Absolute Quantification Of Myocardial Perfusion Research Articles

Lower stress perfusion in patients with myocardial infarction with non-obstructive coronary arteries compared to controls in long-term follow-up with quantitative perfusion mapping

Abstract Introduction Myocardial infarction with non-obstructive coronary arteries (MINOCA) constitutes a heterogenous condition with different coronary, cardiac and non-cardiac etiologies. Cardiovascular magnetic resonance imaging (CMR) has emerged as an important diagnostic tool in recent years and is now recommended in patients with MINOCA as a working diagnosis. However, despite early CMR following admission for MINOCA, no cause can be found in around 25% of all patients. A pathophysiological mechanism may be diffuse global coronary microvascular dysfunction (CMD) which has emerged as an important cause of myocardial ischemia. Quantitative adenosine stress CMR perfusion mapping allows for absolute quantification of myocardial perfusion, reflecting CMD in the absence of obstructive coronary disease in MINOCA patients. Purpose To study the presence of CMD in MINOCA patients with an initial normal CMR scan compared to healthy controls. Methods Patients from the multicenter myocardial infarction in our city with normal Coronaries 2 (SMINC-2) study, with a normal CMR scan 2–4 days after hospitalization, and healthy age- and sex-matched controls underwent stress perfusion at 1.5T (MAGNETOM Aera). Native rest T1 and T2 short-axis maps were acquired. Quantitative perfusion maps were acquired during adenosine stress (140 micrograms/kg/min) and at rest following an intravenous contrast bolus (0.05 mmol/kg of gadoteric acid, Gd-DOTA). Post contrast T1 maps were acquired after intravenous contrast (total dose 0.2 mmol/kg) rendering extracellular volume (ECV) maps. Global native T1, T2, ECV and rest and stress perfusion values were acquired by averaging segmental values per patient. Myocardial perfusion reserve (MPR) was calculated as perfusion in stress divided by rest. Values were presented as mean±standard deviation and compared with the independent t-test in normally distributed data, and with the Mann-Whitney U test in non-normally distributed data. Clinical data regarding cardiovascular risk factors, smoking and medications were presented as numbers (percentages) and compared with Fisher's exact test. Rate pressure product (RPP) was calculated as systolic blood pressure multiplied by heart rate in rest and stress. Results In total, 15 patients (59±16 years old, 60% female), and 15 healthy age- and sex-matched controls, were included. There was a trend towards higher incidence of hypertension in patients compared to controls, however no difference in other risk factors (Table 1). Compared to controls, MINOCA patients had lower perfusion in stress (Figure 1). There was no difference in global native T1, T2, ECV, rest perfusion, MPR or hemodynamic parameters between the MINOCA patients and the controls (p>0.05 for all, Table 1). Conclusions Myocardial stress perfusion is lower in MINOCA patients with a normal initial CMR scan compared to age- and sex-matched controls suggesting CMD as a possible pathophysiological mechanism in MINOCA. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Swedish Heart and Lung Foundation

Rubidium-82 positron emission tomography for detection of acute doxorubicin-induced cardiac effects in lymphoma patients

BackgroundDoxorubicin is a cornerstone in lymphoma treatment, but is limited by dose-dependent cardiotoxicity. Rubidium-82 positron emission tomography (82Rb PET) assesses coronary microvascular function through absolute quantification of myocardial perfusion and myocardial perfusion reserve (MPR). Doxorubicin-induced microvascular injury represents a potential early marker of cardiotoxicity. Methods and resultsWe included 70 lymphoma patients scheduled for doxorubicin-based treatment. Cardiotoxicity was evaluated with 82Rb PET myocardial perfusion imaging during rest and adenosine stress before chemotherapy and shortly after the first doxorubicin exposure. Patients with a MPR decline > 20% were defined as having a low threshold for cardiotoxicity. In the 54 patients with complete data sets, MPR was significantly lower after the initial doxorubicin exposure (2.69 vs 2.51, P = .03). We registered a non-significant decline in stress perfusion (3.18 vs 3.02 ml/g/min, P = .08), but no change in resting myocardial perfusion. There were 13 patients with a low cardiotoxic threshold. These patients had a significantly higher age, but were otherwise similar to the remaining part of the study population. ConclusionDecreases in MPR after initial doxorubicin exposure in lymphoma patients may represent an early marker of doxorubicin-induced cardiotoxicity. The prognostic value of acute doxorubicin-induced changes in MPR remains to be investigated.

