Influence of dobutamine on hemodynamics and coronary blood flow in patients with and without coronary artery disease

The influence of dobutamine on hemodynamics and coronary blood flow was studied in patients after routine cardiac catheterization. The data demonstrated that dobutamine is a powerful inotropic agent at a dose that has a relatively small influence on heart rate. In patients without coronary artery disease dobutamine greatly increased coronary arterial perfusion. In patients with severe coronary artery disease dobutamine resulted in a much smaller increase in coronary perfusion, and the pattern of perfusion became more Inhomogeneous. The results suggest that dobutamine has a potential inotropic value but raise concern about its influence on regional myocardial perfusion in patients with serious coronary artery disease.     

Submaximal exercise testing after acute myocardial infarction: myocardial scintigraphic and electrocardiographic observations.

The relation between global and regional left ventricular function and electrocardiographic signs of ischemia at rest and during submaximal supine exercise was studied in 27 patients 2 to 3 weeks after acute myocardial infarction. Dynamic myocardial scintigraphy was performed at rest and during submaximal exercise utilizing an in vivo method of labeling red blood cells with technetium-99m pertechnetate. Gated radionuclide blood pool scintigrams were obtained in a modified left anterior oblique, and in some patients also in the right anterior oblique projection, to measure left ventricular ejection fraction and segmental wall motion. Electrocardiographic monitoring of heart rate and rhythm was provided during the exercise. The submaximal exercise test was terminated when the patient's heart rate reached 125 beats/min or if angina, malignant ventricular ectopy or electrocardiographic evidence of myocardial ischemia developed before this rate was reached. The data demonstrate that patients with a recent anterior myocardial infarct, in contrast to patients with a recent inferior or nontransmural infarct, manifest a significant reduction in left ventricular ejection fraction with submaximal exercise. Of the eight patients with an anterior infarct, seven had segmental wall motion abnormalities at rest. Four of these eight manifested more severe abnormalities with submaximal exercise; three had abnormalities at rest that did not change with exercise. Four of the eight had a positive electrocardiographic response during exercise (two were taking digoxin). Of these four, only two had more marked wall motion abnormalities with effort. Of the 13 patients with an inferior infarct, 11 had apparently normal wall motion in the modified left anterior oblique projection at rest, including 2 who manifested segmental wall motion abnormalities with submaximal exercise; the 2 remaining patients had wall motion abnormalities at rest that, on exercise, became more marked in one and were unchanged in one. Four of the 13 had a positive electrocardiographic response with exercise (one was taking digoxin); only one of these had a detectably more severe wall motion abnormality with exercise. Of the six patients with a nontransmural infarct, four had no identifiable wall motion abnormalities at rest; in one of these, an abnormality developed with exercise. The remaining two patients had wall motion abnormalities at rest; in one, a positive electrocardiographic ischemic response developed with exercise. Patients with an anterior infarct appear to have a different functional ventricular response to submaximal exercise at the time of hospital discharge than patients with an inferior or nontransmural infarct. To identify ischemic responses with submaximal exercise in these patients one should ideally use both electrocardiographic monitoring and dynamic myocardial scintigraphy.     

Unstable angina pectoris: A randomized study of patients treated medically and surgically

Fifty patients with the clinical syndrome of unstable angina pectoris were evaluated. Twenty-seven were randomized into medical or surgical treatment groups and subsequently followed up. The results of the study reveal that: (1) there is approximately a 16 percent incidence rate of significant left main coronary artery disease in patients with this entity at our institution; (2) 10 percent of patients do not have angiographically significant coronary artery disease; (3) pain relief is better in the surgically treated patients, but the 1 1/2 year survival rate is not significantly different between the groups; (4) 50 percent of the medically treated patients again had the syndrome of unstable angina pectoris in the initial few months of the follow-up period; (5) the operative and late postoperative mortality rate in patients presenting with unstable angina pectoris and left main coronary artery disease in this small group of patients was 43 percent; and (6) four of six patients with this syndrome whose condition was deemed inoperable and who were not randomized died within the subsequent few months.     

Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia

Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 ± 0.11 [mean ± standard deviation] before pacing to 0.67 ± 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by > 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression ≥0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF ≥0.05 (0.46 ± 0.10 to 0.33 ± 0.09, p < 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of > 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.     

