Search PubMed⌕ Search

Biomedical subjects

S R Bergmann

Publications and source records attributed to S R Bergmann.

At least 37 records · Page 2Linked to original sources
PubMed1998

Cardiac positron emission tomography.

Positron emission tomography (PET) is an intrinsically quantitative tool that provides a unique and unparalleled approach for clinicians and researchers to interrogate the heart noninvasively. The ability to label substances of physiological interest with positron-emitting radioisotopes has permitted insight into normal blood flow and metabolism and the alterations that occur with disease states. The efficacies of interventional therapies also have been demonstrated with cardiac PET. PET is unequaled in establishing the presence or absence of coronary artery disease (CAD) as well as for assessment of myocardial viability. Using mathematically and physiologically appropriate models, myocardial blood flow, metabolism, and ligand density and flux can be measured noninvasively, providing physicians and researchers with an exceptional window to the heart. Future advances in both instrumentation as well as radiochemistry and image processing will improve our understanding of the heart under normal conditions as well as with disease and should provide therapeutic approaches to enhancing the treatment of patients with heart disease of diverse etiologies.

Animals↗
PubMed1996

Superiority of C-11 acetate compared with F-18 fluorodeoxyglucose in predicting myocardial functional recovery by positron emission tomography in patients with acute myocardial infarction.

In patients with chronic coronary artery disease, preservation of myocardial oxidative metabolism measured by positron emission tomography (PET) with 11C-acetate is a more accurate predictor of subsequent myocardial functional recovery than is maintenance of glucose metabolism estimated with 18F-fluorodeoxyglucose. However, whether measurements of myocardial oxidative metabolism are more accurate than measurements of glucose metabolism in predicting functional recovery in patients with recent myocardial infarction is unknown. Myocardial oxidative metabolism was measured within 10 days of infarction in 19 patients by analysis of the rate of myocardial clearance of 11C-acetate. Metabolism of glucose was assessed by analysis of the uptake of 18F-fluorodeoxyglucose. Criteria for prediction of the recovery of function based on measurements of oxidative metabolism and glucose metabolism were compared. Threshold criteria with 11C-acetate exhibited superior positive and negative predictive values (89% and 73%, respectively) compared with the criteria of 18F-fluorodeoxyglucose (65% and 57%, respectively) (p <0.025). In addition, the magnitude of functional recovery after revascularization correlated with the severity of the metabolic abnormality present initially. In patients with recent myocardial infarction, the extent of functional recovery can be predicted accurately by measurement of regional oxidative metabolism by PET with 11C-acetate, and these measurements are superior to those of 18-fluorodeoxyglucose.

Acetates↗
PubMed1996

Assessment of blood flow distal to coronary artery stenoses. Correlations between myocardial positron emission tomography and poststenotic intracoronary Doppler flow reserve.

BACKGROUND: Previous studies have correlated quantitative coronary angiographic stenosis severity with positron emission tomography (PET) myocardial perfusion and proximal measurements of intracoronary flow velocities in normal and diseased coronary arteries. The aim of this study was to correlate regional myocardial blood flow (RMBF) derived from [15O]H2O PET with directly measured poststenotic intracoronary Doppler flow velocity data acquired under basal conditions and dipyridamole-induced hyperemia. METHODS AND RESULTS: Eleven consecutive patients 53 +/- 13 years old with ischemic chest pain and isolated proximal left coronary artery stenoses (left anterior descending, 9; left circumflex, 2; mean, 59 +/- 23% diameter stenosis) underwent [15O]H2O myocardial PET and intracoronary Doppler flow velocity studies within 1 week. PET RMBF (mL.g-1.min-1) and myocardial perfusion reserve (MPR) were calculated in poststenotic and normal reference vascular beds. Poststenotic Doppler average peak flow velocities (APV; cm/s) and coronary flow velocity reserve (CFR) were compared with corresponding PET data and quantitative angiographic lesional parameters. PET RMBF and Doppler APV were linearly correlated (r = .60; P < .001), as were poststenotic PET MPR and Doppler CFR (r = .76; P < .0002). Relative coronary flow velocity and MPR ratios between poststenotic and angiographically normal vascular beds were comparably reduced (0.83 +/- 0.25 versus 0.86 +/- 0.21, respectively; P = NS). CONCLUSIONS: Intracoronary Doppler flow velocities acquired distal to isolated left coronary artery stenoses correlated with [15O]H2O PET regional myocardial perfusion and are useful for assessment of the physiological significance of coronary stenoses in humans.

