Hemodynamically significant anomalies include anomalies of origination with interarterial course, anomalous origin from the pulmonary artery,  atresias, and congenital fistulas. (1)

Origin of the coronary artery from the opposite Valsalva sinus (ACAOS) with the interarterial course is the second leading cause of death in young athletes after hypertrophic cardiomyopathy. (2)

Interarterial or "malignant "course is defined as a pathway of the coronary artery between the pulmonary trunk and aorta. Some authors believe that the vessel with this course is susceptible to obstruction during forceful physical activity due to compression by the aorta and pulmonary trunk. (1)

The total prevalence of coronary artery originating from the opposite Valsalva sinus is 1%. (3)

Krasuski et al. found that the risk of sudden cardiac death (SCD) in athletes with ACAOS is 79 times higher than in the general population. (4) On the other hand, Cheezum et al. found that the risk of SCD attributed to ACAOS is the greatest in patients <30 years. Still, this anomaly can cause symptoms in the elderly. (5)

Besides the interarterial course of ACAOS, there are more morphological high-risk features contributing to SCD: ostial stenosis, proximal narrowing of ACAOS (segmental hypoplasia), intramural course of the coronary artery, and acute angle take-off. (2,5,6,)

Depending on the stenosis degree of the ostium of ACAOS, the ostium can be described as oval (stenosis <50%) and slit-like (≥50%).

The intramural course of ACAOS is defined as shared tunica media between two vessels without interposing tunica adventitia. It is best appreciated on the cross-section of ACAOS perpendicular to its course. If the vessel appears elliptical on this cross-section, it has an intramural course; otherwise, the vessel is round. Since the vessel normally courses in the epicardium surrounded by fat, the lack of pericoronary fat sign is suggestive of an intramural course.

Acute angle take-off is the angle <45° between the origin of ACAOS and the aorta. (5-10)

ACAOS can have four possible courses: interarterial, subpulmonic, prepulmonic, and retroaortic. It is important to differentiate between interarterial and subpulmonic course. The former courses above the pulmonary artery valve, and the latter above (9,11,12)

The radiologist's report should include a description of the origin and the pathway of ACAOS, its vascular territory, the dominant vascularization, and additional abnormalities. (13)

After the morphology of the anomalous coronary artery is assessed on CTA, the patient should undergo cardiac functional testing. Symptomatic non-athlete patients require surgery, and asymptomatic do not.

Conservative treatment is not suitable for athletes. (10)

Anomalous origin of the coronary artery from the pulmonary artery is a rare congenital anomaly, with the LCA arising from the pulmonary artery (ALCAPA) being the most common variant and comprising 0.24-0.26% of congenital heart diseases. (8)

ALCAPA syndrome is usually solitary defect. (14)

Depending on the hemodynamic changes that occur after birth, ALCAPA syndrome can be divided into infant and adult type. (8)

Infant type- Immediately after birth, no symptoms occur in the child since the pulmonary arterial pressure equals systemic pressure, resulting in an anterograde flow of blood from the pulmonary artery into the anomalous left coronary artery.

The onset of symptoms occurs usually two months after birth when the pressure in the pulmonary artery starts decreasing. (8,14)

Adult type- In these patients, the sufficient collateral network between RCA and LCA develops, enabling them to survive till adulthood with no/minor symptoms. The blood tends to flow from the high-resistance coronary arteries into the low resistance pulmonary artery leading to left to right shunt (coronary steal phenomenon), and resulting in chronic subendocardial ischemia of the left ventricle, which might lead to infarctions, malignant ventricular dysrhythmias, and SCD. (8,14)

Delayed subendocardial enhancement of the left ventricle on MRI is suggestive of fibrotic scar and predictive for dysrhythmias and SCD. (14)

Coronary artery fistula (CAF) can be congenital and acquired; the former comprises 0.3% of congenital heart diseases.

CAF represents abnormal vascular communication between coronary artery and cardiac chamber or coronary artery and any part of systemic or pulmonary circulation without interposing capillary network.

Since in CAF, there is no capillary network, the blood bypasses the myocardium, creating a "coronary steal "phenomenon.

Most CAFs are asymptomatic, but the larger fistulas can cause significant steal phenomen. Symptoms depend on the extent of the "coronary steal "phenomenon, the development of significant left-to-right or left-to-left shunt and can include mild dyspnea, fatigue, angina, congestive heart failure, and myocardial infarction.

CAF can be classified based on its origin, drainage site, and complexity. The most common fistulas are coronary-cameral, coronary-pulmonary artery, and coronary artery-coronary sinus fistulas. The patent drainage site can be seen as a contrast shunt sign-contrast present into the drainage vessel or chamber, which might not always be depicted due to contrast enhancement timing and other issues. (15)

In coronary artery-coronary sinus fistula, the sinus is dilated. Another differential diagnosis of dilated coronary sinus must be considered (persistent left superior vena cava, unroofed coronary sinus, and TAPVC). (16)

Myocardial bridging represents the intramural course of coronary vessels within the myocardium at varying lengths instead of its normal pathway through the epicardial fat tissue. Most commonly, it involves LAD and rarely causes symptoms. (13,17,18)

Coronary ostial atresia is a rare congenital anomaly that commonly affects LCA. The absence of atherosclerosis is suggestive of this anomaly, though inconclusive. In coronary ostial atresia, developed collateral vessels between the distal patent site and the opposite coronary artery are not dilated since they are present from birth. On the contrary, in the occlusion of the proximal coronary artery due to atherosclerosis, collateral vessels are dilated because they enlarge progressively. The absence of angina is also suggestive of congenital ostial atresia since the developed collateral vessels provide sufficient vascularization. (19)