Effect of coronary reocclusion after initial reperfusion on ventricular function and infarct size.

Reocclusion of a coronary artery after thrombolytic therapy occurs in approximately 12% to 33% of patients; however, there are few experimental data concerning reocclusion. Accordingly, to compare the effects of reocclusion versus sustained occlusion on the myocardium, a canine model (n = 12) of 2 h of left circumflex artery occlusion, 1 h of reperfusion and 1 h of reocclusion was studied. In a control group (n = 11), 3 h of circumflex artery occlusion was followed by 1 h of reperfusion. As a result, both groups had the same total duration of ischemia (3 h) and reperfusion (1 h). Hemodynamic measurements, radioactive microsphere injections and two-dimensional echocardiography were performed at baseline, occlusion and reperfusion for both groups and at the end of reocclusion for the experimental group. In vivo risk area was determined with Evans blue dye and infarct size with triphenyltetrazolium staining methods. Similar decreases in myocardial blood flow after coronary occlusion and similar reperfusion blood flows occurred in both groups. Despite intervening reperfusion in the reocclusion group, no significant difference was found in the infarct size/risk area ratio between the reocclusion and control groups (54.5 +/- 6.9% vs. 48.4 +/- 5.1%, respectively, p = NS). Two-dimensional echocardiography demonstrated a similar degree and extent (159 +/- 9 degrees vs. 153 +/- 12 degrees, p = NS) of left ventricular dysfunction with both the occlusion and reocclusion. In addition, there were no significant differences in global or regional left ventricular function between the two groups. However, reocclusion after reperfusion did produce a further deterioration in ischemic zone wall thickening (9.5 +/- 2.0% to 0.7 +/- 1.8%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of the centerline method for assessment of echocardiographic wall thickening and motion: a comparison with areas of risk.

The ability of the centerline method to discern regional myocardial risk area was evaluated using two-dimensional echocardiographic measurements and coronary artery occlusion in 16 open chest, anesthetized dogs. The centerline method was modified to allow determination of both wall thickening and wall motion at control and during coronary artery occlusion. End-systolic and end-diastolic echocardiographic images were analyzed at 100 equally spaced points around the centerline of the short-axis view of the left ventricle to determine shortening and thickening abnormalities. In vivo risk regions were assessed by microsphere injection during occlusion, and autoradiographic analysis revealed a mean (+/- SD) circumferential risk area of 37.5 +/- 7.7%. Abnormal function was established by three criteria on the basis of the control values for both fractional shortening and wall thickening: 1) less than 2 SD, 2) less than 95% tolerance limits, and 3) dyskinesia. The criterion of less than 2 SD estimated a risk area of 45.9 +/- 16.7% for fractional shortening and 37.2 +/- 16.8% for wall thickening. Although neither value was significantly different from the actual mean value for the risk region, the results for fractional shortening were greater than for wall thickening (p less than 0.01). The less than 95% tolerance limit method significantly underestimated risk area for both shortening (25.6 +/- 15.1%, p less than 0.05) and thickening (19.1 +/- 12.7%, p less than 0.001), as did analysis by dyskinesia (13.1 +/- 12.1% for shortening, p less than 0.001; 20.6 +/- 12.1% for thickening, p less than 0.01). Thus, modification of the centerline method allowed determination of both fractional shortening and wall thickening from echocardiographic images.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of the functional border zone around regionally ischemic myocardium using circumferential flow-function maps.

