Characterization of left ventricular mechanical function during arrhythmias with two dimensional echocardiography: I. premature ventricular contractions

Two dimensional echocardiography was applied experimentally in the closed chest dog to quantitate left ventricular function during and immediately after single premature ventricular contractions induced through threshold stimulation at the apex. Coupling intervals were varied over a range from 35 to 85 percent of the R-R interval during normal sinus rhythm (920 to 980 ms). The quality of tomographic echocardiographic images during premature as well as postextrasystolic beats was found to be satisfactory for quantitating short axis section areas at end-diastole and end-systole. A systolic fractional area change was computed from two dimensional echocardiographic measurements to characterize mid ventricular cardiac function, which correlated significantly with peak left ventricular pressure and maximal first derivative of left ventricular pressure (dP/dt). Marked shortening of coupling intervals reduced fractional shortening during premature systole and enhanced the degree of potentiation during the postextrasystolic beat. By contrast, premature beats with relatively long coupling intervals caused less reduction in contraction and only minor postextrasystolic potentiation.Systolic shortening of left ventricular length as well as transverse diameters were studied in a two dimensional echocardiographic long axis cross section. During long coupling intervals contraction was normal except for distinct regional systolic outward “bulging” in the apical region. In contrast, short coupling intervals were associated with a more significant generalized derangement of ventricular wall motion during systole. It is concluded that the two dimensional echocardiographic method can be used to portray and quantitate global as well as regional left ventricular function during disturbances of cardiac rhythm.     

Heterogeneity of left ventricular segmental wall thickening and excursion in 2-dimensional echocardiograms of normal human subjects

Regional abnormalities of left ventricular (LV) wall thickening and excursion have been demonstrated by 2-dimensional (2-D) echocardiography. However, the variability of normal segmental contraction has not previously been defined. We performed 2-D echocardiography in 12 normal men aged 19 to 27 years. We obtained short-axis images at the level of the mitral valve, chordae tendineae, papillary muscles, and apex at end-diastole and end-systole. A computer-based system divided each short-axis image into 12 cavity and wall segments, and analyzed percent systolic wall thickening along each radius and percent area change of each cavity segment. Overall variability of contraction as well as the contributions of several sources of variability were determined. The overall range of cavity segment area change was 0 to 100% and of segmental wall thickening was 0 to 150% in these normal subjects. Average contraction was similar at different ventricular levels. Significant differences were found between adjacent segments at each level as well as between subjects. Intrathoracic cardiac rotation and motion were minimal; correction for these movements did not significantly alter the variability of contraction as calculated from 2-D echocardiograms. Temporal asynergy of contraction did contribute to variability; correction resulted in a significant alteration in mean segmental area change (from 59 ± 20% [standard deviation] uncorrected to 66 ± 16% corrected, p < 0.001) and in mean segmental wall thickening (58 ± 29% uncorrected to 71 ± 34% corrected, p < 0.01). Substantial interexamination variability also occurred with an average difference in cavity segment area change of 20% per segment and in segmental wall thickening of 29% per segment between 2 analyses by the same observer. Thus, considerable intersegmental and intersubject variability of LV contraction occurs in normal subjects as exhibited on 2-D echocardiograms, exaggerated by technical difficulties in analyzing and reproducing the echocardiographic tracings. Significant differences in segmental wall thickening and endocardial excursion may occur in adjacent segments in normal subjects, and therefore such differences alone may not indicate cardiac disease.     

Dynamic changes in left ventricular regional wall thickness during premature ventricular contraction in conscious dogs

The contractile pattern of the regional left ventricular wall during premature ventricular contraction was analyzed in conscious dogs instrumented with an ultrasonic dimension gauge across the anterior and posterior left ventricular walls. Aortic flow was measured with an electromagnetic flow probe. A single premature ventricular contraction was induced by stimulating either the anterior or posterior wall with varied coupling intervals from 380 to 650 msec. Stroke volume of premature ventricular contraction was significantly smaller than that of premature atrial contraction with identical coupling intervals. In premature contractions, stroke volume was linearly related to coupling intervals. Though there was no isovolumic wall thickening in premature atrial contraction, the wall started to thicken during isovolumic ventricular systole in premature ventricular contraction. There was a clear inverse correlation between the ratio of the isovolumic wall thickening to the total wall thickening and coupling intervals.

