Midpapillary Muscle Level Research Articles

Acute Effects of Pacing at Different Ventricular Sites on Left Ventricular Rotational Mechanics in a Porcine Model.

The purpose of this study was to examine the acute effects of pacing at different ventricular sites on hemodynamics and left ventricular (LV) rotational mechanics using speckle-tracking echocardiography (STE) in a porcine model. A prospective laboratory investigation. University research laboratory. Yorkshire pigs. In 9 pigs, after midline sternotomy, epicardial pacing was performed from the right ventricular outflow tract (RVOT), right ventricular apex (RVA), and LV free wall. Two-dimensional STE and conductance catheter-derived LV pressure-volume measurements were made to determine the impact of pacing from various sites on LV rotational parameters (twist/untwist) and hemodynamics. RVOT pacing caused the least decrease in end-systolic pressure from baseline (-9.5%), when compared with RVA (-19.1%) and LV (-23.4%). Systolic and diastolic parameters (Emax, Tau) also were different among RVOT (4.7±0.8 mmHg/mL, 32±4 ms), RVA (3.9±0.7 mmHg/mL, 37±6 ms), and LV sites (3.6±0.8 mmHg/mL, 42±7 ms). Similar to the effects of pacing on hemodynamics, RVOT pacing better preserved LV twist (11.1±1.8 v 8.6±1.7, 5.9±0.7 °) and untwisting rate (64.6±8.5 v 56.2±5.3, 48.2±8.5 °/s) when compared with RV apical pacing and LV pacing. Furthermore, prolongation of conduction from LV lateral to anteroseptal at LV base (26.5±3.8 v 13.8±3.3 ms, p<0.05) and LV midpapillary muscle level (35.6±5.6 v 14.1±2.4 ms, p<0.05) was observed with LV pacing compared with RVOT pacing. The present data showed that the LV twist/untwist and cardiac systolic and diastolic function were least affected by RVOT pacing. This finding may be explained by the proximity of this location to the native ventricular conduction system.

Restriction of Food Intake Prevents Postinfarction Heart Failure by Enhancing Autophagy in the Surviving Cardiomyocytes

We investigated the effect of restriction of food intake, a potent inducer of autophagy, on postinfarction cardiac remodeling and dysfunction. Myocardial infarction was induced in mice by left coronary artery ligation. At 1 week after infarction, mice were randomly divided into four groups: the control group was fed ad libitum (100%); the food restriction (FR) groups were fed 80%, 60%, or 40% of the mean amount of food consumed by the control mice. After 2 weeks on the respective diets, left ventricular dilatation and hypofunction were apparent in the control group, but both parameters were significantly mitigated in the FR groups, with the 60% FR group showing the strongest therapeutic effect. Cardiomyocyte autophagy was strongly activated in the FR groups, as indicated by up-regulation of microtubule-associated protein 1 light chain 3-II, autophagosome formation, and myocardial ATP content. Chloroquine, an autophagy inhibitor, completely canceled the therapeutic effect of FR. This negative effect was associated with reduced activation of AMP-activated protein kinase and of ULK1 (a homolog of yeast Atg1), both of which were enhanced in hearts from the FR group. In vitro, the AMP-activated protein kinase inhibitor compound C suppressed glucose depletion-induced autophagy in cardiomyocytes, but did not influence activity of chloroquine. Our findings imply that a dietary protocol with FR could be a preventive strategy against postinfarction heart failure.

Evaluation and simplified measurement of infarct size by myocardial contrast echocardiography in a rat model of myocardial infarction

To test the feasibility and accuracy of myocardial contrast echocardiography (MCE) for predicting infarct size (IS) in a rat model of myocardial infarction (MI) and to compare a simplified single plane-based measurement of IS with the conventional three plane-based approach. Fifty male SD rats underwent left anterior descending artery ligation and were evaluated by MCE 8 h post MI. IS was calculated by the single and three plane-based approaches, compared to that determined by triphenyltetrazolium chloride (TTC) staining method. Simplified single plane-based MCE approach and TTC method showed similar IS values (38.48 +/- 16.80% vs. 35.72 +/- 15.33%, P > 0.05) and presented a favorable positive correlation (r = 0.851, P < 0.001). IS values derived from simplified single plane-based approach was also highly significantly correlated with that by the conventional MCE method (r = 0.973, P < 0.001). Bland-Altman plots also displayed satisfactory agreement between them. MCE was validated as a novel technique to quantify infarct area in rats with MI. A single measurement at the mid-papillary muscle level may become a simple, efficient and reliable approach for in vivo IS assessment.

