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Published online before print April 3, 2003, 10.1148/radiol.2272020366
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(Radiology 2003;227:447-452.)
© RSNA, 2003

Cardiac Imaging

Analysis of Cardiopulmonary Transit Times at Contrast Material–enhanced MR Imaging in Patients with Heart Disease1

Christopher J. François, MD, Stephanie M. Shors, MD, Robert O. Bonow, MD and J. Paul Finn, MD

1 From the Department of Radiology (C.J.F., S.M.S., J.P.F.) and Division of Cardiology (R.O.B.), Northwestern University Medical School, Chicago, Ill. Received April 5, 2002; revision requested June 14; final revision received October 11; accepted October 14. Address correspondence to J.P.F., Department of Radiological Sciences, UCLA Medical Center, 10833 LeConte Ave, Los Angeles, CA 90095-1721 (e-mail: pfinn@mednet.ucla.edu).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To build a database of arm-to-aorta circulation times for contrast enhancement and to determine if measured transit times can help in discrimination between patients with and patients without heart disease.

MATERIALS AND METHODS: Findings at test-bolus examinations performed before acquisition of contrast material–enhanced magnetic resonance (MR) angiographic images of the head and neck were retrospectively reviewed. The times from test-bolus injection to first and peak enhancement in regions of interest were recorded in 77 patients with coronary artery disease, left ventricular hypertrophy, and/or impaired left ventricular function and 33 control subjects. Transit times in patients and control subjects were compared with Student t test. Linear regression was performed to measure the correlation coefficient.

RESULTS: Transit times in patients with heart disease, including those with a normal ejection fraction, were significantly prolonged compared with those in control subjects (P < .05). Mean time to peak enhancement in the carotid artery bifurcation was 16.6 seconds ± 1.9 (SD) and 20.8 seconds ± 3.9 in control subjects and patients, respectively. Threshold value of 18 seconds for time to peak signal intensity in the carotid artery bifurcation provided highest combination of sensitivity and specificity. All (11 of 11) patients with an ejection fraction less than 40% and only three (9%) of 33 control subjects had circulation times greater than this threshold. No significant correlation was found between transit times and age, sex, weight, and height.

CONCLUSION: Transit times measured with MR imaging may help in discrimination between patients with and patients without heart disease, independently of other cardiac functional parameters.

© RSNA, 2003

Index terms: Heart, diseases, 51.72, 51.76, 51.78 • Magnetic resonance (MR), contrast enhancement, 51.12142, 51.12143 • Magnetic resonance (MR), vascular studies, 51.12142 • Pulmonary arteries, MR, 944.12942, 944.12943


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Magnetic resonance (MR) imaging provides a convenient and potentially accurate tool for noninvasive measurement of cardiac function. MR imaging yields a combination of spatial, temporal, and contrast resolution superior to that of other imaging methods. Measurements of ventricular mass, ejection fraction (EF), cardiac output, myocardial thickening, and indices of cardiac filling and ejection are reproducibly performed with MR imaging (1). With the increasing use of contrast material–enhanced MR angiography and computed tomographic (CT) angiography, it has become commonplace to use a test bolus of contrast material to measure transit time to a target artery prior to image acquisition (2–7). Other approaches in use with MR angiography and CT angiography include real-time bolus detection (8–10) and automated bolus detection (11–13). Contrast material injection protocols with test doses and three-dimensional MR angiographic sequences are precisely controlled with electronic power injectors, and this control facilitates standardization and reproducibility of measurements (6,7). Similar timing considerations apply to contrast-enhanced MR angiography and CT angiography (14,15), but timing injections for CT angiography require larger contrast material doses, as well as an additional radiation burden (15). Not uncommonly, no timing or bolus-detection schemes are used, and the transit time is simply estimated (14). In situations where timing measurements are not performed, it would be convenient to have a database from which to predict the likely transit time in a patient group.