In premature ventricular contractions with identical coupling intervals, the deformation of thickening characteristics was more pronounced in regions with closer proximity to the ectopic focus. Thus it is concluded that the pump function is depressed in premature ventricular contraction, in part due to the increased ratio of wall thickening during isovolumic systole before the opening of the aortic valve. Isovolumic wall thickening increases along with the shorter coupling intervals and closer proximity to the ectopic focus. These alterations in left ventricular mechanical function due to ectopic contraction might induce serious sequelae, depending upon the ectopic focus in the presence of already depressed regional function.     

Cardiac function and myocardial contractility: a perspective

An experimental study was designed to validate postextrasystolic potentiation assessment of myocardial viability or functional reserve of cardiac segments after acute coronary occlusion. Segmental systolic fractional area changes and wall thickening in pacing-induced postextrasystolic beats were mapped in 12 closed chest dogs by two-dimensional echocardiography during a control period and from 20 minutes to 3 hours after occlusion of the left anterior descending coronary artery. The extent of myocardial ischemic and necrotic zones was evaluated in left ventricular slices and subsegements corresponding to echographic cross sections. During two-dimensional echocardiography, left ventricular segments that were found to be neither ischemic nor necrotic always exhibited a significant augmentation of both fractional area change and wall thickening during the postextrasystolic beat that followed an induced premature contraction with a 42.4% coupling interval. In segments without necrosis but with varying degrees of ischemia, significant postextrasystolic potentiation was also demonstrated, even after 3 hours of occlusion. In contrast, segments that developed more than 80% necrosis failed to potentiate systolic fractional area change after 2 hours, and systolic wall thickening, even after 20 minutes of coronary occlusion. Statistical evaluation revealed a characteristic threshold at 41 to 60% necrosis, beyond which no potentiation of function could be elicited 3 hours after occlusion. Extrapolation from the experimental data suggests that when two-dimensional echographic studies in myocardial ischemia indicate postextrasystolic augmentation of segmental left ventricular function, the latter segments may be assumed to contain only small infarcts or to consist of reversibly ischemic and normal myocardium. Conversely, segments that fail to exhibit postextrasystolic potentiation can be assumed to be more than 60% necrotic.     

Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

A model was developed to study ventricular automaticity and reentry in the heart of open chest dogs during myocardlal ischemia. Atrioventricular (A-V) block and the resultant idioventricular rhythm were induced by surgical destruction of the His bundle, and acute myocardial ischemia was produced by ligation of the left anterior descending coronary artery. The ventricle was paced by basic stimuli, and one or two premature beats were introduced at various coupling Intervals after the 10th basic beat. Two different types of response to these premature beats could be observed: (1) rapidly repetitive beats or fibrillation due to reentry after early premature beats, and (2) the appearance of escape beats from idioventricular automatic fibers after late premature beats.With this model of ventricular reentry and automaticity, the effect of procainamide (group I antiarrhythmic agent) was studied in 12 dogs, and that of lidocaine (group II) in 13 dogs. Both procainamide and lidocaine were effective in decreasing automaticity since they significantly increased postextrasystolic escape intervals of idloventricular beats. Although procainamide failed to abolish the reentrant beats induced by early premature beats in all 12 dogs, lidocaine abolished these beats in 10 of 13 dogs. The results indicate that lidocaine is much more effective than procainamide in preventing ventricular reentrant activity induced by early premature beats.     