Previous studies have suggested that there exists a functional border zone in myocardium at the lateral margins of an ischemic area. The functional border zone is normally perfused but is characterized by abnormal contractile function. To define the spatial characteristics of this border zone, circumferential maps of left ventricular function by two-dimensional echocardiography and of coronary flow using radioactive microspheres were generated in 18 dogs at baseline and after circumflex coronary occlusion. Circumferential left ventricular wall thickening was measured in all dogs at 22.5 degrees intervals over 360 degrees. In seven dogs, the pathologic slice corresponding to the two-dimensional echocardiographic image was circumferentially dissected into 16 segments corresponding to 22.5 degrees intervals and a subendocardial myocardial blood flow map was derived. In the other 11 dogs, autoradiography was performed of the pathologic slice corresponding to the two-dimensional echocardiographic image, and the hypoperfusion zone was directly measured. There was no difference between the circumferential extent of hypoperfusion zones by either perfusion measurement technique in the five dogs that had both techniques performed (140 +/- 12 versus 124 +/- 7 degrees, p = NS). The hypofunctional zone by two-dimensional echocardiography was significantly larger than the hypoperfusion zone (174 +/- 4 versus 125 +/- 26 degrees, p less than 0.0005), indicating that a zone of normally perfused but abnormally contracting muscle surrounds the ischemic area. However, this border zone in our model was small, measuring 49 +/- 34 degrees (approximately 8 to 9 mm on either lateral border). This suggests that the functional border zone lateral to ischemic myocardium exists, but is relatively discrete.

Neutrophil depletion fails to modify myocardial no reflow and functional recovery after coronary reperfusion.

Recent studies suggest that neutrophil accumulation and activation in postischemic myocardium may be responsible for myocardial no reflow, which is characterized by an incomplete restoration of blood flow after reperfusion. To examine this further, 11 open chest, anesthetized dogs received bolus injections of a bovine neutrophil antiserum that produced an average 81 +/- 5% depletion of circulating neutrophils, and 10 control dogs received nonimmune serum. Each animal underwent 2 h of left circumflex artery occlusion followed by 4 h of reperfusion. Simultaneous two-dimensional echocardiography and radioactive microsphere blood flow studies were performed at baseline, 2 h of occlusion and early (approximately 5 min) and 4 h of reperfusion. During occlusion, both groups developed similar reductions in myocardial blood flow and levels of ischemic zone myocardial wall thinning. At early reperfusion, similar levels of hyperemia and regional hypokinesia were observed for both groups. By late reperfusion, both groups experienced significant no reflow in the subendocardium (p less than 0.05) and reduced reflow in the mid-myocardium. Regional depression in ischemic zone function persisted throughout the reperfusion period in both groups. However, infarct size expressed as a percent of left ventricular weight, assessed by triphenyltetrazolium chloride staining, was smaller for the neutrophil depletion group compared with the control group (8.7 +/- 1.3% versus 13.1 +/- 1.8%, p less than 0.05). It is concluded that an 81% neutrophil depletion fails to modify the no reflow phenomenon or improve functional recovery after 2 h of coronary artery occlusion and 4 h of coronary reperfusion despite modification of the ultimate size of necrosis.

Augmentation of regional function in nonischemic myocardium during coronary occlusion measured with two-dimensional echocardiography.

Increased regional left ventricular function frequently occurs in the nonischemic myocardium after acute coronary occlusion. To further define the regional and global effects of this increased remote function in the ischemic left ventricle, 22 dogs were studied with two-dimensional echocardiography before and 1 h after left circumflex coronary artery occlusion. Two groups of dogs were identified with and without compensatory increased regional left ventricular function, defined as regional wall thickening in the nonischemic zone greater than 2 SD above baseline. After coronary occlusion, nonischemic wall thickening was 76 +/- 15% in the hyperfunction group (n = 11) and 45 +/- 14% in the nonhyperfunction group (n = 11) (p less than 0.001). Despite similar left ventricular end-diastolic cavity areas and equivalent degrees of ischemic wall thinning, dogs with increased left ventricular function in the nonischemic myocardium had a smaller extent of circumferential left ventricular dysfunction (136 +/- 33 versus 170 +/- 43 degrees, p less than 0.001) and a higher area ejection fraction (38 +/- 9% versus 27 +/- 6%, p less than 0.001). These functional differences occurred despite similar myocardial areas at risk by autoradiography (41 +/- 6% versus 37 +/- 12%, p = NS). The data suggest that increased left ventricular function in the nonischemic myocardium determines the global functional impact of acute coronary occlusion and, through interaction with adjacent myocardium, modifies the extent of circumferential left ventricular dysfunction.

