Methods

We reviewed retrospectively a database of 8,928 consecutive patients who were referred for CCTA from February 2008 to May 2012 to the Institute of Cardiology in Warsaw, Poland. The computed tomographic reports were analyzed for the presence of ACAOS, and those with (1) right-sided origin of the left main coronary artery (LMCA), (2) right-sided origin of the left anterior descending coronary artery (LAD), (3) right-sided origin of the left circumflex artery (LC), and (4) left-sided origin of the right coronary artery (RCA) were selected for further assessment. Of a total of 8,928 patients, 406 (4%) failed to undergo contrast-enhanced CCTA because of high calcium scores (n = 289), intended noncontrast calcium score assessment (n = 52), significant arrhythmias (n = 48), lack of peripheral venous access or contrast extravasation (n = 9), patient refusal (n = 5), and contrast intolerance (n = 3). The final analysis was thus performed on 8,522 patients. No computed tomographic study with ACAOS was excluded because of poor image quality. Anomalous coronary origin from the noncoronary sinus or the pulmonary trunk, including complex congenital heart defects, was excluded. We reviewed clinical records and obtained follow-up data by telephone interviews and through an electronic database. The institutional ethics committee approved the study, and all patients gave informed consent.

Studies conducted from February 2008 to July 2011 (5,534 patients [65%]) were performed using a first-generation dual-source computed tomographic scanner (Somatom Definition; Siemens Healthcare, Forchheim, Germany), with beam collimation of 64 × 0.6 mm, a gantry rotation time of 330 ms, tube voltage of 80 to 140 kV, pitch of 0.2 to 0.3, and temporal resolution of 83 ms. Unless contraindicated, an intravenous bolus of metoprolol (sequential 2.5 mg doses) was administered to target a heart rate <65 beats/min, and sublingual nitroglycerin (0.8 mg) was given directly before computed tomography. The computed tomographic protocol was extended to the measurement of a coronary artery calcium score if clinically indicated. A retrospective or prospective electrocardiographically gated acquisition protocol was used at the operator’s discretion. To minimize radiation exposure, electrocardiographically gated tube current modulation was applied in all patients. Scan data were reconstructed routinely in mid- to end-systole and diastole (35% to 45% and 65% to 75% of the RR interval). Studies conducted from August 2011 to May 2012 were performed using a second-generation dual-source computed tomographic scanner (Somatom Definition Flash; Siemens Healthcare) using the same protocol (n = 2,093 [25%]) or a high-pitch Flash protocol (n = 895 [10%]), with beam collimation of 64 × 0.6 mm, a gantry rotation time of 280 ms, tube voltage of 80 to 120 kV, pitch of 3.2 to 3.4, and temporal resolution of 75 ms. Image acquisition was prospectively triggered by the patient’s electrocardiogram using a high-pitch spiral protocol, and the data acquisition started at 55% to 60% of the R peak–to–R peak interval. Slice thickness was 0.6 mm, with an increment of 0.4 mm, irrespective of the computed tomographic protocol, and the contrast injection technique was similar for all studies. For acquisition of the volume data set, a bolus of 60 to 120 ml iodinated contrast material (Iomeron 400; Bracco Altana Pharma, Konstanz, Germany) was administered through an antecubital vein at a rate of 6 ml/s. The average effective radiation doses were determined on the basis of the recommended conversion factors as previously described.