Dynamic characterization of premature ventricular beats and ventricular tachycardias

The contraction patterns induced by ectopic ventricular premature beats and ventricular tachycardias occurring in man during left ventriculography were analyzed. These were compared with contraction patterns induced by ventricular premature beats and tachycardias produced in five dogs by epicardial left ventricular apical or basilar stimulation. Two patterns of contraction observed in the animals corresponded to two patterns observed in man. Apically stimulated left ventricular beats produced an “hourglass” type of contraction pattern and were hemodynamically more effective than beats arising from basilar stimulation, which produced an inverse “teardrop” pattern. The same patterns were reproduced by experimental ventricular tachycardias. These observations stress the importance of a normal sequence of ventricular contraction to optimal cardiac function in man and warn against the hazards of misinterpretation of the left ventricular contraction pattern if the beat originates ectopically during ventriculography.     

Recording from the body surface of arrhythmogenic ventricular activity during the S-T segment

Recent experimental reports have documented the delay of epicardial potentials beyond the QRS complex as a result of infarction, and the degree of delay was directly associated with the onset of ventricular arrhythmias. This study describes a method using high amplification, band pass filtering and signal averaging for recording from the body surface these delayed potentials presaging ventricular arrhythmias. This technique, has been used for recording low level cardiac potentials masked by noise. In 10 dogs control records of the electrocardiogram and surface averaged lead were obtained during sinus rhythm, atrial pacing and premature atrial beats. Subsequently, the left anterior descending coronary artery was ligated in each dog. Nine dogs survived the surgical procedure and underwent similar recordings 3 to 6 days after infarction. Electrocardiographic changes were consistent with a recent infarction. During the pacing protocol discrete multiphasic wave forms appeared during the S-T segment of the surface averaged lead, and concomitant changes in the terminal portions of the QRS complex were observed in seven dogs. In five of these dogs ventricular arrhythmias were observed at the faster pacing rates or after closely coupled premature atrial beats. The chest was then reopened and the pacing procedure repeated during recording of direct epicardial electrograms with a multicontact bipolar electrode. This electrogram validated the existence of potentials during the S-T segment in all but one dog and late activity that was not repeatable on a beat to beat basis in another. Thus, when late activity was confirmed with the epicardial electrogram, seven of eight dogs showed a corresponding change in the surface averaged lead. This technique may prove to be a sensitive indicator of abnormal electrical activity preceding ventricular arrhythmias.     

Regional differences in left ventricular response to atrial pacing in the dog: mapping of segmental function by two-dimensional echocardiography

Two-dimensional echocardiography was applied in 10 closed-chest dogs to evaluate, in several left ventricular (LV) short-axis cross sections and subsegments, the regional contractile response to right atrial pacing. Compared with sinus rhythm (81 +/- 10 beats/min), which exhibited a moderate 7.2 +/- 12.0% (mean +/- standard deviation) base-to-apex increment in function, this gradient was significantly augmented to 34 +/- 12% by pacing at a heart rate of 180 beats/min. Measurements of wall thickening and perimeter shortening exhibited similar trends. Differences also were observed in subsegments of individual cross sections: in sinus rhythm the base-to-apex difference in function was relatively minor in the anterior and lateral aspects of the left ventricle (-9.1 +/- 18% and -1.9 +/- 19%), whereas a significant increase was noted in posterior and midseptal zones (18 +/- 17% and 22 +/- 30%). In response to pacing, the anterior and lateral wall base-to-apex gradients were significantly augmented (25 +/- 8% and 35 +/- 34%), but there was no further change in the posterior or septal regions. In conclusion, apical regions of the canine left ventricle responded to right atrial pacing with significant augmentation of contractile function, whereas more basal levels showed little response. Circumferentially, response to atrial pacing was most pronounced in the anterior and lateral segments.     

Early segmental thinning of the left ventricular wall following regional ischemia

To explore possible mechanisms of left ventricular early segmental relaxation, complete occlusion of the left anterior descending coronary artery (LAD) was produced in seven open-chest dogs and partial occlusion of the LAD was produced in six openchest anesthetized dogs. Regional wall thickness was measured both in an ischemic and a normally perfused zone using implanted ultrasonic crystals. Two to three seconds following complete LAD occlusion, thinning of the ischemic wall occurred prematurely during isovolumic relaxation. The extent of premature thinning became more prominent 5 to 10 sec following LAD occlusion. Early thinning of the ischemic wall preceded thinning of the normally perfused wall by 110 ± 10 msec. Partial occlusion of the LAD produced a 33 ± 6% reduction of coronary flow and a 23 ± 4% reduction of systolic wall thickening in the ischemic region. Systolic thickening of the nonischemic wall was unchanged relative to the preocclusion period. Premature early thinning of the mildly ischemic wall preceded thinning of the normally perfused segment by 90 ± 8 msec. The observation that ischemia can produce segmental early thinning of the ventricular wall may have implications in understanding the mechanism of the angiographic observation of the segmental early relaxation phenomena in patients with coronary artery disease.     