Reply to “Letter to the editor: Infarct size measurements are critically important when comparing interventions affecting ventricular remodeling”

Reply to “Letter to the editor: Infarct size measurements are critically important when comparing interventions affecting ventricular remodeling”

Letter to the editor: Infarct size measurements are critically important when comparing interventions affecting ventricular remodeling

REPLY: Dr. Lygate (5) has suggested that the variability observed in infarct size in the surgical mouse myocardial infarction model (10 –70%) (1, 7) mandates larger sample sizes than used in our study (9). Although we agree that variable infarct size certainly occurs with this model, our presented data show clear, statistically significant differences with the given sample sizes. Our protocol may reduce variability in infarct size by careful attention to a proximal ligation of the left coronary immediately at the site where it emerges from under the left atrium as well as by eliminating mice that do not have a clear area of distal blanching of myocardium after immediate ligation (4, 8, 9). The more distal the ligation is made, the more the variability in coronary anatomy of the mouse heart impacts infarct size. Thus the referenced study by Patten et al. (7), which stated that the suture on the left coronary was placed approximately midway between the apex and base of the left ventricle, likely introduced greater variability in infarct size than we observed. Another study referenced by Dr. Lygate further makes this point in that Takagawa et al. (10) systematically created large infarctions by using proximal left coronary ligations (4 mm from apex) and small infarctions by distal ligations (2 mm from apex). We conclude that with careful attention to surgical technique, the range of infarct sizes can be much smaller than the 10 –70% suggested by Dr. Lygate and that with the techniques used in our study, statistically significant results with the stated sample sizes were obtained. Second, Dr. Lygate questions the validity of the infarct size measurements made at the mid-papillary muscle level. This approach is a common technique used in the literature, including a contemporary study (2). Although we certainly concede that absolute quantification of size of the infarction relative to the total left ventricle would require additional sampling, our purpose was to compare two groups of animals assessed in the same fashion at the mid-papillary level. This was the region where the samples were taken for assessment of apoptosis, so it was desirable to have the closest matched regions for apoptosis and infarct size measurements. Using this uniform sampling method, we observed statistically significant differences. Finally, Dr. Lygate raises the question as to whether the decrease in apoptosis, hypertrophy, and fibrosis were direct effects of ESC treatment or simply reflected the reduction in infarct size. Dr. Lygate states that the extent of apoptosis correlates directly with infarct size and cites relevant literature (3, 7); however, these references simply look at apoptosis levels following infarction without intervention. A broader examination of the literature in which intervention groups are compared with control myocardial infarction groups reveals that a correlation between infarct size and the extent of apoptosis is oftentimes not present (2, 6). To begin to address this issue directly for apoptosis in our study, we provided data in Figure 1H (9) showing that there is not a simple correlation between infarct size and apoptotic nuclei and that the two groups of data are clearly separate. Nevertheless, we acknowledge that fully understanding the mechanisms underlying the observed effects will require substantial future studies.

Complimentary effects of chronic pharmacologic manipulation of β-adrenergic receptor (βAR) subtype signaling in rodent dilated ischemic cardiomyopathy

Background: While treatment of dilated cardiomyopathy with β1AR blockers has proven beneficial, the potential added, well-documented benefits of β2AR receptor stimulation, e.g. protection from apoptosis and reduction of arterial elastance with respect to chronic heart failure, have not been addressed. Method: A myocardial infarction (MI) was effected by left descending coronary artery ligation in 88 rats. Five rats were subjected to sham operation (SH). One week later the ligated animals were randomized to treatment groups, insuring equal initial MI size (27% of LV endocardial circumference at end-diastole in echocardiographic short-axis view at mid-papillary muscle level) among the groups: untreated (UT) MI; β1AR blocker, Metoprolol; and β2AR agonist, Fenoterol.

The effect of maternal cocaine exposure on neonatal rat cardiac function.

