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Atypical Chest Pain: Coronary, Aortic, and Pulmonary Vasculature Enhancement at Biphasic Single-Injection 64-Section CT Angiography¹

¹ From the Departments of Radiology (K.G.B., A.H.), Cardiology (R.K., M.G., G.R., W.O.), and Emergency Medicine (M.R., B.O.), and Biostatistics–William Beaumont Research Institute (M.B.), William Beaumont Hospital, 3601 W 13 Mile Rd, Royal Oak, MI 48073; and the Department of Radiology, Henry Dunant Hospital, Athens, Greece (T.G.V.). Received March 11, 2006; revision requested May 10; final revision received June 8; accepted June 22; final version accepted, September 5. Address correspondence to K.G.B. (e-mail: kbis{at}beaumont.edu).

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

 
Purpose: To prospectively evaluate the enhancement of coronary, pulmonary, and thoracic aortic vasculature by using biphasic single-acquisition 64-section computed tomographic (CT) angiography and to prospectively evaluate if differences in right side of the heart and coronary venous enhancement interfere with interpretation of coronary arteries.

Materials and Methods: With internal review board approval and HIPAA compliance, 50 patients (16 men, 34 women; mean age, 51.5 years; range, 30–75 years) with atypical chest pain were referred from the emergency department and were imaged with a 64-section CT scanner after premedication with oral atenolol and/or intravenous metoprolol. Thoracic CT angiography with retrospective gating was subsequently performed with a single biphasic injection of 130 mL of iso-osmolar contrast material (100 mL at 5 mL/sec and 30 mL at 3 mL/sec) in caudal-to-cranial acquisition. Coronary, aortic, and pulmonary arterial attenuation values were obtained. Coronary venous and right atrial enhancement were evaluated to assess whether there was interference with coronary artery evaluation. A two-tailed Friedman test was used to evaluate differences among segments within each artery.

Results: Mean coronary arterial, pulmonary arterial, and aortic attenuation values were significantly higher than the 250-HU threshold (P < .05). Mean pooled coronary arterial (288.9 HU ± 64.8), pulmonary arterial (316.4 HU ± 79.9), and aortic (329.9 HU ± 63.3) attenuation values were significantly higher than the 250-HU threshold (P < .0001). Coronary venous enhancement did not affect depiction or interpretation of coronary arteries. Right atrial streak artifact focally traversed the right coronary artery in only one study.

Conclusion: The aforementioned thoracic CT angiographic protocol provides enhancement of coronary, aortic, and pulmonary vasculature in a single breath hold without interference from right side of the heart streak artifact or coronary venous enhancement.

© RSNA, 2007

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

 
Combined simultaneous evaluation of the pulmonary, coronary, and thoracic aortic vasculature with multidetector computed tomographic (CT) angiography requires tailored imaging and contrast material injection protocols. A single comprehensive protocol that could accomplish combined evaluation would be highly desirable for rapid and cost-effective work-up of emergency department patients with atypical chest pain. Thus, the purpose of our study was to prospectively evaluate the enhancement of the coronary, pulmonary, and thoracic aortic vasculature by using biphasic single-acquisition 64-section CT angiography and to prospectively evaluate if differences in right side of the heart and coronary venous enhancement interfere with the interpretation of coronary arteries.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

 
Patients
From February 2005 to May 2005, 50 emergency department patients (16 men, 34 women; mean age (± standard deviation), 51.5 years ± 10.6; age range, 30–75 years) with atypical chest pain were prospectively evaluated. The study was approved by our internal review board and was compliant with the Health Insurance Portability and Accountability Act. The study, including radiation risks, was explained to the patients before informed consent was obtained.

Inclusion criteria.—Patients with atypical chest pain or other symptoms suggestive of acute cardiac ischemia were included. The definition for atypical chest pain was a low Thrombolysis in Myocardial Infarction risk score (<3), as described by Antman et al (1). Other inclusion criteria included the ability to provide informed consent and age 18 years or older.