Alterations in ventricular contraction pattern in the Wolff-Parkinson-White syndrome. Detection by echocardiography.

The effects of abnormal ventricular activation upon the contractile pattern of the ventricles in patients with the Wolff-Parkinson-White syndrome (WPW) remain uncertain. Therefore we compared the motion of the anterior right ventricular wall (RV), the interventricular septum (IVS), and left ventricular posterior wall (LVPW) on echogram in nine patients with WPW and one patient with a coronary sinus pacemaker (CSP) to 20 normal subjects. Normal subjects manifested posterior RV motion which began and reached maximal excursion at 175 and 366 msec (group mean), respectively, after the onset of the QRS complex; posterior movement of the IVS which started and peaked at 90 and 30 msec, respectively; and anterior contraction of the LVPW which began and peaked at 159 and 406 msec, respectively. Five of seven patients with Type A WPW demonstrated a localized area of premature contraction of the LVPW occuring during the initial 100 msec interval following the onset of the QRS complex which was accompanied by paradoxic anterior motion of the IVS. Thereby in Type A patients initial and maximal posterior motion of the IVS occurred later, 230 (P less than 0.001) and 400 (P less than 0.05) msec, and anterior motion of the LVPW occurred earlier, 75 (P less than 0.001) and 367 (P less than 0.05) msec as compared to normal. The amplitude and duration of early contraction could be related to the prominence of the delta wave during atrial pacing. Similar premature contraction was also observed in the patient with CSP during paced beats. One Type B WPW patient exhibited abnormal IVS motion while the additional patient manifested premature LVPW contraction similat to that seen in Type A patients. The contractile pattern of the right ventricular anterior wall was recorded in five of seven Type A Wolff-Parkinson-White patients and manifested prolongation of the interval from the onset of the QRS complex to the initial posterior movement (group mean 234 msec, P less than 0.05) as compared to normal. Thus echocardiography can be used to confirm the diagnosis and to improve understanding of the pathophysiology of the Wolff-Parkinson-White syndrome.     

Study on the relationship between myocardial ischemia assessed by 24-hour ambulatory electrocardiogram and ventricular premature beat originating from different positions in older adults

BackgroundMyocardial ischemia is a common reason of ventricular premature beat, and it plays an important role in arrhythmia in older adults. We could often see the report about the diagnosis and radiofrequency catheter ablation of ventricular arrhythmia from the right ventricular outflow tract, Haissaguerre et al. (2002) [1], Miyamoto et al. (2010) [2], Nakagawa et al. (2008) [3], Zhu et al. (1995) [4]. However, no study to date has examined the relation of myocardial ischemia and ventricular premature beat originating from different positions. In this article, we studied the incidences of myocardial ischemia of ventricular premature beats originating from different positions in older adults.MethodsWe located the original positions of ventricular premature beats according to the shape of the wide and malformed QRS waves in 12 leads synchronizing ECG. We used synchronism 12-lead ambulatory 24 hour electrocardiograms to examine 531 aged patients with ventricular premature beats, calculated the incidences of myocardial ischemia of the ventricular premature beats originating from different positions.ResultsThe incidence of myocardial ischemia of ventricular premature beats from the right ventricular outflow and the left ventricular outflow were 52.31% and 51.42% respectively. The incidence of myocardial ischemia of ventricular premature beat from the right ventricle anterior wall and the left ventricle anterior wall were 53.57% and 73.47% respectively. The incidence of myocardial ischemia of ventricular premature beat from the right ventricular apex and the left ventricular apex were 55.10% and 74.42% respectively. The total incidence of myocardial ischemia of right ventricular premature beats and left ventricular beats were 52.92% and 61.65% respectively.ConclusionsThe total incidence of myocardial ischemia of left ventricular premature beats was higher than that of right ventricular premature beats. The highest incidence of myocardial ischemia of ventricular premature beats was that from the left ventricular apex and anterior wall. The incidence of myocardial ischemia of ventricular premature beats was more than 50% in older adults.     