Fetal cocaine exposure has been associated with a variety of cardiovascular dysfunctions in humans. We treated pregnant rats with either saline or cocaine at 60 mg/kg by gastric lavage for the entire gestational period and for 14 days after parturition. We then performed high-frequency transthoracic echocardiography to determine whether cocaine exposure affected neonatal cardiac contractile function in vivo in 7- and 14-day-old neonatal rats. All studies were performed in the unsedated, conscious state. Heart rate (HR) and systolic function, expressed as fractional area of change at the midpapillary muscle level, were calculated from two-dimensional images. Resting HR was faster in the cocaine-exposed group at both ages, but baseline contractile function was not different between control (CTL) and cocaine-exposed (COC) neonatal rats. Dobutamine induced a significant increase in HR in all groups at only the largest dose tested (Day 7 CTL HR increased from 438 +/- 3 bpm to 462 +/- 10 bpm; Day 7 COC HR increased from 466 +/- 3 bpm to 493 +/- 7 bpm; Day 14 CTL HR increased from 443 +/- 4 bpm to 487 +/- 4 bpm; Day 14 COC HR increased from 477 +/- 4 bpm to 501 +/- 5 bpm). Dobutamine elicited a significant increase in contractile response at both Day 7 (from 76.6% +/- 0.6% to 81.5% +/- 0.7%) and Day 14 in CTL (from 78.2% +/- 0.7% to 81.9% +/- 0.7%), but not in COC, animals (from 76.7% +/- 0.8% to 78.9% +/- 0.8% at Day 7 and from 76.8% +/- 1.1% to 79.3% +/- 0.8% at Day 14). Epinephrine induced a significant increase in contractile response in CTL, but not in COC, rats at Day 7 and had no effect on fractional area of change at 14 days of age in either CTL or COC animals. Our results indicate that perinatal cocaine exposure does not modify resting contractile function but attenuates the contractile response to beta-adrenoceptor stimulation in the neonatal rat. These results suggest that perinatal cocaine exposure may lead to decreased responsiveness to inotropic drugs during the early neonatal period.

An experimental intraoperative quantitative echocardiographic study of myocardial perfusion in dogs

Myocardial contrast echocardiography is a valuable technique for demonstration and delineation of regions of myocardial underperfusion secondary to coronary occlusion and/or significant coronary stenosis. Various contrast materials have been used. The aim of this study was to determine whether myocardial contrast echocardiography by the original contrast agent AQ-DDT (albumin based), produced in the Institute for Cardiovascular Diseases, Clinical Center of Serbia in Belgrade can be used in the detection and quantification of regions of myocardial perfusion defects. In 14 adult open chest dogs the perfusion defect was produced by selective coronary ligations (30 seconds) and was observed with epicardial contrast two-dimensional echocardiography. For administration of contrast a modified pigtail catheter was positioned in the aorta just above the aortic valves. In this way the perfusion regions of the left main and right coronary artery were included. The left anterior descending and left circumflex artery could not be selectively injected with contrast agent and their individual perfusion areas were not clearly demonstrated. In all cases contrast echocardiography images of the left ventricle were obtained in a short-axis cross-sectional view at the mid-papillary muscle level. Forty-two injections of AQ-DDT for perfusion analysis were done, and were recorded on a VHS recorder. Quantification of the quality in demonstrating myocardial perfusion was scored as good, poor or without visual echocardiographic effect, by an investigator experienced in echocardiography, immediately and one month later. There was 100% agreement in the scoring. Our results indicated that agent AQ-DDT produces a good contrast effect (echocardiography visualization) in dogs and has the potential to demonstrate regional perfusion defects of the myocardium. Its potential role in human medicine, for diagnosis and evaluation of the results of interventional therapy, especially during aortocoronary bypass graft surgery, should be evaluated.

Assessment of myocardial ischemia and infarction by intravenous myocardial contrast echocardiography with perfluorocarbon microbubbles

OBJECTIVE: To assess the value of myocardial contrast echocardiography (MCE) with intermittent second harmonic technique and perfluorocarbon microbubbles in identifying myocardial ischemia and infarction. METHODS: Open-chest dogs were performed by intravenous MCE with perfluorocarbon microbubbles after 3 h of left anterior descending coronary artery (LAD) occlusion. The parameters of time-intensity curve were measured and compared between the normal and ischemic myocardial area at short-axis view of left ventricule midpapillary muscle level. The infarct size assessed by MCE was compared with the gross pathologic specimen stained with triphenyltetrazolium chloride (TTC). RESULTS: The peak intensity (PI), T1/2, and area under curve (AUC) in the ischemic area were significantly different versus the normal area 13.5+/-1.9 compared with 22.5+/-2.4; 16.6+/-0.9 compared with 9.7+/-0.5; 231.6+/-14.9 compared with 405.6+/-12.3 P<0.02). The percents of the no flow area determined by MCE had correlation with those by TTC stain(r=0.89, P=0.01). CONCLUSION: Intermittent second harmonic MCE using intravenous injection of perfluorocarbon microbubbles could assess myocardial perfusion, diagnose ischemia, and define myocardial infarct size.

