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Biomedical subjects

W C Little

Publications and source records attributed to W C Little.

At least 109 records · Page 6Linked to original sources
PubMed1986

Comparison of the cardiovascular effects of intravenous and intraaortic protamine in the conscious and anesthetized dog.

Controversy exists as to whether intraaortic (IA) administration of protamine sulfate has less adverse effects than the intravenous (IV) route. The effect of protamine on contractility is not well established. Therefore, 9 dogs underwent chronic instrumentation to monitor aortic pressure (AP), left ventricular (LV) pressure, central venous pressure, cardiac index (CI), heart rate, stroke volume index (SVI), systemic vascular resistance index, and LV volume. The end-systolic LV pressure-volume relationship was used as a load-independent measure of contractility. Each dog was administered IV and IA protamine on separate occasions after pretreatment with heparin. Studies were performed with and without anesthesia. In the awake studies, analysis of variance showed greater decreases in mean AP (p less than .03), CI (p less than .05), and SVI (p less than .02) with IA protamine infusion. In the anesthetized animals, there were no significant differences between IA and IV administration of protamine. Protamine did not decrease contractility in any group. We conclude that IA administration of protamine offers no advantage over IV administration in the dog. Protamine does not decrease contractility when given by either route.

Analysis of Variance↗
PubMed1986

Comparison of in situ and in vitro studies of pericardial pressure-volume relation in dogs.

Whether the material properties of the pericardial membrane are the key determinants of the in situ pericardial pressure-volume relation is not known. Although both the pressure-volume relation of the intact pericardium and the stress-strain relation of isolated pericardial samples are nonlinear, it is not clear how closely these phenomena are related. To directly examine this question we compared the pressure-volume, pressure-normalized volume, and stress-strain relations of pericardia from six dogs tested both in situ and in vitro. The curves generated under the two sets of conditions were different. The transition from the compliant to the noncompliant portion of the curve was more acute under in vitro conditions. Nonlinear regression analysis using a monoexponential function of the form Y = alpha (e beta chi-1) showed beta, the proportionality constant for the slope of the curve, to be larger for each form of analysis under in vitro testing conditions as follows: 0.002 +/- 0.009 vs. 0.078 +/- 0.029, P less than 0.002 for pressure-volume; 3.52 +/- 1.75 vs. 11.03 +/- 5.31, P less than 0.005 for pressure-normalized volume; and 19.6 +/- 6.6 vs. 62.3 +/- 18.8, P less than 0.001 for stress-strain. These differences in the pressure-volume relation of the intrapericardial space in situ and the isolated pericardium in vitro suggest that pericardial attachments present in situ may buffer the loading of the membrane itself. We conclude that the pressure-volume relation of the intrapericardial space is only partly determined by the properties of the isolated pericardium alone and is also influenced by other components of the intact pericardium.

Animals↗
PubMed1986

The effect of vasoactive agents on the left ventricular end-systolic pressure-volume relation in closed-chest dogs.

The left ventricular end-systolic pressure-volume relation has received intense interest as a relatively load-insensitive measure of cardiac performance. In clinical studies, pharmacologic manipulation of blood pressure has been used to determine this relation. Since previous studies have shown that acute changes in the resistance and impedance of the arterial circulation influence the left ventricular end-systolic pressure-volume relation, the use of vasoactive drugs in its determination may affect the results achieved. This study was undertaken to determine whether clinically used vasoactive drugs influence the left ventricular end-systolic pressure-volume relation. Sixteen dogs were previously instrumented with micromanometer pressure transducers and three sets of piezoelectric crystals to permit determination of left ventricular pressure and volume. The dogs were studied after autonomic blockade and sedation. End-systolic pressure-volume relations were generated by caval occlusion at control levels of blood pressure, after infusion of a vasopressor (methoxamine, n = 6; angiotensin II, n = 10), and then after infusion of nitroprusside. A composite end-systolic pressure-volume relation was also constructed with the use of control, vasopressor, and vasodilator points in each dog. Angiotensin II resulted in a leftward shift in the relation (Vo decreased from 14.32 +/- 7.3 to 8.04 +/- 10.4 ml, p less than .05) with no significant effect on slope. Methoxamine shifted the relation to the left (Vo decreased from 13.98 +/- 8.74 to -0.47 +/- 12.06 ml, p less than .05) and also reduced the slope (5.41 +/- 3.09 vs 8.28 +/- 3.94 mm Hg/ml, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Effect of regional ischemia on the left ventricular end-systolic pressure-volume relation in chronically instrumented dogs.