Immediate rebound followed by deterioration of regional left ventricular function with coronary reperfusion.

The immediate and early effects of coronary artery reperfusion initiated 1 and 3 hours after coronary artery occlusion were evaluated by two-dimensional echocardiographic measurements of overall and regional left ventricular function. A total of 29 anesthetized open chest dogs underwent one of the following: 1 hour occlusion followed by reperfusion (Group I, n = 9), 3 hour occlusion followed by reperfusion (Group II, n = 12) or 5 hour occlusion without reperfusion (Group III, n = 8). Serial two-dimensional echocardiography was performed at baseline; at 1, 3 and 5 hours of coronary occlusion; within 5 minutes of reperfusion; and at 2 hours of reperfusion. After occlusion, all groups manifested significant (p less than 0.01) increases in left ventricular diastolic and systolic area and decreases in left ventricular area ejection fraction. With coronary reperfusion, there was no improvement in these global variables in Groups I and II. However, immediately after reperfusion, there was improvement in the regional extent of dysfunction (Group I, 138 +/- 35 to 66 +/- 62 degrees, p less than 0.05; Group II, 156 +/- 51 to 85 +/- 77 degrees, p less than 0.05) as well as improvement in the regional degree of dyskinesia (p less than 0.05). These regional improvements were transient and resolved by 2 hours of coronary reperfusion. This immediate rebound of function was not associated with the duration of coronary occlusion, hemodynamic variables or ultimate infarct size. Thus, in the anesthetized open chest dog model, coronary artery reperfusion at 1 or 3 hours produces an immediate but transient improvement in regional systolic myocardial function.

Superoxide dismutase does not cause scar thinning after myocardial infarction.

Previous studies demonstrated that treatment with superoxide dismutase, a scavenger of superoxide anions, limits the extent of myocardial injury in a canine preparation of regional myocardial ischemia and reperfusion. Little is known, however, about the effects of superoxide dismutase on the healing of a myocardial infarct. Therefore, this study was performed to determine whether treatment with superoxide dismutase during myocardial ischemia impairs formation of scar tissue after infarction. Dogs received 2 hour infusions of superoxide dismutase or albumin (controls) by way of the left atrium beginning 15 minutes before and ending 15 minutes after a 90 minute occlusion of the left circumflex coronary artery. Six weeks later the animals were killed. Two-dimensional echocardiography was performed before surgery and before induced death. Wall thickening in the central ischemic zone was decreased at 6 weeks compared with baseline studies (p less than 0.05), but the decrease was similar for both groups. The hydroxyproline concentrations (microgram/mg dry weight) of the scar tissue in the superoxide dismutase and control groups, respectively, were 35.3 +/- 3.8 and 28.7 +/- 5.0 (p less than 0.05). The ratios of the scar thickness to normal wall thickness were superoxide dismutase 0.91 +/- 0.03 and control 0.89 +/- 0.03 (p greater than 0.05). Thus, superoxide dismutase had no adverse effect on wall thickening or scar formation assessed 6 weeks after myocardial infarction, and may be useful to limit oxygen radical-mediated damage during reperfusion of the ischemic myocardium.

Prevention of subsequent exercise-induced periinfarct ischemia by emergency coronary angioplasty in acute myocardial infarction: comparison with intracoronary streptokinase.