Beat-to-beat Augmentation of Left Ventricular Function by Intraaortic Counterpulsation

Measuring the effects of intraaortic balloon counterpulsation (IABP) in single cardiac beats may permit an improved understanding of the physiologic mechanisms by which IABP improves the circulation. The objective of the study was to use trans- esophageal echocardiography in combination with hemodynamic measurements to test the hypothesis that IABP improves global left ventricular systolic function selectively in the IABP-augmented cardiac beats by acutely decreasing left ventricular afterload. Twenty-seven studies in which the IABP-to-R wave trigger ratio was serially changed from 1:1, 1:2, 1:4, 0:1 (IABP off) and back to 1:1 were performed in 20 anesthetized cardiac surgical patients during IABP support. Left ventricular short-axis end-diastolic cross-sectional area, end-systolic area, mean end-systolic wall thickness, and ejection time were measured by transesophageal echocardiography at the midpapillary muscle level. Aortic pressure was measured simultaneously from the central lumen of the intraaortic balloon catheter. These measurements were used to calculate the fractional area change, end-systolic meridional wall stress, and heart rate-corrected velocity of circumferential fiber shortening. The echocardiographic and hemodynamic parameters of left ventricular preload, afterload, and systolic function immediately after balloon deflation (IABP-augmented cardiac beats) were compared to the parameters measured during nonaugmented cardiac beats to determine the beat-to-beat effects of IABP on left ventricular function. IABP-augmented cardiac beats had a decreased systolic arterial pressure and end-systolic meridional wall stress and increased diastolic blood pressure, fractional area change, and velocity of circumferential fiber shortening compared to nonaugmented cardiac beats. IABP did not cause significant beat-to-beat changes in heart rate, pulmonary artery diastolic pressure, or central venous pressure. The improvement in left ventricular systolic function associated with IABP-augmented cardiac beats correlated with the decrease in end-systolic meridional wall stress for that cardiac beat. Beat-to-beat echocardiographic and hemodynamic measurements performed in anesthetized cardiac surgical patients during IABP support demonstrated improved left ventricular systolic function and decreased left ventricular systolic wall stress in the cardiac beats immediately after balloon deflation. The relationship between left ventricular systolic function and left ventricular systolic wall stress during IABP support suggests that afterload reduction was an important mechanism by which IABP instantaneously improved circulatory function in anesthetized cardiac surgical patients.

950-96 Quantification of Left Ventricular Function by Applying Signal Averaging to Echocardiographic Automated Border Detection

The acoustic quantification technique for automated detection of endocardial boundaries currently provides continuous left ventricular (LV) area or volume signals and beat-to-beat ejection fraction. However, due to displacement of the heart relative to the predefined region of interest, gain settings may become inappropriate, resulting in a distortion of individual waveforms and a wide beat-to-beat variability. To circumvent these limitations, we developed an algorithm for the evaluation of LV function using signal averaging, based on the stochastic sign change as a criterion for temporal beat alignment and rejection of artifacts. Left ventricular area signals obtained from the short axis view at the mid papillary muscle level in 8 normal subjects were digitized over a period of 100 sec and subjected to signal processing. End-diastolic and end-systolic area, stroke area and fractional area change were measured directly from the average waveform. Peak ejection and peak filling rates, and time to peak filling rate were obtained from the time derivative of the average waveform. The proposed algorithm was initially evaluated by studying the variability in the above parameters caused by different template waveform selections and different averaging threshold settings, which were found to result in a variability below 5% in parameters measured directly from the average waveform, and up to 10% in those obtained from the time derivative. Subsequently, the feasibility of an automated version of the algorithm, based on objective operator independent criteria, was evaluated, and parameters obtained were found to be in excellent agreement with those obtained using manual approach. In summary, this algorithm provides a fast. easy and objective method for noise reduction in acoustic quantification signals. This algorithm may improve the on-line noninvasive assessment of systolic and diastolic LV function.