The slope of the left ventricular end-systolic pressure-volume relation has been proposed as a sensitive index of left ventricular function since it increases in response to positive inotropic agents and decreases with global depression of contractility. The effect of a segmental depression of left ventricular contractile function produced by circumflex coronary artery occlusion on the left ventricular end-systolic pressure-volume relation was evaluated in seven chronically instrumented dogs. Left ventricular volume was calculated from three ultrasonically measured, orthogonal left ventricular endocardial dimensions. Left ventricular pressure was measured with a micromanometer. The left ventricular end-systolic pressure-volume relation was generated by occlusion of the inferior vena cava, before and after inducing regional ischemia, in the presence of autonomic blockade with propranolol and atropine. The end-systolic data in each dog, before and after coronary occlusion, were fit to the equation, P = E(V - V0), with r greater than or equal to 0.95 in all cases. Coronary occlusion shifted the left ventricular end-systolic pressure-volume relation to the right in each animal. During regional ischemia, the volume intercept (V0) increased from 10.1 +/- 7.8 to 20.4 +/- 9.8 ml (mean +/- SD) (p less than 0.005). The slope (E) of the left ventricular end-systolic pressure-volume relation was relatively unchanged. It is concluded that in intact dogs, regional left ventricular ischemia resulting from coronary occlusion produces a rightward shift of the left ventricular end-systolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Altered effect of the Valsalva maneuver on left ventricular volume in patients with cardiomyopathy.

The failure of the blood pressure to fall during the late strain pase of the Valsalva maneuver in patients with heart failure may result from the left ventricle operating on a flat portion of its function curve or from maintenance of left ventricular volume despite decreased systemic venous return. To test these possibilities, we studied the effect of the Valsalva maneuver (40 cm H2O for 15 sec) on left ventricular volume in 12 normal subjects with a mean left ventricular ejection fraction of 0.65 +/- 0.07 (+/- SD) and in eight patients with nonischemic cardiomyopathy, evidence of pulmonary congestion, and a mean left ventricular ejection fraction of 0.23 +/- 0.09. Left ventricular volume and right ventricular area were determined by apical two-dimensional echocardiography. In both groups the right ventricular end-diastolic area decreased during the late strain phase of the Valsalva maneuver. In normal subjects it decreased from 9.3 +/- 1.5 to 5.6 +/- 1.6 cm2 (p less than .001) and in patients it decreased from 13 +/- 2.2 to 10 +/- 2.9 cm2 (p less than .001). In normal subjects, left ventricular end-diastolic volume decreased from the control level during the Valsalva maneuver, and this was apparent in both the four-chamber (96 +/- 21 to 68 +/- 18 ml, p less than .01) and two-chamber views (97 +/- 15 to 56 +/- 20 ml, p less than .01). In the patients, left ventricular end-diastolic volume was not significantly different from control in either view (199 +/- 70 to 195 +/- 78 and 214 +/- 77 to 218 +/- 86 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Simultaneous determination of left ventricular end-systolic pressure-volume and pressure-dimension relationships in closed-chest dogs.

The left ventricular end-systolic pressure-volume relationship is a load-insensitive measure of left ventricular performance. The relationship at end-systole between left ventricular pressure and dimension is more easily obtained, but the conflicting results of previous studies make it unclear if it has the same properties as the left ventricular end-systolic pressure-volume relationship. To address this issue, 11 dogs were instrumented to measure left ventricular pressure and three orthogonal left ventricular dimensions. Left ventricular pressure and dimensions were varied by use of caval occlusion. Left ventricular volume was calculated as an ellipsoid. The left ventricular end-systolic pressure-volume relationship and each of the three end-systolic pressure-dimension relations were described by straight lines (r = .97 +/- .02, mean +/- SD). In six animals, dobutamine produced similar significant increases (p less than .01) in the slope of the end-systolic pressure-volume relationship (244 +/- 61% of control), the end-systolic pressure-anterior-posterior dimension relationship (248 +/- 89%), the end-systolic pressure--septal-lateral dimension relationship (211 +/- 95%), and the end-systolic pressure-basal-apical dimension relationship (210 +/- 85%). The intercepts at zero pressure were relatively unchanged by dobutamine. In contrast, occlusion of the distal left anterior descending coronary artery in five animals produced a rightward shift of the left ventricular end-systolic pressure-volume relationship and the pressure--basal-apical dimension relationship, while the pressure--anterior-posterior dimension and pressure--septal-lateral dimension relationships were relatively unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The left ventricular dP/dtmax-end-diastolic volume relation in closed-chest dogs.