Exclusion criteria.—Electrocardiographic (ECG) evidence of ischemia; positive cardiac markers (troponin I, serum myoglobin level, and/or creatinine phosphokinase–MB fraction); known preexisting coronary artery disease; renal insufficiency (serum creatinine level >1.6 mg/dL [141.4 µmol/L]) or renal failure requiring dialysis; atrial fibrillation or other markedly irregular rhythm; inability to provide informed consent; psychologic unsuitability or extreme claustrophobia; pregnancy or unknown pregnancy status; age younger than 18 years; clinical instability as deemed by the attending physician; known allergy to iodinated contrast material; inability to tolerate ß-blockers, including patients with chronic obstructive pulmonary disease or asthma requiring maintenance with inhaled bronchodilators or steroids; complete heart block; second-degree atrioventricular block; and CT imaging or contrast material administration within the past 48 hours.

Patient Preparation and Imaging Protocol
All 50 patients were imaged without complications with a 64-section CT scanner (Siemens Medical Solutions, Forcheim, Germany). An upper-extremity 20-gauge intravenous catheter was placed in an antecubital vein for venous access. Fifty to 100 mg (30–60 minutes prior to the procedure) of oral atenolol (Tenormin; AstraZeneca Pharmaceuticals, Wilmington, Del) and/or 5–10 mg boluses every 15 minutes (up to 50 mg) of intravenous metoprolol (Lopressor; AstraZeneca Pharmaceuticals) was administered to achieve a target heart rate of 65 beats per minute or fewer. Precontrast scanning for calcium scoring was performed by using a standard, prospective, ECG-triggered (55% of R-R interval) protocol (3-mm section thickness and collimation, 120 kVp, variable tube current [range, 40–80 mAs], 0.24-second scanning time). Scanning for calcium scoring was performed as part of the imaging protocol for coronary CT angiography at our institution. Sublingual nitroglycerin (0.4 mg Nitroquick; Ethex, St Louis, Mo) was administered for coronary vasodilation after completion of scanning. Bolus timing was performed by scanning the mid–ascending aorta (9.6-mm section thickness, 120 kVp, variable tube current [range, 40–80 mAs], 0.33-second scanning time) 10 seconds after injection of 20 mL of iodixanol (Visipaque, 320 mg of iodine per milliliter; GE Healthcare, Princeton, NJ) at 5 mL/sec, followed by a 50-mL saline flush at 5 mL/sec with a dual power injector (Stellant; Medrad, Indianola, Pa). Contrast material was prewarmed to body temperature in incubators prior to use and was subsequently warmed with injector-head electrodes. We then immediately injected 100 mL of iodixanol at 5 mL/sec followed by 30 mL at 3 mL/sec and, subsequently, a 50-mL saline flush at 3 mL/sec. The initial phase of contrast enhancement (100 mL of contrast material at 5 mL/sec) was chosen, as this is the typical protocol for coronary CT angiography.

Since in our experience this coronary protocol results in little enhancement of the right side of the heart and pulmonary arterial anatomy with a cranial-to-caudal acquisition, we chose to use a caudal-to-cranial acquisition with an additional 30 mL of contrast material. The additional contrast material volume results in a prolonged time for contrast material injection to ensure adequate enhancement of the pulmonary arterial anatomy. Our mean time for reaching peak aortic enhancement with the 20-mL test bolus was 15 seconds. The addition of the 5-second delay before data acquisition coupled with a maximum data acquisition time of 15 seconds resulted in a time of 35 seconds (15 seconds for mean time to reach peak aortic enhancement plus 5 seconds for delay plus 15 seconds for imaging time), in which active vascular contrast material flow is required for adequate pulmonary enhancement. The time of active contrast material flow with this biphasic protocol was 30 seconds (20 seconds for the 100-mL volume and 10 seconds for the 30-mL volume). This does not include the time during which the saline flush (16 seconds) pushed the remaining contrast material in the upper extremity and central thoracic venous volume.

The CT angiographic examination began 5 seconds after aortic peak enhancement by using a single breath-hold caudal-to-cranial acquisition. A 5-second imaging delay relative to the time of peak aortic enhancement was used, since the use of a test bolus is known to underestimate (compared with bolus tracking) the peak enhancement by a mean time of 6 seconds (2). A caudal-to-cranial acquisition was performed to ensure that the lung bases and lower lobe vasculature were imaged during contrast material infusion. This is typical for pulmonary embolism protocols (3,4). Since ECG pulsing for tube current modulation was not used, the thorax was covered from the lung bases to just above (1–2 cm) the aortic arch. This resulted in exclusion of the apical segments of the thorax.

