Computed tomographic analysis of the effects of hyperosmolar mannitol and methylprednisolone on myocardial infarct size.

Using contrast-enhanced computed tomography, the effects of hyperosmolar mannitol and methylprednisolone on experimentally produced myocardial infarcts were evaluated serially over the course of approximately 1 month. Infarct size, initial perfusion defect (jeopardized segment) and noninfarcted muscle mass were determined in three groups of conditioned mongrel dogs. Group 1 (n = 11) served as the control group, groups 2 and 3 were pretreated with mannitol (375 mg/kg, n = 10) or methylprednisolone (7.5 mg/kg, n = 11). Each animal in the treatment groups was treated with identical doses of the originally administered agent twice daily for 7 days after coronary occlusion. Each group developed increases in the noninfarcted muscle mass of the left ventricle (compensatory hypertrophy). The mean increase averaged more than 20% over 30 days when all groups were included together. Infarct size was smaller in both of the treatment groups. However, at 4 days after infarction, mannitol-treated dogs had a mean infarct size that was 68 +/- 8% (+/- standard error of the mean) of the size of control infarcts (p less than 0.01) and methylprednisolone-treated dogs had a mean infarct size that was 77 +/- 6% of the size of control infarcts (p less than 0.01) (referenced to the initial perfusion defect). At 30 days, these differences were less substantial (though still significant), 88 +/- 4% and 85 +/- 5%, respectively. Pharmacologic interventions can be shown to alter the size of an acute myocardial infarction, particularly when examined over the time course of infarct healing.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of beta-adrenergic blockade on the natural progression of myocardial infarct size and compensatory hypertrophy.

Using contrast-enhanced computed tomography, the effects of beta-adrenergic blockade were assessed on experimentally produced myocardial infarcts in dogs evaluated serially over the course of approximately 1 month. Infarct size, initial perfusion defect (jeopardized segment) and noninfarcted muscle mass were studied in two groups of conditioned mongrel dogs. Group 1 (n = 11) served as the control group and Group 2 (n = 10) was pretreated with propranolol (2 mg/kg). Each animal in the propranolol-treated group was given identical amounts of the agent twice daily for 7 days after coronary occlusion. Both groups developed increases in the noninfarcted muscle mass of the left ventricle (compensatory hypertrophy). The mean increase averaged 19.8% over 30 days when the two groups were included together. Infarct size was smaller in the propranolol-treated group, and averaged 28% less (p less than 0.05) than that of the control group 30 days after initial myocardial infarction. Thus, pharmacologic interventions were shown by computed tomography to alter the size of an acute experimental myocardial infarct, particularly when examined over the time course of infarct healing. Moreover, compensatory hypertrophy occurred in both the control and propranolol-treated groups.

Myocardial infarct size determined by computed transmission tomography in canine infarcts of various ages and in the presence of coronary reperfusion.

Thirty-one dogs underwent in vivo scanning with computed transmission tomography; 15 dogs were studied within 7 days (mean 4) after coronary occlusion, 10 dogs 21 to 25 days (mean 28) after occlusion and 6 dogs 4 days after coronary reperfusion of a 2 to 3 hour coronary ligation. Ungated scans (1 cm in depth) of the left ventricle were obtained from apex to base to determine infarct size. In all animals with documented (postmortem) infarction (n = 26), contrast medium caused delayed enhancement of the entire infarct or the periphery of the infarct. Infarct size was calculated from scans showing contrast enhancement of the infarct. Infarct size was also determined from the postmortem heart using histochemical morphometry (nitroblue tetrazolium) and then compared with infarct size derived from tomography using the outer margin of the contrast-enhanced periphery of the infarct as the border of the infarct. Infarct size calculated by the tomographic technique (excluding the animals without an infarct) correlated well with infarct size determined at autopsy (r = 0.90, p less than 0.001). The tomographic estimate (18.2 +/- 11.3 g) of infarct size was similar to autopsy values (18.6 +/- 11.8 g, p = NS). Thus, ungated computed transmission tomographic imaging of the heart can reliably estimate infarct size in a variety of potential clinical circumstances, particularly when the area of rim enhancement of the infarct is included within the presumed infarct region.