All selected computed tomographic scans were analyzed off-line on a dedicated workstation (Leonardo; Siemens Healthcare) by a consensus of 2 experienced observers blinded to all patient data. The origin and course of ACAOS were evaluated using multiplanar reconstructions and 3-dimensional volume-rendered images. The proximal ACAOS course was classified into the following pathways: anterior (prepulmonary), interarterial (between the aorta and the pulmonary artery), septal (posterior to the right ventricular outflow tract within the myocardium of interventricular septum), and retroaortic. Malignant ACAOS was defined if all of the following anatomic features were recorded, as previously described : a slitlike ostium (≥50% luminal narrowing of coronary orifice), an acute angle of takeoff (defined as an angle ≤30° between the plane longitudinal to the proximal ACAOS and the tangential plane of the aortic root at the level of the ACAOS in axial multiplanar reconstruction), a proximal intramural course within the aortic wall, and significant lateral compression (≥50% luminal narrowing) between the aorta and the pulmonary trunk in the diastolic and/or systolic phase of the heart cycle. Additionally, we assessed the presence of significant systolic compression of ACAOS running intraseptally. Significant coronary artery disease was defined as ≥50% luminal stenosis by visual assessment in ≥1 major coronary artery on CCTA.

Continuous data are reported as mean ± SD and categorical data as frequencies and percentages. Nonparametric Mann-Whitney tests were used to assess differences between continuous variables. Differences in categorical data were analyzed using Fisher’s exact test. Significance was defined as a p value <0.05, and analysis was performed using SPSS version 15.0 (SPSS, Inc., Chicago, Illinois).

Results

Of the 8,522 subjects, 7,447 (87%) and 1,075 (13%) underwent computed tomography because of suspected and known coronary artery disease, respectively. The median age was 60 ± 11 years (range 12 to 93), and 4,222 patients (49%) were male.

The prevalence of ACAOS was 0.84% (72 of 8,522). Among the 72 patients, there was a total of 73 ACAOS (1 patient had 2 coronary anomalies: LAD and LC originating separately from the right aortic sinus). Clinical characteristics are listed in Table 1 . The median age was 55 ± 12 years (range 23 to 85), and 37 patients were men (51%). Thirty-eight patients (53%) underwent CCTA because of atypical chest pain, whereas 32 patients (44%) had typical angina. Two patients (3%) were admitted with diagnoses of acute coronary syndromes, both of whom had left-sided RCAs with significant interarterial compression and slitlike ostia (the first patient had normal coronary arteries and an intramural RCA course, whereas the second patient had 2-vessel disease with distal occlusion of the LAD and a significant stenosis in the proximal LC). There were no differences in gender distribution (51% vs 49% male, p = 0.813) or the prevalence of significant coronary artery disease as detected by CCTA (29% vs 34%, p = 0.385) between patients with and without ACAOS. In contrast, patients with ACAOS were significantly younger compared with those without ACAOS (55 ± 12 vs 60 ± 11 years, p = 0.002).

Right-sided LC was the most common ACAOS in our population, followed by left-sided RCA, with computed tomographic prevalence of 0.39% (33 of 8,522) and 0.23% (20 of 8,522), respectively. The proximal course and potentially malignant anatomic characteristics of ACAOS are listed in Table 2 . Anomalous LMCAs and LADs showed most commonly intraseptal courses, followed by anterior and interarterial courses. There were neither LMCA nor LAD cases running posterior to the aorta. In contrast, anomalous LCs ( Figure 1 ) showed retroaortic courses in 32 of 33 patients (97%), and the RCA always took an interarterial course. None of the anomalous LMCAs or LADs with anterior courses showed malignant anatomic features. Although LMCAs and LADs with septal courses lacked slitlike ostia or intramural aortic courses, we identified 2 LADs (22%) with significant compression within the myocardium during systole. Of the 32 LCs with retroaortic courses, only 2 (6%) showed intramural courses and acute angles of takeoff. Of the 24 ACAOS (0.28%) with interarterial courses, most of 20 cases (0.23%) were attributed to left-sided RCAs, of which 12 (0.14%) showed significant interarterial compression. In contrast to anomalous RCAs, none of the LMCAs ( Figure 2 ), LADs, or LCs with interarterial courses revealed significant vessel compression, slitlike ostia, or intramural aortic courses, and RCAs ( Figure 3 ) showed a significantly higher prevalence of malignant anatomic features (62% vs 12%, p <0.001) compared with the remaining ACAOS with interarterial courses. We identified 6 anomalous RCAs demonstrating all 4 malignant features of the proximal vessel course but no associated coronary artery disease ( Table 3 ).

