Relationship between regional myocardial blood flow and thallium-201 distribution in the presence of coronary artery stenosis and dipyridamole-induced vasodilation.

This study assesses the relationship between the distribution of thallium-201 and myocardial blood flow during coronary vasodilation induced by intravenous dipyridamole in canine models of partial and complete coronary artery stenosis. 10 dogs were chronically instrumented with catheters in the left atrium and aorta and with a balloon occluder and electromagnetic flow probe on the proximal left circumflex coronary artery. Regional myocardial blood flow was measured during control conditions with radioisotope-labeled microspheres, and the phasic reactive hyperemic response to a 20-s transient occlusion was then recorded. Dipyridamole was then infused intravenously until phasic coronary blood flow increased to match peak hyperemic values. The left circumflex coronary artery was either partially occluded to reduce phasic blood flow to control values (group 1) or it was completely occluded (group 2), and thallium-201 and a second microsphere label were injected. 5 min later, the animals were sacrificed, the left ventricle was sectioned into 1-2-g samples, and thallium-201 activity and regional myocardial blood flow were measured. Curvilinear regression analyses between thallium-201 localization and myocardial blood flow during dipyridamole infusion demonstrated a slightly better fit to a second- as compared with a first-order model, indicating a slight roll-off of thallium activity as myocardial blood flow increases. During the dipyridamole infusion, the increases in phasic blood flow, the distributions of regional myocardial blood flow, and the relationships between thallium-201 localization and regional blood flow were comparable to values previously observed in exercising dogs with similar occlusions. These data provide basic validation that supports the use of intravenous dipyridamole and thallium-201 as an alternative to exercise stress and thallium-201 for evaluating the effects of coronary occlusive lesions on the distribution of regional myocardial blood flow.

Myocardial blood flow distribution during ischemia-induced coronary vasodilation in the unanesthetized dog.

This study was designed to determine whether coronary vasodilation distal to a flow-limiting coronary artery stenosis could result in redistribution of myocardial blood flow to produce subendocardial underperfusion. Studies were performed in 10 awake dogs chronically prepared with electromagnetic flow-meters and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow was measured using radionuclide-labeled microspheres, 7-10 mum in diameter, injected into the left atrium. A 5(-s) coronary artery occlusion was followed by reactive hyperemia with excess inflow of arterial blood effecting 375+/-20% repayment of the blood flow debt incurred during occlusion. When, after a 5(-s) occlusion, the occluder was only partially released to hold arterial inflow to the preocclusion level for 20 s before complete release, the delayed reactive hyperemia was augmented (mean blood flow repayment = 610+/-45%, P < 0.01). This augmentation of the reactive hyperemia suggested that ischemia was continuing during the interval of coronary vasodilation when coronary inflow was at the preocclusion level. Measurements of regional myocardial blood flow demonstrated that endocardial flow slightly exceeded epicardial flow during control conditions. When arterial inflow was limited to the preocclusion rate during vasodilation after a 5(-s) total coronary artery occlusion, however, flow to the subepicardial myocardium was increased at the expense of underperfusion of the subendocardial myocardium. Thus, in the presence of a flow-limiting proximal coronary artery stenosis, ischemia-induced coronary vasodilation resulted in redistribution of myocardial blood flow with production of subendocardial ischemia in the presence of a net volume of arterial inflow which, if properly distributed, would have been adequate to prevent myocardial ischemia.

Regional myocardial blood flow in awake dogs.

