Significant Difference in Acute Coronary Lesions in Patients on Therapeutic Statin Therapy Compared to Those Without

Background Statin therapy has been shown to alter coronary plaque via decreasing lipid-rich pools, substituting with fibrocalcific plaque. We propose that acute coronary lesions in patients on therapeutic statin therapy, compared with patients not on statin therapy with elevated low-density lipoprotein (LDL) levels, will have features typically not associated with lipid-rich disease, such as lengthy fibrocalcific lesions, stent failure (in-stent restenosis and stent thrombosis), and/or bypass graft degeneration. Methods Charts and coronary angiograms of 143 consecutive patients from May 2016 to December 2018 with Type 1 Myocardial Infarction Fourth Universal Definition were retrospectively reviewed. Patients were divided into two groups: group 1, those on statin therapy with an LDL < 100 mg/dL, and group 2, those not on statin therapy with an LDL ≥ 100 mg/dL at the time of an acute coronary syndrome. Acute lesion characteristics and angioplasty techniques/equipment were recorded. Results There were 56 patients in group 1 and 39 patients in group 2. Group 1 patients, compared with group 2, were more likely to have moderate-severe vessel calcification (55.4% vs 10.3%; p < 0.01), lesion length greater than 20 mm (51.8% vs 23.1%; p = 0.019), stent failure (39.3% vs 7.7%; p < 0.01), and bypass graft failure (23.2% vs 7.7%; p = 0.04). Coronary interventions in group 1, compared with group 2, more often required adjunctive angioplasty techniques, including the need for multiple coronary wires, guide extender, thrombectomy, and circulatory support (51.8% vs 7.7%; p < 0.01). There was no significant difference between the number of culprit vessels, including the specific coronary culprit vessel identified between both groups. Conclusion Acute coronary lesions in patients on therapeutic statin therapy, compared to those not on statin therapy with an elevated LDL, tend to be longer, more calcific with increased vessel tortuosity and angulation, as well as from a stent or bypass graft failure mechanism. Furthermore, there is a signal for heightened procedural complexity in the arm with statin therapy. These clinical findings are likely the result of the altered natural history of plaque pathophysiology seen with statin therapy.