Differential effects of left anterior descending coronary occlusion on left and right ventricular anterior wall thickening in the conscious pig.

OBJECTIVE: In humans, the left anterior descending coronary artery supplies the left ventricular wall, anterior septum and the paraseptal part of the right ventricular anterior wall. Our aim was to study the effects of acute left anterior descending coronary occlusion on wall thickening in the regions of the left and right ventricular anterior walls supplied by the artery, and in remote, non-ischaemic regions of both ventricles. METHODS: Systolic wall thickening (defined as percent thickening with respect to end diastolic wall thickness) was studied in eight conscious pigs every 15 s during 1 min of acute left anterior descending coronary occlusion by a cuff occluder, and every 30 s during 4 min of reperfusion. Pigs were instrumented with ultrasonic microcrystals measuring wall thickness in the anterior walls (left anterior descending artery territory) and lateral walls (left circumflex or right coronary artery territory) of both ventricles, and a left ventricular pressure microtransducer. RESULTS: During control and reperfusion, both anterior walls displayed similar systolic thickening. During coronary occlusion, the left ventricular anterior wall showed paradoxical systolic thinning (dyskinesia) whereas the right ventricular anterior wall showed only hypokinesia. CONCLUSIONS: In the presence of equal blood flow deprivation, the right ventricular anterior wall supplied by the left anterior descending coronary artery displays a significantly lesser degree of functional impairment than the left ventricular anterior wall supplied by the same artery. This differential effect may be due to mechanical unloading of the right ventricular anterior wall resulting from left ventricular anterior wall ischaemia. This afterload reduction due to decreased mechanical interaction between the two walls would allow the right ventricular anterior wall to express its contractile reserve in the form of systolic thickening.     

Computer analysis of cross sectional echocardiogram for quantitative evaluation of left ventricular asynergy in myocardial infarction.

Left ventricular asynergy in myocardial infarction was assessed quantitatively by computer analysis of the cross sectional echocardiogram. Short axis cross sectional images of the left ventricle at the levels of the mitral valve, papillary muscle, and apex were recorded by a phased array sector scanner in 30 patients with healed myocardial infarction and 15 normal controls. Endocardial and epicardial short axis images of the left ventricle were transferred from video tape to a minicomputer through the interface circuits, then digitised and processed automatically by a minicomputer. Automatic edge detection of the endocardial and epicardial wall was performed by applying sequential steps including smoothing, second derivative technique, dynamic thresholding, and approximation of boundaries by a spline curve. To quantify regional wall motion, the short axis cross sectional left ventricular wall of each level was divided into eight octants with eight axes at 45 degrees angles from the initial standard axis which was constructed from the geometric centre of the end diastolic left ventricular cavity to the posterior end of the right side of the interventricular septum. Segmental hemiaxis, segmental area, segmental wall thickness, and those changes during cardiac cycle were measured and calculated in each segment automatically by a computer. Regional contractility of the left ventricle was evaluated by percentage systolic changes of the segmental hemiaxis, area, and wall thickness. These values were significantly reduced in the infarcted left ventricular wall as defined by left ventriculography and electrocardiography. Moreover, percentage hemiaxis changes obtained by quantitative left ventriculography described by Herman and colleagues correlated well with those using our analytical method of cross sectional echocardiography in the corresponding segments. The geometric centre of the left ventricular cavity determined by the computer moved slightly towards the anterior wall during systole in normal subjects, possibly reflecting the anterior swinging motion of the heart. The geometric centre of the left ventricular cavity in myocardial infarction moved towards the infarcted wall, showing that the floating reference system was inferior to the fixed reference system for the quantification of abnormal wall motion in myocardial infarction. In conclusion, a computer analysis of the short axis cross sectional echocardiogram of the left ventricle using the fixed reference system has shown its ability to evaluate left ventricular contraction abnormalities, especially systolic wall thickening, which is relatively free of arbitrary interpretation of the wall motion caused by the anterior swinging motion of the heart.     

Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction.

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.     

Initiation of ventricular tachycardia by interpolated ventricular premature depolarizations

Programmed electrical stimulation of the heart was performed in a 47 year old man with prior myocardial infarction and recurrent sustained ventricular tachycardia that was refractory to standard medical therapy. The tachycardia could be provoked by regular atrial pacing at a rate of 100/min, regular ventricular pacing at the same rate and regular atrial pacing at a rate of 200/min in the presence of 2:1 atrioventricular block. All three techniques resulted in an interval of approximately 600 ms between successive ventricular depolarizations. Single interpolated ventricular premature depolarizations delivered during sinus rhythm were followed by a postextrasystolic conducted sinus beat that initiated ventricular tachycardia. However, when the same interpolated ventricular premature depolarization was followed by a ventricular fusion beat no tachycardia ensued. This study therefore emphasizes the importance of heart rate and the pattern of ventricular activation in determining whether ventricular tachycardia can be provoked by programmed electrical stimulation of the heart.     

Systolic direct ventricular interaction affects left ventricular contraction and relaxation in the intact dog circulation

Changes in right ventricular systolic function directly influence left ventricular systolic function. Most of our knowledge of this systolic direct ventricular interaction comes from studies of isolated hearts, which suggest that changes in right ventricular size only affect left ventricular systolic function at low pressures and volumes. However, almost nothing is known about systolic direct ventricular interaction in a heart functioning in situ as a part of the intact circulation. We used sudden constriction of the pulmonary artery to assess the immediate effect of a change in right ventricular pressure and contraction pattern on left ventricular contraction and relaxation on the beat following the pulmonary artery constriction in anesthetized open-chest dogs. By focusing on this first beat, we were able to avoid the confounding effect of series ventricular interaction, which changes left ventricular filling and, thus, indirectly influences left ventricular function. At baseline left ventricular end-diastolic pressure of 9.6 +/- 2.1 mm Hg (mean +/- SD), sudden pulmonary artery constriction increased left ventricular peak systolic pressure by 3 +/- 2 mm Hg (2% change), left ventricular stroke volume by 2 +/- 2 ml (8% change), and monoexponential time constant of left ventricular pressure fall during relaxation by 9 +/- 6 msec (22% change). This increased left ventricular relaxation time constant was associated with altered regional segment length changes in the posterior and anterior left ventricular free walls during relaxation. We conclude that systolic direct ventricular interaction affects left ventricular systolic function and relaxation under normal conditions in the intact circulation.     

Computer analysis of cross sectional echocardiogram for quantitative evaluation of left ventricular asynergy in myocardial infarction

Left ventricular asynergy in myocardial infarction was assessed quantitatively by computer analysis of the cross sectional echocardiogram. Short axis cross sectional images of the left ventricle at the levels of the mitral valve, papillary muscle, and apex were recorded by a phased array sector scanner in 30 patients with healed myocardial infarction and 15 normal controls. Endocardial and epicardial short axis images of the left ventricle were transferred from video tape to a minicomputer through the interface circuits, then digitised and processed automatically by a minicomputer. Automatic edge detection of the endocardial and epicardial wall was performed by applying sequential steps including smoothing, second derivative technique, dynamic thresholding, and approximation of boundaries by a spline curve. To quantify regional wall motion, the short axis cross sectional left ventricular wall of each level was divided into eight octants with eight axes at 45 degrees angles from the initial standard axis which was constructed from the geometric centre of the end diastolic left ventricular cavity to the posterior end of the right side of the interventricular septum. Segmental hemiaxis, segmental area, segmental wall thickness, and those changes during cardiac cycle were measured and calculated in each segment automatically by a computer. Regional contractility of the left ventricle was evaluated by percentage systolic changes of the segmental hemiaxis, area, and wall thickness. These values were significantly reduced in the infarcted left ventricular wall as defined by left ventriculography and electrocardiography. Moreover, percentage hemiaxis changes obtained by quantitative left ventriculography described by Herman and colleagues correlated well with those using our analytical method of cross sectional echocardiography in the corresponding segments. The geometric centre of the left ventricular cavity determined by the computer moved slightly towards the anterior wall during systole in normal subjects, possibly reflecting the anterior swinging motion of the heart. The geometric centre of the left ventricular cavity in myocardial infarction moved towards the infarcted wall, showing that the floating reference system was inferior to the fixed reference system for the quantification of abnormal wall motion in myocardial infarction. In conclusion, a computer analysis of the short axis cross sectional echocardiogram of the left ventricle using the fixed reference system has shown its ability to evaluate left ventricular contraction abnormalities, especially systolic wall thickening, which is relatively free of arbitrary interpretation of the wall motion caused by the anterior swinging motion of the heart.     