To compare the efficacy of emergency percutaneous transluminal coronary angioplasty and intracoronary streptokinase in preventing exercise-induced periinfarct ischemia, 28 patients presenting within 12 hours of the onset of symptoms of acute myocardial infarction were prospectively randomized. Of these, 14 patients were treated with emergency angioplasty and 14 patients received intracoronary streptokinase. Recatheterization and submaximal exercise thallium-201 single photon emission computed tomography were performed before hospital discharge. Periinfarct ischemia was defined as a reversible thallium defect adjacent to a fixed defect assessed qualitatively. Successful reperfusion was achieved in 86% of patients treated with emergency angioplasty and 86% of patients treated with intracoronary streptokinase (p = NS). Residual stenosis of the infarct-related coronary artery shown at predischarge angiography was 43.8 +/- 31.4% for the angioplasty group and 75.0 +/- 15.6% for the streptokinase group (p less than 0.05). Of the angioplasty group, 9% developed exercise-induced periinfarct ischemia compared with 60% of the streptokinase group (p less than 0.05). Thus, patients with acute myocardial infarction treated with emergency angioplasty had significantly less severe residual coronary stenosis and exercise-induced periinfarct ischemia than did those treated with intracoronary streptokinase. These results suggest further application of coronary angioplasty in the management of acute myocardial infarction.

Impact of radionuclide techniques on evaluation of patients with ischemic heart disease.

Radiotracer studies of the heart have become clinically important in the last decade, especially for evaluation of patients with known or suspected ischemic heart disease. Radionuclide ventriculography provides quantitative measures of biventricular function and regional wall motion. Recent technical advances include the development of computer programs for analyzing diastolic function, parametric imaging methods such as "phase" analysis and methods for calculating absolute ventricular volumes. Thallium-201 scans provide maps of regional myocardial perfusion. Recent advances include development of computer programs to quantitate regional thallium-201 uptake and to calculate thallium-201 turnover rates and the development of tomographic imaging systems. Technetium-99m pyrophosphate localizes in irreversibly damaged myocardium and provides a method for diagnosing, localizing and sizing acute myocardial infarcts. Recent applications include tomographic imaging to improve image contrast and development of criteria to identify high risk patients after infarction. Two important trends affecting the application of all the radionuclide studies in clinical cardiologic practice are the increasing use of decision analysis for incorporating results of multiple tests into single diagnostic probability statements, and the use of diagnostic algorithms that include the radionuclide studies to optimize the cost effectiveness of evaluation of patients with ischemic heart disease.

Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

Repeated neurogenic pressor episodes by hindquarter compression were elicited in nine experimental dogs. Conscious dogs underwent 6 hours of compression every day over a period of 9 weeks. The average mean blood pressure increase during the compression periods was 25 mm Hg, but after decompression the blood pressure promptly returned to baseline values. This blood pressure response was constant and did not change over the 9-week period. The blood pressure increase was associated with a significant increase of plasma norepinephrine values. After validity of the model was established, echocardiographic measurements were performed at baseline and after 3, 6, and 9 weeks of compression in six experimental and six time-control dogs. Concentric left ventricular hypertrophy was already detectable at 3 weeks, and at the ninth week, the left ventricular mass was 28% above the baseline value. The left ventricular mass in time-control dogs remained unchanged over the same period of time. The time-left ventricular mass curves in experimental dogs were significantly different (by profile analysis), had different means (p less than 0.005), were not parallel (p less than 0.0006), and the overall group difference was highly significant (p less than 0.00001). Since left ventricular hypertrophy, a poor prognostic sign in clinical situations, can evolve before established hypertension, present therapeutic recommendations based on permanently elevated blood pressure values may not be entirely justified.

Coronary artery spasm in the denervated transplanted human heart: a clue to underlying mechanisms.

The mechanism of coronary artery spasm has been poorly understood but there has been some suggestion that cardiac autonomic innervation may play an important role. We report coronary artery spasm in a 43 year old man two years after he had received a transplant. Provocative pharmacologic testing suggested functional denervation of the patient's heart. Thus, coronary artery spasm can occur in the transplanted, denervated human heart. Autonomic innervation of the heart is not essential in all cases of coronary spasm, and circulating catecholamines and/or metabolic of hormonal products may play an important role.

Surgery for life-threatening ventricular tachyarrhythmias.