ECG pulsing was not used so as to allow review of systolic and early diastolic data with adequate signal, if needed. Retrospective ECG gating was used with the following parameters: 0.6-mm collimation, 0.33-second tube rotation time, 120-kVp tube voltage, 750–850-mAs effective tube current, and 0.2 pitch. Single-sector reconstructions of coronary arteries were performed by the technologist at 65% and 35% of the R-R interval for all studies but were then modified to a different phase if there were motion artifacts. This was directed (K.G.B.) with a "preview" series, whereby one transverse section was reconstructed at every 10% of the R-R interval at the level of the motion artifact. Fixed 65% and 35% reconstructions were obtained to minimize the postprocessing time by the technologist. Subsequently, additional reconstructions were made from the raw data to display the noncoronary structures.

The respective reconstruction field of view, section thickness, reconstruction increment, and kernel were 15–22 cm, 0.6 mm, 0.3 mm, and B25-f smooth for coronary arteries; 35–42 cm, 2 mm, 1 mm, B31-f medium smooth for thoracic aorta, pulmonary arteries, and thoracic soft tissues; and 35–42 cm, 3 mm, 2 mm, B70 f very sharp for the lungs. Reconstructions were performed by a technologist on a workstation (Wizard; Siemens Medical Solutions) and were then transferred to another workstation (Terarecon, San Mateo, Calif) for analysis (K.G.B., 4 years of experience in cardiac CT) with multiplanar reformations and maximum intensity projections (MIPs). The Terarecon workstation was also used for measuring peak and mean attenuation values (in Hounsfield units) for all vascular segments.

Vascular Enhancement Measurements
A full width at half maximum technique (5) was used for all vascular segments to set the window width and window level for appropriately delineating the vascular lumen edge. A threshold value of 250 HU (6,7) was chosen as the target enhancement value considered to be diagnostic for assessment of the three vascular beds. Patients were evaluated prospectively with the idea that the presence of artifacts or disease involving a particular vascular segment would result in exclusion of that particular segment from analysis. Each vascular segment to be measured was displayed perpendicular to its long axis by using a magnification factor of 3.5 (coronary and pulmonary arteries) or 2 (aorta). A circular region of interest (1–5-mm diameter for coronary arteries, 3–20 mm for pulmonary arteries, 20–45 mm for aorta) that incorporated the vascular target was initially used to obtain a peak attenuation value for subsequent adjustment of the window to 0 and the level to 50% this peak. Two linear perpendicular measurements were then made to acquire the peak and mean attenuation values, which were then averaged for that particular level.

Coronary measurements were performed in consensus (K.G.B., 15 years chest CT experience after training and 4 years cardiac CT experience after training; T.G.V., 10 years chest CT experience after training and 2 years cardiac CT experience after training) by using the American Heart Association (8) definitions of anatomy at proximal, middle, and distal segments of the right coronary artery (RCA) and left anterior descending (LAD) coronary artery. The American Heart Association anatomy definition, however, does not allow segmentation of the left circumflex (LCX) coronary artery into proximal, middle, and distal components. To obtain measurements similar to those of the RCA and LAD, the LCX was segmented into proximal, middle, and distal components by using the following definitions: proximal, beyond left main bifurcation or trifurcation; middle, halfway down the posterior atrioventricular groove; and distal, proximal aspect of the last obtuse marginal branch.

Pulmonary arterial measurements were performed (T.G.V.) at the following levels: truncus anterior, left upper lobe, right main, left main, right lower lobe medial basilar segmental, and left lower lobe anteromedial basilar segmental. Aortic measurements were performed (T.G.V.) at the proximal brachiocephalic trunk, mid–ascending aorta, proximal portion of the descending aorta (just beyond the arch segment), and distal portion of the descending aorta (at the level of the posterior costophrenic sulcus).