Expert consensus on blood pressure management in hypertensive disorders of pregnancy (2019)

Objective: To compare the incidence of coronary microvascular disease (CMVD) between patients with non-obstructive and obstructive coronary arteries. Methods: We retrospectively analyzed 97 patients with angina pectoris, who underwent the absolute quantitative PET examination of myocardial perfusion and coronary anatomy examination within 90 days. All patients were divided into two groups: non-obstructive group (72 cases, no stenosis ≥50% in all three coronary arteries) and obstructive group (25 cases, at least one coronary stenosis ≥50%; and at least one coronary stenosis<50%). Quantitative parameters derived from PET including rest myocardial blood flow (RMBF), stress myocardial blood flow (SMBF), coronary flow reserve (CFR) and cardiovascular risk factors were compared between the two groups. CMVD was defined as CFR<2.90 and SMBF<2.17 ml·min(-1)·g(-1). Results: Incidence of CMVD was significant higher in the non-obstructive coronary arteries of the obstructive group than in the non-obstructive coronary arteries of non-obstructive group (47.1% (16/34) vs. 25.5% (55/216), χ(2)=6.738, P=0.009) while incidence of CMVD was similar between non-obstructive and obstructive patients ((44% (11/25) vs. 33.3% (24/72), χ(2)=0.915, P=0.339). RMBF ((0.83±0.14) ml·min(-1)·g(-1) vs. (0.82±0.17) ml·min(-1)·g(-1)), SMBF ((2.13±0.60) ml·min(-1)·g(-1) vs. (1.91±0.50) ml·min(-1)·g(-1)) and CFR (2.59±0.66 vs. 2.36±0.47) were similar between the two groups (all P>0.05). Conclusions: CMVD can occur in non-obstructive coronary arteries in both patients with non-occlusive coronary arteries and patients with obstructive coronary arteries. Prevalence of CMVD is significantly higher in patients with obstructive coronary arteries than in patients with non-obstructive coronary arteries. The CMVD severity is similar between the two groups.目的： 比较非阻塞及阻塞性冠状动脉（冠脉）疾病患者的冠脉微血管疾病（CMVD）发生情况。 方法： 回顾性分析2015年12月至2019年12月在山西医科大学附属第一医院成功完成(13)N-氨水正电子发射计算机断层显像（PET）心肌血流绝对定量检查并在PET检查90 d内完成冠脉造影或CTA的97例疑诊CMVD患者，根据造影及CTA结果将患者分为非阻塞组（72例，3支冠脉均不存在狭窄≥50%的病变）和阻塞组（25例，至少存在1支冠脉狭窄≥50%，且至少存在1支冠脉狭窄<50%），以冠脉血流储备（CFR）<2.90且负荷心肌血流量（SMBF）<2.17 ml·min(-1)·g(-1)为CMVD的判定标准，从血管及患者层面分析两组患者非阻塞性冠脉的CMVD发生情况，并比较两组间发生CMVD的冠脉支配区的静息心肌血流量（RMBF）、SMBF及CFR。 结果： 在血管层面，阻塞组非阻塞性冠脉存在CMVD的比例高于非阻塞组[47.1%（16/34）比25.5%（55/216），χ(2)=6.738，P=0.009]。在患者层面，两组发生CMVD的比例差异无统计学意义[（44%（11/25）比33.3%（24/72），χ(2)=0.915，P=0.339]。两组间发生CMVD的冠脉支配区的RMBF[（0.83±0.14）ml·min(-1)·g(-1)比（0.82±0.17）ml·min(-1)·g(-1)]、SMBF[（2.13±0.60）ml·min(-1)·g(-1)比（1.91±0.50）ml·min(-1)·g(-1)]及CFR（2.59±0.66比2.36±0.47）比较，差异均无统计学意义（P>0.05）。 结论： 非阻塞与阻塞性冠脉疾病患者的非阻塞性冠脉均可存在CMVD，后者的CMVD检出率更高，两者CMVD的严重程度基本一致。.