CCTA of a right-sided LC. (A) Oblique multiplanar reconstruction of the LC taking a retroaortic course (arrowhead) . The proximal LC does not show ostial stenosis or an intramural course. (B) Sagittal multiplanar reconstruction of wide LC cross-sectional lumen (arrowhead) without visible compression between the aorta and the left atrium. (C) Curved multiplanar reconstruction of the LC (arrowhead) running posterior to the aorta. (D) Volume-rendered reconstruction of the LC (arrowhead) . Ao = aorta; LA = left atrium; LV = left ventricle; PA = pulmonary artery.

CCTA of a right-sided LMCA. (A) Oblique multiplanar reconstruction of the LMCA originating from the right aortic sinus with an interarterial course (arrowhead) . (B) Sagittal multiplanar reconstruction showing wide cross-sectional lumen of the LMCA (arrowhead) . (C) Curved multiplanar reconstruction of the LMCA (arrowhead) without ostial stenosis or intramural course. (D) Volume-rendered reconstruction of the LMCA (arrowhead) . Ao = aorta; PA = pulmonary artery.

CCTA of a left-sided RCA. (A) Axial multiplanar reconstruction of the RCA originating from the left aortic sinus with an interarterial course. Note that the proximal RCA has ostial narrowing (arrowhead) and intramural course within the aortic wall. (B) Sagittal multiplanar reconstruction showing interarterial compression of the RCA (arrowhead) . Note that the RCA is bulging outside the aortic wall causing a typical indentation in the pulmonary trunk. (C) Curved multiplanar reconstruction of the RCA (arrowhead) . (D) Volume-rendered reconstruction of the RCA with tangential ostial stenosis (arrowhead) . Ao = aorta; PA = pulmonary artery.

Table 3

Clinical and computed tomographic characteristics of 24 patients with anomalous coronary arteries originating from the opposite sinus of Valsalva and an interarterial course

Patient	ACAOS	Age (yrs)	Gender	Symptoms at Referral	Slitlike Ostium	Acute Angle of Takeoff	Intramural Course	Significant Compression	4 Malignant Features Present
1	RCA	27	M	Atypical chest pain	+	+	0	+	0
2	RCA	35	M	Atypical chest pain	0	+	0	0	0
3	RCA	41	M	Atypical chest pain	+	+	+	+	+
4	RCA	42	F	Atypical chest pain	0	+	+	0	0
5	RCA	42	M	Acute coronary syndrome	+	+	+	+	+
6	RCA	48	M	Atypical chest pain	0	+	+	0	0
7	RCA	51	F	Angina	+	+	+	+	+
8	RCA	52	F	Angina	+	0	0	+	0
9	RCA	56	M	Atypical chest pain	0	+	+	0	0
10	RCA	57	F	Atypical chest pain	+	0	0	+	0
11	RCA	58	M	Atypical chest pain	+	+	+	+	+
12	RCA	59	M	Angina	+	+	0	+	0
13	RCA	59	F	Angina	+	+	+	+	+
14	RCA	61	M	Acute coronary syndrome	+	+	0	+	0
15	RCA	62	F	Atypical chest pain	+	0	0	0	0
16	RCA	64	M	Angina	+	+	+	+	+
17	RCA	65	M	Atypical chest pain	+	0	0	+	0
18	RCA	67	F	Atypical chest pain	0	0	+	0	0
19	RCA	69	F	Angina	0	+	0	0	0
20	RCA	75	M	Angina	0	+	0	0	0
21	LMCA	50	M	Atypical chest pain	0	0	0	0	0
22	LMCA	74	F	Atypical chest pain	0	+	0	0	0
23	LAD	85	F	Atypical chest pain	0	0	0	0	0
24	LC	56	M	Angina	0	+	0	0	0

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