The pulmonary arteries were also depicted with 5-mm coronal and sagittal MIPs (K.G.B.) by using the Terarecon workstation and were quantitatively assessed for the presence of a gradient in attenuation between the lower lobe segmental artery and the more central right and left main pulmonary arterial segments. A substantial gradient was arbitrarily defined as a difference of more than 100 HU for the mean and the peak attenuation values. The sagittal 5-mm MIPs were also used (K.G.B.) to evaluate enhancement uniformity by identifying the presence or absence of a gradient (>100 HU difference for mean and peak attenuation values) between the descending aorta and distal aorta segments.

Cardiac Venous and Right Side of the Heart Enhancement
To assess whether differences in enhancement of the cardiac veins at caudal-to-cranial acquisition affected the display and analysis of the subjacent coronary arteries, enhancement of the cardiac veins was graded (relative to the subjacent coronary arterial enhancement) on a scale of 0–3 as follows: 0, none; 1, mild; 2, moderate (less than arterial); and 3, substantial (equal to arterial). The great cardiac vein subjacent to the proximal and middle LAD and the middle cardiac vein subjacent to the posterior descending artery (PDA), as well as the coronary sinus within the posterior atrioventricular groove, were evaluated on 5-mm MIPs. When cardiac venous enhancement was present, three-dimensional volume-rendered images and 5-mm MIPs in a variety of planes were used to assess (K.G.B.) if the enhancement interfered with the evaluation of subjacent arterial coronary anatomy. Furthermore, given the higher right atrial enhancement, the associated streak artifact was graded on a scale of 0–3 by evaluating transverse 5-mm MIP sections extending from the superior vena cava (SVC) through the right side of the heart as follows: 0, none; 1, mild; 2, moderate (no interference with RCA analysis); and 3, severe (interference with RCA analysis).

Statistical Analysis
Averages of the mean attenuation values were compared among the proximal, middle, and distal segments within the coronary, pulmonary, and aortic arterial anatomy individually. The two-tailed (significantly greater than and less than 250 HU) Friedman test was used to evaluate differences among the segments within each artery. Since the mean attenuation values for each segment for the three arteries were obtained from the same patient, these measurements are not independent of each other, and in fact are all highly correlated. Also, at the preliminary analysis, none of the measurements were normally distributed, thereby indicating that parametric tests were inappropriate to use. Hence, this analysis was performed by using the nonparametric Friedman test. The P values reported were based on asymptotic computational algorithms and were rounded to four decimal places. Asymptotic computational algorithm tests are used when the sample size is sufficiently large.

P values less than .05 (probability of type I error) were considered to indicate a significant difference. No power analysis was performed for determining sample size. Rather, the analysis of vascular attenuation was performed in the arbitrarily chosen number of 50 patients that were studied between February 2005 and May 2005. Statistical analysis was performed by using SAS for Windows (version 9.1.3; SAS Institute, Cary, NC), Service Pak 2 (Microsoft, Redmond, Wash), and StatXact version 6.3.0 (Cytel Software, Cambridge, Mass) with Cytel Studio version 6.3.0 (Cytel Software).

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

 
Because of the artifacts that could result in inaccurate attenuation measurements, eight patients were excluded from coronary analysis for the following reasons: extensive coronary artery calcium (two patients), cardiac rhythm abnormalities (two patients), breathing artifacts (three patients), and gross patient motion (one patient). As such, 42 patients were included for the coronary study analysis. Because of breathing artifacts (three patients) and gross patient motion (one patient), 46 patients were included for both the pulmonary and aortic studies. Various vascular targets were further excluded from enhancement measurements if the anatomy was not clearly defined or was less than 1 mm in diameter, the latter of which was the case for the middle and distal LCX segments in right dominant systems and the distal LAD.