I investigated the relation of the maximum rate of left ventricular pressure rise to the end-diastolic volume and the comparison of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to the end-systolic pressure-volume relation, using the time-varying elastance model. These studies were performed in 11 dogs chronically instrumented to measure left ventricular pressure and determine left ventricular volume from three orthogonal dimensions. During vena caval occlusions, the relations between the maximum rate of left ventricular pressure rise and end-diastolic volume were described by straight lines (r = 0.97 +/- 0.01, mean +/- SD). Dobutamine increased the slope of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to 358 +/- 94% of control. This increase was greater than the 244 +/- 61% increase in the slope of the end-systolic pressure-volume relation (P less than 0.005). The volume intercepts of the maximum rate of left ventricular pressure rise-end-diastolic volume relation and end-systolic pressure-volume relation were similar and were not significantly altered by dobutamine. The ratio of the slope of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to the slope of the end-systolic pressure-volume relation divided by the time from end-diastole to end-systole was similar before (2.2 +/- 0.7) and after dobutamine (2.3 +/- 0.7, P = NS). Angiotensin II did not significantly alter the maximum rate of left ventricular pressure rise-end-diastolic volume relation generated by caval occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Effect of alteration of left ventricular activation sequence on the left ventricular end-systolic pressure-volume relation in closed-chest dogs.

We investigated the effect of pacing from the atrium and various ventricular sites on the left ventricular end-systolic pressure-volume relation following autonomic blockade in a total of 10 dogs chronically instrumented to measure left ventricular pressure and determine left ventricular volume from three ultrasonic endocardial dimensions. During ventricular pacing, left ventricular end-diastolic volume, stroke volume, and end-systolic pressure were decreased, while the end-systolic volume was relatively unchanged. Left ventricular end-systolic pressure-volume relations were generated by vena caval occlusions during pacing at a constant rate from the left atria, and the epicardium of the right ventricular free wall, right ventricular apex, and left ventricular free wall. The left ventricular end-systolic pressure-volume relations were described by straight lines for each site (r greater than 0.96 and SEE less than 2.9 mm Hg in all but one instance). Compared to atrial pacing, the left ventricular end-systolic pressure-volume relations were shifted (P less than 0.001) to the right during pacing from ventricular sites. During atrial pacing, the volume intercept of the left ventricular end-systolic pressure-volume relation was 16.0 +/- 7.2 ml (mean +/- SD), and increased to 18.7 +/- 7.8 ml (P less than 0.05) during pacing from the right ventricular free wall, to 19.6 +/- 7.7 ml (P less than 0.05) during pacing from the right ventricular apex, and to 20.0 +/- 7.5 ml (P less than 0.05) during pacing from the left ventricular free wall. These volume intercepts correlated roughly with the extent of dyssynchronous activation as estimated by the QRS duration (r = 0.59 to 0.93) and the time for left ventricular endocardial activation (r = 0.92 and 0.95). During ventricular pacing, the slope of the left ventricular end-systolic pressure-volume relation changed only slightly. Similar results were obtained during pacing from right ventricular endocardial sites. We conclude that alterations of the normal activation sequence produced by ventricular pacing depress left ventricular pumping function independent of loading conditions, as indicated by a rightward shift of the left ventricular end-systolic pressure-volume relation. The extent of this shift appears to be in proportion to the degree of dyssynchronous activation. The decreased stroke volume during ventricular pacing is due both to a decreased end-diastolic volume (decreased preload) and the rightward shift of the end-systolic pressure-volume relation (decreased pump function).