Effects of transient coronary ischemia and reperfusion on myocardial edema formation and in vitro magnetic relaxation times.

The effects of transient ischemia and reperfusion on regional myocardial function, salvage and swelling have been systematically analyzed in experimental canine preparations. The results of these interventions on myocardial in vitro measurements of magnetic relaxation times (T1 = magnetization recovery, T2 = spin echo) are of significant importance with respect to future nuclear magnetic resonance tomographic imaging. Thus, using a pulsed magnetic resonance spectrometer (10.7 MHz), myocardial tissue samples from two groups of dogs were evaluated. In group 1 (n = six dogs), the left anterior descending artery was occluded for 3 hours before sacrifice; in group 2 (six dogs), 3 hours of occlusion was followed by 1 hour of reperfusion. Multiple tissue samples from normal and ischemic (or ischemic and reperfused) myocardium were obtained for measurement of T1, T2 and % water content (wet weight--dry weight/wet weight). Water content increased with ischemia (78 +/- 4%) and reperfusion (81 +/- 4%) (both p less than 0.01 versus control values). Values for T1 increased with ischemia (598 +/- 39 versus 487 +/- 23 ms in normal tissue from the same heart, p less than 0.01). Even greater T1 changes occurred in the animals with reperfusion (654 +/- 52 ms, p less than 0.01 versus the intra-animal control values). Changes in T2 were similar but less marked (ischemic zone 43.9 +/- 1.0 versus 41.2 +/- 1.0 ms in nonischemic tissue in the corresponding heart, p less than 0.05; reperfusion zone 48.3 +/- 3.5 versus 41.9 +/- 2.3 ms in the normal zone, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Right and left ventricular dysfunction in patients with chronic obstructive lung disease. Assessment by first-pass radionuclide angiography.

To evaluate the relationship between right and left ventricular function in patients with obstructive lund disease, we studied 10 normal subjects (group 1) and 37 patients with chronic obstructive pulmonary disease by first pass radionuclide angiography. These 37 patients were divided into three groups: nine with mild chronic obstructive pulmonary disease (group 2), 20 with severe chronic obstructive pulmonary disease (group 3) and eight with severe chronic obstructive pulmonary disease and primary left ventricular disease (group 4). In each subject right ventricular ejection fraction (RVEF), left ventricular ejection fraction (LVEF) and ejection fraction during first third of systole (first third LVEF) were calculated. (For table: see text.) p less than 0.05 versus 1. All subjects in group 2 had normal left ventricular and right ventricular function. In group 3, 11 of 10 (55 per cent) had a low RVEF and three of 20 (15 per cent) a low LVEF. However eight of 20 in this group (40 per cent) had a depressed first-third LVEF. The correlation between decline in RVEF and first-third LVEF was good r = 0.73. We conclude that (1) certain indices of early systolic left ventricular ejection are abnormal in many patients with chronic obstructive pulmonary disease and correlate with the decline in right ventricular function; (2) this is not seen in patients with mild chronic obstructive pulmonary disease and is worse in patients with underlying left-sided heart disease.

Thallium scintigraphy in experimental toxic pulmonary edema: relationship to extravascular pulmonary fluid.

Pulmonary fluid volumes (PBV = lung blood volume; EVLW = extravascular lung water) were examined to define the effects of oleic acid injury and then to examine the relationship between edema formation and accumulation of pulmonary thallium. In six dogs, pulmonary fluid compartments were monitored during the induction of pulmonary injury by oleic acid (0.15 cc/kg i.v.). By 30 min after the injection, EVLW had doubled (p less than 0.01); it continued to increase slowly for 180 min, whereas PBV declined. In six anesthetized dogs, we made similar measurements in an identical preparation and compared pulmonary fluid volumes with pulmonary counts derived from sequential thallium (1-1.3 mCi) scintigrams obtained after the injection of oleic acid (0.12-0.15 ml/kg). Measures of EVLW and PBV were obtained sequentially along with thallium scintigrams. There was a linear relationship between EVLW and pulmonary counts alone, or when pulmonary counts were normalized to myocardial activity. We conclude that sequential thallium scintigrams provide useful information about the degree of change of EVLW over time in a model of noncardiogenic pulmonary edema.