More interestingly, circulation times potentially contain important information about the interplay between cardiac function, pulmonary vascular impedance, and blood volume (16–19). Although findings in previous studies with contrast-enhanced MR angiography indicated that transit time is highly variable from patient to patient (2–7), few researchers have specifically examined the relationship between circulatory transit times and cardiovascular status.

Circulation times calculated by using conventional angiography (17), nuclear angiocardiography (18–20), digital angiography (21), and noninvasive indicator-dilution methods (22) have been used to measure cardiac output, to detect intracardiac shunts, and to evaluate left ventricular disease. We hypothesized that patients with a history of cardiac disease would have longer transit times than would control subjects and that patients with more severe heart failure would have the longest transit times. The implication is that circulation time, easily measured with MR imaging, may provide an additional, independent index of cardiocirculatory status in patients with heart disease. Thus, the purpose of our study was to build a database of arm-to-aorta transit times across a spectrum of patient groups for a priori estimates with MR angiography and CT angiography and to analyze transit times in patients with and patients without heart disease.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Bolus-timing examinations were performed in patients who underwent contrast-enhanced MR angiography of the head and neck for clinically accepted indications during a 6-month period. Findings at these examinations were retrospectively analyzed after protocol approval by the university institutional review board. Informed consent was not required.

Patient Selection
Data from 167 bolus-timing examinations were reviewed by an author (C.J.F.) blindly, independently, and prior to review of the clinical records. The medical records of the subjects were analyzed by the same author for a history of coronary artery disease (CAD), left ventricular (LV) hypertrophy, or impaired LV function. It was noted if patients with these abnormalities had coexisting hypertension, peripheral vascular disease, chronic obstructive pulmonary disease, or diabetes mellitus. Subjects were considered to have a history of CAD if they had 70% or greater narrowing in one or more major epicardial coronary arteries as seen at coronary angiography, a history of myocardial infarction documented by using electrocardiography or cardiac enzyme levels, or a history of coronary revascularization. Estimates of EF and LV hypertrophy were obtained with echocardiographic or nuclear angiocardiographic reports; patients with an abnormal early-to-late diastolic filling ratio (23) were considered to have diastolic dysfunction. Seventy-seven patients (Table 1) who had a history of CAD (n = 47), LV hypertrophy (n = 49), diastolic dysfunction (n = 38), or an EF of less than 50% (n = 22) and 33 control subjects who were referred for contrast-enhanced MR angiography of the head and neck and had no history of cardiovascular, cerebrovascular, or peripheral vascular disease were included in the analysis. Sixty-six percent (31 of 47) of the patients with CAD, 71% (35 of 49) of the patients with LV hypertrophy, and 79% (30 of 38) of the patients with diastolic dysfunction had a normal EF. Of the 22 patients with an EF of less than 50%, 12 (55%) had an EF of less than 40%.


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  		TABLE 1. Characteristics of Groups among 77 Patients

 
Timing Examinations
All examinations were performed by using a 1.5-T MR system (Magnetom Symphony or Sonata; Siemens Medical Solutions, Iselin, NJ). A 2-mL bolus of gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) and a 20-mL flush of normal saline were administered with an electronic power injector (Spectris; Medrad, Indianola, Pa) into an antecubital vein at a rate of 2 mL/sec. Coronal single-shot turbo fast low-angle shot images, which included the heart, aortic arch, carotid artery bifurcation, and internal jugular vein were acquired at 1-second intervals for 40–60 seconds following injection of contrast agent and saline flush. Image acquisition and contrast material infusion were started simultaneously. Heart rates were not recorded during timing examinations.

The times to first appearance of enhancement and to peak enhancement in the pulmonary artery, ascending aorta, carotid artery bifurcation, and internal jugular vein were recorded in each patient by the same author who reviewed data and medical records by using interactive region-of-interest selection. The size of the region of interest was 50% of the structure being analyzed. An increase of 20% in signal intensity compared with mean baseline signal intensity was used to determine the first appearance of contrast medium.