Animals↗
PubMed1984

Accurate estimates of absolute left ventricular volumes from equilibrium radionuclide angiographic count data using a simple geometric attenuation correction.

To simplify and clarify the methods of obtaining attenuation-corrected equilibrium radionuclide angiographic estimates of absolute left ventricular volumes, 27 patients who also had biplane contrast cineangiography were evaluated. Background-corrected left ventricular end-diastolic and end-systolic counts were obtained by semiautomated variable and hand-drawn regions of interest and were normalized to cardiac cycles processed, frame rate and blood sample counts. Blood sample counts were acquired on (d degree) and at a distance (d') from the collimator. A simple geometric attenuation correction was performed to obtain absolute left ventricular volume estimates. Using blood sample counts obtained at d degree or d', the attentuation-corrected radionuclide left ventricular end-diastolic volume estimates using both region of interest selection methods correlated with the cineangiographic end-diastolic volumes (r = 0.95 to 0.96). However, both mean radionuclide semiautomated variable left ventricular end-diastolic volumes (179 +/- 100 [+/- 1 standard deviation] and 185 +/- 102 ml, p less than 0.001) were smaller than the average cineangiographic end-diastolic volume (217 +/- 102 ml), and both mean hand-drawn left ventricular end-diastolic volumes (212 +/- 104 and 220 +/- 106 ml) did not differ from the average cineangiographic end-diastolic volume. Using the blood sample counts obtained at d degree or d', the attenuation-corrected radionuclide left ventricular end-systolic volume estimates using both region of interest selection methods correlated with the cineangiographic end-systolic volumes (r = 0.96 to 0.98). Also, using blood sample counts at d degree, the mean radionuclide semiautomated variable left ventricular end-systolic volume (116 +/- 98 ml, p less than 0.05) was less than the average cineangiographic end-systolic volume (128 +/- 98 ml), and the other radionuclide end-systolic volumes did not differ from the average cineangiographic end-systolic volume. Therefore, it is concluded that: 1) a simple geometric attenuation-correction of radionuclide left ventricular end-diastolic and end-systolic count data provides accurate estimates of biplane cineangiographic end-diastolic and end-systolic volumes; and 2) the hand-drawn region of interest selection method, unlike the semiautomated variable method that underestimates end-diastolic and end-systolic volumes, provides more accurate estimates of biplane cineangiographic left ventricular volumes irrespective of the distance blood sample counts are acquired from the collimator.

Adult↗
PubMed1984

Effect of right ventricular pressure on the end-diastolic left ventricular pressure-volume relationship before and after chronic right ventricular pressure overload in dogs without pericardia.

We studied the effect of chronic right ventricular pressure overload on diastolic ventricular interdependence in dogs without pericardia, instrumented to measure left ventricular pressure, right ventricular pressure, and 3 left ventricular dimensions. We studied 12 dogs before (control) and nine dogs after 6 weeks of pulmonary artery constriction producing systolic right ventricular pressure greater than or equal to 70 mm Hg. Compared to control, following pulmonary artery band there was greater (P less than 0.01) interventricular septal mass (53 +/- 15 vs. 35 +/- 7 mg, mean +/- SD), thickness (15 +/- 2 vs. 10 +/- 1 mm), and ratio of the surface area of the interventricular septal to total left ventricular surface area (0.38 +/- 0.03 vs. 0.33 +/- 0.02), but unchanged left ventricular free wall mass (81 +/- 12 vs. 84 +/- 14 mg) and thickness (11 +/- 2 vs. 11 +/- 2 mm). End-diastolic right and left ventricular pressures and left ventricular volume were varied by vena cava and pulmonary artery occlusions and releases. Volume was calculated as an ellipsoid and the data in each dog fit to: left ventricular pressure = a0 + a1V + a2V2 + a3V3 + a4V4 + bPRV, r greater than or equal to 0.91 in each dog. During control, b was similar, whether calculated from both pulmonary artery and vena cava occlusions (0.47 +/- 0.09) or from vena cava occlusions alone (0.43 +/- 0.11), and was greater than the ratio of the interventricular septal surface area to left ventricular surface area (0.33 +/- 0.02, P less than 0.05). Following the pulmonary artery band, b decreased to 0.21 +/- 0.10 (P less than 0.05) and was less than the ratio of interventricular septal surface area to the left ventricular surface area which increased to 0.38 +/- 0.03 (P less than 0.05). We conclude that the effect of alterations in right ventricular pressure on the end-diastolic left ventricular pressure volume relationship, independent of the pericardium, is reduced following the pulmonary artery band that produces interventricular septal hypertrophy. These results are consistent with the hypothesis that the effect of alterations of right ventricular pressure on the diastolic left ventricular pressure-volume relationship depends on the relative elastance of the interventricular septum and left ventricular free wall, and not simply on the ratio of the interventricular septal surface area to the left ventricular surface area.