Quantification of myocardial perfusion with spiral pulse sequences

Background The quest to quantify myocardial perfusion has been largely motivated by the desire to obtain quantitative, observer-independent, and reproducible measures of myocardial perfusion. Spiral pulse sequences have multiple advantages for myocardial perfusion imaging including high acquisition efficiency, high signal to noise (SNR) and robustness to motion. We have developed a spiral pulse sequence with an integrated single-shot arterial input function (AIF) capable of performing absolute quantification of myocardial perfusion.

Quantification of Absolute Myocardial Perfusion in Patients With Coronary Artery Disease: Comparison Between Cardiovascular Magnetic Resonance and Positron Emission Tomography

The aim of this study was to compare fully quantitative cardiovascular magnetic resonance (CMR) and positron emission tomography (PET) myocardial perfusion and myocardial perfusion reserve (MPR) measurements in patients with coronary artery disease (CAD). Absolute quantification of myocardial perfusion and MPR with PET have proven diagnostic and prognostic roles in patients with CAD. Quantitative CMR perfusion imaging has been established more recently and has been validated against PET in normal hearts. However, there are no studies comparing fully quantitative CMR against PET perfusion imaging in patients with CAD. Forty-one patients with known or suspected CAD prospectively underwent quantitative (13)N-ammonia PET and CMR perfusion imaging before coronary angiography. The CMR-derived MPR (MPR(CMR)) correlated well with PET-derived measurements (MPR(PET)) (r = 0.75, p < 0.0001). MPR(CMR) and MPR(PET) for the 2 lowest scoring segments in each coronary territory also correlated strongly (r = 0.79, p < 0.0001). Absolute CMR perfusion values correlated significantly, but weakly, with PET values both at rest (r = 0.32; p = 0.002) and during stress (r = 0.37; p < 0.0001). Area under the receiver-operating characteristic curve for MPR(PET) to detect significant CAD was 0.83 (95% confidence interval: 0.73 to 0.94) and for MPR(CMR) was 0.83 (95% confidence interval: 0.74 to 0.92). An MPR(PET) ≤1.44 predicted significant CAD with 82% sensitivity and 87% specificity, and MPR(CMR) ≤1.45 predicted significant CAD with 82% sensitivity and 81% specificity. There is good correlation between MPR(CMR) and MPR(PET.) For the detection of significant CAD, MPR(PET) and MPR(CMR) seem comparable and very accurate. However, absolute perfusion values from PET and CMR are only weakly correlated; therefore, although quantitative CMR is clinically useful, further refinements are still required.

The diagnostic accuracy of quantitative CMR perfusion imaging may not be the same for all coronary arteries