Among 203 left ventricular aneurysmectomies performed since 1970, the operative mortality rate was 18.7 percent. In 49 patients (24 percent), left ventricular aneurysmectomy was performed for refractory life-threatening ventricular arrhythmias. Eight additional patients had coronary bypass grafting without ventricular aneurysmectomy. One of these patients had bypass grafting followed later by ventricular aneurysmectomy. All 56 patients had underlying coronary artery disease. The operative mortality rate was 19.6 percent. In patients with a recent myocardial infarction, the rate was 60 percent, whereas it was 11 percent in patients with a remote myocardial infarction. Other high risk variables in these patients included coronary bypass grafting without myocardial resection, and an elevated left ventricular end-diastolic pressure. The late mortality rate was 17.9 percent, but only one of these deaths was sudden and unexpected. The 35 long-term survivors have been followed up for a mean of 40.7 months (range 7 to 92 months). Of these, 20 remain on antiarrhythmic medications for palpitation or documented ventricular premature complexes, whereas 15 are free of detectable rhythm disturbances and do not require antiarrhythmic agents. Only 4 of 35 (11 percent) have had recurrent documented ventricular tachycardia. Left ventricular aneurysmectomy may be performed for refractory ventricular tachyarrhythmias with an acceptable operative mortality, particularly if the patient has survived longer than 6 weeks after myocardial infarction. Although epicardial mapping techniques may be useful in localizing the reentrant pathway of the ventricular tachycardia, ventricular aneurysmectomy without mapping techniques produces a satisfactory clinical result in the vast majority of long-term survivors.

Transient left ventricular filling abnormalities (diastolic stunning) after acute myocardial infarction.

A variety of experimental studies suggest that diastolic left ventricular (LV) function changes after acute myocardial infarction (AMI), but limited data exist on these changes in humans. To assess diastolic filling after AMI, 60 patients underwent Doppler echocardiographic examination within 24 hours of AMI. Of 54 patients who also underwent catheterization, 45 (83%) were successfully reperfused. A subgroup of 17 patients underwent a follow-up Doppler examination at 7 days after infarction, whereas 15 patients with stable exertional angina served as control subjects. There was no significant difference in age, gender, incidence of systemic hypertension or diabetes mellitus, heart rate, mean arterial pressure or severity of coronary artery disease between the infarct and control groups. The infarct group had a lower velocity time integral total (9.9 +/- 0.4 cm vs 12.0 +/- 0.9 cm, p less than 0.001), a lower velocity time integral E (5.8 +/- 0.3 cm vs 6.8 +/- 0.5 cm, p less than 0.01) and a lower velocity time integral 0.333 (3.5 +/- 0.4 cm vs 6.1 +/- 0.5 cm, p less than 0.01) than the control group. In addition, velocity time integral A/total was significantly greater in the infarction group (0.44 +/- 0.03 vs 0.35 +/- 0.04, p less than 0.01) compared to the control group. The follow-up subgroup showed an increase in velocity time integral total (p less than 0.01), velocity time integral E (p less than 0.05) and velocity time integral 0.333/total (p less than 0.05) over the first 7 days after infarction. The final recovery values at 7 days were not significantly different from those of the coronary artery disease group.(ABSTRACT TRUNCATED AT 250 WORDS)

Importance of overweight in studies of left ventricular hypertrophy and diastolic function in mild systemic hypertension.