Adult↗
PubMed1996

Detection of cardiac transplant rejection with 111In-labeled lymphocytes and gamma scintigraphy.

BACKGROUND: Cardiac transplantation is an increasingly important treatment for patients with end-stage heart failure. Rejection is one of the major limitations, and currently, serial endomyocardial biopsies are required to diagnose rejection. In the year after transplantation, patients routinely undergo 12, 14, or more biopsies. Infiltration of lymphocytes into the graft is a central feature of rejection. Previous studies from our laboratory have demonstrated the feasibility of detecting early rejection noninvasively with gamma scintigraphy after administration of autologous lymphocytes labeled with 111In. METHODS AND RESULTS: Eight patients were studied at the time of routine biopsy an average of 4.5 months after cardiac transplantation. Autologous lymphocytes were isolated and labeled with 111In. Forty-eight to 72 hours later, patients underwent planar scintigraphic imaging. Myocardial accumulation of labeled lymphocytes was quantified (indium excess, IE) with a previously described and validated technique. Animal studies have shown that an IE > or = 0.07 is associated with rejection. Two of four patients with biopsy grade 0 or 1A rejection had no excess accumulation of labeled lymphocytes. The other two patients with biopsy grade 0 or 1A had an average IE of 0.13 +/- 0.04 (SD), which may actually represent the higher sensitivity of the scintigraphic approach, since the whole myocardium is interrograted. All four patients with biopsy grade 1B rejection had increased accumulation of labeled lymphocytes (IE = 0.18 +/- 0.06, P = .06 compared with all patients with grade 0 or 1A biopsies). CONCLUSIONS: The development of a sensitive, specific, and noninvasive method of diagnosing cardiac allograft rejection in humans might obviate the need for endomyocardial biopsy as well as improve the accuracy of diagnosis. The results suggest that scintigraphic detection of labeled lymphocytes is a promising approach for the noninvasive detection of cardiac transplant rejection. In addition, the approach should permit the assessment of the efficacy of antirejection therapy.

Adult↗
PubMed1996

Delineation of myocardial stunning and hibernation by positron emission tomography in advanced coronary artery disease.

With positron emission tomography, the resting flow abnormalities underlying reversible left ventricular dysfunction in 17 patients with chronic coronary artery disease were delineated. The level of flow in reversible dysfuncTional segments (i.e., those demonstrating improvement after revascularization) was markedly variable, ranging from 0.32 to 1.25 ml/gm/min. In 20 of these segments, flow was preserved, whereas in 12 segments, flow was reduced, when compared with that in, age-matched controls. Preservation of flow was associated with preservation of myocardial oxygen consumption and no alterations in myocardial substrate use. In contrast, a reduction in flow resulted in a decrease myocardial oxygen consumption and an increase in myocardial glucose use. Thus resting reversible left ventricular dysfunction in patients with chronic coronary artery disease can reflect a diversity of resting flow abnormalities. Moreover, myocardial perfusion at rest is frequently within normal limits, suggesting that the reversible mechanical dysfunction in these patients is attributable to intermittent myocardial stunning and not hibernation.

Adult↗
PubMed1996

Regional myocardial perfusion assessed with generator-produced copper-62-PTSM and PET.

UNLABELLED: We have previously demonstrated that myocardial perfusion can be estimated accurately in experimental animals with the generator-produced positron-emitting tracer, 62Cu-pyruvaldehyde bis (N4-methylthio- semicarbazone)(62Cu-PTSM) and PET. This study evaluated the feasibility of quantifying regional myocardial blood flow using 62Cu-PTSM and PET in human subjects. METHODS: Regional perfusion was estimated using a previously described and validated two-compartment model from dynamic PET scans obtained after an intravenous bolus of 62Cu-PTSM in 10 healthy volunteers and in 6 patients with coronary artery disease at rest: and in 9 of the volunteers and 4 of the patients after administration of dipyridamole intravenously. Flow estimates were compared with those obtained using H2(15)O. RESULTS: Contrast was high between myocardium and blood or lung with 62Cu-PTSM, resulting in high-quality myocardial images. Liver uptake was also high. At flows of up to 1.5 ml/g/min, flow estimated with 62Cu-PTSM correlated closely with estimates obtained with H2(15)O (y = 0.71x .21, n = 169 regional comparisons, r = 0.66, p < 0.55), but this relationship was not maintained at higher flows. CONCLUSION: The results demonstrate that quantification of myocardial perfusion with 62Cu-PTSM is feasible in human subjects but cannot be used to estimate hyperemic flows due most likely to the strong binding of the tracer to human serum albumin. Copper-62-PTSM congeners with less avidity for human albumin may prove more suitable for evaluation of hyperemic flows.