946-106 Papillary Muscle Perfusion Assessed with Myocardial Contrast Echocardiography in Humans

Papillary muscle perfusion assessed with myocardial contrast echocardiography was compared with coronary anatomy as identified by coronary arteriography in 114 pts without coronary artery disease. Myocardial contrast echocardiographywas performed by imaging the parasternal short axis view at the mid papillary muscle level during the right (RCA) and left intracoronary arterial (LCA) injection of sonicated Hexabrix or hand agitated Urografin. The anterolateral papillary muscle was opacified in 113 of 114 (99%) pts with LCA injection and in only 1 of 114 (1%) pt with RCA injection. The posteromedial papillary muscle was opacified in 37 of 114 (32%) pts with LCA injection, in 72 of 114 (63%) pts with RCA injection and in 5 of 114 (5%) pts both with LCA and RCA injection. Both papillary muscle and its adjacent LV wall were opacified with same coronary arterial injection in 94 of 114 (82%) pts, however, they were opacified with different coronary arterial injection in 20 of 114 (18%) pts. (1)The papillary muscle is usually supplied by either LCA or RCA in most subjects, but it may be supplied by both RCA and LCA (approximately 5 %). (2) The papillary muscle may be supplied by the other artery than that supplies the adjacent area. (3) Thus, there are considerable variabilities in the papillary muscle perfusion.

Influence of pacing-induced myocardial ischemia on left atrial regurgitant jet: A transesophageal echocardiographic study

Objectives. We investigated the influence of pacing-induced myocardial ischemia on systolic regurgitant jet in the left atrium, using simultaneous transesophageal echocardiography and transesophageal atrial pacing.Background. In vitro studies have shown that ischemia-induced mitral regurgitation may occur as a result of mitral leaflet malcoaptation or (global) left ventricular dysfunction. However, no transesophageal echocardiographic study has thus far been performed to demonstrate the mechanism and extent of mitral regurgitation during myocardial ischemia in patients.Methods. In 24 patients (mean [±SD] age 57 ± 10 years) with (15 patients) and without (9 control subjects) coronary artery disease, heart rate, blood pressure and systolic regurgitant jet were assessed before and immediately after pacing. Pacing was increased stepwise up to 160 beats/min to provoke wall motion abnormalities while the left ventricular short axis was monitored at the midpapillary muscle level. Other variables obtained before and at peak pacing included left ventricular end-diastolic and end-systolic areas and left ventricular end-diastolic and end-systolic endocardial segmental lengths.Results. Heart rate and blood pressure before and after pacing were not significantly different in control subjects or in patients. At baseline, a jet was present in all but three control subjects. New or increased anterior or posterior wall motion abnormalities were observed during pacing in seven and eight patients, respectively. End-systolic left ventricular areas and segment lengths were significantly reduced in control subjects compared with patients with coronary artery disease at peak pacing (p < 0.05). The increase in systolic regurgitant jet was significantly greater in patients (2.0 ± 1.1 to 3.1 ± 1.8 cm2vs. 0.7 ± 0.7 to 0.9 ± 0.9 cm2[after pacing], p < 0.01). This effect was greater in patients with posterior than with anterior wall motion abnormalities (3.5 ± 1.6 vs. 2.1 ± 1.2 cm2[after pacing], p < 0.05).Conclusions. Quantitative changes in geometry and function of the left ventricle caused by pacing-induced myocardial ischemia augments systolic regurgitant jet size. An increase in the jet during atrial pacing is associated with new or increased wall motion abnormalities, especially of the posterior wall. Pacing-induced anterior wall motion abnormalities appear not to be related directly to an increase in the jet.

Are wall thickening measurements reproducible?

An early transesophageal echocardiography (TEE) study reported that there was high inter- and intraobserver variability in measurements of wall thickening (WT). This study reevaluated TEE for the measurement of WT in the transverse plane and, for the first time, evaluated it in the longitudinal plane. Ten patients were studied with a biplane TEE probe inserted and positioned to obtain a transverse short-axis (SA) view of the left ventricle at the midpapillary muscle level. A longitudinal transgastric long-axis (LA) view of the left ventricle was then obtained. This measurement sequence was performed four times in each patient. Off-line analysis was performed independently by two observers. In each tomographic cut of the ventricle, four locations for measurement were defined. WT was measured in three consecutive beats, and the results averaged (WT1). The observers repeated the measurements (WT2) 2 wk later, and the intra- and interobserver differences (mm) were calculated. Average differences for the intraobserver comparisons of wall thickening were small (0.08-0.24 mm), but the high standard deviations (1.17-2.44 mm) suggest significant variability between individual measurements. Thus it appears that measurements of wall thickening with small mean intraobserver bias may be possible, but to offset the potential for variability, multiple measurements are necessary. Also, careful standardization of location and edge definition is important to limit interobserver variability.

