Endothelial and Smooth Muscle Cells Dysfunction Distal to Recanalized Chronic Total Coronary Occlusions and the Relationship With the Collateral Connection Grade

Objectives This study sought to assess the vascular function in patients with chronic total coronary occlusions (CTO) immediately after successful percutaneous recanalization and its relation with the pre-existing collateral circulation. Background CTOs represent a long-acting occlusion of a coronary vessel, in which the progressively developed collateral circulation may limit ischemia and symptoms. However, it is unknown if the coronary segment distal to the occlusion has a preserved vascular function. Methods We prospectively enrolled 19 consecutive patients, after percutaneous coronary intervention of a CTO. Luminal diameter, measured by quantitative coronary angiography, and coronary blood flow at level of epicardial coronary artery distal to the treated CTO was assessed before and after administration of acetylcholine (Ach), adenosine, and nitroglycerin (NTG). Collaterals were assessed angiographically by grading of Rentrop and of collateral connections (CC1: threadlike continuous connection; CC2: side branch-like connection). Results Overall, Ach and adenosine caused coronary artery vasoconstriction (p = 0.001 and p = 0.004, respectively), whereas NTG failed to induce vasodilation (p = 0.084). Coronary blood flow significantly decreased with Ach (p = 0.005), significantly increased with NTG (p = 0.035), and did not change with adenosine (p = 0.470). Patients with CC2 collaterals (n = 8) had less vasoconstriction response and reduction in coronary blood flow after Ach (p = 0.005 and p = 0.008, respectively), and better vasomotor response to NTG (p = 0.029) than patients with CC1 collaterals (n = 11). Conclusions Significant endothelial and smooth muscle dysfunction is present in the distal segments of successfully recanalized CTOs, and that seems to be more pronounced in the presence of a low grading of collateral circulation. (J Am Coll Cardiol Intv 2012;5:170-8) (C) 2012 by the American College of Cardiology Foundation