Short- and long-term influence of beta-adrenergic antagonists after acute myocardial infarction

After coronary arterial occlusion, catecholamines are released from storage depots in the left ventricle and injured myocardial cells are exposed to relatively high concentrations of catecholamines during the evolutionary period in which cell injury is becoming progressively more severe. In addition, in experimental animal models, there is a substantial increase in beta-adrenergic receptor density without any alteration in affinity within 1 hour of permanent coronary arterial occlusion. Recent data suggest that alpha-adrenergic receptor density increases within 30 to 60 minutes after coronary arterial occlusion in experimental animal models. The administration of catecholamines during the early phases of evolving myocardial injury can result in heightened adrenergic biochemical responses in severely injured compared with normally perfused tissue in the hearts of experimental animals. Thus, there is adequate rationale for anticipating that beta-adrenergic antagonists would protect ischemic myocardium and potentially reduce the incidence of life-threatening arrhythmias in individuals with evolving acute myocardial infarction (AMI). Studies in animal models demonstrate that the administration of beta-adrenergic antagonists in the first few minutes after coronary artery occlusion may reduce the ultimate extent of myocardial necrosis. Clinical data from several different trials in which beta-adrenergic antagonists were administered to (1) protect ischemic myocardium and preserve ventricular function and (2) reduce the severity of serious ventricular arrhythmias in patients with AMI are reviewed. The effects of longer-term administration of beta-adrenergic antagonists in patients after AMI in prolonging life and reducing risk of reinfarction are presented.     

Detection of myoglobin by radioimmmunoassay in human sera: its usefulness and limitations as an emergency room screening test for acute myocardial infarction

The results indicate that serum myoglobin determinations may be obtained by radioimmunoassay utilizing time periods for the testing which allow more useful clinical evaluation of patients. The data also demonstrate, however, that there are important temporal considerations in using serum myoglobin levels for the detection of acute myocardial infarcts and, if this test is used to determine in the Emergency Room whether patients have had acute myocardial infarcts, these limitations will have to be kept in mind. In addition, three other patient subgroups that might be expected to have elevated serum myoglobin levels by radioimmunoassay have been determined. These include patients with shock (irrespective of etiology), patients with severe renal insufficiency, i.e., those with serum creatinine levels equal to or greater than 8 mg. per cent, and possibly patients who have been on alcohol binges immediately prior to being seen in the Emergency Room.     

Measurement of myocardial infarct size by technetium pyrophosphate single-photon tomography

The primary determinant of prognosis after acute myocardial infarction (AMI) is the size of the acute infarct. The present study evaluates 46 patients with different infarct distributions and sizes to test the hypothesis that single photon emission computed tomography with technetium-99m pyrophosphate (Tc-99m-PPi) and blood pool overlay allows measurements of AMI size that provide insight into prognosis irrespective of infarct location. Identical Tc-99m-PPi and ungated blood pool projections were acquired over 180 degrees with a rotating gamma camera. Reconstructed sections were color-coded and superimposed for purposes of infarct localization. Areas of increased pyrophosphate uptake within myocardial infarcts were thresholded at 65% of peak activity. The blood pool was thresholded at 50% and subtracted so as to determine an endocardial border for the left ventricle. Using this method, myocardial infarcts weighed 2.5 to 81.2 g. The correlation of infarct mass with prognosis showed that patients without previous AMI and with acute infarcts that weighed more than 40 g had an increased frequency of death and congestive heart failure (p less than 0.001). The correlation of measured infarct mass with peak serum creatine kinase level was significant (r = 0.83, p less than 0.001; y = 0.015x + 13.20). The correlation coefficients for anterior, inferior and nontransmural AMI were not significantly different from those for the entire group. In conclusion, tomographically determined infarct mass data correlate with subsequent clinical prognosis, and Tc-99m-PPi tomography with blood pool overlay is a safe and effective means of sizing infarcts in patients with AMI.     

Effect of verapamil and nifedipine on left ventricular function at rest and during exercise in patients with Prinzmetal''s variant angina pectoris

To assess the effects of verapamil and nifedipine on left ventricular function at rest and during exercise in patients with Prinzmetal's variant angina pectoris, 10 patients (6 men and 4 women with a mean age of 52 years) with variant angina were each treated for 2 month periods with placebo, verapamil (400 ± 80 mg/day, mean ± standard deviation [SD]) and nifedipine (82 ± 31 mg/day). During the final week of each 2 month treatment period equilibrium gated blood pool scintigraphy was performed at rest and during exercise. At rest, heart rate during verapamil therapy was lower than during treatment with nifedipine; systolic blood pressure and left ventricular volumes and ejection fraction were similar for the three interventions. The maximal work load achieved was similar during placebo, verapamil and nifedipine therapy. At the maximal work load common to all three exercise studies, heart rate and systolic blood pressure were lower with verapamil than with placebo and nifedipine; ventricular volumes and ejection fraction were similar with the three agents. Thus, in patients with variant angina and a wide range of left ventricular function at rest, neither verapamil nor nifedipine significantly alters left ventricular volumes or ejection fraction at rest or during exercise.     