Background Absolute quantification of myocardial perfusion with cardiac magnetic resonance (CMR) is an emerging technique and its diagnostic accuracy remains to be fully established. Furthermore it is not known whether there are any differences in the accuracy of coronary artery disease (CAD) detection between coronary arteries. Methods 41 patients with known or suspected CAD underwent 1.5T perfusion imaging prior to coronary angiography. Perfusion imaging k-t balanced Turbo Field Echo sequence, shortest TE (range 1.35-1.54ms), shortest TR (range 2.64-3.12ms), 50°flip angle; 90° prepulse, 100ms prepulse delay and typical acquired resolution 1.7x1.9x10mm. 3 short axis slices were acquired every heartbeat. Stress imaging preceded rest by 14±2 minutes. A dual bolus (0.01mmol/kg then 0.1mmol/kg 20 seconds later) of contrast agent was used. Blinded experts performed all data analysis. Mean segmental perfusion values were obtained using dedicated prototype Philips ViewForum software and Fermi deconvolution. Each segment was assigned to a perfusion territory according to standard definitions. Myocardial perfusion reserve (MPR) was defined as stress perfusion divided by rest perfusion. The mean of the 2 lowest MPR for each perfusion territory was used for analysis. X-ray angiography Quantitative coronary angiography (QCA) was performed on all arteries ≥2mm and a mean diameter stenosis ≥70% regarded as significant. The accuracy of MPR to detect significant CAD as defined by QCA was determined by receiver-operating characteristic (ROC) curves. Results

Absolute Quantification of Myocardial Perfusion

Coronary artery disease (CAD) remains the main cause of death in the western world, despite the considerable improvements in its diagnosis and therapy in the past few decades.1 Today, CAD is widely understood to constitute an advanced stage of atherosclerosis,2 that is to say, an inflammatory pathology involving both coronary and extracoronary arteries.3 The diagnosis of CAD is frequently based on morphological observations obtained through invasive coronary angiography (ICA), whereby the presence of at least 1 coronary artery stenosis of at least 50% and a history of myocardial infarction are considered to be diagnostic. It is increasingly appreciated that perfusion imaging brings additional prognostic value compared with morphological imaging alone.4 In particular, perfusion defects can occur at any stage of atherosclerotic disease, from the earliest signs of endothelial dysfunction5,6 to the debut of nonobstructive plaques in coronary arteries,7 and in cases of intermediate or high-grade coronary artery stenoses.8 In those patients with myocardial perfusion abnormalities, individual risk for coronary events increases with the size of perfusion defects, irrespective of the nature of underlying structural or functional changes causing these perfusion defects.9 Thus, myocardial perfusion abnormalities can be understood as the functional consequence of a broad range of present atherosclerotic vessel alterations, bearing considerable significance for the diagnostic and prognostic work-up of CAD. Article see p 678 In daily clinical routine, diagnostic myocardial perfusion is most frequently estimated by single-photon emission CT (SPECT) using 99Tc-labeled radiopharmaceuticals, whereby the tracer uptake in the left ventricular myocardium is analyzed semiquantitatively. Compared with SPECT, PET presents advantages with respect to spatial and temporal resolution, leading to higher sensitivity for the detection of perfusion defects.10 Furthermore, PET perfusion tracers, such as 13N-ammonia or 15O-water, have a higher extraction from the blood …

Cardiac PET/CT for the evaluation of known or suspected coronary artery disease.

Positron emission tomography (PET) is increasingly being applied in the evaluation of myocardial perfusion. Cardiac PET can be performed with an increasing variety of cyclotron- and generator-produced radiotracers. Compared with single photon emission computed tomography, PET offers lower radiation exposure, fewer artifacts, improved spatial resolution, and, most important, improved diagnostic performance. With its capacity to quantify rest-peak stress left ventricular systolic function as well as coronary flow reserve, PET is superior to other methods for the detection of multivessel coronary artery disease and, potentially, for risk stratification. Coronary artery calcium scoring may be included for further risk stratification in patients with normal perfusion imaging findings. Furthermore, PET allows quantification of absolute myocardial perfusion, which also carries substantial prognostic value. Hybrid PET-computed tomography scanners allow functional evaluation of myocardial perfusion combined with anatomic characterization of the epicardial coronary arteries, thereby offering great potential for both diagnosis and management. Additional studies to further validate the prognostic value and cost effectiveness of PET are warranted.

