoven network. The interior septal fibers are activated nearly simultaneously with equidistant points on the border fibers. The apparent conduction velocity of the border fibers was 1.8 m/sec as opposed to 1.45 m/sec in the interior network. The bridging strands provide a shortcut across the chamber to upper portions of the free wall and septum. The pattern of activation of M cells is represented by concentric rings with an island of earliest activation (at 15 to 25 msec) in the central septum. The M cells latest to be activated are at the tips of the papillary muscles and the upper septum below the valves. Interruption of one group of border fibers may delay by 5 to 8 msec activation of P and M cells of the upper paraseptal free wall and upper septum. Lesions in the interior network delay by 2 to 4 msec activation of the P and M cells of comparatively small areas of the septum. Activation of the mid-papillary free walls, the bases of the papillary muscles and the lower septum is not affected by proximal lesions partially interrupting the bundle branch. Transection of both groups of border fibers does not produce complete block. The left bundle branch is best represented as a fan-shaped network of interwoven fibers whose diverging border fibers are specialized for rapid, distant transport.