Abstract

Background: Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) effectively reduces angina symptoms and improves quality of life, but the frequency of new or residual angina (RA) in follow-up after CTO PCI and its relationship with titration of anti-anginal medications (AAM) has not been described. Methods: In consecutive CTO PCI patients treated at 12 centers in the OPEN CTO registry, angina symptoms were assessed 6 months after the index PCI using the Seattle Angina Questionnaire (SAQ) Angina Frequency scale (a score <100 defined new or residual angina). AAMs were recorded at discharge and 1 and 6 months after the index CTO PCI. AAM escalation was defined as an increase in the number or dosage of AAMs between discharge and 6-month follow-up. The proportion of patients who had escalation of AAM by 6-month follow-up was compared among those with and without 6-month angina, and analyses were repeated after stratification by the ultimate technical success of their CTO PCI (including follow-up procedures), achievement of physiologically complete revascularization during the index procedure, and presence or absence of angina at baseline. Results: Of 901 patients undergoing CTO PCI, 197 (21.9%) reported angina at 6-months. Of patients with RA, 54 (27.4%) had de-escalation, 118 (59.9%) had no change, and 25 (12.7%) had escalation of their AAM by 6 month follow-up. Although patients with residual angina were more likely to have escalation of AAMs, only 12.7% of patients with residual angina had escalation of their AAM regimens in follow-up. Results were similar when stratifying patients by the ultimate success of the CTO PCI, completeness of physiologic revascularization, and presence or absence of angina at baseline (Figure). Conclusions: One in 5 patients reported angina 6-months after CTO PCI. Although patients with new or residual angina were more likely to have escalation of AAMs in follow-up compared to those without residual symptoms, only one in 7 patients with residual angina had escalation of AAMs. These results were similar in key subgroups. Although it is unclear whether this finding reflects maximal tolerated therapy at baseline or therapeutic inertia, these findings suggest an important potential opportunity to further improve symptom control in complex stable ischemic heart disease.

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