In vitro magnetic relaxation times of the ischemic and reperfused rabbit kidney: concise communication.

To assess the effects of renal ischemia and reperfusion on in vitro magnetic relaxation times (T1 = magnetization recovery, T2 = spin echo), we evaluated the spectroscopic characteristics of the renal cortex from 25 rabbits. Eight served as controls (Group 1), nine had one renal pedicle ligated for 1 hr (Group 2), and eight (Group 3) were occluded for 1 hr and reperfused for 30 min. For intra-animal comparison purposes, % H2O content, T1 (msec), and T2 (msec) of the ischemic (reperfused) kidney were normalized to the values from the normal kidney within the same animal. Renal ischemia consistently increased water content, which was exaggerated by reperfusion. In association with ischemia, T1 fell, and with reperfusion T1 lengthened. T2 increased with ischemia and declined from the peak ischemic effects with reperfusion.

Analysis of phase-angle histograms from equilibrium radionuclide studies: correlation with semiquantitative grading of wall motion.

Quantitative wall motion assessment from gated radionuclide left ventriculograms using phase analysis was studied in 14 subjects (6 normal volunteers and 8 patients with previous acute myocardial infarction). The standard deviation and skewness of the phase-angle histograms were determined from both global and segmental left ventricular (LV) regions of interest (septal, apical and posterolateral). Studies were performed at rest, after administration of atropine and after combined administration of phenylephrine and atropine. Both the standard deviation and skewness showed significant correlations with semiquantitative wall motion scoring. From the global analyses, the highest correlations were found after atropine administration (r = 0.86, p less than 0.001 for standard deviation and r = 0.72, p less than 0.001 for skewness). Nevertheless, deterioration in global wall motion scores correlated poorly with directional changes in standard deviation (r = 0.06, difference not significant) or skewness (r = 0.33, p less than 0.05). No significant correlation between skewness or change in skewness and wall motion scores were found with the segmental analyses. The maximal correlation between segmental standard deviation and segmental wall motion grading was again noted after atropine administration (r = 0.68, p less than 0.001), but deterioration in grading did not correlate with similar deterioration of the standard deviation (r = -0.05, difference not significant). Based on 90% confidence limits for normal standard deviation and skewness, an abnormal standard deviation (greater than 14.5) identified 13 of 28 wall motion disorders (sensitivity 46%), whereas an abnormal skewness (greater than 1.4) identified 1 of 28 wall motion disorders (sensitivity 4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Digital intravenous ventriculography: analysis and validation of wall thickness changes during ischemia and inotropic stimulation in dogs.

To assess regional ventricular wall thickening, we studied 8 open-chest dogs using digital intravenous ventriculography at a control stage, after subtotal and total coronary occlusion, and then after isoproterenol administration. In 3 dogs, 2 pairs of myocardial thickness crystals were implanted. Correlations of measures of wall thickness and percentage of wall thickening with crystal measures were excellent at the base (r greater than or equal to 0.97) and near the apex (r greater than or equal to 0.97). Four areas of the inferoapical wall muscle were measured: the base, mid-wall, distal wall, and apex. Four chamber dimensions were also examined: the long axis, base decreased with ischemia. At completion occlusion, it was -24.6 +/- 6% at the base, -27.3 +/- 5% at the mid-wall, -27.1 +/- 5% at the distal wall, and -24.7 +/- 5% at the apex. Percent thickening decreased with occlusion, although greater at the base and mid-wall than at the distal wall and apex. With isoproterenol, end-diastolic thickness increased only at the apex, with little change at the base, distal wall, and mid-wall. Percent thickening increased. In general, ischemia produced increases in end-diastolic hemichords with little change in the long axis. Isoproterenol reduced the hemichords, although the long axis did not change. We conclude the digital intravenous ventriculograms can be used to assess changes in wall thickness with high degrees of accuracy. Asymmetric thickening occurred at rest, with ischemia and with inotropic stimulation, being greatest at the apex and least at the base.

Analysis of ventricular emptying and filling indexes during acute increases in arterial pressure.