Effects of ortho-iodo sodium benzoate on acute myocardial ischemia, hemodynamic function, and infarct size after coronary artery occlusion in dogs

Ortho-iodo sodium benzoate (OISB) decreases the affinity of blood for oxygen, thus enhancing potential tissue oxygen delivery. To test the hypothesis that a change in oxygen affinity would ameliorate regional myocardial ischemic injury resulting from occlusion of the left anterior descending (LAD) coronary artery, experiments were carried out in 55 anesthetized dogs which received an intravenous infusion of OISB. In Protocol I studies (n = 9), preocclusion intravenous infusion of OISB (500 mg/kg) reduced epicardial S-T segment elevation 15 minutes after coronary occlusion, while a similar volume of normal saline solution did not affect this index of ischemic damage. In Protocol II experiments, 34 dogs were randomized to either an OISB or saline group, after which the LAD was ligated, the chest closed, and the animal allowed to recover from anesthesia. Myocardial infarction (MI) size was assessed after the animal died or was killed 8 to 24 hours later, and was found to be 29% smaller in dogs receiving OISB. In 6 dogs, blood P50 (the partial oxygen pressure at which hemoglobin is 50% saturated with oxygen) was increased by OISB infusion, confirming that its administration effected a rightward shift in the oxyhemoglobin dissociation curve. Protocol III studies assessed the effects of OISB on cardiac hemodynamic function and acute myocardial ischemic damage when infusion was begun 15 minutes after LAD occlusion: average epicardial S-T segment elevation was not altered by saline solution, but decreased when OISB was infused during the last 15 minutes of myocardial ischemia. Reductions in heart rate, left ventricular dP/dt, and cardiac output were observed in 7 dogs during OISB infusion, but there were no changes in these measurements during coronary occlusion in 5 dogs receiving a constant infusion of saline solution. There were no changes in regional myocardial blood flow (microsphere technique) to either ischemic or nonischemic zones in either the saline control or OISB treatment groups. Thus, both acute myocardial ischemic injury (assessed by epicardial electrocardiographic mapping) and ultimate MI size are reduced when OISB is infused before experimental coronary artery occlusion. OISB also reduces myocardial ischemic injury when its administration is begun 15 minutes after coronary occlusion, while effecting decreases in heart rate, left ventricular contractility, and cardiac output.     

Effect of chronic oral digoxin therapy on ventricular function at rest and peak exercise in patients with ischemic heart disease: Assessment with equilibrium gated blood pool imaging

The effect of chronic digoxin therapy on left ventricular ejection fraction, left ventricular volumes and cardiac output was assessed using multigated blood pool imaging both at rest and during supine exercise in 14 patients with known ischemic heart disease. Digoxin had no significant effect on ejection fraction at rest or at peak exercise. Neither exercise nor digoxin therapy had a significant influence on stroke volume index. Cardiac index was also not significantly influenced by digoxin either at rest (3.1 ± 1.15 without digoxin versus 2.9 ± 1.03 liters/min per m² during digoxin therapy) or at peak exercise (5.1 ± 2.08 versus 5.1 ± 2.04 liters/min per m², respectively), although the increase in heart rate resulted in a significant increase in cardiac index with exercise in each state (p <0.01).End-diastolic and end-systolic volume indexes both tended to be smaller at rest after digoxin therapy than before, but this difference was not significant. In the eight patients with an ejection fraction at rest of less than 0.50 (range 0.15 to 0.47), both end-diastolic and end-systolic volume indexes increased significantly with exercise (p <0.05) irrespective of therapy with digoxin. Conversely, in the six patients with a well preserved (greater than 0.50) ejection fraction at rest, digoxin prevented the exerciseinduced increase in end-diastolic and end-systolic volume indexes, and at peak exercise end-systolic volume index was significantly smaller during digoxin therapy than before it (p <0.05).It is concluded that chronic digoxin therapy in patients with stable ischemic heart disease (1) does not have a significant deleterious functional effect on the nonfailing heart, and (2) does not result in a significant change in left ventricular function at rest, but that it (3) does provide improved ventricular function at peak exercise in patients with well preserved left ventricular function at rest.     