Incidence and time course of left ventricular dilation in the early convalescent stage of reperfused anterior wall acute myocardial infarction

The incidence and early process of left ventricular (LV) dilation in 52 patients with reperfused anterior wall acute myocardial infarction (AMI) were assessed. All patients achieved coronary reflow within 24 hours of the onset and had a patent infarct-related artery in the convalescent stage. Left ventriculography was performed at pre-reflow and 25 days (mean) later to determine LV end-diastolic volume (ml) with the area/length method. Short-axis echo images at the midpapillary muscle level were recorded at days 1, 7, 14, and 28 of the AMI. With use of the papillary muscles as the internal landmarkers, the LV wall was divided into the anterior and posterior segments, and length and thickness of each segment were determined. Among 52 patients, 10 (19%) had a ≥20% increase in end-diastolic volume in the convalescent stage. Echocardiographic studies demonstrated that there were no significant changes in lengths and thicknesses of the anterior and posterior segments during follow-up study relative to his or her baseline value in 42 patients without LV dilation. In the patients with LV dilation, however, the anterior segment exhibited a mean increase of 25% in its length with a mean decrease of 21% in its thickness at day 7 relative to their baseline values, but no progressive expansion was observed after day 7. A mean increase of 7% in the posterior segment length without reduction in its thickness first became evident at day 28. It is concluded that (1) LV dilation is observed in a relatively small population of patients (19%) with reperfused anterior wall AMI, and (2) in patients with LV dilation, infarct expansion progresses until day 7, followed by the secondary eccentric hypertrophy of the noninfarcted segment being evident at day 28 of the AMI.

Transesophageal Echocardiographic Evaluation of Left Ventricular Function During Intraaortic Balloon Pump Counterpulsation

Transesophageal echocardiography was used to study the effects of intraaortic balloon pump counter pulsation (IABP) on left ventricular dimensions and function in 16 hypotensive patients after cardiac surgery. The short-axis cross section at midpapillary muscle level was used to determine systolic and diastolic dimensions. We found a significant decrease in end-systolic and end-diastolic area and increase in fractional area change during IABP-supported circulation. Regional area ejection fraction analysis demonstrated an improvement during IABP of impaired (particularly severely impaired) function at baseline. We conclude that both regional and global left ventricular function improve by the use of IABP in conjunction with a decrease of left ventricular size.

Prognostic value of biventricular function in hypotensive patients after cardiac surgery as assessed by transesophageal echocardiography

In patients after cardiac surgery, hypotension, defined as a mean arterial pressure less than 65 mmHg despite adequate filling pressures and positive inotropic medication, poses a problem. In addition, it is often difficult to determine whether these patients have suffered irreversible myocardial injury or if they are likely to recover. In this study, left and right ventricular function, as assessed by transesophageal echocardiography (TEE), was related to mortality both (1) quantitatively, using fractional area change (FAC), and (2) qualitatively, using a segmental wall motion analysis, which assigned a score to myocardial wall segments, in order to determine whether this technique can be used to predict survival. Mortality rate was very high in patients with biventricular and especially right ventricular failure (FAC < 35%). Left and right ventricular wall motion abnormality indices were significantly better in survivors compared to nonsurvivors, but no distinct cut-off value could be determined. A wall motion index derived from only 6 segments at the mid-papillary muscle level was found to be as reliable as one based on 16 segments of the entire left ventricle. Thus, TEE provided information about the degree of left and right ventricular dysfunction by using a single cross-section at the papillary muscle level. It identified patients at high risk of death, ie, those with compromised right and biventricular function.

Detection of Acute Myocardial Infarction by Evaluation of Ultrasonic Gray Levels in Dogs.