Adult↗
PubMed1996

Quantitation of myocardial fatty acid metabolism using PET.

UNLABELLED: Abnormalities of fatty acid metabolism in the heart presage contractile dysfunction and arrhythmias. This study was performed to determine whether myocardial fatty acid metabolism could be quantified noninvasively using PET and 1-(11)C-palmitate. METHODS: Anesthetized dogs were studied during control conditions; during administration of dobutamine; after oxfenicine; and during infusion of glucose. Dynamic PET data after administration of 1-(11)C-palmitate were fitted to a four-compartment mathematical model. RESULTS: Modeled rates of palmitate utilization correlated closely with directly measured myocardial palmitate and total long-chain fatty acid utilization (r = 0.93 and 0.96, respectively, p < 0.001 for each) over a wide range of arterial fatty acid levels and altered patterns of myocardial substrate use (fatty acid extraction fraction ranging from 1% to 56%, glucose extraction fraction from 1% to 16% and myocardial fatty acid utilization from 1 to 484 nmole/g/ min). The percent of fatty acid undergoing oxidation could also be measured. CONCLUSION: The results demonstrate the ability to quantify myocardial fatty acid utilization with PET. The approach is readily applicable for the determination of fatty acid metabolism noninvasively in patients.

Animals↗
PubMed1995

Visualization of thrombi in pulmonary arteries with radiolabeled, enzymatically inactivated tissue-type plasminogen activator.

BACKGROUND: Despite the high frequency of pulmonary thromboembolism and its significant morbidity and mortality, diagnosis remains suboptimal. We have been developing a method for prompt detection with the use of radiolabeled, inactivated tissue-type plasminogen activator (TPA) and performed the present study to determine whether its use permits rapid scintigraphic visualization of pulmonary thrombi in vivo. METHODS AND RESULTS: The thrombolytic, but not fibrin-binding, property of TPA was inactivated with a tripeptide chloromethyl ketone (YPACK) that had already been iodinated with 123I to radiolabel the TPA. Pulmonary arterial thrombosis was induced in nine dogs with the use of guide wires modified to provide thrombogenic tips. 123I-YPACK-TPA (1.1 to 7.8 mCi, 0.5 to 7.8 mg) was infused for 5 minutes into either the systemic or the pulmonary circulation. Clearance of radioactivity from the blood was rapid and indistinguishable from that of unlabeled, thrombolytically active TPA, with only 6.7 +/- 1.0% (mean +/- SEM) of peak radioactivity remaining after 60 minutes and minimal release of labeled fragments from the liver during this interval. Thrombi were visualized with single photon emission computed tomography and/or planar imaging 40 to 120 minutes after infusion of tracer in all seven animals given at least 3.7 mCi of 123I-YPACK-TPA. Ratios of radioactivity in thrombus (wet mass, 610 +/- 64 mg) to blood were high (14 +/- 3:1). CONCLUSIONS: The use of radiolabeled TPA in which thrombolytic activity is inactivated permits prompt scintigraphic detection of thrombi in pulmonary arteries in vivo.

Amino Acid Chloromethyl Ketones↗
PubMed1995

Species-dependent binding of copper(II) bis(thiosemicarbazone) radiopharmaceuticals to serum albumin.