The similarity of changes in segmental contraction patterns induced by postextrasystolic potentiation and nitroglycerin.

Despite a fundamental difference in their underlying mechanisms, both postextrasystolic potentiation (PESP) and administration of nitroglycerin (TNG) have been utilized to predict reversibility of abnormal segmental wall motion in patients with ischemic heart disease. To determine whether these interventions induce the same changes in segmental contraction pattern, we analyzed biplane ventriculograms of 14 patients who had an adequately visualized PESP beat on a basal ventriculogram as well as a post-TNG ventriculogram. Four segments in each plane were defined and the area ejection fraction of each segment was calculated for a basal sinus, PESP, and post-TNG beat. To correct for global differences in the response to PESP and TNG, we normalized each segmental ejection fraction (NSEF) by the ventricular ejection fraction for that beat and then compared the differences in NSEF from the basal value after PESP and TNG. Eleven patients demonstrated similar responses to both interventions. The three patients whose responses were discordant had elevated or unchanged left ventricular systolic or end-diastolic pressures at the time of the TNG ventriculogram. Our data suggest that, provided these pressures are lower than basal values at the time of the TNG ventriculogram, PESP and TNG will induce similar changes in segmental contraction patterns. Seven patients with similar responses had a PESP beat on their post-TNG ventriculogram. Changes in NSEF after PESP+TNG were identical to those after either intervention. This implies that the combination of interventions does not induce further changes in segmental contraction pattern beyond that produced by either intervention alone.     

Overestimation of infarct size by quantitative two-dimensional echocardiography: the role of tethering and of analytic procedures

Analyses of regional left ventricular systolic wall motion or thickening overestimate infarct size. We used quantitative two-dimensional echocardiographic analysis of systolic thickening and contrast two-dimensional echocardiography to evaluate causes for that overestimation. The following possibilities were considered: "tethering," defined as dysfunction of contrast-enhancing myocardium adjacent to ischemic or contrast-negative regions, and the role of standard center of mass analysis algorithms, which may overestimate wall motion abnormalities because of the axis shift produced by simultaneous systolic expansion of the ischemic segment and systolic contraction of the nonischemic segment. In the short-axis view in 12 animals, the echo contrast defect (ECD) occupied 32 +/- 7% of the left ventricular circumference. Extent of dysfunction by the center of mass analysis was 39 +/- 5% of the left ventricular circumference and correlation with ECD size was .68 (SEE = 5.2%). Thus 8 +/- 6% of the circumference of the left ventricle was assessed to be dysfunctional yet enhanced with contrast. Tethering accounted for only half of this (4 +/- 4% of left ventricular circumference) and involved less than 1 cm on either side of the ECD. The remaining overestimation by the center of mass analysis correlated significantly (r = .89, p less than .01) with the amount of systolic expansion of the ECD. This expansion of the ECD (increase in angle subtended by the ECD of 11 +/- 8%) was produced by the systolic shift in the center of mass toward the dysfunctional segment from contraction of the opposite, nonischemic segment.(ABSTRACT TRUNCATED AT 250 WORDS)