Coronary Artery Enhancement
Mean coronary arterial attenuation values for proximal, middle, and distal coronary segments were 299.0 HU ± 62.9, 328.4 HU ± 61.8, and 308.6 HU ± 61.3 for RCA; 287.0 HU ± 57.6, 264.5 HU ± 45.2, and 198.1 HU ± 43.7 for the LAD; and 305.2 HU ± 54.9, 290.0 HU ± 35.1, and 286.1 HU ± 68.9 for the LCX. Attenuation values for all coronary vascular targets were significantly higher than 250 HU (P < .05), excluding the distal LCX and the distal LAD. The mean pooled coronary arterial attenuation value of 288.9 HU ± 64.8 was significantly higher than 250 HU (P < .0001) (Table 1).

View larger version (77K): [in this window] [in a new window] [Download PPT slide]   Figure 1a: Uniform thoracic aorta and pulmonary arterial enhancement. (a) Coronal and (b) sagittal 5-mm MIPs show uniform enhancement of thoracic aorta without streak or cardiac motion artifacts. (c) Coronal 30-mm MIP shows uniform enhancement of pulmonary arteries. Calcified left hilar and subcarinal nodes are incidental findings.

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 1b: Uniform thoracic aorta and pulmonary arterial enhancement. (a) Coronal and (b) sagittal 5-mm MIPs show uniform enhancement of thoracic aorta without streak or cardiac motion artifacts. (c) Coronal 30-mm MIP shows uniform enhancement of pulmonary arteries. Calcified left hilar and subcarinal nodes are incidental findings.

View larger version (85K): [in this window] [in a new window] [Download PPT slide]   Figure 1c: Uniform thoracic aorta and pulmonary arterial enhancement. (a) Coronal and (b) sagittal 5-mm MIPs show uniform enhancement of thoracic aorta without streak or cardiac motion artifacts. (c) Coronal 30-mm MIP shows uniform enhancement of pulmonary arteries. Calcified left hilar and subcarinal nodes are incidental findings.

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 2a: Pulmonary arterial enhancement gradient. (a) Coronal and (b) sagittal 5-mm MIPs of pulmonary arteries obtained from larger-field-of-view reconstructions reveal difference in enhancement between basilar segmental and more central pulmonary arteries. This attenuation gradient was seen in six of 46 studies. However, the more central attenuation values are of sufficient diagnostic quality for detection of emboli.

View larger version (127K): [in this window] [in a new window] [Download PPT slide]   Figure 2b: Pulmonary arterial enhancement gradient. (a) Coronal and (b) sagittal 5-mm MIPs of pulmonary arteries obtained from larger-field-of-view reconstructions reveal difference in enhancement between basilar segmental and more central pulmonary arteries. This attenuation gradient was seen in six of 46 studies. However, the more central attenuation values are of sufficient diagnostic quality for detection of emboli.

View larger version (140K): [in this window] [in a new window] [Download PPT slide]   Figure 3a: Middle cardiac vein enhancement and right dominant coronary anatomy. (a, b) Left anterior oblique 5-mm MIPs show the course (proximal in a, middle and distal in b) of dominant RCA (arrows). (c) Transverse 5-mm MIP shows PDA (black arrows). High attenuation of right atrium and ventricle does not obscure arterial anatomy. There is only mild enhancement of middle cardiac vein (white arrows), which does not interfere with visualization of subjacent PDA.

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 3b: Middle cardiac vein enhancement and right dominant coronary anatomy. (a, b) Left anterior oblique 5-mm MIPs show the course (proximal in a, middle and distal in b) of dominant RCA (arrows). (c) Transverse 5-mm MIP shows PDA (black arrows). High attenuation of right atrium and ventricle does not obscure arterial anatomy. There is only mild enhancement of middle cardiac vein (white arrows), which does not interfere with visualization of subjacent PDA.

View larger version (133K): [in this window] [in a new window] [Download PPT slide]   Figure 3c: Middle cardiac vein enhancement and right dominant coronary anatomy. (a, b) Left anterior oblique 5-mm MIPs show the course (proximal in a, middle and distal in b) of dominant RCA (arrows). (c) Transverse 5-mm MIP shows PDA (black arrows). High attenuation of right atrium and ventricle does not obscure arterial anatomy. There is only mild enhancement of middle cardiac vein (white arrows), which does not interfere with visualization of subjacent PDA.