UNLABELLED: Copper-62-labeled pyruvaldehyde bis(N4-methylthiosemicarbazonato)-copper(II) (Cu-PTSM) is a generator-based PET radiopharmaceutical under investigation for use in evaluation of tissue perfusion. Despite promising results from animals, problems have been encountered in the use of 62Cu-PTSM to quantitate myocardial perfusion in humans at high flow rates, possibly due to species-dependent interactions of the tracer with serum albumin. METHODS: Ultrafiltration and plasma/erythrocyte partitioning studies were performed to assess the protein binding of 67Cu-labeled Cu-PTSM and six related copper(II) bis(thiosemicarbazone) complexes. RESULTS: These studies reveal significant interspecies variability in the strength of Cu-PTSM binding to serum albumin, with 67Cu-PTSM binding much more strongly to human albumin than to dog albumin. Most of the related Cu(II)-bis(thiosemicarbazone) complexes examined exhibit interspecies variability of albumin binding similar to that observed with Cu-PTSM. Two such complexes, Cu-ETS and Cu-n-PrTS, however, were identified that exhibit no preferential association with human serum albumin. CONCLUSION: Copper-62-PTSM exhibits substantial interspecies variability in the strength of its binding to serum albumin, which appears to explain the problems encountered in using animal data to predict 62Cu-PTSM behavior in humans. The 62Cu-ETS and 62Cu-n-PrTS complexes may be viable alternatives to 62Cu-PTSM for PET studies to evaluate quantitatively myocardial blood flow in humans.

Animals↗
PubMed1995

Heterogeneity of myocardial perfusion provides the physiological basis of perfusable tissue index.

UNLABELLED: Assessment of viable from nonviable myocardium is critical for the care of patients being considered for revascularization procedures. Recently, the perfusable tissue index (PTI) has been proposed as an index of myocardial viability. METHODS: Computer simulations were performed for homogeneously and heterogeneously perfused tissue over a wide range of flows (0.04-6.4 ml/g/min) using both bolus and infusion inputs. RESULTS: PTI estimated from simulated homogeneously perfused tissue did reflect the amount of tissue being perfused independent of absolute level of flow, type of input or model configuration, whereas PTI obtained from simulated heterogeneously perfused tissue was consistently lower than the simulated "true" PTI and varied with flow, type of input function and model configuration. Flow estimated with 15O-water was not significantly different from that measured with radio labeled microspheres. CONCLUSION: Oxygen-15-water can diffuse into both acutely and chronically ischemic myocardium irrespective of its functional status. The results suggest that PTI is most likely an index of the heterogeneity of myocardial flow rather than an index of the amount of tissue being perfused. Its utility for delineating myocardial viability is thus related to the amount of tissue perfused that has low absolute levels of perfusion or high degrees of flow heterogeneity.

Analysis of Variance↗
PubMed1994

Synthesis and tissue biodistribution of [omega-11C]palmitic acid. A novel PET imaging agent for cardiac fatty acid metabolism.

In order to diagnose patients with medium-chain acyl-CoA dehydrogenase deficiency with a noninvasive diagnostic technique such as positron emission tomography, we have developed a synthesis of [omega-11C]palmitic acid. The radiochemical synthesis was achieved by coupling an alkylfuran Grignard reagent (7) with [11C]methyl iodide, followed by rapid oxidative cleavage of the furan ring to the carboxylate using ruthenium tetraoxide. Tissue biodistribution studies in rats comparing [omega-11C]palmitic acid and [1-11C]palmitic acid show that the %ID/g and %ID/organ in the heart tissue after administration of [omega-11C]palmitic acid is approximately 50% greater than after administration of [1-11C]palmitic acid, due to the diminished metabolism of the [omega-11C]palmitic acid. These studies show as well, low uptake in nontarget tissues (blood, lung, kidney, and muscle). PET images of a dog heart obtained after administration of [omega-11C]-and [1-11C]palmitic acid show virtually identical uptake and distribution in the myocardium. The differing cardiac washout of labeled palmitates measured by dynamic PET studies may allow diagnosis of disorders in cardiac fatty acid metabolism.

Acyl-CoA Dehydrogenase↗
PubMed1994

Ischemic preconditioning stimulates anaerobic glycolysis in the isolated rabbit heart.

Preconditioning decreases ischemic injury, preserves tissue ATP content, and enhances the salutary effects of reperfusion. To evaluate whether preserved ATP is related to reduced utilization or increased production, 28 paced isolated rabbit hearts, perfused at constant flow, were subjected to 3 min of transient no-flow ischemia followed 12 min later by 1 h of low-flow ischemia and 45 min of reperfusion. Results were compared with those from 34 control hearts subjected to ischemia and reperfusion without preconditioning. Preconditioning delayed the onset of ischemic contracture and decreased its amplitude. At the end of ischemia, tissue ATP content was higher in hearts subjected to preconditioning (9.8 +/- 3.3 vs. 4.5 +/- 1.1 mumol/g dry wt; P < 0.01), accounted for by increased anaerobic ATP production using exogenous glucose. Preconditioning decreased ischemic damage (creatine kinase release 373 +/- 199 vs. 587 +/- 291 U/g dry wt; P < 0.05) and resulted in better functional recovery with reperfusion (74 +/- 11% of baseline developed pressure vs. 60 +/- 23%; P < 0.05). Thus preconditioning appears to protect ischemic myocardium by enhancing anaerobic glycolytic production of ATP using exogenous glucose.