Statistical Analysis
The correlation between transit times and patient age, height, sex, weight, body mass index, and body surface area was evaluated by using Pearson correlation coefficients. Because circulation time is inversely related to cardiac output, we analyzed the correlation between (1/transit time) and echocardiographically estimated EF. Average transit times in all patients and in each patient subgroup were compared with those in the control group and with each other by using the Student t test. To select a threshold value to distinguish between normal and abnormal transit times, receiver operator characteristic curves (24) were generated by plotting sensitivity versus (1 - specificity).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Control subjects were younger (mean age, 43.2 years ± 15.1 [SD] vs 67.6 years ± 13.1), shorter (mean height, 167.0 cm ± 8.8 vs 169.7 cm ± 10.8), and weighed less (mean weight, 75.2 kg ± 16.1 vs 80.0 kg ± 17.1) than patients with disease. While 56% (43 of 77) of patients were men, only 31% (10 of 33) of control subjects were men. The mean bolus arrival times for all subjects were 15.8 seconds ± 3.3 and 24.8 seconds ± 4.6 at the carotid artery bifurcation and internal jugular vein, respectively, and the mean peak intensity times were 19.6 seconds ± 4.0 and 29.2 seconds ± 5.0 at the carotid artery bifurcation and internal jugular vein, respectively. The mean time from first appearance of contrast medium in the pulmonary artery to first appearance in the aorta was 4.9 seconds ± 1.0 in control subjects and 6.1 seconds ± 2.1 (P < .001) in patients. The mean time from peak signal intensity in the pulmonary artery to peak signal intensity in the aorta was 6.0 seconds ± 1.4 in control subjects and 7.5 seconds ± 2.4 (P < .001) in patients. No significant correlation was seen between patient age, sex, height, weight, body mass index, body surface area, or EF (Fig 1) and transit times at any level.



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  		Figure 1. Graph shows a weak correlation between 1/(time to peak signal intensity in the carotid artery bifurcation) and EF (P < .001).

 
Transit times were significantly prolonged (P < .05) for all noncontrol patients at each area of interest (Table 2, Fig 2). The longest transit times were observed in patients with an EF of less than 50%. Even though many of the patients with CAD or LV hypertrophy had an EF of less than 50% (Table 1), the difference in mean transit times between control subjects and patients with CAD or LV hypertrophy was still significant (P < .05) even if they had a normal EF (Table 3). Normalized distribution curves (Fig 3) suggest that patients and control subjects form two distinct populations on the basis of transit times. These curves also illustrated that transit times in patients with an EF of greater than 50% and CAD or LV hypertrophy were greater than they were in control subjects.


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  		TABLE 2. Mean Transit Times in Control Subjects and Patients

 


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  		Figure 2. Graphs show distribution of transit times in the carotid artery bifurcation. Between control subjects and patients, there is overlap in times; however, the mean transit times are significantly greater in patients than they are in control subjects (P < .001). A, Time to first appearance. B, Time to peak signal intensity.

 

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  		TABLE 3. Mean Transit Times in Patients with EF Greater than 50% and CAD or LV Hypertrophy

 


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  		Figure 3. Normalized distribution curves of times to peak signal intensity in the carotid artery bifurcation in control subjects and in patients with an EF of less than 50% versus EF greater than 50%. A, Patients with CAD. B, Patients with LV hypertrophy (LVH). Patients with an EF of less than 50% have the longest transit times; however, even patients with an EF of greater than 50% and CAD or LV hypertrophy have, on average, a transit time significantly (P < .05) prolonged compared with that of control subjects.

 
When we compared transit times in patients with diastolic dysfunction and an EF of greater than 50% to transit times in patients with an EF of less than 40%, we found that the difference in transit times from antecubital vein to pulmonary artery was not significant (P = .23 and .11 for first appearance and peak signal intensity, respectively) (Fig 4). However, there was a significant difference in transit times between these groups when the transit time was measured at the ascending aorta, carotid artery bifurcation, or internal jugular vein (Table 2, Fig 4).