Comparison of intravascular and extracellular contrast media for absolute quantification of myocardial rest‐perfusion using high‐resolution MRI

To use the contrast agent gadofosveset for absolute quantification of myocardial perfusion and compare it with gadobenate dimeglumine (Gd-BOPTA) using a high-resolution generalized autocalibrating partially parallel acquisition (GRAPPA) sequence. Ten healthy volunteers were examined twice at two different dates with a first-pass perfusion examination at rest using prebolus technique. We used a 1.5 T scanner and a 32 channel heart-array coil with a steady-state free precession (SSFP) true fast imaging with steady state precession (trueFISP) GRAPPA sequence (acceleration-factor 3). Manual delineation of the myocardial contours was performed and absolute quantification was performed after baseline and contamination correction. At the first appointment, 1cc/4cc of the extracellular contrast agent Gd-BOPTA were administered, on the second date, 1cc/4cc of the blood pool contrast agent (CA) gadofosveset. At each date the examination was repeated after a 15-minute time interval. Using gadofosveset perfusion the value (in cc/g/min) at rest was 0.66 ± 0.25 (mean ± standard deviation) for the first, and 0.55 ± 0.24 for the second CA application; for Gd-BOPTA it was 0.62 ± 0.25 and 0.45 ± 0.23. No significant difference was found between the acquired perfusion values. The apparent mean residence time in the myocardium was 23 seconds for gadofosveset and 19.5 seconds for Gd-BOPTA. Neither signal-to-noise ratio (SNR) nor subjectively rated image contrast showed a significant difference. The application of gadofosveset for an absolute quantification of myocardial perfusion is possible. Yet the acquired perfusion values show no significant differences to those determined with Gd-BOPTA, maintained the same SNR and comparable perfusion values, and did not picture the expected concentration time-course for an intravasal CA in the first pass.

Abstract 5820: The Clinical Value of Absolute Quantification of Myocardial Perfusion in The Detection of Coronary Artery Disease. A Study Using Positron Emission Tomography to Detect Multi-vessel Disease

Background: Perfusion imaging is standard technique in the detection of CAD. However, the analysis is based on assessment of relative perfusion defects that has known limitations in the detection of multi-vessel disease. Typically only the most severe perfusion abnormalities are detected but not less severe defects or balanced disease. PET measures myocardial perfusion in absolute terms potentially being able to avoid these drawbacks but the value of quantitation has not been shown in clinical studies. Aims: To evaluate the accuracy of absolute quantification of myocardial perfusion in the diagnosis and the detection of multivessel CAD. Patients and methods: 83 consecutive patients with moderate (30–70%) pretest likelihood of CAD were enrolled. PET perfusion imaging at rest and during adenosine stress were performed using O-15-water. The studies were analyzed using validated quantitative model and software. Both standard relative perfusion images and images that were scaled to known absolute scale (0.0–3.5 ml/min/g) were produced. The images were analyzed by two experienced readers blinded to clinical data, image scaling and invasive coronary angiography (ICA). The regions were classified as normal (&gt;70% of uptake), mildly abnormal (50–70%) and severely abnormal (&lt; 50%) in each vascular territory and compared against ICA. Results: The PPV, NPV and accuracy of absolute perfusion in the detection of any CAD were 87%, 97%, 92% respectively. The corresponding values in the detection of multi-vessel disease were 94%, 96% and 95%. When standard relative images were used the respective values for multi-vessel disease were 33%, 69% and 60% against ICA. Relative analysis was able to detect only 39% of patients with multi-vessel disease. In addition, regional perfusion was often (31%) falsely interpreted as multi-vessel disease while preserved absolute perfusion was able to exclude significant stenoses. Conclusions: The measurement of myocardial perfusion in absolute terms has significant impact on the interpretation of myocardial perfusion. Standard relative analysis is able to detect only small fraction of patients with multi-vessel disease and also quite commonly variability in perfusion is falsely interpreted as a sign of multi-vessel disease.

