Introduction Fractional flow reserve (FFR) guided angioplasty has been shown to have a beneficial effect on clinical outcome in patients with multi-vessel coronary disease. However, multi-vessel disease is frequently accompanied by a chronic total occlusion (CTO). We have limited understanding of the effect of the donation of a collateral supply to collateral dependent myocardium on the FFR. Marked changes in non-target vessel FFR post recanalisation of CTOs have been reported, but the consistency of this phenomenon remains uncertain and changes in haemodynamic indices immediately post-angioplasty might be confounded by the effect of the vessel trauma of angioplasty on the microvasculature. If the phenomenon is consistent, we might expect haemodynamics in a vessel donating collaterals to a CTO to be dependent on the extent of angiographic collateral flow originating from it.

Methods Prior to CTO angioplasty in 22 patients, simultaneous pressure and flow were measured at rest and during hyperaemia in the distal and proximal segment of each non-target vessel. Absolute coronary flow, coronary flow reserve, hyperaemic microvascular resistance and fractional flow reserve were calculated. Blinded to haemodynamic measurements, the major collateral donor vessel was selected and each vessel was graded by the size of the largest collateral branch which originated from it by collateral connexion (CC) grade (0 = no continuous connexion, 1 = threadlike connexion, 2 = side branch like connexion). Haemodynamic measurements were compared between the major and minor collateral donor vessels using a paired t-test.

Results All patients had right dominant coronary anatomy. The target vessel was the left anterior descending artery (LAD) in 9 patients, circumflex artery (LCx) in 2 and right coronary artery (RCA) in 11. All target vessels were filled by a modified Rentrop grade of >2 (2 n = 12, 3 n = 10). Angiographic characteristics are listed in Table 1 and haemodynamic measurements are listed in Table 2. In spite of clearly increased angiographic collateral donation, we did not identify any associated significant difference between haemodynamic indices.

Conclusion The mechanism for a large rise in non-target vessel FFR post CTO angioplasty must involve one or more of a fall in absolute flow, a fall in coronary flow reserve or an increase in microvascular resistance. One would expect that change to move towards the norm for a vessel donating fewer collateral branches. The absence of a difference in any of these haemodynamic indices between paired non-target vessels with differing CC grades (and therefore different extents of collateral ‘donation’) would suggest thatthe large changes in FFR which have been reported might only represent a publication biassed measurement extreme, rather than the rule.