BACKGROUND: Statins are reportedly effective in the primary and secondary prevention of cardiovascular disease, mainly due to their ability to aggressively reduce low-density lipoprotein cholesterol (LDL-C) levels. However, patients sometimes exhibit the so-called "statin escape" phenomenon. The purpose of our study was to investigate the impact of the statin escape phenomenon on long-term clinical outcomes in patients with acute myocardial infarction (AMI). METHOD: This was a subgroup analysis of 1144 patients from the Nagoya Acute Myocardial Infarction Study (NAMIS) treated between January 2004 and December 2012. We analyzed 660 patients who initiated statin treatment after AMI. Statin escape phenomenon was defined as an increase in the LDL-C levels during the 9-month treatment period by >10% of the initial values after 4 weeks of initiating statin treatment. Patients were divided into two groups depending on whether they exhibited the statin escape phenomenon, with 474 patients in the non-escape group and 186 patients in the escape group. RESULT: Compared to the non-escape group, the escape group showed significantly lower LDL-C levels at 4 weeks after treatment initiation (81.3 ± 20.1 mg/dL vs. 101.1 ± 25.4 mg/dL, P < 0.01). By contrast, the escape group showed significantly higher LDL-C levels at 9 months after treatment initiation (105.8 ± 28.3 mg/dL vs. 90.3 ± 22.6 mg/dL, P < 0.01). Major adverse cardiac and cerebrovascular events (MACCE; a composite of all-cause death, MI, and stroke) were more frequent in the escape group than in the non-escape group (10.8% vs. 6.1%, P = 0.03). Multivariate analysis showed that statin escape phenomenon was an independent predictor of MACCE (hazard ratio: 2.02, 95% confidence interval: 1.11-3.66, P = 0.02). CONCLUSION: Statin escape phenomenon may be an independent predictor of long-term clinical outcomes in AMI patients.
BACKGROUND: Statins are reportedly effective in the primary and secondary prevention of cardiovascular disease, mainly due to their ability to aggressively reduce low-density lipoprotein cholesterol (LDL-C) levels. However, patients sometimes exhibit the so-called "statin escape" phenomenon. The purpose of our study was to investigate the impact of the statin escape phenomenon on long-term clinical outcomes in patients with acute myocardial infarction (AMI). METHOD: This was a subgroup analysis of 1144 patients from the Nagoya Acute Myocardial Infarction Study (NAMIS) treated between January 2004 and December 2012. We analyzed 660 patients who initiated statin treatment after AMI. Statin escape phenomenon was defined as an increase in the LDL-C levels during the 9-month treatment period by >10% of the initial values after 4 weeks of initiating statin treatment. Patients were divided into two groups depending on whether they exhibited the statin escape phenomenon, with 474 patients in the non-escape group and 186 patients in the escape group. RESULT: Compared to the non-escape group, the escape group showed significantly lower LDL-C levels at 4 weeks after treatment initiation (81.3 ± 20.1 mg/dL vs. 101.1 ± 25.4 mg/dL, P < 0.01). By contrast, the escape group showed significantly higher LDL-C levels at 9 months after treatment initiation (105.8 ± 28.3 mg/dL vs. 90.3 ± 22.6 mg/dL, P < 0.01). Major adverse cardiac and cerebrovascular events (MACCE; a composite of all-cause death, MI, and stroke) were more frequent in the escape group than in the non-escape group (10.8% vs. 6.1%, P = 0.03). Multivariate analysis showed that statin escape phenomenon was an independent predictor of MACCE (hazard ratio: 2.02, 95% confidence interval: 1.11-3.66, P = 0.02). CONCLUSION: Statin escape phenomenon may be an independent predictor of long-term clinical outcomes in AMI patients.