New Technology for Noninvasive Evaluation of Coronary Artery Disease

Cardiac computed tomography (CT) and positron emission tomography (PET) are emerging as powerful noninvasive imaging tools for the evaluation of atherosclerosis in patients with known or suspected coronary artery disease (CAD). Unlike invasive coronary angiography, CT coronary angiography (CTA) not only assesses disease within the coronary lumen but can also provide direct qualitative and quantitative information about nonobstructive atherosclerotic plaque burden within the vessel wall. Thus, it is possible that CTA-based patient evaluation may provide more clinically relevant information on which to base risk assessments compared with conventional “lumenography.” On the other hand, PET is rapidly growing as a powerful and efficient alternative to conventional single-photon emission CT (SPECT) imaging to evaluate regional myocardial perfusion and metabolism in patients with CAD. In addition, PET scanners are now being converted to hybrid PET/CT devices, which, in the setting of CAD, offer the potential for a comprehensive noninvasive cardiac evaluation of anatomy and function. This review will discuss current and potential future applications of cardiovascular CT, PET, and hybrid PET/CT, with a particular focus on ischemic heart disease. The information provided by noninvasive imaging generally falls into 1 of 3 categories: myocardial perfusion, left ventricular (LV) function, or coronary artery anatomy. The clinical utility, value, and role of a noninvasive modality are based on 2 test characteristics: What type of information is provided (eg, stress perfusion, stress and/or rest LV function, coronary anatomy), and what is the accuracy of the information provided. For example, SPECT and PET both provide stress and rest perfusion information, but the latter will be a superior clinical tool if the imaging data better represent the actual defect size and are subject to less artifact. The advantage of PET over SPECT will be further enhanced, as will be discussed later, if it provides additional clinically relevant information not …

The quantification of absolute myocardial perfusion in humans by contrast echocardiography: Algorithm and validation

We sought to test whether myocardial blood flow (MBF) can be quantified by myocardial contrast echocardiography (MCE) using a volumetric model of ultrasound contrast agent (UCA) kinetics for the description of refill curves after ultrasound-induced microsphere destruction. Absolute myocardial perfusion or MBF (ml.min(-1).g(-1)) is the gold standard to assess myocardial blood supply, and so far it could not be obtained by ultrasound. The volumetric model yielded MBF = rBV.beta/rho(T), where rho(T) equals tissue density. The relative myocardial blood volume rBV and its exchange frequency beta were derived from UCA refill sequences. Healthy volunteers underwent MCE and positron emission tomography (PET) at rest (group I: n = 15; group II: n = 5) and during adenosine-induced hyperemia (group II). Fifteen patients with coronary artery disease underwent simultaneous MCE and intracoronary Doppler measurements before and during intracoronary adenosine injection. In vitro experiments confirmed the volumetric model and the reliable determination of rBV and beta for physiologic flow velocities. In group I, 187 of 240 segments were analyzable by MCE, and a linear relation was found between MCE and PET perfusion data (y = 0.899x + 0.079; r(2) = 0.88). In group II, resting and hyperemic perfusion data showed good agreement between MCE and PET (y = 1.011x + 0.124; r(2) = 0.92). In patients, coronary stenosis varied between 0% to 89%, and myocardial perfusion reserve was in good agreement with coronary flow velocity reserve (y = 0.92x + 0.14; r(2) = 0.73). The volumetric model of UCA kinetics allows the quantification of MBF in humans using MCE and provides the basis for the noninvasive and quantitative assessment of coronary artery disease.

1036-157 Quantification of absolute myocardial perfusion by contrast echocardiography: Algorithm, in vitro and in vivo validation

1036-157 Quantification of absolute myocardial perfusion by contrast echocardiography: Algorithm, in vitro and in vivo validation

P600 Absolute quantification of myocardial perfusion using real-time myocardial contrast echocardiography: an in vitro study and first in vivo results

P600 Absolute quantification of myocardial perfusion using real-time myocardial contrast echocardiography: an in vitro study and first in vivo results

Quantification of absolute myocardial perfusion at rest and during exercise with positron emission tomography after human cardiac transplantation