The objectives of this study were to test the hypothesis in awake dogs that during control conditions endocardial vessels are maximally dilated and to determine whether variables introduced by general anesthesia and thoracotomy modify distribution of myocardial blood flow or impair capacity for augmentation of flow in response to a coronary vasodilator stimulus. Myocardial blood flow was measured in relatively small, 2-3 g, left ventricular epicardial and endocardial samples by using 7-10-mum radioisotope-labeled microspheres during control conditions and during infusion of adenosine in dosages which produced maximum increases in coronary blood flow. Measurements were made initially in awake resting animals and were repeated after pentobarbital anesthesia, thoracotomy, and pericardiotomy. Blood flow (mean+/-SEM) in the epicardium and endocardium, respectively, was 0.75+/-0.06 and 0.83+/-0.06 during control conditions and 4.98+/-0.28 and 4.49+/-0.27 cm(3)/min/g during adenosine. These data demonstrate considerable capacity for vasodilation in both myocardial layers and thus refute the hypothesis that endocardial vessels are maximally dilated during control conditions. During control conditions blood flow within epicardial and endocardial layers was essentially homogeneous around the circumference of the left ventricle. In contrast to previous studies in anesthetized animals, however, transmural gradients were present in most regions, i.e., endocardium: epicardium ratio (endo/epi) 1.06-1.16. During adenosine, circumferential epicardial flows were homogeneous; however, circumferential endocardial flows were inhomogeneous and increased less than epicardial flows, endo/epi 0.81-0.99.Anesthesia, thoracotomy, and pericardiotomy increased epicardial and endocardial flow, mean values 1.08+/-0.10 and 1.11+/-0.08 cm(3)/min/g, respectively. Transmural gradients remained in only papillary muscle regions. Adenosine increased epicardial flow comparably before and after anesthesia. Although adenosine increased endocardial flow three- to fourfold after anesthesia, the increase was considerably less than epicardial flow, i.e., endo/epi 0.63-0.78.

Pressure-flow studies in man: effect of atrial systole on ventricular function in mitral stenosis.

The effect of atrial contraction on left ventricular function in six patients with varying degrees of mitral stenosis was determined by utilizing the pressure gradient technique to measure instantaneous aortic blood flow and pressure. Aortic flow was measured as ventricular rate was controlled by right ventricular pacing to create A-V (atrioventricular) dissociation at varying rates (90-150 beats/min). At each heart rate, beats with preceding P waves, effective atrial systole, were grouped according to the duration of the P-R interval. Beats without P waves served as controls. There was always a significant increase in stroke volume, created by effective atrial systole, but the P-R interval at which it took place was different for each patient. There was no difference in the stroke volume for beats preceded by P waves having a P-R interval within the range of 0.05-0.20 sec. These beats were grouped for each patient, subjected to regression analysis, and compared to control beats. The absolute and percent change created by effective atrial systole was inversely proportional to the severity of the disease as determined by mitral valve orifice size. Effective atrial systole plays less of a role in augmenting left ventricular function in patients with mitral stenosis than in patients with normal valves.

Regional myocardial blood flow during graded treadmill exercise in the dog.

Regional myocardial blood flow was measured in nine dogs at rest and during three levels of treadmill exercise by using left atrial injections of 7-10-mum radioactive microspheres. At rest, heart rate was 76 plus or minus 3 beats/min (mean plus or minus SEM), mean left ventricular myocardial flow was 0.94 plus or minus 0.09 ml/min/g and endocardial flow (endo) exceeded epicardial flow (epi) in all regions (endo/epi equals 1.12-1.33). When treadmill exercise was regulated to increase heart rates from 152 plus or minus 3 to 190 plus or minus 3 to 240 plus or minus 6 beats/min, myocardial blood flow (MBF) to all regions of the left ventricle increased linearly with heart rate (HR) from 1.83 plus or minus 0.11 to 2.75 plus or minus 0.22 to 3.90 plus or minus 0.26 ml/min/g (MBF EQUALs 0.0175 HR - 0.523 PLUS OR MINUS 0.614, R EQUALS 0.87). Exercise abolished the gradient of blood flow favoring the left ventricular endocardium at rest, so that the endo/epi flow ratios were not significantly different from 1.00. Right ventricular flows were consistently less than corresponding left ventricular flows, but showed a similar linear increase with heart rate. Right ventricular endo/epi ratios were not different from 1.00 either at rest or during exercise. Thus, exercise resulted in increased myocardial blood flow to all regions of the left and right ventricles with maintenance of subendocardial flow equal to subepicardial flow.

Local effects of acute cellular injury on regional myocardial blood flow.