Using equilibrium radionuclide angiography, an evaluation was made of the response of left ventricular ejection and filling rates at rest and during acute increases in afterload in 8 normal volunteer subjects and 10 patients with previous transmural myocardial infarctions. Using the postatropine point for comparison, normal patients increased ejection time and decreased peak ejection rate (-3.90 +/- 0.49 vol/s to -3.41 +/- 0.95 vol/s) and peak filling rate (3.94 +/- 0.88 vol/s to 3.51 +/- 0.38 vol/s). Infarct patients had similar responses, although all indexes were lower than the corresponding values in the normal subjects. At rest, the ratio of peak filling to emptying rate was similar in the normal subjects and the infarct patients (1.01 +/- 0.24 versus 0.99 +/- 0.25, respectively) and maintained that relationship after atropine (0.91 +/- 0.11 versus 0.81 +/- 0.21) and at the peak increase in arterial pressure (1.07 +/- 0.21 versus 1.02 +/- 0.32). The ratio of time to peak filling/time to peak emptying behaved in similar fashion regardless of the differences in the absolute values. In this study, left ventricular filling and emptying behaved in a similar fashion in response to the alteration in arterial pressure in normal subjects and in patients with previous myocardial infarctions.

Comparative effects of ionic and nonionic contrast materials on indexes of isovolumic contraction and relaxation in humans.

The effects of contrast media on left ventricular (LV) relaxation as assessed by the time constant of isovolumic relaxation have not previously been studied. A new nonionic contrast agent (iohexol) has been shown to have fewer deleterious effects than standard ionic agents. Nineteen patients received iohexol and sodium meglumine diatrizoate (Renografin-76) in a double-blind, crossover study during left and right coronary arteriography and with simultaneous high-fidelity micromanometer measurements of LV pressure. Neither agent induced significant changes in LV end-diastolic pressure after right or left coronary arteriography. After right coronary arteriography, neither agent produced significant deterioration of peak positive dP/dt or (dP/dt)/DP40 (dP/dt at a developed pressure of 40 mm Hg). However, after right coronary arteriography both agents caused a transient deterioration in peak negative dP/dt and the time constant of isovolumic relaxation (p less than 0.05 at 20 seconds after arteriography). After left coronary arteriography, sodium meglumine diatrizoate induced deterioration of systemic blood pressure (p less than 0.05), peak positive dP/dt (p less than 0.01), (dP/dt)/DP40 (p less than 0.05), peak negative dP/dt (p less than 0.01) and the relaxation time constant (p less than 0.01). These effects were not induced by iohexol. Thus, nonionic contrast media exert negligible alterations on LV function when used for coronary arteriography. The findings are of potential clinical importance in view of the large number of patients with depressed LV function who undergo coronary arteriography.

In vivo assessment by computed tomography of the natural progression of infarct size, left ventricular muscle mass and function after acute myocardial infarction in the dog.

Quantification of myocardial infarct (MI) size is of prognostic importance in patients with acute ischemic damage. Evaluation of the efficacy of interventions for salvage of ischemic myocardium depends on the accurate estimation of the ischemic area and a knowledge of the natural progression of the infarct. Computerized transmission tomography (CTT) is a reliable in vivo technique for estimating infarct size. We serially studied 8 dogs over approximately 1 month after occlusion of the left anterior descending coronary artery using both ungated and prospectively electrocardiogram-gated CTT. Scans were obtained 20 minutes after occlusion and then several more times until the dogs were killed. Using the ungated CTT scans, infarct size increased from 0 to 4 days (+ 65 +/- 20%, mean +/- standard error of the mean, p less than 0.05), then progressively decreased. The initial perfusion defect overestimated the eventual MI size at 1 month by 33 +/- 15% (p less than 0.05). The MI size at necropsy correlated well (r = 0.98, p less than 0.001) with CTT MI size determined just before sacrifice. Non-infarcted left ventricular (LV) muscle mass increased significantly (27 +/- 7% greater at 1 month compared with day 0, p less than 0.01) over time, presumably representing compensatory LV hypertrophy. The LV muscle mass at necropsy correlated well (r = 0.94, p less than 0.001) with CTT LV muscle mass just before sacrifice.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic and electrocardiographic effects in man of a new nonionic contrast agent (iohexol): advantages over standard ionic agents.