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  		Figure 4. Graphs show time to peak signal intensity in patients with diastolic and systolic dysfunction. A, Transit time in the pulmonary artery. B, Transit time in the carotid artery bifurcation. There was no statistically significant difference in mean peak transit times to the pulmonary artery between patients with diastolic or systolic dysfunction. However, the difference in mean peak transit times to the carotid artery bifurcation was significant.

 
By plotting sensitivity against specificity, we were able to select threshold values that maximized the accuracy of the circulation time to distinguish between normal and abnormal (Fig 5). For time to peak signal intensity in the carotid artery bifurcation, a threshold circulation time of 18 seconds provided a specificity of 90.4% and a sensitivity of 75.0%, 84.8%, 85.7%, and 100% for patients with LV hypertrophy, CAD, an EF of less than 50%, and an EF of less than 40%, respectively.



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  		Figure 5. ROC curves with transit times measured at various regions in the circulation. A, Time to first appearance. B, Peak signal intensity transit time. Dashed line = test of no discriminative ability, AO = ascending aorta, CA = carotid artery bifurcation, FPR = false-positive rate, IJ = internal jugular vein, PA = pulmonary artery, TPR = true-positive rate.

 
Data were available in two patients with regard to findings at test-bolus examinations performed on two separate occasions. Patient 1 was a 68-year-old man with CAD, LV hypertrophy, and an estimated EF of 30% who underwent the examinations with an interval of 2 months between them. The time to peak signal intensity in the carotid artery bifurcation was 23 seconds on both occasions. Patient 2 was a 56-year-old man with hypertension and an estimated EF of 55% who the underwent examinations with an interval of 1 month between them. The time to peak signal intensity in the carotid artery bifurcation was 16 seconds on both occasions.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The results of this study clearly show that the presence of ischemic and hypertensive heart disease is associated with a measurable prolongation in transit time, which is easily estimated by using a test bolus of gadolinium-based contrast material. Mean first appearance and peak intensity times at the carotid artery bifurcation in control subjects were 13.1 seconds ± 1.5 and 16.6 seconds ± 1.9, respectively, and 16.9 seconds ± 3.2 and 20.8 seconds ± 3.9, respectively, in patients with heart disease. As in previous studies (2–7), we observed a wide range of transit times: 10–27 seconds for first appearance and 12–33 seconds for peak intensity at the carotid artery bifurcation.

The wide variability in transit times supports the need to accurately time image acquisition during the time of maximal arterial enhancement. Although performance of a test-bolus examination prior to performance of contrast-enhanced MR imaging is simple and routine, a test-bolus examination with CT angiography (15) has the disadvantages of added radiation burden and contrast material load (timing injections for CT angiography typically require at least 15 mL of contrast material). The data from the current study provide a reference that could be used to estimate the bolus arrival time at the carotid artery bifurcation in patients with and patients without cardiac disease, and this reference is applicable to both MR angiography and CT angiography. For example, if a patient had a history of CAD, LV hypertrophy, or a low EF, one could expect the time to peak signal intensity in the carotid artery bifurcation to be 20.8 seconds, whereas in patients without these conditions the time to peak signal intensity would be only 16.6 seconds.

Although differences in cardiovascular function are cited as reasons for performance of a test-bolus examination prior to MR angiography, to our knowledge, findings of this study are the first to indicate a significant difference in transit times between patients with and patients without established cardiac disease. The mean times from bolus injection to first appearance and peak signal intensity in the carotid artery bifurcation are within 1 SD of the values previously reported in the literature (2,4,9,10). In the only study (2) of which we are aware in which the researchers attempted to distinguish between patients with and patients without cardiopulmonary disease, no statistically significant difference in carotid artery bifurcation transit times was observed between patients and control subjects.