The relations of Metropolitan Life Insurance Co. Relative Weight values and blood pressure (BP) to minimal forearm vascular resistance, ventricular septal and posterior wall thickness, left ventricular (LV) mass index and cardiac diastolic function were assessed in 31 men, 37 +/- 2 (mean +/- standard error of the mean) years of age. Eighteen patients with untreated mild hypertension were compared with 13 normotensive control subjects of similar age and weight. The hypertensives had higher clinic (137 +/- 3/96 +/- 2 vs 121 +/- 4/81 +/- 3 mm Hg, p less than 0.001/less than 0.001) and home (p less than 0.001) BP. Despite higher BP, the hypertensives did not have significantly greater values than normotensives, respectively, for minimal forearm vascular resistance (2.20 +/- 0.12 vs 2.04 +/- 0.11 U), ventricular septal (9.9 +/- 0.5 vs 10.2 +/- 0.3 mm) and posterior wall thickness (10.2 +/- 0.4 vs 10.0 +/- 0.3 mm) or LV mass index (106 +/- 6 vs 107 +/- 6 g/m2). Furthermore, diastolic peak filling rate, an index of LV diastolic function, was virtually identical in the 2 groups (2.71 +/- 0.14 vs 2.69 +/- 0.07 liters/s, difference not significant). Correlates of peak filling rate included relative weight (r = -0.62, p less than 0.001), posterior wall thickness (r = -0.51, p less than 0.01) and age (r = -0.45, p less than 0.05). Relative weight also correlated significantly with posterior wall (r = 0.59, p less than 0.005), ventricular septal (r = 0.47, p less than 0.005) and LV mass index (r = 0.38, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Prognostic significance of exercise-induced left ventricular dysfunction in chronic aortic regurgitation.

Twenty-three patients with hemodynamically significant aortic regurgitation (AR) underwent gated equilibrium radionuclide angiography to assess rest and exercise left ventricular ejection fraction (LVEF) before and after aortic valve replacement. Preoperatively, LVEF decreased from 54 +/- 3% at rest to 45 +/- 3% during exercise (p less than 0.001). Two patients died at operation. Postoperatively, after 5.7 +/- 1.6 months, LVEF was 62 +/- 5% at rest and 60 +/- 4% during exercise (difference not significant). Exercise LVEF improved significantly postoperatively (p less than 0.01). The patients were followed for a mean of 30 months (range 1 to 56), after valve replacement and during this period, 13 patients were in functional class I, 5 patients were in class II and 2 patients were in class III. One late death occurred and was unrelated to myocardial failure. Thus, in most patients with AR, exercise LVEF improves after aortic valve replacement. A preoperative decrease in LVEF during exercise in patients with significant AR does not predict a poor postoperative outcome.

Pulsed Doppler assessment of left ventricular diastolic filling in coronary artery disease before and immediately after coronary angioplasty.

To determine if left ventricular (LV) diastolic filling abnormalities are detectable by Doppler echocardiography in patients with coronary artery disease (CAD), 34 patients with CAD and 24 normal, age-matched control subjects underwent mitral valve pulsed Doppler examination. At catheterization, all CAD patients had typical angina, at least 70% diameter narrowing of 1 major coronary artery, ejection fraction of 50% or more and no valvular heart disease. Seventeen CAD patients underwent coronary angioplasty and had a Doppler examination 1 day before and 1 day after the procedure. Doppler diastolic time intervals, peak velocities at rapid filling (E velocity), atrial contraction (A velocity) and the ratio peak E/peak A velocities were measured. The following areas under the Doppler velocity envelope and their percentage of the total area were calculated: first third of diastole (0.33 area), triangular area under the peak E velocity (E area), and triangular area under the peak A velocity (A area). Patients with CAD and normal subjects were significantly different (p less than 0.01) in peak E velocity (CAD 0.60 +/- 0.12 m/s, normal 0.68 +/- 0.12 m/s), peak A velocity (CAD 0.59 +/- 0.12 m/s, normal 0.48 +/- 0.11 m/s), ratio peak E/peak A velocities (CAD 1.0 +/- 0.27, normal 1.5 +/- 0.32), A area (CAD 0.052 +/- 0.015 m, normal 0.036 +/- 0.010 m), ratio E area/A area (CAD 1.7 +/- 0.53, normal 2.5 +/- 0.69), and all area fractions. In the CAD patients who had undergone coronary angioplasty, no differences were found in any Doppler index before and immediately after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive quantification of jeopardized myocardial mass in dogs using 2-dimensional echocardiography and thallium-201 tomography.