Iohexol is a new, nonionic contrast material that has been shown in animal studies to hold great promise as an agent for coronary arteriography and ventriculography with fewer adverse hemodynamic effects than standard ionic media. At present, it has not been studied systematically in man. Fifty patients referred for elective cardiac catheterization were randomized to receive either iohexol or meglumine sodium diatrizoate (Renografin-76). Both operator and patient were blinded as to which agent was being used. Hemodynamic variables measured were pulmonary artery wedge pressure and systemic blood pressure. In addition, the following electrocardiographic indexes were evaluated: S-T segment shifts, changes in Q-T interval, changes in T-wave amplitude, and changes in heart rate. These variables were measured after left ventriculography and after both left and right coronary arteriography. Both iohexol and sodium meglumine diatrizoate produced small transient elevations in pulmonary artery wedge pressure. Systemic hypotension occurred with both agents but was more profound and longer-lasting with sodium meglumine diatrizoate. Iohexol injection resulted in no electrocardiographic changes, whereas sodium meglumine diatrizoate produced marked Q-T prolongation, as well as changes in T-wave amplitude and heart rate. Iohexol was well tolerated by the patients, and radiographic opacification was good to excellent in all cases. Thus, iohexol produces fewer deleterious hemodynamic and electrocardiographic changes than sodium meglumine diatrizoate when studied in a typical adult population requiring diagnostic cardiac catheterization. This favorable preliminary experience in man has potential widespread importance because of the large number of patients undergoing angiographic procedures.

Radionuclide analysis of peak filling rate, filling fraction, and time to peak filling rate. Response to supine bicycle exercise in normal subjects and patients with coronary disease.

Using gated equilibrium radionuclide angiography, variables of diastolic filling were analyzed at rest and during supine bicycle exercise in normal subjects (Group 1, n = 18), coronary patients with normal resting ejection fractions (Group 2, n = 26), and coronary patients with reduced resting ejection fractions (Group 3, n = 8). Indexes analyzed were peak filling rate and filling fraction during the first third of diastole. At rest, the peak filling rate was significantly lower in coronary patients than in normal subjects (3.18 +/- 0.82 end-diastolic volume [EDV]/s in Group 1 versus 2.41 +/- 0.66 EDV/s in Group 2, p less than 0.005; and 1.34 +/- 0.26 EDV/s in Group 3, p less than 0.001 versus Group 1). These differences persisted at peak exercise. Coronary patients also had significantly lower filling fractions at rest and during exercise than did normal control subjects. The time from end-systole to peak filling rate was longer at rest in patients in Group 2 (203 +/- 52 ms) than in subjects in Group 1 (172 +/- 50 ms, p less than 0.025). This remained true when the time to peak filling was normalized by the R-R interval. Although the exercise time to peak filling was longer in coronary patients in both Groups 2 and 3 than in Group 1, these differences were not apparent when the interval was normalized by the R-R interval. Thus, abnormalities in peak filling rate and filling fraction exist in patients with coronary disease both at rest and during exercise, but large overlaps exist between normal and coronary patients. Caution is advised in comparing the timing of events during diastole because apparent group differences may be related in part to rest or exercise heart rate.

Sensitivity and specificity of nuclear phase analysis versus ejection fraction in coronary artery disease.

Phase standard deviation (SD) and skew characteristics of the first Fourier harmonic of equilibrium radionuclide volume curves were examined and compared during rest and during supine bicycle exercise with ejection fraction (EF) changes and the development of ischemia in 17 control subjects and in 2 groups of patients (n = 57) with coronary artery disease (CAD). Group I comprised 37 patients with CAD; IA was a subgroup of 20 patients with previous myocardial infarction (MI) and IB a subgroup of 17 patients with CAD without MI (all with coronary stenosis greater than 75% diameter narrowing). Group II comprised 20 patients with CAD who had undergone coronary bypass surgery. In the Group I subjects, phase SD was the most sensitive indicator of CAD at rest (Group I, 56%; Group IA, 70%, and Group IB, 29%), and the EF was the most sensitive indicator at submaximal (Group I, 78%; Group IA, 86%, and Group IB, 64%) and maximal exercise (Group I, 70%; Group IA, 93%, and Group IB, 53%). When phase SD and skewness were combined with EF changes, little increase in sensitivity occurred in Group I (rest 61%, submaximal exercise 88% and maximal exercise 76%). The results from Group II subgroups were qualitatively similar to those observed with Group I subgroups. These data reveal a marginally improved sensitivity for detection of CAD during supine bicycle radionuclide ventriculography when phase measurements were added to changes in global EF values.