Our findings of a delayed transit time in patients with cardiovascular disease are consistent with results of prior studies in nuclear cardiography (18–20). In a study of cardiopulmonary transit times in 10 healthy subjects, Jones et al (18) found that the first appearance of radionuclide in the ascending aorta occurred 5.6 seconds after the first appearance of it in the pulmonary artery. This is slightly longer than, but within 1 SD of, our observation of a mean time of 4.9 seconds ± 1.0 from the time of first appearance in the pulmonary artery to first appearance in the ascending aorta.

Many physiologic variables affect the circulation of an indicator through the vascular system, including its volume of distribution and blood flow (25). For inert hydrophilic extracellular tracers such as gadopentetate dimeglumine, the volume of distribution at the first pass is the total plasma volume that the tracer passes through from the site of injection to the site of detection; to determine the volume of distribution, one must ignore a small effect due to first-pass lung extraction into the interstitial fluid space. Because of the relatively high spatial and temporal resolution possible with MR imaging, estimates of pulmonary blood volume should be derivable from cardiac output and pulmonary arteriovenous transit time (18).

The scatter in the transit time-EF plot observed in the current study may reflect differences in cardiopulmonary blood volume and cardiac output at the time of the study. Although in the current study we did not address treatment protocols among patient groups, varying levels of response to intercurrent diuretic, antihypertensive, or cardiac failure therapy may have contributed to the spread of transit times. We were not able to address these potentially confounding issues in the current study, and the influence of treatment on cardiopulmonary transit times in patients with cardiac impairment remains to be evaluated with MR imaging.

The delayed circulation times in patients with diastolic dysfunction suggest that a significant amount of the delay in patients with CAD or LV hypertrophy could be due to inadequate diastolic filling. Patients with LV hypertrophy or chronic CAD have left ventricles that function with conditions of increased end-diastolic pressure and decreased end-diastolic volume (26,27). These compliance changes often occur prior to deterioration in systolic EF and effectively add to cardiopulmonary impedance. No significant difference between patients with systolic dysfunction and diastolic dysfunction was observed in circulation times measured to the pulmonary artery, whereas a significant difference was observed when circulation times to the aorta, carotid artery bifurcation, and internal jugular vein were measured.

Although we have data from only two patients that address the reproducibility of the test measurements over time, the results suggest that MR angiographic transit time is reproducible. With the threshold values we derived on the basis of receiver operating characteristic curve analysis, we were able to obtain very high specificity while the sensitivity was variable. It is possible that if we had been able to control for confounding factors such as blood volume, heart rate, and medical therapy, we may have observed more consistent transit times in our patient population, which would have increased the measured sensitivity.

This study had several limitations. We did not record heart rate at the time of the bolus-timing examinations. However, Hany et al (3) found no correlation between heart rate and abdominal aorta transit time. The major independent determinants of transit time are cardiac output and cardiopulmonary blood volume. Heart rate is relevant, therefore, only insofar as it is associated with changes in cardiac output. Another limitation of our case-control study was that the control group was not age-, sex-, or weight-matched with the patient group with disease. Subjects in the control group were younger, weighed less, and tended to be women. However, it is not clear that matching the control group to the patient group would have had any effect on the results. Findings in our study and in previous studies (2,3) showed no significant correlation between age, sex, or weight and transit time. Furthermore, our control group consisted of subjects referred for contrast-enhanced MR angiography of the head and neck. Although review of their medical records and radiographic files did not reveal any history or presence of vascular disease, it is possible that healthy subjects would have even shorter transit times.

In the current study, we did not measure mean transit times, which would benefit from deconvolution (28,29) or singular value decomposition (29,30) of the input function of the right side of the heart. Although we only reported time to first appearance and time to peak signal intensity, it has been previously established (21) that peak-to-peak transit times are closely correlated to mean transit times. We made no attempt to derive cardiopulmonary impulse response curves in our study. However, when combined with the anatomic precision possible with MR imaging, such an analysis may provide unique information about the pulmonary microcirculation in disease. This is the subject of ongoing study in our laboratory.

