452 Saline-induced coronary hyperaemia is mediated by intravascular haemolysis

Aims Absolute coronary blood flow can be measured by intracoronary continuous thermodilution of saline through the lateral side holes of a dedicated infusion catheter placed in the proximal segment of the coronary artery. A room-temperature saline infusion rate at 15–20 ml/min induces an immediate, steady-state, maximal microvascular vasodilation. The mechanism of this hyperemic response remains unclear. The aim of the present study is to test whether local haemolysis is a potential mechanism of coronary hyperaemia. Methods and results Twelve patients undergoing left and right catheterization were included. The left coronary artery and the coronary sinus were selectively cannulated. Absolute resting and hyperemic coronary flow were measured using the continuous intracoronary thermodilution of saline through a dedicated infusion catheter (RayFlow®). Arterial and venous samples were collected from the coronary artery and the coronary sinus in five phases: baseline (BL); resting flow measurement (Rest, saline infusion at 10 ml/min); hyperaemia (Hyperaemia, saline infusion at 20 ml/min); post-hyperaemia [Post-Hyperaemia, 2 min after the cessation of saline infusion; and control phase (Control, during infusion of saline through the guide catheter at 30 mL/min). Haemolysis was visually detected only in the centrifugated venous blood samples collected during the Hyperaemia phase. As compared to Rest, during Hyperaemia both LDH [131.50 ± 21.89 U/dL (Rest) and 258.33 ± 57.40 U/dl (Hyperaemia), P < 0.001] and plasma-free haemoglobin [PFHb, 4.92 ± 3.82 mg/dl (Rest) and 108.42 ± 46.58 mg/dl (Hyperaemia), P < 0.001] significantly increased in the coronary sinus. The percentage of haemolysis was significantly higher during the hyperaemia phase [0.04 ± 0.02% (Rest) vs. 0.89 ± 0.34% (Hyperaemia), P < 0.001]. Conclusions Saline-induced hyperaemia through a dedicated intracoronary infusion catheter is associated with haemolysis. Vasodilatory compounds released locally, like ATP, are likely ultimately responsible for localized microvascular vasodilation. The role of other substances released by erythrocytes in inducing hyperaemia cannot be excluded and requires further investigations.