This study was designed to examine local effects of acute cellular injury on regional myocardial blood flow. Studies were carried out in awake dogs chronically prepared with indwelling catheters in the aorta and left atrium and an occluder on the left circumflex coronary artery. Regional myocardial blood flow was measured by using 7-10-mum radioisotope-labeled microspheres after reestablishing inflow to a region subjected to a 2-h complete coronary occlusion. Microspheres were injected 15 s, 15 min, 4 h, and 3 days after reperfusion to assess effects of cell injury at varying intervals after reperfusion. Effects of acute cellular injury on blood flow were assessed by determining the relationship between regional blood flow and the extent of subsequent cellular necrosis measured in multiple tissue samples, weight 1-2 g, from the entire ischemic zone. The extent of cellular necrosis was determined from histological sections of each tissue sample. Prolonged ischemia effected local tissue responses which altered perfusion as a function of the interval after reperfusion and the subsequent extent of myocardial necrosis. Although the net response in each region immediately after reperfusion was vasodilation, the hyperemia in regions which subsequently suffered cellular necrosis was attenuated in direct proportion to the extent of subsequent infarction. Blood flow to acutely injured regions remained equal to, or in excess of, flow to nonischemic regions 15 min after reperfusion, but at 4 h and 3 days after reperfusion, flow was significantly decreased in regions with greater than 50% infarction. Thus, these data indicate that prolonged ischemia initiates tissue responses which progressively reduce myocardial perfusion after reperfusion. These effects on tissue perfusion may result from normal responses to irreversible injury and (or) abnormal responses to reversible and thus, potentially alterable, ischemic injury.

Effects of inhibition of nitric oxide formation on basal vasomotion and endothelium-dependent responses of the coronary arteries in awake dogs.

The role of nitric oxide in basal vasomotor tone and stimulated endothelium-dependent dilations in the coronary arteries in chronically instrumented awake dogs was studied by examining the consequences of inhibiting endogenous nitric oxide formation with the specific inhibitor of nitric oxide formation, NG-monomethyl-L-arginine (L-NMMA). In four awake dogs, coronary dimension crystals were chronically implanted on the circumflex artery for the measurement of epicardial coronary diameter, and Doppler flow probes were implanted for quantitation of phasic coronary blood flow (vasomotion of distal regulatory resistance vessels). Basal epicardial coronary diameter, acetylcholine-stimulated endothelium-dependent dilation, and flow-induced endothelium-dependent dilation of the epicardial arteries and phasic blood flow were recorded before, and after 5, 15, 50, and 120 mg/kg of L-NMMA. L-NMMA induced a dose-related increase in basal epicardial coronary vasomotor tone. There was an accompanying increase in aortic pressure and a decrease in heart rate. At doses greater than or equal to 50 mg/kg, rest phasic coronary blood flow was also decreased. Left ventricular end-diastolic pressure and contractility were not significantly changed. In contrast, the flow-induced or acetylcholine-stimulated endothelium-dependent responses were attenuated only after infusion of the highest does of L-NMMA (120 mg/kg). The changes in the basal vasomotor tone and acetylcholine-stimulated endothelium-dependent responses returned towards the control states in the presence of L-arginine (660 mg/kg). These data support the view that nitric oxide plays a significant role in modulating basal vasomotion and endothelial-dependent dilation stimulated by acetylcholine or increase in blood flow in epicardial coronary arteries and also influence the regulation of coronary blood flow during physiologic conditions.

Effects of nitroglycerin on transmural myocardial blood flow in the unanesthetized dog.

This study was designed to determin the effect of nitroglycerin upon transmural distribution of myocardial blood flow in the awake dog during normal conditions and in the presence of ischemia-induced coronary vasodilation. Studies were performed in chronically prepared dogs with electromagnetic flowmeters and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow was estimated by using radionuclide-labeled microspheres, 7-10 mum in diameter, injected into the left atrium. During control conditions endocardial flow (0.86 plus or minus SEM 0.05 ml/min per g) slightly exceeded epicardial flow (0.72 plus or minus 0.03 ml/min per g, P smaller than 0.05), and this distribution of flow was not significantly altered by nitroglycerin. After a 5-s coronary artery occlusion, reactive hyperemia occurred with excess inflow of arterial blood effecting 360 plus or minus 15% repayment of the blood flow debt incurred during occlusion. When arterial inflow was limited to the preocclusion rate during coronary vasodilation after a 5-s total coronary artery occlusion, flow to the subepicardial myocardium was increased at the expense of underperfusion of the subendocardial myocardium, and the delayed reactive hyperemia was markedly augmented (mean blood flow debt repayment =775plus or minus 105%, P smaller than 0.01). Tese data suggested that subendocardial underperfusion during the interval of coronary vasodilation in the presence of a flow-limiting proximal coronary artery stenosis caused continuing subendocardial ischemia which resulted in augmentation of the reactive hyperemic response. In this experimental model both the redistribution of myocardial blood flow which occurred during an interval of restricted arterial inflow after a 5-s coronary artery occlusion and augmentation of the subsequent reactive hyperemic response were returned toward normal by nitroglycerin. This effect of nitroglycerin may have resulted, at least in part, from its ability to vasodilate the penetrating arteries which deliver blood from the epicardial surface to the subendocardium.