Animals↗
PubMed1984

Evaluation of left ventricular contractile performance utilizing end-systolic pressure-volume relationships in conscious dogs.

The relationship between left ventricular end-systolic pressure and volume has been proposed as a model of left ventricular contraction which may be useful for quantifying inotropic state independent of preload and afterload. Although the model has been well-validated in isolated hearts, systematic evaluation in conscious animals with an intact peripheral circulation has been limited. Accordingly, we derived end-systolic pressure-volume relationships in twelve conscious dogs, chronically instrumented to measure left ventricular pressure and dimensions from endocardial ultrasonic crystals in three orthogonal axes. We examined the linearity of the end-systolic pressure-volume relationship, its response to alterations of inotropic state and the peripheral circulation, and the influence of beta-adrenergic reflexes. End-systolic pressure-volume relationships were constructed by linear regression of end-systolic pressure-volume coordinates produced by transient inferior vena caval occlusions during atrial pacing. The relations were highly linear; of 127 inferior vena caval occlusions, the correlation coefficient was 0.96 +/- 0.05 (mean +/- SD). The slope of the end-systolic pressure-volume relationship was not significantly altered either by a moderate resistive afterload induced by angiotensin II infusion, or by a moderate increase in preload produced by dextran, but was increased from 4.7 +/- 2.3 to 6.5 +/- 2.2 mm Hg/ml (P less than 0.05) in response to the positive inotropic stimulus of dobutamine. The volume intercept at zero end-systolic pressure was unaffected by dextran or dobutamine, but was decreased from 12 +/- 8 to 5 +/- 11 ml (P less than 0.01) by angiotensin II infusion, indicating a leftward shift of the end-systolic pressure-volume relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1984

Mechanism of anterior ST segment depression during acute inferior myocardial infarction. Observations during coronary thrombolysis.

Anterior ST segment depression, found in 13 of 17 patients with acute inferior myocardial infarctions, resolved promptly in all 11 patients whose occluded right coronary arteries were opened with an infusion of streptokinase. Failure of streptokinase to open the artery produced no change in the electrocardiogram. Five of the patients with anterior ST segment depression had normal left anterior descending coronary arteries. In the other patients opening the right coronary artery normalized the anterior ST segments without resulting in collateral flow to the anterior wall, or changing blood pressure or heart rate. Anterior ST depression was a manifestation of the inferior infarction and was not due to anterior ischemia.

Adult↗
PubMed1984

Estimates of left-ventricular volumes by equilibrium radionuclide angiography: importance of attenuation correction.

To compare the accuracy of attenuated and attenuation-corrected equilibrium radionuclide angiographic (RNA) left ventricular (LV) volume estimates, we studied 23 consecutive patients with biplane contrast cineangiography (CINE). Attenuated RNA end-diastolic (ED) and end-systolic (ES) volumes were calculated from background-corrected ED and ES counts obtained from hand-drawn regions of interest that were normalized to cardiac cycles processed, frame rate, and blood activity. A simple, geometric attenuation correction was performed to obtain attenuation-corrected RNA LV volumes. The attenuated and attenuation-corrected RNA LV EDV estimates correlated with the CINE LV EDVs ; however, the attenuation-corrected RNA LV EDV estimates correlated more closely. Also, the average attenuation-corrected RNA LV EDV did not differ significantly from the mean CINE LV EDV. Attenuated and attenuation-corrected RNA LV ESV estimates also correlated with the CINE LV ESVs , but the attenuation-corrected RNA LV ESV estimates correlated more closely. Also, the average attenuation-corrected RNA LV ESV did not differ significantly from the mean biplane CINE LV ESV.

