The role of coronary collaterals in chronic total occlusions

Abstract

A chronic total occlusion (CTO) describes a completely occluded coronary artery. This type of lesion is found in about 18% of all significant lesions in patients with coronary artery disease. A system of collateral connections are observed in almost all of these lesions, which have the capacity to prevent myocardial necrosis and may even uphold metabolic supply to the territory distal to an occlusion to maintain full contractile capacity. During exercise these collaterals are limited in their functional reserve, and more than 90% of patients with a well collateralized occlusion will experience ischemia. in the absence of ideal animal models that mimic the human collateral circulation, we need to rely on studies in man. The knowledge of collateral physiology in man has increased considerably over the past two decades with the advent of intracoronary sensors of coronary pressure and flow velocity. A number of basic physiologic questions have been answered by these studies. The blood supply through coronary arteries depends on a complex array of in general serial resistance systems, with an additional array of multiple parallel resistances on the collateral level. There seems to be a great interindividual variability in the ability to recruit preformed collateral connections in the case of an epicardial occlusion. Collateral function can develop to a similar functional level in patients post myocardial infarction with large akinetic territories as it does in patients with normal preserved regional function. The presence of viability is thus not a prerequisite for collateral development. The question of practical relevance in the era of interventional therapy of chronic occlusions is also, whether a patient with coronary artery disease will remain protected by collaterals after removing the obstruction in the collateralized artery, or whether collaterals regress and lose their functional capacity. Both developments are observed again mainly depending of individual predisposition.

Figures

Fig. (1)

Schematic presentation of the electric analog model of coronary and collateral circulation (left), and of the experimental setup (right). Mean aortic pressure (PAo) is recorded via the guiding catheter. Pressure at the takeoff of the collateral in the donor artery (PD) is recorded before recanalization, as well as the coronary flow reserve (CFR)D in the donor artery. Collateral blood flow velocity (APVOccl) and pressure (POccl) are recorded distal to the occlusion before balloon dilatation, and CFRR in the recanalized artery at the end of the procedure. The resistance of the occlusion (ROccl) is infinitesimal, and resistance indexes are calculated to describe the donor (RD) and collateral resistance (RC), and the microvascular resistance distal to the occlusion (RP). PRA = mean right atrial pressure. Reprint from 27 with permission.

Fig. (2)

The distribution of fractional flow reserve (FFR) measured distal to a CTO during systemic adenosine infusion, based on data published in 30. The dotted line indicates the mean value of all 94 measurements of 0.29.

Fig. (3)

Dynamics of the angiographic appearance of collaterals. A 50 year old patient with chronic occlusion of the right coronary artery (RCA) (A, open arrow) and the circumflex artery (LCX) (B, open arrow). Collaterals supply both CTOs. The RCA CTO extends proximal until the distal bifurcation at the crux cordis, and receives both ipsilateral collaterals from the proximal RCA (A, closed arrow, CC2 size) and contralateral collaterals from the left coronary system via septal branches (B, closed arrow, CC2 size). The LCX CTO is filled distally via ipsilateral bridging collaterals along the CTO (B). The RCA was then recanalized, and the final image shows already no longer a filling of the ipsilateral collateral (C). Distally a branch is marked by a dashed arrow. Four months later the patient was re-examined to perform the recanalization of the LCX CTO. At that time the RCA branch is now fully developed as a major contralateral collateral towards the LCX CTO (D, dashed arrow), while the ipsilateral collaterals visible on B as bridging collaterals are no longer visible (E), and the antegrade filling of the LCX distal to the CTO is obscured now by contralateral collateral washout.