Mechanism and significance of a decrease in ejection fraction during exercise in patients with coronary artery disease and left ventricular dysfunction at rest.

The purpose of this study was to determine whether an exercise-induced decrease in ejection fraction in patients with coronary artery disease and left ventricular dysfunction at rest represents ischemia or the nonspecific response of a compromised left ventricle to exercise stress. Accordingly, radionuclide ejection fraction responses of 246 patients with coronary artery disease and an ejection fraction at rest of less than 0.50 were compared with those of a "nonischemic" control group of 48 patients with idiopathic dilated cardiomyopathy and a similar degree of ventricular dysfunction. The significance of the ejection fraction response in the group with coronary artery disease was further examined by relating it to the angiographic extent of coronary artery disease, severity of angina, incidence of chest pain and electrocardiographic ST segment depression during exercise and long-term prognosis. The ejection fraction decreased by greater than or equal to 0.01 and greater than or equal to 0.05 during exercise in 48 and 28%, respectively, of the patients with coronary artery disease compared with only 8 and 2%, respectively, of the patients with cardiomyopathy. When exercise was limited by fatigue at a submaximal heart rate, the ejection fraction decreased in 25% of the patients with coronary artery disease but in none of the patients with cardiomyopathy. Patients with coronary artery disease whose ejection fraction decreased during exercise had a significantly higher incidence of three vessel disease, exercise-induced chest pain or ST depression and late mortality than did patients whose ejection fraction did not decrease. These relations were confirmed equally in subgroups of patients with moderate (ejection fraction 0.30 to 0.49) and severe (ejection fraction less than 0.30) left ventricular dysfunction. Thus, in patients with coronary artery disease and left ventricular dysfunction at rest, a decrease in ejection fraction during exercise is more likely to indicate ischemia than a nonspecific left ventricular response to exercise stress. In the individual patient, a decrease of 0.05 or greater, or a decrease during submaximal exercise, appears to be highly specific for ischemia. A decrease in ejection fraction identifies a subgroup of patients with a high prevalence of multivessel coronary artery disease and a high risk of death during long-term follow-up on medical therapy.

Value and limitation of biplane rest and exercise radionuclide angiography for assessing individual bypass grafts: a prospective study.

This prospective study evaluated the ability of serial biplane rest and exercise radionuclide angiography to predict the status of individual coronary bypass grafts in 20 patients 2 to 6 months after surgery. The preoperative coronary angiogram was used to assign vessels to 10 regions of distribution on the radionuclide angiogram. Predictions of graft adequacy for individual vessels were based on a detailed assessment of rest and exercise wall motion in their regions of supply. Of 59 grafts, 38 were judged adequate (patent with less than 75% stenosis) and 21 inadequate by postoperative catheterization. Radionuclide prediction of graft status was possible for 32 of the 59 grafts, including 19 of 24 left anterior descending, 7 of 19 circumflex and 6 of 16 right coronary artery grafts. The status of the remaining 27 grafts could not be assessed because of normal wall motion in their region of supply both pre- and postoperatively (22 vessels) or because a region of supply was not represented on the biplane radionuclide angiogram (5 vessels). Of the 32 predictions made, 25 (78%) were correct, including 13 (93%) of 14 predictions of graft adequacy and 12 (67%) of 18 predictions of graft inadequacy. The single incorrect prediction of graft adequacy resulted from improved exercise wall motion in a region supplied by a graft judged as having a 75% anastomotic stenosis. Most incorrect predictions of graft inadequacy were due to new septal or other rest wall motion abnormalities postoperatively. The comparison of pre- and postoperative studies was essential to maintain the predictive ability of the test. Thus, a detailed analysis of regional wall motion by rest and exercise radionuclide angiography can be used to predict the status of individual coronary artery bypass grafts. Reliable predictions can be made for most successful anterior descending grafts, and may permit cardiac catheterization to be deferred in certain cases. However, the method is limited by the need to perform preoperative exercise studies, by the low number of right and circumflex coronary artery grafts that can be evaluated and by the poor specificity of predictions of graft failure.

Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism.

Invasive cardiopulmonary exercise testing was performed in 7 patients who presented with congestive heart failure, normal left ventricular ejection fraction and no significant coronary or valvular heart disease and in 10 age-matched normal subjects. Compared with the normal subjects, patients demonstrates severe exercise intolerance with a 48% reduction in peak oxygen consumption (11.6 +/- 4.0 versus 22.7 +/- 6.1 ml/kg per min; p less than 0.001), primarily due to a 41% reduction in peak cardiac index (4.2 +/- 1.4 versus 7.1 +/- 1.1 liters/min per m2; p less than 0.001). In patients compared with normal subjects, peak left ventricular stroke volume index (34 +/- 9 versus 46 +/- 7 ml/min per m2; p less than 0.01) and end-diastolic volume index (56 +/- 14 versus 68 +/- 12 ml/min per m2; p less than 0.08) were reduced, whereas peak ejection fraction and end-systolic volume index were not different. In patients, the change in end-diastolic volume index during exercise correlated strongly with the change in stroke volume index (r = 0.97; p less than 0.0001) and cardiac index (r = 0.80; p less than 0.03). Pulmonary wedge pressure was markedly increased at peak exercise in patients compared with normal subjects (25.7 +/- 9.1 versus 7.1 +/- 4.4 mm Hg; p less than 0.0001). Patients demonstrated a shift of the left ventricular end-diastolic pressure-volume relation upward and to the left at rest. Increases in left ventricular filling pressure during exercise were not accompanied by increases in end-diastolic volume, indicating a limitation to left ventricular filling.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute myocardial infarction and MB creatine phosphokinase. Relationship between onset of symptoms of infarction and appearance and disappearance of enzyme.

Sixty-six patients admitted to the coronary care unit within 12 hours of the onset of symptoms of acute myocardial infarction (AMI) were subjected to blood sampling at one- to two-hour intervals for analysis of creatine phosphokinase (CPK) and lactic dehydrogenase (LDH) enzymes and isoenzymes. Complete MB CPK curves were obtained in 27 patients, and these were analyzed for optimum times for sampling and minimum number of analyses for detection of AMI. The present study indicates that (1) optimum detection of AMI can be achieved by analysis for MB CPK in a minimum of two samples obtained at 12 and 24 hours after onset of symptoms of AMI; (2) negative results of analyses for MB CPK in samples obtained before 12 hours or after 24 hours should not be used to exclude the diagnosis of AMI; and (3) a total CPK value within the normal range is not a reliable screening test to exclude analysis of MB CPK.

Effect of increases in afterload before and after coronary occlusion in awake dogs.

Ventricular function curves relating stroke work and left ventricular end-diastolic pressure were generated in awake dogs during increases in preload produced by infusion of fluid and during increases in afterload produced by administration of phenylephrine. The ventricular function curves produced by preloading were steeply upsloping whereas those produced by afterloading were essentially horizontal. Coronary occlusion produced downward displacement of these horizontal curves, but no change in slope. This increases in afterload did not help to demonstrate the functional impairment produced by coronary occlusion.

Chronic stable angina monotherapy. Nifedipine versus propranolol.