Adult↗
PubMed1983

Angiographic evidence of hemorrhagic myocardial infarction after intracoronary thrombolysis with streptokinase.

The reperfusion of acutely ischemic myocardium by intracoronary streptokinase thrombolysis is an exciting new therapy for acute myocardial infarction (MI). It appears that successful thrombolysis and reperfusion in the first few hours after acute coronary occlusion may salvage myocardium and possibly improve prognosis. A potential adverse effect of reperfusion is the production of hemorrhage in the area of myocardial necrosis. We report on a patient with prompt, successful coronary thrombolysis by streptokinase infusion who showed angiographic evidence of a hemorrhagic MI.

Aged↗
PubMed1983

Thrombolytic therapy of acute myocardial infarction.

Thrombotic coronary artery occlusion is now recognized as the usual cause of acute myocardial infarction. The thrombus usually forms at the site of intimal disruption over an atherosclerotic plaque. Following coronary occlusion, myocardial necrosis begins within 40 minutes in the subendocardium and progresses outward toward the epicardium over the next several hours. The intracoronary infusion of streptokinase will produce lysis of the occluding thrombus in up to 80% of patients. It appears that reperfusion with streptokinase in the first few hours following the onset of the myocardial infarction produces a small increase in late left ventricular function, though ECG and enzyme evidence of acute myocardial infarction are not prevented. The improvement in left ventricular function is variable from patient to patient and has not been demonstrated in all the randomized studies to date. The time limit for myocardial salvage may not be the same in all patients. The greatest benefit is probably achieved with reperfusion in the first 4-6 hours, although some benefit may occur as late as 18 hours after the onset of infarction. Many patients who receive intracoronary infusion of streptokinase develop a systemic lytic state, though serious bleeding complications in carefully selected patients are infrequent. High-dose IV streptokinase is easier, cheaper, and quicker to initiate than intracoronary streptokinase but is probably less effective than the intracoronary route in producing rapid lysis of the occluding coronary thrombus. The optimal dose and rate of administration of IV streptokinase have not been determined. The final role and ultimate benefit of thrombolytic therapy of myocardial infarction have not yet been determined, but some of the issues may be clarified by the larger randomized trials now under way. It appears, at present, that the use of intracoronary streptokinase may have a role in the treatment of selected patients with acute myocardial infarctions in institutions with the facilities and the personnel necessary to perform this procedure safely. In the future, thrombolytic therapy may also have a place in the treatment of selected patients with unstable angina and post-myocardial infarction angina. The future availability of more selective thrombolytic agents may make the early IV therapy of myocardial infarction a safer, more effective option and expand the indications for thrombolytic therapy.

Coronary Disease↗
PubMed1982

Mechanism of abnormal interventricular septal motion during delayed left ventricular activation.

To evaluate the mechanism of the abnormal motion of the interventricular septum (IVS) seen echocardiographically in some patients with relatively delayed ventricular activation, we simultaneously recorded high-fidelity left and right ventricular pressures and electrograms and echocardiograms of the IVS in nine open-chest dogs. During sinus rhythm and during left IVS pacing, the IVS was activated from left to right, preejection left ventricular pressure exceeded right ventricular pressure, and IVS motion was normal. During right ventricular pacing from the outflow tract, apex, free wall or right IVS was activated from right to left, right ventricular pressure increased before left ventricular pressure and simultaneously there was an abrupt posterior IVS motion. Simultaneous pacing from the right IVS and left ventricular free wall activated the IVS from right to left and produced a normal transseptal preejection pressure gradient and normal IVS motion. Simultaneous pacing from the left IVS and right ventricular free wall activated the IVS from left to right, and produced abrupt preejection posterior IVS motion coincident with an altered transseptal pressure gradient. During right ventricular pacing, IVS motion after the abrupt preejection posterior movement was variable. Anterior motion was associated with a greater asynchrony of right and left ventricular contraction than was normal posterior motion. We conclude that abrupt preejection posterior IVS motion seen with delayed left ventricular activation from right ventricular pacing is due to passive IVS displacement from an altered transseptal pressure gradient, and subsequent IVS motion depends on the degree of asynchrony between right and left ventricular contraction.

Animals↗