Iodine-123 phenylpentadecanoic acid: Detection of acute myocardial infarction and injury in dogs using an iodinated fatty acid and single-photon emission tomography

The ability of an iodinated fatty acid, iodine-123 Phenylpentadecanoic acid (1–123 PPA), and single-photon emission computed tomography (SPECT) to detect myocardium injured by temporary or permanent coronary arterial occlusion was evaluated. In 5 control dogs, 11 dogs that underwent 90 to 120 minutes of fixed left anterior descending coronary artery (LAD) occlusion, and 8 dogs that underwent 90 minutes of temporary LAD occlusion and up to 90 minutes of reflow, 2 to 6 mCi of 1–123 PPA were injected and the dogs were imaged with SPECT. Control dogs showed relatively uniform uptake and clearance of 1–123 PPA in similar left ventricular (LV) regions. Dogs with permanent LAD occlusion were identified by computer algorithm as having regions of decreased 1–123 PPA uptake in the infarct-related area and a reduced rate of 1–123 PPA clearance (−9.4% in infarct sectors [washin], +3.7% in sectors adjacent to the area of infarction, and +15.4% in control LV sectors [p <0.01]). Dogs with temporary LAD occlusion and reperfusion had decreased clearance of 1–123 PPA from the regions with infarction; 1–123 PPA clearance was −5.2 ± 16.4% in infarct sectors, 12.7 ± 7.4% in periinfarct zones, and 30.4 ± 12% in control LV regions. These data demonstrate that tomographic analysis of 1–123 PPA uptake and clearance permits the relatively noninvasive detection of LV myocardium injured by permanent or temporary LAD occlusion and reperfusion.     

Nongeometric determination of left ventricular volumes from equilibrium blood pool scans

This study assesses the utility of a scintigraphic, nongeometric technique for the determination of left ventricular volumes. Accordingly, gated blood pool scintigraphy and cineangiography were performed within a 24 hour period in 22 patients. Scintigraphic volume measurements were calculated from individual frames of a modified 35 ° left anterior oblique projection using an algorithm designed to consider (1) the background-corrected left ventricular activity normalized for activity per milliliter of peripheral venous blood; (2) total study time; (3) number of frames acquired per cardiac cycle; and (4) percent of the cardiac cycle acquired. Angiographic volumes were calculated by the area-length method and the Kennedy regression equation. There was an excellent correlation between scintigraphic and angiographic methods for all volume measurements grouped together (r = 0.985, standard error of the estimate [SEE] = 14.6 ml) as well as for segregated end-diastolic volumes (r = 0.985, SEE = 16.2 ml) and end-systolic volumes (r = 0.988, SEE = 14.7 ml). Prospective testing of the independent ability of scintigraphy to estimate ventricular volumes was provided for by studying an additional 13 patients, and good agreement was found between scintigraphic and angiographic determinations of left ventricular end-systolic and end-diastolic volumes. Thus, radio nuclide techniques, which are independent of geometric assumptions, may be utilized for the quantitation of left ventricular volumes.     

Regional coronary flow with increased right ventricular output in anesthetized dogs

In this study of acute right ventricular volume overloading in anesthetized dogs, right ventricular coronary blood flow increased, probably in response to the effect of increased right ventricular pressure on myocardial oxygen needs. Left-to-right shunts with small elevations in right ventricular pressure had compensatory coronary vasodilatation which increased coronary flow. However, shunts with right ventricular hypertension had no further fall in coronary resistance and failed to have an additional increase in coronary flow. This suggests that with acute right ventricular volume overloading the presence of right ventricular hypertension increases myocardial oxygen needs but limits the ability of the coronary vessels to increase flow. Should myocardial oxygen needs increase and the coronary vessels be unable to increase myocardial perfusion, relative coronary insufficiency may occur.     