Comparison of digital intravenous ventriculography with direct left ventriculography for quantitation of left ventricular volumes and ejection fractions.

Digital images of the left ventricle obtained at 30 frames/second from continuous fluoroscopy after intravenous injection of contrast medium (digital intravenous ventriculography) were used to estimate left ventricular (LV) volumes and ejection fraction with use of several techniques for identifying the ventriculographic silhouette. The digital technique was compared with direct contrast left ventriculography in 26 patients undergoing diagnostic cardiac catheterization. End-diastolic and end-systolic volumes calculated from digital intravenous and direct left ventriculograms were obtained with use of a standard area-length formula. Both end-diastolic volume (EDV) (r = 0.88, y = 1.06x - 17.1 ml) and end-systolic volume (ESV) (r = 0.89, y = 0.96x + 0.43 ml) determined from digital intravenous ventriculography (mask mode images) correlated closely with those obtained by direct left ventriculography. Combining the EDV and ESV to define the relation between the 2 techniques yielded an even closer correlation (r = 0.96). There was also good correlation between the 2 techniques for measurement of ejection fraction (r = 0.81, standard error of the estimate 6.7%). Measurements from direct left ventriculography were frequently invalidated by ventricular arrhythmias during the time of opacification of the left ventricle; this was rarely the case for digital intravenous ventriculography. It is concluded that area-length estimates of LV volumes and ejection fraction can be accurately obtained from digital processing of fluoroscopic LV images after intravenous injection of contrast medium.

Phenylephrine stress in the evaluation of patients with congestive cardiomyopathies.

To analyze the effects of acute elevations in arterial blood pressure on pulmonary blood volume (PBV) and left ventricular function, 21 outpatients with congestive cardiomyopathies and stable condition and eight normal control subjects were studied using equilibrium radionuclide angiography during the infusion of phenylephrine. The myopathy patients were subdivided into seven patients who developed rales during phenylephrine infusion and 14 who did not. All of the myopathy subjects had reduced ejection fractions and enlarged end-diastolic volumes at rest. With phenylephrine, the patients who developed rales (Group 1) and those who did not (Group 2) had similar changes in left ventricular parameters (ie, ejection fraction declined and end-diastolic volume increased). With phenylephrine, however, the patients with rales had marked increases in radionuclide estimates of PBV (48.2 +/- 1.2 to 71.2 +/- 4.1 units, P less than .01, a mean increase of 48%), while in the subjects without rales, PBV increased from 48 +/- 11 to 54.6 +/- 2.2 (P less than .05, a mean increase of only 14%). Normal individuals (Group 3) had a qualitatively similar response to phenylephrine as did the myopathy patients (a decline in ejection fraction and an increase in end-diastolic volume), with no significant change in PBV. Noninvasive phenylephrine radionuclide imaging may help characterize patients with varying forms of congestive cardiomyopathies, direct appropriate therapy, and help explain the pathophysiology of clinical findings.

Thallium pulmonary scintigraphy. Relationship to pulmonary fluid volumes during left atrial hypertension and the acute release of pressure.