The maximal exercise capacity of cardiac transplant recipients is reduced compared with that of normal subjects. To determine if this reduced exercise capacity is related to inadequate myocardial perfusion during exercise, myocardial perfusion was measured noninvasively with use of positron emission tomography and nitrogen (N)-13 ammonia. Twelve transplant recipients with no angiographic evidence of accelerated coronary atherosclerosis were studied. Serial N-13 ammonia imaging was performed at rest and during supine bicycle exercise. The results were compared with those from 10 normal volunteers with a low probability of having cardiac disease. A two-compartment kinetic model for estimating myocardial perfusion was applied to the data.Transplant recipients achieved a significantly lower exercise work load than did the volunteers (42 ± 16 vs. 128 ± 22 W), but a higher venous lactate concentration (31.3 ± 14.9 vs. 13.7 ±4.1 mg/100 ml). Despite the difference in exercise work load, there was no significant difference in the cardiac work achieved by transplant recipients and normal subjects as evidenced by similar rate-pressure products of 24,000 ± 3,400 versus 21,300 ±2,800 beats/min per mm Hg, respectively. In addition, myocardial blood flow during exercise was not significantly different between the two groups (1.70 ± 0.60 vs. 1.56 ± 0.71 ml/min per g, respectively).This study demonstrates that the myocardial flow response to the physiologic stress of exercise is appropriate in transplant recipients and does not appear to explain the decreased exercise capacity in these patients.

13N ammonia myocardial imaging at rest and with exercise in normal volunteers. Quantification of absolute myocardial perfusion with dynamic positron emission tomography.

Positron emission tomography (PET) was applied to the measurement of myocardial perfusion using the perfusion tracer 13N-labeled ammonia. 13N ammonia was delivered intravenously to 13 healthy volunteers both at rest and during supine bicycle exercise. Dynamic PET imaging was obtained in three cross-sectional planes for 10 minutes commencing with each injection. The left ventricle was divided into eight sectors, and a small region of interest was assigned to the left ventricular blood pool to obtain the arterial input function. The net extraction of 13N ammonia was obtained for each sector by dividing the tissue 13N concentration at 10 minutes by the integral of the input function from the time of injection to 10 minutes. With this approach for calculating net extractions, rest and exercise net extractions were not significantly different from each other. To obviate possible overestimation of the true 13N ammonia input function by contamination by 13N-labeled compounds other than 13N ammonia or by spillover from myocardium into blood pool, the net extractions were calculated using only the first 90 seconds of the blood and tissue time-activity curves. This approach for calculating net extractions yielded significant differences between rest and exercise, with an average ratio of exercise to rest of 1.38 +/- 0.34. Nonetheless, the increase was less than predicted from the average 2.7-2.8-fold increase in double product at peak exercise or the 1.7-fold increase in double product at 1 minute after exercise. However, when the first 90 seconds of dynamic data were fit with a two compartment tracer kinetic model, average perfusion rates of 0.75 +/- 0.43 ml/min/g at rest and 1.50 +/- 0.74 ml/min/g with exercise were obtained. This average increase in perfusion of 2.2-fold corresponded to similar average increases in double product. Thus, the noninvasive technique of PET imaging with 13N ammonia shows promise for future applications in determining absolute flows in patients with coronary artery disease.

The dependence of accumulation of 13NH3 by myocardium on metabolic factors and its implications for quantitative assessment of perfusion.