In conclusion, findings of this case-control study indicated that although the longest transit times were observed in patients with poor systolic function, prolonged transit times were observed in patients with LV hypertrophy or CAD and a normal EF. Transit time measured by using a bolus of contrast material at MR angiography has potential as a simple and reproducible index of underlying cardiovascular status, independent of other measures of cardiac function.


   FOOTNOTES
 
Abbreviations: CAD = coronary artery disease, EF = ejection fraction, LV = left ventricular

Author contributions: Guarantor of integrity of entire study, J.P.F.; study concepts, all authors; study design, C.J.F., J.P.F.; literature research, C.J.F., S.M.S.; clinical studies, C.J.F.; data acquisition, C.J.F.; data analysis/interpretation, C.J.F., J.P.F.; statistical analysis, C.J.F.; manuscript preparation and definition of intellectual content, C.J.F., J.P.F.; manuscript editing, R.O.B., J.P.F.; manuscript revision/review and final version approval, all authors.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. van der Geest RJ, Reiber JHC. Quantification in cardiac MRI. J Magn Reson Imaging 1999; 10:602-608.[CrossRef][Medline]
  2. Krinsky G, Kaminer E, Lee VS, Rofsky NM, Weinreb JC. The effects of apnea on timing examinations for optimization of gadolinium-enhanced MRA of the thoracic aorta and arch vessels. J Comput Assist Tomogr 1998; 22:677-681.[CrossRef][Medline]
  3. Hany TF, McKinnon GC, Leung DA, Pfammatter T, Debatin JF. Optimization of contrast timing for breath-hold three-dimensional MR angiography. J Magn Reson Imaging 1997; 7:551-556.[Medline]
  4. Kim JK, Farb RI, Wright GA. Test bolus examination in the carotid artery at dynamic gadolinium-enhanced MR angiography. Radiology 1998; 206:283-289.[Abstract/Free Full Text]
  5. Levy RA, Prince MR. Arterial-phase three-dimensional contrast-enhanced MR angiography of the carotid arteries. AJR Am J Roentgenol 1996; 167:211-215.[Abstract/Free Full Text]
  6. Earls JP, Rofsky NM, DeCorato DR, Krinsky GA, Weinreb JC. Breath-hold single-dose gadolinium-enhanced three-dimensional MR aortography: usefulness of a timing examination and MR power injector. Radiology 1996; 201:705-710.[Abstract/Free Full Text]
  7. Earls JP, Rofsky NM, DeCorato DR, Krinsky GA, Weinreb JC. Hepatic arterial-phase dynamic gadolinium-enhanced MR imaging: optimization with a test examination and a power injector. Radiology 1997; 202:268-273.[Abstract/Free Full Text]
  8. Wilman AH, Riederer SJ, King BF, Debbins JP, Rossman PJ, Ehman RL. Fluoroscopically triggered contrast-enhanced three-dimensional MR angiography with elliptical centric view order: application to the renal arteries. Radiology 1997; 205:137-146.[Abstract/Free Full Text]
  9. Huston J, Fain SB, Reiderer SJ, Wilman AH, Bernstein MA, Busse RF. Carotid arteries: maximizing arterial to venous contrast in fluoroscopically triggered contrast-enhanced MR angiography with elliptic centric view ordering. Radiology 1999; 211:265-273.[Abstract/Free Full Text]
  10. Riederer SJ, Bernstein MA, Breen JF, et al. Three-dimensional contrast-enhanced MR angiography with real-time fluoroscopic triggering: design specifications and technical reliability in 330 patient studies. Radiology 2000; 215:584-593.[Abstract/Free Full Text]
  11. Prince MR, Chenevert TL, Foo TKF, Londy FJ, Ward JS, Maki JH. Contrast-enhanced abdominal MR angiography: optimization of imaging delay time by automating the detection of contrast material arrival in the aorta. Radiology 1997; 203:109-114.[Abstract/Free Full Text]
