Collateral Coronary Circulation in the Absence of Obstructive Coronary Artery Disease

Collateral coronary blood flow has been shown to be protective in function,1–4 and its presence is almost always a sine qua non of significant obstructive coronary artery disease.2 The theories behind collateral vessel development remain controversial. However, post mortem studies of normal hearts demonstrating the presence of small channels that interconnect the coronary arteries5,6 favor the hypothesis that these channels normally exist and become angiographically visible when they become larger as a response to obstructive coronary artery disease. In all such cases, the coronary arterial stenosis is evident. We present two cases wherein a large collateral connected the two coronary arteries, which were free of angiographically visible disease. We believe that these two cases represent a developmental variant and are distinct from the collaterals seen in the presence of coronary obstruction. Case Report. Patient #1. A 53-year-old male bus driver presented with atypical chest pain. He was a smoker but had no other risk factors, and his physical examination and laboratory parameters were unremarkable. The electrocardiogram showed T-wave inversion in leads VI–V4. In view of his occupation, history of smoking and abnormal resting electrocardiogram, he was referred for coronary angiography. Since the right radial artery was judged to be small but adequate, and the Allens test clearly demonstrated adequate ulnar blood flow, a radial approach was planned. A 4 French (Fr) sheath was inserted into the right radial artery, and both coronary arteries were cannulated with a 4 Fr Amplatz left catheter. The right and left coronary arteries were smooth and free of angiographically visible disease. There was no evidence of pressure damping during cannulation of the arteries, and reflux of contrast into the aorta during the coronary injections was observed. A large vessel was seen during injection of the left coronary artery that connected the distal circumflex artery and the right coronary artery at its crux. This vessel ran in the atrioventricular groove and filled the entire distal segment of the right coronary artery. During the right coronary injections, this vessel was seen to fill the entire left coronary arterial bed, with "reflux" of contrast from the left coronary ostium into the aorta (Figure 1). This suggested a large and low resistance communication between the two coronary arterial beds. Ventriculography was performed with a 4 Fr pigtail catheter and showed no regional wall motion abnormality and a calculated 67% ejection fraction. The patient was discharged four hours after the procedure. Patient #2. A 78-year-old male with no coronary risk factors underwent coronary angiography as part of a work-up for significant paravalvar aortic regurgitation. The right radial artery was used to secure vascular access and a 5 Fr sheath was inserted into the artery. Coronary angiography was performed with a 5 Fr Amplatz catheter. The right and left coronary arteries were normal, with a collateral vessel that connected the distal right coronary artery and the distal circumflex coronary artery, and ran in the atrioventricular groove (Figure 2). We had no information about coronary angiography before surgery. This vessel was angiographically equivalent to that seen in Patient #1. During the coronary injections, there was no evidence of pressure damping and free reflux of contrast was observed from both coronary ostia during the right coronary arterial injection. Ventriculography was not performed. Discussion. Coronary collateral circulation in the presence of obstructive coronary artery disease has been well described. In the presence of a significant lesion, the perfusion pressure in the distal vascular bed falls, which causes myocardial ischemia and leads to the recruitment of collateral arteries. These collaterals increase in size and subsequently become angiographically visible. These vessels are generally tortuous, taper toward the recipient artery, have a variable location and are usually well demarcated from the supplying and recipient arteries. In addition to a significant stenosis of the coronary arteries, anemia, cardiac hypertrophy and hypoxia can also contribute to the development of collateral coronary circulation. In our patient, none of the above listed factors were present. The presence of collaterals in patients with apparently normal coronary arteries has been anecdotal7–11 and was first described by Cheng.7 The development of the coronary arteries has been described.12 During angiogenesis, two vascular rings develop in the interventricular and atrioventricular grooves. Interruption of these vascular rings gives rise to the final coronary arterial pattern. The interventricular ring gives rise to the posterior descending and left anterior descending arteries, and the atrioventricular ring gives rise to the right coronary and circumflex arteries. This occurs simultaneously with the development of the aortic origin of the coronary arteries and their venous drainage. In light of the above developmental sequence, the absence of a coronary lesion, and the course of the vessels in the atrioventricular groove, we believe that the cases we describe represent a developmental anomaly secondary to a failure of resorption of part of the early vascular ring. In both cases, the vessel was smooth, straight and non-tapering, and it was not possible to judge where the native coronary artery ended and the collateral vessel commenced. Of the cases reported,8–11 three vessels ran in the atrioventricular groove and one in the interventricular groove. The course of the vessel did not appear to be intersulcal in only one case;7 this patient had chronic obstructive lung disease and corpulmonale, with an electrocardiogram showing severe right ventricular hypertrophy and severely elevated pulmonary arterial pressures at right heart catheterization. Right ventricular angiography revealed marked ventricular and conus hypertrophy and moderate tricuspid regurgitation. The vessel connected the conus branch of the right coronary artery and the proximal left anterior descending artery. This vessel was clearly tortuous, had a diminishing caliber as it reached the left anterior descending artery and was not intersulcal in location. The author suggests that this vessel may have developed as a consequence of hypoxia, polycythemia and right ventricular hypertrophy. In conclusion, we believe that collateral coronary vessels are of two types, congenital and acquired. The acquired forms arise as a consequence of coronary stenosis or are in relation to ventricular hypertrophy and hypoxia. The angiographic appearance clearly separates the congenital and acquired forms. The absence of coronary arterial stenosis, intersulcal location, nontapering appearance, absence of tortuosity, and the absence of a clear delineation of the collateral favor a congenital origin. In contrast, the presence of coronary stenosis, tortuosity, tapering appearance, nonsulcal location, and the ability to delineate the collateral vessel favor an acquired coronary collateral vessel. We believe that the cases presented here and those reported by others8–11 are congenital collateral arteries, with the exception of the case reported by Chen.7 Second, the presence of collaterals does not always imply the presence of obstructive coronary artery disease. The uncommon presence of such collaterals in normal subjects may have a protective role if the patient develops coronary artery disease.

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