Nongeometric determination of right ventricular volumes from equilibrium blood pool scans

It has previously been shown that left ventricular volumes can be measured accurately from radionuclide gated blood pool scintigrams by quantttating the background-corrected and volume-normalized ventricular activity at end-diastole and end-systole. To determine if this same technique can be applied to the calculation of right ventricular volumes, simultaneous measurements of right ventricular stroke volume were performed using gated scintigraphy and the thermodilution technique in 60 patients without clinical or hemodynamic evidence of right-sided regurgitation. Three techniques for the acquisition of the radionuclide studies were evaluated. The best correlation between scintigraphic and thermodilution determinations of stroke volume was obtained for studies acquired with a 25 ° rotating slant hole collimator positioned in a 10 to 15 ° left anterior oblique projection with the collimator slant directed toward the cardiac apex along the axis of the interventricular septum: Thermodilution stroke volume = 4.2 (scintigraphic stroke volume) + 10.3 ml (correlation coefficient [r] = 0.88; standard error of the estimate = 9.3 ml; probability [p] < 0.0001). This scintigraphic acquisition technique was superior to (1) a straight bore collimator positioned in a septal projection (30 to 50 ° left anterior oblique with 15 ° caudal tilt), and (2) a 25 ° slant hole collimator positioned in a similar septal projection with the collimator slant directed caudally. This method was evaluated prospectively in an additional 14 patients, and there was excellent agreement between stroke volumes obtained with thermodilution and scintigraphic methods (r = 0.96, p < 0.001). In addition, measurements of right ventricular ejection fraction by the equilibrium method agreed closely with those obtained with a gated first pass technique (r = 0.94, p < 0.001, n = 14). With use of the scintigraphic right ventricular ejection fraction and the relation between scintigraphic and thermodilution measurements of right ventricular stroke volume, right ventricular end-diastolic and end-systolic volumes can be estimated. Thus, nongeometric radionuclide techniques may be used for the quantitation of right ventricular volumes.     

Thallium-201 myocardial perfusion studies in patients with the mitral valve prolapse syndrome

To determine whether regional myocardial ischemia plays a role in patients with the mitral valve prolapse syndrome, we examined myocardial perfusion with exercise stress testing and thallium-201 myocardial scintigraphy. Twelve patients were studied, 11 women and one man aged 18 to 56 years, mean age 30 years. In all patients, mitral valve prolapse was documented by echocardiography or phonocardiography. Patients over 35 years of age underwent cardiac catheterization. Electrocardograms disclosed abnormalities during maximal exercise in eight of the 12 patients. In two patients, angina developed during exercise. Thallium-201 (²⁰¹TI) scintigrams were normal in the 11 patients with presumed or documented normal coronary arteries. One patient, in whom an apical defect was demonstrated on scintigraphy, had significant disease of the left main and left anterior descending coronary artery. Repeat testing after successful aortocoronary bypass grafting revealed improved exercise capacity and a normal ²⁰¹TI myocardial scintigram. The data indicate that patients with mitral valve prolapse alone do not have regional myocardial ischemia and that the presence of a defect on ²⁰¹TI myocardial scintigraphy following maximal stress testing would suggest the existence of concomitant coronary artery disease.     

Left ventricular functional alterations at rest and during submaximal exercise in patients with recent myocardial infarction

Submaximal exercise testing with radionuclide ventriculography was performed in 117 patients prior to hospital discharge 16.7 ± 6.7 days (SD) following acute myocardial infarction. The hypothesis tested in this study was that patients with different locations and types of infarction have different functional responses to submaximal exercise prior to discharge. The distribution of the myocardial infarctions were anterior transmural in 33, Inferior transmural in 39, anterior nontransmural in 23, inferior nontransmural in 19, and indeterminant in three. Patients with transmural infarction generally had significantly larger resting left ventricular volumes at enddiastole and end-systole and lower ejection fractions and systolic blood pressure/end-systolic volume Indexes than patients with nontransmural infarctions (p < 0.05). During submaximal exercise, the change in end-systolic volume was significantly different in these two groups. When patients were separated further into anterior and inferior transmural subgroups, the patients with anterior transmural infarction had significantly lower left ventricular ejection fractions and higher right ventricular ejection fractions than the group with inferior transmural Infarction (p < 0.05). In response to exercise, the group with anterior transmural infarction had a significant decrease in left ventricular ejection fraction and a blunted systolic blood pressure/left ventricular end-systolic volume index, in comparison to patients with inferior myocardial infarction (p < 0.05); this was the only group to have a significant increase in end-systolic volume. The group variance for the parameters studied was large, particularly during exercise when the individual responses were frequently directionally opposite from the group means. The group with anterior transmural infarction was the most homogenous, with 26 of 33 having a directionally abnormal response to submaximal exercise. It was concluded that the group with anterior transmural infarction generally displayed the most abnormal left ventricular function. However, despite significant group differences in resting ventricular function with different infarcts, the intragroup variability at rest and in response to exercise was too great to permit an accurate prediction of the subject's resting ventricular performance or to permit a prediction of exercise response based solely on location of the infarct.     