A placebo-controlled, double-blind, crossover study was conducted to determine the effects of nifedipine (60 to 90 mg per day) monotherapy and propranolol (240 mg per day) monotherapy on symptoms, angina threshold, and cardiac function in patients with chronic stable angina. Following a two-week placebo period, patients were randomly assigned to receive either nifedipine or propranolol for a five-week treatment period, after which they crossed over to the alternative regimen. All 21 patients were men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. New York Heart Association functional class improved in patients taking either nifedipine or propranolol, and nitroglycerin consumption decreased with both treatments compared with placebo. Nifedipine significantly delayed the onset of chest pain and 1 mm of ST-segment depression during bicycle exercise; increases with propranolol were smaller and not statistically significant. Nine patients had a preferential clinical response to nifedipine compared with six patients to propranolol; this was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvement in radionuclide ejection fraction at identical work loads. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14 percent (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is more effective on several measurements than propranolol when administered as single drug therapy in stable angina and has the advantage of preserving cardiac output during exercise.

Comparison of 180 degrees and 360 degrees data collection in thallium-20 1 imaging using single-photon emission computerized tomography (SPECT): concise communication.

Thallium-201 imaging using SPECT is being done with 180 degrees (RAO to LPO) data collection in some centers with single-gamma camera systems. Using our SPECT system with two gamma cameras, we have compared the effects of 180 degrees data collection without attenuation correction against 360 degrees collection with attenuation correction, using phantoms and patients. With a heart phantom in a chest phantom, TI-201 activities simulating "normal myocardium," "ischemia," "infarction," and "background" were placed in object contrast ratios (with respect to background) of 5.0, 2.0, and -1.0, respectively. The 180 degrees data gave image contrast ratios of 1.6, 0.2, and -0.8, and the 260 degrees data gave ratios of 1.5, 0.8, and -0.3, respectively. Uniform activity throughout the heart gave similar image contrast with both data-collection methods, but there was more variability with the 180 degrees collection than with 360 degrees collection. Since attenuation correction is available with the 260 degrees collection, the effects of attenuation are seen only on the 180 degrees collection images. In eight patients the image contrasts from the 180 degrees and 260 degrees collections are similar. For our two-camera SPECT system, the 360 degrees collection permits attenuation correction, has less variability in counting statistics, and gives contrast ratios like those of 180 degrees collection.

Disproportionate effects of regional hypokinesis on radionuclide ejection fraction: compensation using attenuation-corrected ventricular volumes.

This study evaluates the potential effects of regional hypokinesis on measurements of global ejection fraction (EF) as determined by radionuclide angiographic techniques. Studies were performed in a two-compartment left-ventricular (LV) model that allowed stimulation of global, anterior-region, or posterior-region hypokinesis in a torso chamber with heart-to-background activity similar to that in clinical studies. Radionuclide techniques accurately measured changes in EF during global hypokinesis but progressively underestimated true EF during increasing anterior-region hypokinesis, and progressively overestimated true EF during increasing posterior hypokinesis. When EF (y-axis) was plotted against true EF (x-axis) for a 240-ml model, from linear regression equations, the slopes and intercepts were significantly different for anterior and posterior hypokinesis. The disproportionate effects of regional hypokinesis increased with LV size. Accurate EF was computed during regional hypokinesis by determining absolute LV volumes from count rates corrected for attenuation, depth, background activity and blood-pool activity. Thus, the disproportionate effects of regional hypokinesis on EF were corrected by considering differential count attenuation.

Myocardial perfusion imaging using thallium-201: a new algorithm for calculation of background activity.

A method is presented for calculating a background image to be subtracted from TI-201 myocardial perfusion images. The method was derived from experimental measurements of background components in which hearts of animals injected with TI-201 were replaced with hearts from nonradioactive animals. The algorithm generates a background image that accounts for TI-201 activity in surrounding tissues and within the cardiac chamber. Comparison of the computer-generated background images with background images of the experimental models showed a mean difference of about 3% (range 1-6%). Clinical images using this method of background generation and subtraction are presented.

Relation between regional distribution of thallium-201 and myocardial blood flow in normal, acutely ischemic, and infarcted myocardium.