View larger version (142K): [in this window] [in a new window] [Download PPT slide]   Figure 4a: Great cardiac vein enhancement and LAD anatomy. (a) Right anterior oblique 5-mm MIP of LAD (arrows). (b) Left anterior oblique caudal and (c) transverse oblique cranial 5-mm MIPs show the course of LAD (large arrow) and diagonal branch (arrowhead) with moderate enhancement of great cardiac vein (small arrows), which does not interfere with depiction of LAD or its diagonal branch.

View larger version (136K): [in this window] [in a new window] [Download PPT slide]   Figure 4b: Great cardiac vein enhancement and LAD anatomy. (a) Right anterior oblique 5-mm MIP of LAD (arrows). (b) Left anterior oblique caudal and (c) transverse oblique cranial 5-mm MIPs show the course of LAD (large arrow) and diagonal branch (arrowhead) with moderate enhancement of great cardiac vein (small arrows), which does not interfere with depiction of LAD or its diagonal branch.

View larger version (156K): [in this window] [in a new window] [Download PPT slide]   Figure 4c: Great cardiac vein enhancement and LAD anatomy. (a) Right anterior oblique 5-mm MIP of LAD (arrows). (b) Left anterior oblique caudal and (c) transverse oblique cranial 5-mm MIPs show the course of LAD (large arrow) and diagonal branch (arrowhead) with moderate enhancement of great cardiac vein (small arrows), which does not interfere with depiction of LAD or its diagonal branch.

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 5a: Coronary sinus enhancement and LCX anatomy. (a) Transverse oblique caudal 5-mm MIP shows the course of LCX (large arrows) and coronary sinus (small arrows). (b) Left anterior oblique 5-mm MIP shows that moderate enhancement of the coronary sinus (white arrows) does not obscure the descent of atrioventricular groove artery (black arrow).

View larger version (135K): [in this window] [in a new window] [Download PPT slide]   Figure 5b: Coronary sinus enhancement and LCX anatomy. (a) Transverse oblique caudal 5-mm MIP shows the course of LCX (large arrows) and coronary sinus (small arrows). (b) Left anterior oblique 5-mm MIP shows that moderate enhancement of the coronary sinus (white arrows) does not obscure the descent of atrioventricular groove artery (black arrow).

View larger version (136K): [in this window] [in a new window] [Download PPT slide]   Figure 6a: Right atrial streak artifact. (a) Transverse 5-mm MIP of RCA shows focal right atrial streak artifact (arrow). (b) Left anterior oblique 5-mm MIP of RCA (white arrows) shows focal streak artifact (black arrow) that traverses through the middle part of RCA.

View larger version (153K): [in this window] [in a new window] [Download PPT slide]   Figure 6b: Right atrial streak artifact. (a) Transverse 5-mm MIP of RCA shows focal right atrial streak artifact (arrow). (b) Left anterior oblique 5-mm MIP of RCA (white arrows) shows focal streak artifact (black arrow) that traverses through the middle part of RCA.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

Previous studies on contrast material delivery dynamics have focused on the enhancement profiles in a single vascular territory, that is, the aorta (10,12) or the pulmonary arteries (7,13,14). To our knowledge, a single-injection CT angiographic protocol that would provide uniform and simultaneous enhancement along the z-axis in coronary, thoracic aortic, and pulmonary arterial vasculature has not been described. With respect to optimal CT angiographic enhancement of the pulmonary vasculature, Jones and Wittram (7) defined attenuation of greater than 250 HU to be adequate. Becker et al (6) considered 250–300 HU as adequate for CT coronary angiography. In our study, the mean values for the coronary segments ranged from 264 to 328 HU, with the exception of the distal LAD, which had a mean value of 198 HU. The explanation for this lower value is, most likely, the small caliber of the vessel at its distal part. The middle and distal LCX segments were insufficiently sampled, as their anatomy was frequently less than 1 mm in the right dominant systems analyzed. Mean attenuation values for pulmonary vasculature ranged from 299.0 to 331.1 HU, and those for the aortic vasculature ranged from 331.1 to 347.5 HU.