The study tested whether an experimental myocardial infarction can be detected from two-dimensional echocardiograms (2DE) by analysis of regional gray levels. The mid-left anterior descending coronary artery was ligated for 3 hours in 14 dogs (group 1) and for 5 hours in 6 dogs (group 2). 2DE were performed before, and after 3 and 5 hours of coronary artery ligation. The ultrasonic amplitude of the control and infarcted regions were obtained from digitized 2DE in the short axis view, at the mid-papillary muscle level. The mean gray levels (+/- SD) of the control and infarcted regions were compared during end-diastolic stop frames. After sacrifice, the hearts were cut into 1 cm thick slices and stained with 1% triphenyl tetrazolium chloride (TTC) solution. The myocardium was then studied by light microscopy. Computerized tomographic scans were also obtained in vitro from 3 hearts of both groups. There was no difference in mean gray levels of the control region during the experiments. However, in the region of wall motion abnormality (area of infarction), the mean gray levels increased from 49.9 +/- 3.5 (before ligation) to 62.0 +/- 7.4 (after 3 hours of ligation, p less than 0.005) in 10 group 1 dogs, but no differences were seen in mean gray levels (49.6 +/- 3.8 vs 50.4 +/- 4.0) in those without a myocardial infarction in 4 group 1 dogs; gray levels also increased from 50.4 +/- 2.9 (before ligation) to 58.6 +/- 6.1 (after 3 hours of ligation, p less than 0.05) and to 65.0 +/- 4.2 (after 5 hours of ligation, p less than 0.005) in group 2 dogs. The area of left ventricular asynergy corresponded precisely to the area of myocardial infarction, determined by both TTC staining and the computerized tomographic scans. The light microscopy of the infarcted area also demonstrated interstitial edema and polymorphonuclear cell infiltration.

Intraoperative Monitoring of Regional Wall Motion Abnormalities for Detecting Myocardial Ischemia by Transesophageal Echocardiography

Transesophageal two-dimensional echocardiography has been used for intraoperative monitoring of regional wall motion of the left ventricle. Regional wall motion abnormality is a sensitive indicator of myocardial ischemia and the use of two-dimensional transesophageal echocardiography may have a substantial advantage for early detection of myocardial infarction and thus for initiating timely and appropriate therapy in preventing postoperative myocardial ischemia. With an expected increase in the use of intraoperative transesophageal echocardiography for monitoring regional wall motion, we described the practical aspects of transesophageal echocardiography: (1) insertion technique of transesophageal echocardiographic probe; (2) the technique for obtaining an optimal short-axis view of the left ventricle; and (3) the method for evaluating regional wall-motion abnormality and myocardial ischemia. Regional wall motion abnormality is best monitored at the mid-papillary muscle level where all three coronary arteries meet. In obtaining this view, the transesophageal echocardiographic probe was found to be predominantly located in the stomach. Failure in obtaining short-axis view of the left ventricle at this level occurred in patients with left ventricular dilatation or obesity. Because of the anatomical reason, the echocardiographic transducer cannot reach a proper plane. In anesthetized patients, air can be pushed into the stomach during induction and may disturb the visualization. The pitfalls in examining regional wall motion abnormalities include: (1) shifting of the center of left ventricular contraction; (2) inadequate direction of the scanning plane; and (3) paradoxical septal movement. Three cases are presented to demonstrate the usefulness of transesophageal echocardiography in managing coronary artery surgical patients.

Comparison of Transesophageal Echocardiographic and Scintigraphic Estimates of Left Ventricular End-Diastolic Volume Index and Ejection Fraction in Patients Following Coronary Artery Bypass Grafting

Transesophageal echocardiography (TEE) has become a commonly used monitor of left ventricular (LV) function and filling during cardiac surgery. Its use is based on the assumption that changes in LV short-axis ID reflect changes in LV volume. To study the ability of TEE to estimate LV volume and ejection immediately following CABG, 10 patients were studied using blood pool scintigraphy, TEE, and thermodilution cardiac output (CO). A single TEE short-axis cross-sectional image of the LV at the midpapillary muscle level was used for area analysis. Between 1 and 5 h postoperatively, simultaneous data sets (scintigraphy, TEE, and CO) were obtained three to five times in each patient. End-diastolic (EDa) and end-systolic (ESa) areas were measured by light pen. Ejection fraction area (EFa) was calculated (EFa = (EDa - ESa)/EDa). When EFa was compared with EF by scintigraphy, correlation was good (r = 0.82 SEE = 0.07). EDa was taken as an indicator of LV volume and compared with LVEDVI which was derived from EF by scintigraphy and CO. Correlation between EDa and LVEDVI was fair (r = 0.74 SEE = 3.75). The authors conclude that immediately following CABG, a single cross-sectional TEE image provides a reasonable estimate of EF but not LVEDVI.