Myocardial localization of thallium-201 was compared with direct measurements of myocardial perfusion in normal, acutely ischemic, and recently infarcted myocardium. Studies were performed in 6 chronically instrumented dogs that were subjected to myocardial infarction by occlusion of the proximal left circumflex coronary artery. Four days after myocardial infarction, thallium-201 and 9 +/- 1 micrometer niobium-95-labelled microspheres were injected simultaneously after acute left anterior descending coronary arterial occlusion; the animals were killed 5 minutes later and the entire left ventricle was sectioned into 1 to 2 g samples. Regression analyses between thallium-201 activity and regional myocardial blood flow using all myocardial samples demonstrated a very close linear relation in each dog; r values were 0.98 or greater, indicating that the initial localization of thallium-201 in acutely ischemic and recently infarcted myocardium as a function of regional blood flow was essentially identical. Consequently, in each dog the regional distribution of thallium-201 closely approximated myocardial perfusion over a wide range of blood flow and potentially different local metabolic conditions that may be encountered in the clinical use of the isotope.

Stroke volume increases by similar mechanisms during upright exercise in normal men and women.

To define the effects of gender on stroke volume control during upright exercise in normal subjects, we examined central hemodynamics in 34 men and 27 women during staged bicycle ergometry. Central hemodynamics were assessed by right-sided cardiac catheterization and simultaneous radionuclide angiography. Left ventricular end-diastolic and end-systolic volumes were calculated from the stroke volume (by direct Fick) and the corresponding left ventricular ejection fraction. Men were larger than women (1.85 +/- 0.11 vs 1.65 +/- 0.13 m2, p less than 0.001) but groups were matched for age (39 +/- 12 vs 36 +/- 9 years, p = 0.27). Oxygen consumption at peak exercise was higher in men than in women (2.51 +/- 0.50 vs 1.74 +/- 0.30 liters/min, p less than 0.001) but was not different when adjusted for body weight (31.5 +/- 8.1 vs 28.4 +/- 6.4 ml/kg/min, p = 0.14), indicating similar levels of overall fitness in the 2 groups. At rest and during submaximal and maximal exercise, stroke volume and left ventricular end-diastolic and end-systolic volumes were higher in men than in women, but there were no intergroup differences in stroke volume index, left ventricular ejection fraction, and left ventricular end-diastolic or end-systolic volume indexes. Comparison of derived regression equations of cardiac index, stroke volume index and left ventricular end-diastolic and end-systolic volume indexes revealed no differences in the time course or magnitude of changes with respect to oxygen consumption, expressed as percentage of peak oxygen consumption, in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The ventilatory threshold: quantitative analysis of reproducibility and relation to arterial lactate concentration in normal subjects and in patients with chronic congestive heart failure.

The present study evaluates optimal ventilatory criteria and exercise protocols for determining the ventilatory threshold, and assesses the day-to-day reproducibility of the ventilatory threshold and its relation to peak oxygen uptake VO2 and blood lactate concentration in normal subjects and patients with stable chronic congestive heart failure (CHF). Eighteen normal subjects and 18 patients underwent rapid (1-minute stage) and gradual (3-minute stage) bicycle exercise tests on consecutive days. The ventilatory threshold was determined from computer-generated printouts of expired gas variables measured breath by breath. Interobserver variability of ventilatory threshold was small in both normal (0.66 +/- 0.85 ml/min/kg) and CHF patients (0.50 +/- 0.46 ml/min/kg). Variability in the normal subjects was lower for the rapid exercise protocol (0.66 +/- 0.85 ml/min/kg) than the gradual protocol (1.72 +/- 1.63 ml/min/kg) (p less than 0.05), but both protocols produced similar results in the CHF group. Day-to-day reproducibility of ventilatory threshold was high (r = 0.91, standard error of the estimate 1.74 ml/min/kg) and was similar to that of peak VO2 (r = 0.95, standard error of the estimate 3.31 ml/min/kg). The use of co-plotted ventilatory equivalents for oxygen and carbon dioxide yielded ventilatory threshold values comparable to values obtained by using multiple parameters (r = 0.94, p less than 0.0001). Although the ventilatory threshold did not predict a precise lactate level for individual subjects, the lactate increment at the ventilatory threshold occurred within a narrow range in both normal subjects and patients with CHF; the increase was 7.5 +/- 4.5 mg/dl and 7.7 +/- 4.1 mg/dl, respectively, indicating a relation to initial increases in blood lactate.