Anatomical variations and anomalies of coronary arteries (AVACA) are uncommon but important findings to recognize [1]. Imaging of coronary arteries by coronary computed tomography angiography (CCTA) has emerged as a noninvasive alternative to the diagnostic coronary catheter angiogram [2]. It is an accurate diagnostic modality with high spatial and temporal resolutions along with capabilities of three-dimensional and extraluminal evaluation of the coronary arteries [3–5].

The definitions of normal morphology, anatomical variation, and anomaly vary from one reference to another. Angelini and coworkers defined them based on the prevalence among an unselected population [6]. They defined “normal” as any morphologic feature observed in >1% of an unselected population, “normal variant” as a relatively unusual alternative morphological feature seen in >1% of that population, and “anomaly” as a morphological feature present in <1% of the same population. They reported that the incidence of coronary anomalies was 5.6% in a continuous series of 1950 angiograms. In another study that utilized CCTA, the prevalence was 18% [7]. Awareness of AVACA is crucial, given several related possible consequences, including misdiagnosis, myocardial ischemia, increased risk of coronary atherosclerotic disease and bacterial endocarditis, secondary aortic valve disease, ischemic cardiomyopathy, volume overload, technical difficulties during coronary angioplasty, complications during cardiac surgery, and sudden cardiac death [6].

AVACA has been linked to increased symptoms and sequelae, such as chest pain, dyspnea, syncope, ventricular fibrillation, myocardial infarction, cardiomyopathy, and sudden death [6]. Yet, the opposite may not necessarily be accurate. Investigating symptomatic patients for the presence of AVACA may or may not reveal a significant increase in its prevalence compared to an asymptomatic population. The consequences of AVACA mentioned above increase the chance of developing symptoms, which may lead to a higher discovery of anomalies among symptomatic patients. Therefore, it was hypothesized in this study that symptomatic cardiac patients have a higher prevalence of AVACA. This study aimed to investigate this hypothesis in a large number of symptomatic patients and compare the results to published results of asymptomatic populations.

The Institutional Research Ethics Committee approved this study and waived informed consent for patients’ anonymous data. This retrospective study included all symptomatic patients with CCTA in a tertiary care hospital in South Saudi Arabia (Assir Province) for seven years, from January 01, 2010, to December 31, 2016. The patients’ symptoms included one or more of the following: chest pain, shortness of breath, palpitation, and syncope. Patients with a coronary artery bypass graft (CABG) surgery or poor scan quality were excluded, because in such cases native coronary artery anatomy may be altered or inaccurately evaluated. To eliminate interobserver variations, all CCTAs were interpreted by one radiologist with ten years of post-board experience.

All studies were performed on a 64-slice CT scanner (Lightspeed VCT, General Electric, Milwaukee, WI, USA). The targeted heart rate in order to perform the scans was less than 65 beats per minute. Beta blockers (or, if contraindicated, calcium channel blockers) were prescribed by cardiologists to achieve the targeted heart rate as needed. In some cases, the target heart rate was not achieved, and they were excluded from this study if the radiologist deemed the scan quality poor. The test bolus technique was used for the timing of the scans. A dual-head power injector was used to inject 20 milliliters (ml) of Iobitridol (350 milligrams of iodine/ml) intravenous (IV) contrast (Xenetix, Guerbet, Roissy, France) at a rate of 5 ml/second, followed by 40 ml of normal saline at a rate of 5 ml/second for the bolus timing phase. For the CCTA phase, 50–70 ml of the same type of IV contrast was injected, followed by 40 ml of normal saline at the same rate. The scanning of CCTA was prospectively ECG-gated during breath-holding with a target phase of data acquisition at 75% of the R-R interval. Other parameters included a tube rotation time of 0.35 s, slice thickness of 0.625 mm, beam collimation of 40 mm at 120 kV, and tube current of 300–700 mA depending on the patient’s body size.

The CCTA images of all patients were viewed, processed, and analyzed on the same workstation (Advantage Window, General Electric, Milwaukie, WI, USA). An electronic data collection sheet was created with Google Sheets software (Google LLC, Mountain View, CA, USA), which was used to perform the statistical calculations by creating different formulas for the needed results. For each patient; age, gender, and percentage of the maximum stenosis of the coronary arteries were recorded.