Differences in coronary venous and right side of the heart enhancement patterns did not interfere with evaluation of the coronary arteries in our study. In the majority (62%) of studies, the middle cardiac vein yielded only mild enhancement (grade 1), which did not interfere with the depiction or interpretation of the PDA. Although not studied by us, the middle cardiac vein would be expected to enhance more if the acquisition was cranial to caudal. The great cardiac vein had moderate (grade 2) (55% of patients) followed by mild enhancement (grade 1) (43% of patients); however, this did not interfere with the depiction or interpretation of the proximal LAD nor its diagonal branches. Although not evaluated in our study, the great cardiac vein would be expected to have less enhancement if the acquisition was cranial to caudal. The majority (76%) of cases yielded only mild enhancement of the coronary sinus, which did not interfere with the depiction or interpretation of the LCX, atrioventricular-groove artery, or obtuse marginal branches. Finally, no study had cardiac venous enhancement equivalent to that of arterial enhancement. Streak artifact from the right atrium was present in the majority of studies and was mostly projected toward the tricuspid valve. However, the RCA was focally obscured in only one study.

In the majority (40 of 46, 87%) of studies, there was uniform enhancement of the pulmonary arteries as viewed on coronal and sagittal MIPs. The remainder of studies (six of 46, 13%) demonstrated an attenuation gradient between the basilar segmental and the more central main right and left pulmonary arteries. Although not studied by us, the attenuation could be due to a more rapid circulation of contrast material in patients with a higher cardiac output. It should be noted that aortic enhancement between the distal descending aorta and the proximal descending aorta was visually uniform in all studies except one, where there was a visual decrease in attenuation proximally.

There were limitations of our study. Many patients, as well as particular vascular segments, were eliminated from analysis; however, this was performed prospectively to eliminate the influence of artifacts and disease on vascular attenuation. Imaging protocol–related limitations, such as the use of scanning for calcium scoring and the lack of ECG pulsing, result in radiation exposure and are thus no longer implemented with our clinical protocol for the evaluation of emergency department patients with atypical chest pain. Likewise, the exclusion of the apical segments of the thorax above the aortic arch was needed because of ECG pulsing. Also, the protocol is specific for the scanner used. Recently, dual and simultaneous injection of contrast material and saline with a variety of dilution options have been described to substantially decrease right side of the heart streak artifact (15). This option can be implemented in the future for addressing the issue of streak artifact, which can obscure the RCA. The total contrast material volume (150 mL) was more than the average volume (80–100 mL) that is typically used with standard coronary CT angiographic protocols. Currently, however, the 20-mL test bolus has been eliminated, and real-time bolus tracking (16) is used to trigger data acquisition. This is reported to optimize vascular enhancement with reduced contrast material volumes (16). Finally, comparison of the biphasic protocol with a uniphasic protocol with the same scanner was not performed.

In conclusion, we have presented a single-acquisition single-injection biphasic multidetector CT angiographic protocol for simultaneous imaging of the coronary arteries, thoracic aorta, and pulmonary arteries in patients with atypical chest pain. The results of this protocol are promising; however, further hardware and software improvements of increased temporal and spatial resolution and contrast material delivery schemes should further improve depiction of the intrathoracic vasculature, including distal coronary arteries at reduced contrast material volumes. Finally, studies are needed to assess how such a protocol performs in a large series of patients for identifying the cause of chest pain.

	ADVANCE IN KNOWLEDGE

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

 

• We describe a multidetector CT angiographic protocol that provides simultaneous enhancement of the coronary arteries, pulmonary arteries, and thoracic aorta in a single breath-hold acquisition for the evaluation of emergency department patients with atypical chest pain.
  

	FOOTNOTES

 

Abbreviations: ECG = electrocardiography • LAD = left anterior descending • LCX = left circumflex • MIP = maximum intensity projection • PDA = posterior descending artery • RCA = right coronary artery

Authors stated no financial relationship to disclose.

Author contributions: Guarantors of integrity of entire study, T.G.V., K.G.B.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, T.G.V., K.G.B.; clinical studies, T.G.V., K.G.B., A.H., R.K., M.G., G.R.; statistical analysis, M.B.; and manuscript editing, T.G.V., K.G.B.

	References

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION ADVANCE IN KNOWLEDGE References

 

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