Alterations in left ventricular volumes and ejection fraction at rest and during exercise in patients with aortic regurgitation

This study was performed (1) to determine the changes in left ventricular volumes during exercise in patients with aortic regurgitation, and (2) to evaluate the importance of these alterations in characterizing left ventricular function in these patients. In 15 normal subjects (Group I) and in 17 patients with aortic regurgitation (Group II), left ventricular end-diastolic volume index, end-systolic volume index, ejection fraction and the ratio of peak systolic blood pressure to end-systolic volume index were measured at rest and during supine exercise. The patients with aortic regurgitation were classified into two groups on the basis of symptoms and chest radiographs: Group IIA, minimal or no symptoms, no cardiomegaly or pulmonary venous congestion; Group IIB, definite symptoms, with cardiomegaly and pulmonary venous congestion. Patients with aortic regurgitation had greater left ventricular end-diastolic and end-systolic volume indexes at rest and during exercise (p <0.05) than did normal subjects. During exercise, left ventricular end-diastolic volume index increased in normal subjects (53 ± 13 ml/m² [mean ± standard deviation] at rest, 67 ± 18 ml/m² during exercise, p <0.01), demonstrated a heterogeneous response in patients in Group IIA and increased in patients in Group IIB (180 ± 96 ml/m² at rest, 209 ± 102 ml/m² during exercise, p <0.05). During exercise, left ventricular end-systolic volume index decreased in normal subjects (18 ± 5 ml/m² at rest, $\text{15}\text{\$}\text{?}\text{6}$ ml/m² with exercise, p <0.01), increased in patients in Group IIB (82 ± 60 ml/m² at rest, 118 ± 93 ml/m² during exercise, p <0.05), and showed a variable response in those in Group IIA. At rest, left ventricular ejection fraction was similar in the three groups, but during exercise it increased in Group I (0.71 ± 0.07 at rest, 0.82 ± 0.07 with exercise, p <0.001), was unchanged in Group IIA and decreased in Group IIB (0.59 ± 0.15 at rest, 0.50 ± 0.16 during exercise, p <0.05). During exercise, there was an inverse relation between changes in left ventricular ejection fraction and endsystolic volume, but no relation between changes in end-diastolic volume and ejection fraction. Changes in the systolic pressure-volume ratio provided no more information than changes in end-systolic volume alone. Thus, abnormal alterations in left ventricular volumes occur during exercise in patients with aortic regurgitation and may be helpful in the further characterization of left ventricular performance in these patients.     

Direct measurement of cardiac output by gated equilibrium blood pool scintigraphy: Validation of scintigraphic volume measurements by a nongeometric technique

A nongeometric technique for the determination of left ventricular volumes from the count data derived from gated equilibrium blood pool scans was previously described and validated by the demonstration of an excellent correlation between the derived data and angiographically determined left ventricular volumes. To provide a further prospective evaluation of this method and to validate its ability to determine stroke volume and cardiac output by a technique that is itself independent of geometric assumptions, simultaneous measurements of cardiac output by the thermodilution technique and gated scintigraphy were performed in 21 patients without valve regurgitation or intracardiac shunts. To substantiate the reliability of scintigraphic measurements at high levels of cardiac output, seven patients had multiple measurements of cardiac output at rest and during an infusion of isoproterenol. There was an excellent correlation between thermodilution and scintigraphic values for cardiac output (scan cardiac output = 0.99 thermodilution cardiac output ? 0.005 liters/min; n = 31, standard error of the estimate [SEE]= 0.175 liters/min, r = 0.97) as well as between thermodilution and scintigraphic stroke volumes (scan stroke volume = 1.03 thermodilution stroke volume ? 2.8 ml; n = 31, SEE = 2.5 ml, r = 0.95). In addition, the relation between scintigraphic and angiographic measurements of left ventricular volumes continued to be excellent: In 15 patients with technically adequate angiograms, scintigraphic left ventricular volume = 0.90 angiographic left ventricular volume + 7 ml (n = 30, SEE = 10 ml, r = 0.91). Thus, this study further validates the nongeometric method of measuring left ventricular volumes with gated scintigraphy and demonstrates its ability to measure left ventricular stroke volume and cardiac output reliably.