To evaluate the relationship between thallium-201 lung activity and pulmonary fluid volumes, we compared thallium pulmonary scintigrams with measures of intravascular (PBV), extravascular (EVLW) and total lung water (TLW) during gradual left atrial (LA) hypertension and then serially after the acute release of pressure. The study group was composed of nine mongrel dogs who were each studied at seven levels of elevated LA pressure, and then every 15 minutes for 2 hours after the acute release of pressure. During LA pressure (congestion phase) elevation, lung counts (normalized for myocardial activity), correlated best with TLW (r = .91), rather than PBV (r = .84) or EVLW (r = .81). After the release of pressure (recovery phase), lung counts correlated well with EVLW (r = .92) and TLW (r = .82), but not with PBV (r = .28). Postmortem lung counts from 197 separate lung sections correlated well with the corresponding wet weight/dry weight ratio from that section (r = .81). Thus, we conclude that changes in pulmonary thallium emissions during cardiogenic pulmonary edema relate to corresponding changes in pulmonary fluid volumes. During congestion, the confounding effects of nonlinear increases in EVLW and PBV make thallium emissions more a marker of TLW than either the intravascular or extravascular pulmonary fluid compartment. After pressure release, PBV immediately returns to normal, at which time EVLW and pulmonary emissions correlate closely. These latter data, more applicable to postexercise stress thallium data, lend support to the hypothesis that elevated pulmonary emissions during postexercise thallium scintigrams reflect elevations in EVLW that develop during exercise.

Effect of patient imaging angle on apparent cardiac volumes and the potential impact on measurement of valvular regurgitant fractions.

The accurate measurement of cardiac chamber volume is of major importance in assessing cardiac performance. Accurate equilibrium radionuclide volume estimations are difficult to obtain, due to the geometry of the chambers, and the physical characteristics of the imaging system. The purpose of this study was to examine the effects of imaging projections on relative cardiac chamber volumes, indexes, and stroke volume ratios. Twenty-two male patients, free of clinical evidence of disease, were studied. A series of four 2-minute acquisitions were made with the patient successively imaged in the anterior, 30 degrees left anterior oblique (LAO), 45 degrees LAO, and 60 degrees LAO projections with 15 degrees of caudal inclination. Filtered stroke volume and original images were used by the operator to assign right ventricular (RV), left ventricular (LV), and a combined right and left ventricular (TOT) regions-of-interest. From the data we determined end-diastolic counts (EDC), end-systolic counts (ESC), stroke counts (SC), ejection fractions (EF), and R/L stroke count ratios. The following changes were observed as the projection was moved from the anterior to 60 degrees LAO: 1) all RV parameters decreased in value, including, RVEDC (P less than .001), RVESC (P less than .01), RVESC (P less than .01) and RVEF (P less than .001); 2) LVEDC and LVESC (both P less than .01) increased while LVEF decreased (P less than .004); and 3) the R/L stroke count ratio decreased (P less than .001). Variability could be explained by 1) chamber overlap and geometry; 2) patient variability; and 3) intrachamber, interchamber and chest wall photon attenuation and scatter. We suggest that close attention to detail, with computer assistance, to optimally position the patient may reduce the effect of inherent limitations in radionuclide volumetric measurements, thus improving the reliability and usefulness of existing studies.

Regional myocardial blood flow, edema formation, and magnetic relaxation times during acute myocardial ischemia in the canine.

This study was designed to measure early changes in myocardial perfusion after acute coronary occlusion, and to examine the relationships among blood flow, myocardial edema, and magnetic relaxation times of ex vivo myocardial tissue. In ten dogs, the left anterior descending coronary artery was occluded for 4 hours prior to sacrifice of the animals. Regional myocardial blood flow was measured using radiolabeled microspheres (15 micron), which were injected into the left atrium 5 minutes prior to sacrifice. Multiple subendocardial tissue samples from the left ventricular free wall were obtained for measurement of magnetic relaxation times, percent water content and tissue radioactivity. Mild, moderate, and severe ischemia were defined as reductions in myocardial blood flow to 30% to 50%, 15% to 30%, and less than or equal to 15% of control, respectively. Myocardial water content was increased with mild ischemia (79.6 +/- 0.7%), moderate ischemia (79.9 +/- 0.4%), and severe ischemia (80.3 +/- 0.6%), all P less than .005 vs. control. T1 relaxation times rose with mild (544 +/- 10 msec, P less than .005 vs. control), moderate (543 +/- 11 msec, P less than .005 vs. control), and severe ischemia (574 +/- 10 msec, P less than .001 vs. control). T2 relaxation times behaved in a similar manner, being prolonged in the mildly, moderately, and severely ischemic groups (38.3 +/- 0.3, 38.1 +/- 0.3 and 38.2 +/- 0.3 msec, respectively; all P less than .001 vs. control).(ABSTRACT TRUNCATED AT 250 WORDS)