Abstract 2721: Therapeutic Effect of Drag Reducing Polymers on Coronary Flow Reserve
Background: We have shown in dogs that during coronary stenosis (STN), drag reducing polymers (DRP) reduce microvascular resistance, restore perfusion, and improve flow reserve to the stenotic bed. It is known that coronary STN impairs flow reserve in the adjacent collateral-supplying bed. We studied the effects of DRPs on flow reserve in an adjacent non-stenotic artery and its relationship to DRP-induced improvements in flow reserve in a stenotic bed.
Methods: Flow probes were placed on the left anterior descending (LAD) and circumflex (CX) arteries in 10 dogs. Hyperemia (HYPER) was induced with an A2A receptor agonist. A non flow limiting LAD STN was created (gradient 17 ± 3 mmHg). Ultraharmonic myocardial contrast echo (MCE) was performed at: Baseline; STN; HYPER; HYPER + STN; and HYPER + STN + DRP. MCE data in the LAD and CX regions were fit to: y=A(1-e−βt), where ‘A’ and ‘β’ are intramycardial blood volume and RBC velocity, and A x β reflects flow. Probe flow, ‘β,’ and ‘A’ reserve were calculated as the ratio of each parameter during HYPER to its baseline value.
Results: LAD STN decreased LAD flow reserve relative to baseline (3.8 ± 0.3 to 1.5 ± 0.1 p<0.005), which was associated with a decrease in β reserve (1.7 ± 0.3 to 0.8 ± 0.1, p <0.03) and trend towards decreased ‘A’ reserve. During HYPER + STN, DRP increased LAD β reserve (p<0.03), resulting in an increase in MCE hyperemic flow relative to STN + HYPER (p<0.05); this occurred with no change in epicardial LAD probe flow. LAD STN decreased CX probe flow during HYPER (125 ± 19 to 110 ± 18 ml/min, p<0.05); DRP further decreased CX probe flow (110 ± 18 to 88 ± 16 ml/min, p<0.0005). Thus, CX flow reserve decreased vs. baseline (from 4.1 ± 0.3 to 3.0 ± 0.3, p<0.005) and further decreased with DRP (3.0 ± 0.3 to 2.4 ± 0.2, p<0.003).
Conclusions: Coronary STN impairs flow reserve in the adjacent non-stenotic collateral-supplying coronary artery. DRPs improve flow reserve in the STN bed, but at the expense of further flow reserve impairment in the non-stenotic coronary. Because anterograde flow via the STN artery does not increase, DRPs most likely recruit collateral flow from the adjacent bed, and this is responsible for the divergent changes in flow reserve. This has important therapeutic implications for patients with coronary artery disease.