Adenosine Triphosphate↗
PubMed1994

Rate of glycolysis during ischemia determines extent of ischemic injury and functional recovery after reperfusion.

The efficacy of increasing glycolysis during ischemia for enhancing the salutary effects of reperfusion was evaluated in isolated perfused rabbit hearts subjected to low-flow ischemia followed by reperfusion. Control hearts were perfused with buffer containing 0.4 mM palmitate, 5 mM glucose, and 70 mU/l insulin. Additional groups of hearts were perfused with double glucose/insulin and 1 mM dichloroacetate or were subjected to substrate priming to increase preischemic glycogen content. Ischemic contracture was completely prevented in hearts perfused with high glucose/insulin and was delayed markedly by either dichloroacetate or enhanced preischemic glycogen [45 +/- 14 and 31 +/- 20 min, respectively; P < 0.01 each vs. control (11 +/- 10 min)] and inversely related to the rate of lactate production. With reperfusion, recovery of developed pressure was 56 +/- 23% of baseline in control hearts, 90 +/- 8% in hearts receiving high glucose/insulin, 92 +/- 5% in hearts receiving dichloroacetate, and 79 +/- 19% in hearts with increased glycogen (P < 0.05 each vs. control hearts). Creatine kinase release was reduced by > 55% in treated hearts. Thus enhancement of glycolysis by diverse mechanisms during ischemia decreased ischemic damage and improved the recovery of contractile function with reperfusion.

Animals↗
PubMed1994

Enhancement of regional myocardial efficiency and persistence of perfusion, oxidative, and functional reserve with paired pacing of stunned myocardium.

BACKGROUND: Stunned myocardium reflects postreperfusion dysfunction in myocardium that is destined to ultimately fully recover. Most investigators attribute postreperfusion stunning to a primary defect in excitation-contraction coupling or to an altered sensitivity of the myofilaments to calcium. The aim of the present study was to evaluate the interrelation between myocardial perfusion, oxidative metabolism, and function in an effort to better characterize the phenomenon of myocardial stunning, to define the regional efficiency of stunned myocardium, and to characterize its reserve capacity. METHODS AND RESULTS: Regional myocardial perfusion (measured with radiolabeled microspheres), myocardial oxygen consumption (MVO2) (quantified with positron emission tomography using 1-11C-acetate), and myocardial function (assessed with two-dimensional echocardiography) were evaluated in 12 anesthetized, closed-chest dogs subjected to 15 minutes of left anterior descending coronary artery occlusion followed by reperfusion. To evaluate flow, oxidative, and functional reserve after measurements were obtained 1 hour after reperfusion, dogs were subjected to paired pacing (an inotropic stimulus that does not alter systemic hemodynamics), and measurements were repeated. One hour after reperfusion, stunned myocardium was characterized by near-normal levels of myocardial perfusion (0.57 +/- 0.13 mL/g per minute, 81 +/- 13% of that in remote, normal regions) but severe dyskinesis (echo score, 2.6 +/- 0.7; percent wall thickening, 14 +/- 20%). Despite the low level of contractile function, MVO2 averaged 1.72 +/- 0.7 mumol/g per minute, 71 +/- 27% of that observed in remote myocardium. Regional myocardial efficiency (systolic wall thickening divided by MVO2) was markedly diminished. With paired pacing, myocardial perfusion increased proportional to that in remote myocardium, systolic function improved (echo score, 1.4 +/- 0.7; percent wall thickening, 30 +/- 15%), and regional MVO2 nearly doubled (to 3.41 +/- 1.82 mumol/g per minute, P < .05 for each paired measurement). Importantly, with paired pacing, regional myocardial efficiency nearly normalized in reperfused myocardium. CONCLUSIONS: Stunned myocardium is characterized by near-normal levels of perfusion and oxygen consumption despite marked dyskinesis. Myocardial efficiency is poor. With inotropic stimulation (in the present study, paired pacing), reperfused myocardium demonstrated considerable perfusion, oxidative, and functional reserve and a dramatic improvement in myocardial efficiency. These results may have implications for the treatment of postreperfusion pump failure.