HomeCirculationVol. 61, No. 1The dependence of accumulation of 13NH3 by myocardium on metabolic factors and its implications for quantitative assessment of perfusion. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBThe dependence of accumulation of 13NH3 by myocardium on metabolic factors and its implications for quantitative assessment of perfusion. S R Bergmann, S Hack, T Tewson, M J Welch, and B E Sobel S R BergmannS R Bergmann Search for more papers by this author , S HackS Hack Search for more papers by this author , T TewsonT Tewson Search for more papers by this author , M J WelchM J Welch Search for more papers by this author , and B E SobelB E Sobel Search for more papers by this author Originally published1 Jan 1980https://doi.org/10.1161/01.CIR.61.1.34Circulation. 1980;61:34–43 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByBol A, Melin J, Vanoverschelde J, Baudhuin T, Vogelaers D, De Pauw M, Michel C, Luxen A, Labar D and Cogneau M (1993) Direct comparison of [13N]ammonia and [15O]water estimates of perfusion with quantification of regional myocardial blood flow by microspheres., Circulation, 87:2, (512-525), Online publication date: 1-Feb-1993.Vanoverschelde J, Melin J, Bol A, Vanbutsele R, Cogneau M, Labar D, Robert A, Michel C and Wijns W (1992) Regional oxidative metabolism in patients after recovery from reperfused anterior myocardial infarction. Relation to regional blood flow and glucose uptake., Circulation, 85:1, (9-21), Online publication date: 1-Jan-1992.Araujo L, Lammertsma A, Rhodes C, McFalls E, Iida H, Rechavia E, Galassi A, De Silva R, Jones T and Maseri A (1991) Noninvasive quantification of regional myocardial blood flow in coronary artery disease with oxygen-15-labeled carbon dioxide inhalation and positron emission tomography., Circulation, 83:3, (875-885), Online publication date: 1-Mar-1991.Bonow R, Berman D, Gibbons R, Johnson L, Rumberger J, Schwaiger M and Wackers F (1991) Cardiac positron emission tomography. A report for health professionals from the Committee on Advanced Cardiac Imaging and Technology of the Council on Clinical Cardiology, American Heart Association., Circulation, 84:1, (447-454), Online publication date: 1-Jul-1991.Shelton M, Green M, Mathias C, Welch M and Bergmann S (1990) Assessment of regional myocardial and renal blood flow with copper-PTSM and positron emission tomography., Circulation, 82:3, (990-997), Online publication date: 1-Sep-1990.Krivokapich J, Smith G, Huang S, Hoffman E, Ratib O, Phelps M and Schelbert H (1989) 13N ammonia myocardial imaging at rest and with exercise in normal volunteers. Quantification of absolute myocardial perfusion with dynamic positron emission tomography., Circulation, 80:5, (1328-1337), Online publication date: 1-Nov-1989.Walsh M, Bergmann S, Steele R, Kenzora J, Ter-Pogossian M, Sobel B and Geltman E (1988) Delineation of impaired regional myocardial perfusion by positron emission tomography with H2(15)O., Circulation, 78:3, (612-620), Online publication date: 1-Sep-1988.Marcus M, Wilson R and White C (1987) Methods of measurement of myocardial blood flow in patients: a critical review., Circulation, 76:2, (245-253), Online publication date: 1-Aug-1987.Krivokapich J, Keen R, Phelps M, Shine K and Barrio J (1987) Effects of anoxia on kinetics of [13N] glutamate and 13NH3 metabolism in rabbit myocardium., Circulation Research, 60:4, (505-516), Online publication date: 1-Apr-1987.Knabb R, Fox K, Sobel B and Bergmann S (1985) Characterization of the functional significance of subcritical coronary stenoses with H(2)15O and positron-emission tomography., Circulation, 71:6, (1271-1278), Online publication date: 1-Jun-1985.Perloff J, Henze E and Schelbert H (1984) Alterations in regional myocardial metabolism, perfusion, and wall motion in Duchenne muscular dystrophy studied by radionuclide imaging., Circulation, 69:1, (33-42), Online publication date: 1-Jan-1984.Schelbert H, Phelps M, Huang S, MacDonald N, Hansen H, Selin C and Kuhl D (1981) N-13 ammonia as an indicator of myocardial blood flow., Circulation, 63:6, (1259-1272), Online publication date: 1-Jun-1981. January 1, 1980Vol 61, Issue 1Article InformationMetrics Download: 58 Copyright © 1980 by American Heart Associationhttps://doi.org/10.1161/01.CIR.61.1.34 Originally publishedJanuary 1, 1980 PDF download