Abstract 16364: The Lipid Paradox: Lowest Level of LDL-C Associated with Increased In-Hospital Mortality in Patients Following Acute Myocardial Infarction

Abstract

Background: Lipoprotein levels are recognized as independent risk factors for long-term cardiovascular (CV) events in patients with acute myocardial infarction (AMI). During the acute phase reaction following AMI, previous studies have reported trends of decreased LDL-C, increased triglycerides (TG), and variable HDL-C levels, often proportional to the severity of myocardial necrosis. However, the association between LDL-C and HDL-C levels and in-hospital mortality has not been well established.

Methods: NRMI 4-5 records from 2002 to 2006 were analyzed in patients hospitalized for AMI with lipid samples measured within 24 h of presentation. The relationship between lipid levels and in-hospital all-cause mortality was evaluated using multivariable-adjusted logistic regression models.

Results: Lipid levels were measured in 114 584 patients with mean LDL-C 104.3 ± 37.7, HDL-C 40.6 ± 13.6, and TG 150.0 ± 97.4 (mg/dL). Compared with the lowest quartile of LDL-C (<77 mg/dL), there was a lower risk of in-hospital mortality in the 2nd, 3rd, and 4th quartiles (adj. odds ratio [OR] = 0.79, 0.80 and 0.86, respectively; P ≤ 0.001). For HDL-C, only those in the lowest quartile (<31 mg/dL) had a higher risk of in-hospital mortality (adj. OR = 1.20; P < 0.001) compared with the highest quartile (≥47 mg/dL).

Conclusion: In this nationally representative AMI cohort, the lowest quartiles of LDL-C and HDL-C were associated with increased risk of all-cause in-hospital mortality. Consistent with previous analyses, lowest HDL-C levels were associated with increased in-hospital mortality. However, results of the in-hospital LDL-C and mortality analysis suggest a lipid paradox and are contrary to accepted findings outside of the acute setting. Further evaluation of this lipid paradox in the acute setting is warranted, including exploration of the relationship between very low levels of LDL-C, myocardial necrosis, and subsequent adverse CV events.