Animals↗
PubMed1994

The relative importance of myocardial energy metabolism compared with ischemic contracture in the determination of ischemic injury in isolated perfused rabbit hearts.

The mechanical effects of ischemic contracture may be important in the development of irreversible cellular damage as it increases mechanical stress on sarcolemmal membranes and restricts endocardial perfusion. To assess the relative importance of these mechanical effects compared with decreased energy supply in the development of irreversible injury, the effects of inhibiting ischemic contracture with 2,3-butanedione monoxime (BDM), an agent that disrupts excitation-contraction coupling, were delineated in isovolumically contracting isolated rabbit hearts. Administration of 20 mmol/L BDM in 12 hearts subjected to 60 minutes of low-flow ischemia prevented ischemic contracture (left ventricular end-diastolic pressure [LVEDP], 12 +/- 3 compared with 48 +/- 14 mm Hg in 20 control hearts; P < .001), reduced membrane damage (creatine kinase [CK] release, -54% compared with control hearts; P < .05), and enhanced functional recovery during reperfusion (left ventricular developed pressure [LVDP], 86 +/- 10% of baseline compared with 56 +/- 23% in control hearts; P < .01). These observations were not related to increased intracavitary pressure and its effects on flow distribution, since venting the left ventricle in additional hearts did not result in improved function during reperfusion. Although it would be tempting to conclude that BDM protected ischemic myocardium by preventing ischemic contracture, administration of BDM was also associated with reduced depletion of ATP during ischemia, perhaps related to diminished energy demand. To distinguish between the relative importance of inhibiting contracture from provision of adequate energy, the period of ischemia was extended to 120 minutes. BDM still prevented ischemic contracture (LVEDP, 10 +/- 6 mm Hg) and preserved ATP stores, but it did not prevent membrane damage (CK release, 483 +/- 254 U/g dry weight) or contractile failure during reperfusion (LVDP, 68 +/- 7% of baseline). In contrast, increasing the rate of anaerobic glycolysis during ischemia by doubling glucose and insulin in the presence of BDM markedly decreased membrane damage (CK release, 114 +/- 72 U/g dry weight; P < .05) and contractile failure during reperfusion (LVDP, 88 +/- 7% recovery of baseline; P < .01). These results suggest that insufficient energy production is primarily responsible for myocardial ischemic damage, whereas mechanical effects of ischemic contracture appear to play only a minor role.

Animals↗
PubMed1994

Effects of time discrepancies between input and myocardial time-activity curves on estimates of regional myocardial perfusion with PET.

UNLABELLED: Estimates of myocardial perfusion with PET using kinetic models require faithful recording of radioactivity content in blood and myocardium. Typically the arterial time-activity curve is obtained by placing a region of interest (ROIs) within the left atrial or left ventricular cavity. However, curves generated from these regions appear earlier in time than tissue time-activity curves obtained from ROIs within the myocardial tissue, and such time discrepancies can lead to errors in flow estimates. METHODS: The magnitude of these time discrepancies and their effect on estimates of regional myocardial perfusion using oxygen-15-water were measured in 30 normal subjects evaluated at rest and again after administration of dipyridamole. RESULTS: Under baseline conditions, the left atrial curve appeared 0.97 +/- 0.67 (s.d.) before the ascending aorta input curve (p < 0.05) and estimated perfusion decreased from 1.28 +/- 0.28 ml/g/min using the left atrial curve uncorrected for time to 0.98 +/- 0.27 ml/g/min after correction (p < 0.05). After dipyridamole, the left atrial curve appeared 0.68 +/- 0.72 sec before the ascending aorta curve (p < 0.05) and estimated perfusion decreased from 3.60 +/- 1.40 ml/g/min using the left atrial curve uncorrected for time to 3.24 +/- 1.26 ml/g/min using the time-corrected curve (p < 0.05). Because the magnitude of time discrepancies between the left ventricular and ascending aortic curves was less (0.25 +/- 0.34 and 0.19 +/- 0.23 sec at rest and after dipyridamole, respectively), effects on flow estimates were more modest. CONCLUSIONS: The results of this study demonstrate that time discrepancies between input and tissue time-activity curves can affect estimates of myocardial flow. Correction for this potential source of error is proposed.

Adult↗