The evaluation of jeopardized myocardial mass is important in defining the effect of interventions during myocardial infarction. To quantitate the in vivo mass at risk, 2-dimensional echocardiography (2-D echo) and thallium-201 single-photon emission computed tomography (SPECT) was performed in 10 closed-chest dogs after circumflex coronary artery occlusion. The 2-D images were manually digitized to compute left ventricular (LV) mass using a modified Simpson's rule algorithm. This measure of LV mass correlated well with the actual LV mass (r = 0.97). Perfused myocardial mass was estimated from thallium SPECT images 4 hours after occlusion using a region-growing algorithm. After the dogs were killed, the jeopardized mass was outlined using a dual perfusion staining technique using triphenyltetrazolium chloride and Evans blue dye. The actual perfused mass was well estimated by the thallium images (r = 0.96). The noninvasively determined mass at risk was calculated as: 2-D mass--thallium SPECT mass, and correlated well with the pathologically determined mass at risk (r = 0.91). Thus, the jeopardized mass may be determined noninvasively by using 2-D echo and thallium-201 tomography. This approach may provide further information regarding the effect of intervention therapy on jeopardized myocardium.

Automatic computer processing of digital 2-dimensional echocardiograms.

Quantitative studies of left ventricular function using 2-dimensional echocardiography have been limited because of a lack of computerized methods to automatically analyze the echocardiographic images. Previous computer efforts have been directed at digitizing the video output of the 2-D echocardiogram, but this digitizing method has significant limitations. A direct digitization method that produces improvement in signal-to-noise ratio and, subsequently, improved automatic detection of endocardial and epicardial borders, was developed. With definition of these edges, left ventricular global and regional analysis is possible frame by frame so that dynamic changes in cardiac function may be assessed throughout the cardiac cycle. Further technologic advances in 2-D echocardiographic acquisition and image processing should allow computer processing of 2-D echocardiographic data in real time.

Two dimensional echocardiographic quantification of infarct size alteration by pharmacologic agents.

In 27 closed chest dogs left ventricular wall motion abnormalities assessed quantitatively with two dimensional echocardiography were used as a measure of myocardial infarct size, and the change in extent of segmental wall motion abnormalities due to drug intervention early after infarction was evaluated. The extent of wall motion abnormalities was measured with echocardiography before and at 20 and 40 minutes and 5 1/2 hours after coronary occlusion. Three subgroups of dogs received, respectively, an infusion of nitroglycerin, phenylephrine or saline solution. Infarct size was measured with technetium pyrophosphate scintigraphy of the excised left ventricle. The infarct size correlated well with the extent of wall motion abnormalities before death. Wall motion was initially similar among the three groups but was significantly improved after treatment with nitroglycerin (P less than 0.025), remained stable with continued saline infusion and worsened significantly (P less than 0.05) after treatment with phenylephrine. Two dimensional echocardiography can be used to quantify experimental canine myocardial infarction and assess the effect of nitroglycerin.

Detection of entrapped intracardiac air with intraoperative echocardiography.

Embolization of entrapped intracardiac air represents a significant risk to the patient undergoing open heart surgery. To date, there have been no menas available to ensure that the heart is free of air prior to restoration of the circulation. To assess whether M mode echocardiography can accurately detect intracardiac air, we studied 10 dogs during cardiopulmonary bypass. Randomly, air was or was not injected into the left ventricular cavity of the fibrillating heart. Intracardiac air could be recognized by the presence of a stippled granular pattern, or a loss of the discrete linear echoes or decreased far field echoes, or any combination of these three. In all, 131 random observations were made. When 1.0 cc of air was injected, sensitivity and specificity were both 100 percent, but when 0.2 cc was injected, sensitivity and specificity decreased to 86 and 58 percent, respectively. thus, M mode echocardiography appears to provide a sensitive and specific tool for detecting intracardiac air.