  12. Foo TKF, Saranathan M, Prince MR, Chenevert TL. Automated detection of bolus arrival and initiation of data acquisition in fast, three-dimensional, gadolinium-enhanced MR angiography. Radiology 1997; 203:275-280.[Abstract/Free Full Text]
  13. Ho VB, Foo TKF. Optimization of gadolinium-enhanced magnetic resonance angiography using an automated bolus-detection algorithm (MR SmartPrep). Invest Radiol 1998; 9:512-523.
  14. Rubin GD, Dake MD, Napel SA, McDonnell CH, Jeffrey RB. Three-dimensional spiral CT angiography of the abdomen: initial clinical experience. Radiology 1993; 186:147-152.[Abstract/Free Full Text]
  15. Fleischmann D, Rubin GD, Bankier AA, Hittmair K. Improved uniformity of aortic enhancement with customized contrast medium injection protocols at CT angiography. Radiology 2000; 214:363-371.[Abstract/Free Full Text]
  16. Selzer A, Dunlap RW, Wray HW, Russell J. A critical appraisal of the circulation time test. Arch Intern Med 1968; 122:491-495.[CrossRef][Medline]
  17. Ganz W, Swan HJ. Measurement of blood flow by thermodilution. Am J Cardiol 1972; 29:241-246.[CrossRef][Medline]
  18. Jones RH, Sabiston DC, Bates BB, Morris JJ, Anderson PA, Goodrich JK. Quantitative radionuclide angiocardiography for determination of chamber to chamber cardiac transit times. Am J Cardiol 1972; 30:855-864.[CrossRef][Medline]
  19. Leitl GP, Buchanan JW, Wagner HN. Monitoring cardiac function with nuclear techniques. Am J Cardiol 1980; 46:1125-1132.[CrossRef][Medline]
  20. Slutsky RA. Pulmonary blood volume: the response to afterload in normal subjects and patients with previous myocardial infarction. Invest Radiol 1982; 17:241-248.[CrossRef][Medline]
  21. Slutsky RA, Carey PH, Bhargava V, Higgins CB. A comparison of peak-to-peak pulmonary transit time determined by digital intravenous angiography with standard dye-dilution techniques in anesthetized dogs. Invest Radiol 1982; 17:362-366.[Medline]
  22. Kasravi B, Boehmer JP, Leuenberger UA. A non-invasive method for estimating cardiac output using lung to finger circulation time of oxygen. Am J Cardiol 1998; 82:915-917.[CrossRef][Medline]
  23. Little WC, Braunwald E. Assessment of cardiac function. In: Braunwald E, eds. Heart disease: a textbook of cardiovascular medicine. 6th ed. Philadelphia, Pa: Saunders, 2001; 496-497.
  24. Metz CE. Basic principles of ROC analysis. Semin Nucl Med 1978; 8:283-298.[Medline]
  25. Peters AM. Fundamentals of tracer kinetics for radiologists. Br J Radiol 1998; 71:1116-1129.[Abstract]
  26. Lorell BH, Carabello BA. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation 2000; 102:470-479.[Free Full Text]
  27. Gersh BJ, Braunwald E, Bonow RO. Chronic coronary artery disease. In: Braunwald E, eds. Heart disease: a textbook of cardiovascular medicine. 6th ed. Philadelphia, Pa: Saunders, 2001; 1282.
  28. Weisskoff RM, Chesler D, Boxerman JL, Rosen BR. Pitfalls in MR measurement of tissue blood flow with intravascular tracers: which mean transit time? Magn Reson Med 1993; 29:553-559.[Medline]
  29. Ostergaard L, Weisskoff RM, Chesler DA, Gyldented C, Rosen BR. High resolution measurement of cerebral blood flow using intravascular tracer bolus passages. I. Mathematical approach and statistical analysis. Magn Reson Med 1996; 36:715-725.
  30. Calamante F, Gadian DG, Connelly A. Delay and dispersion effects in dynamic susceptibility contrast MRI: simulations using singular value decomposition. Magn Reson Med 2000; 44:466-473.[CrossRef][Medline]



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