The evaluated coronary anatomical variations (CAVs) included short left main coronary artery (LMCA) of ≤5 mm, division pattern of LMCA with the presence of ramus intermedius (trifurcation and quadrifurcation), and non-right coronary dominance (Fig. 1).

The right coronary dominance is the posterior descending artery (PDA) supplied by the right coronary artery (RCA). Left-sided dominance is defined as PDA supplied by the left circumflex artery (LCX), while bilateral dominance is when PDA is supplied by both RCA and LCX.

Coronary artery anomalies (CAAs) were classified into five groups. Group 1 included anomalies of the origin of the coronary arteries, defined as an origin, not from the corresponding sinus of Valsalva or higher than the junctional zone. Absent LMCA, with two separate origins of LAD and LCX, was classified in group 1 (Fig. 2).

Group 2 included a myocardial bridge (MB), defined as a major epicardial artery running into the myocardium (Fig. 3).

Group 3 included the anomalous course of the coronary arteries (Fig. 4).

Excessive tortuosity of the coronary arteries was classified in group 3. Intrinsic anomalies, including ectasia and aneurysm of coronary arteries, were classified in group 4. Ectasia and aneurysm were defined as a dilatation of more than 1.5 times the normal diameter of the artery, diffusely (≥50% of the artery length) or focally (<50% of the artery length), respectively. Group 5 included termination anomalies (fistulas) of the coronary artery. If a CAA definition applied to more than one group, it would be classified in all corresponding groups; for example, an RCA, originating from the left coronary cusp and passing in the interarterial groove, was classified in groups 1 and 3.

A total of 527 symptomatic patients had CCTA during a period of seven years, from January 01, 2010, to December 31, 2016. After applying the two exclusion criteria (patients with CABG and poor scan quality), 20 patients were excluded, leaving 507 patients in this study. There were 306 (60.4%) males and 201 (39.6%) females with a mean age of 57.4 years (SD 12.7) ranging from 23–95 years. A total of 297 (58.6%) patients had no stenosis of the coronary arteries in the CCTA, and 210 (41.4%) had stenosis caused by atherosclerosis, with luminal stenosis averaging 49.7% and ranging from 15%–100%.

The total number of patients with CAV and CAA was 217 (42.8%): this included 79 (36.4%) females and 138 (63.6%) males with 277 variations and anomalies.

Table 1 summarizes the results of CAV. Right coronary dominance was present in 437 patients (86.2%), left side dominance was present in 54 patients (10.6%), and bilateral dominance, when RCA and LCX supply the PDA, was present in 16 patients (3.2%).

The mean length of the left main coronary artery (LMCA) was 10 mm (SD 4.8), ranging from zero (absent LMCA with two separate origins of the left anterior descending (LAD) artery and LCX) to 25 mm. If we exclude the cases of absent LMCA, the mean length would be 10.4 mm (range 3–25 mm). The LMCA was absent in 9 (1.8%) patients. Short LMCA, defined as a length of 5 mm or less, was present in 23 (4.5%) patients. The total number of patients with absent or short LMCA was 32 (6.3%). In this study, absent LMCA was counted in group 1 of CAA, whereas short LMCA was counted as CAV. Trifurcation and quadrifurcation of LMCA were present in 36 (7.1%) patients and one patient (0.2%), respectively.

There were 137 (27%) patients with CAA [90 (65.7%) males, 47 (34.3%) females, mean age 55.4 years, range 26–86 years], with a total of 147 CAAs (29%) because 10 (2%) patients had more than one type of CAA. Of 137 patients with CAA, 54 (39.4%) had stenosis in CCTA (mean stenosis 45.7%, range 15%–95%).

The CAA was classified into five groups (Table 2).

The most common CAA was MB (group 2), which was seen in 109 patients, representing 79.6% of CAA and 21.5% of the total study population. It was present in 23.9% (73/306) of males and 17.9% (36/201) of females. MB of LAD was the most common (in 104 patients, 95.4%), followed by ramus intermedius bridging in three (2.8%) patients and RCA bridging in two (1.8%) (Fig. 2). If MB is excluded, the prevalence of CAA in this study population would be 7.1% (36 anomalies). Coronary ectasia was present in one (0.2%) patient, representing (0.7%) of all CAA patients. There were no cases of coronary artery aneurysms or fistulas.