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HR, 0.467; 95% CI, 0.223–0.976; P=0.043). Statin-naïve/ LDL-C <100 mg/dl patients was associated with increased shortterm mortality. Although the mechanisms of the cholesterol paradox are not clearly understood, they may be related to confounding by baseline characteristics.3 However, in the present study, the combination of statin treatment and LDL-C ≥100 mg/dl was an independent predictor for lower in-hospital mortality after adjustment for general risk factors for CAD and other clinical factors.8 It is possible that a low LDL-C level may be associated with illness that leads to higher all-cause mortality, and higher LDL-C levels may reflect better nutritional and health status, which are likely related to better tolerance of acute medical stress. In a previous study, lipid-lowering therapy was underused in ACS patients with lower LDL-C levels.3 Tsai et al9 evaluated the effects of statin therapy in patients with ACS whose serum LDL-C level was ≤80 mg/dl. The incidence of events in the statin-treated group was 9.5%, which was significantly lower than the 29% incidence in the untreated group. In another study, Lee et al10 investigated the clinical outcomes of statin therapy in patients with AMI whose LDL-C levels were <70 mg/dl, and found that statin therapy was associated with improved clinical outcome. Consistent with these reports, statin therapy results in better clinical outcomes in AMI patients with lower LDL-C levels. Thus, although low LDL-C on admission may be a marker for worse clinical outcomes, early lipid-lowering therapy with statin during hospitalization may be necessary to improve short-term prognosis in patients with ACS, regardless of their LDL-C levels. Intensive lipid-lowering therapy with statins significantly reduces the risk of coronary events compared with moderate lipid-lowering therapy.6,11 The concept of “the lower, the better” was based on these previous reports, and the American College of Cardiology/American Heart Association (ACC/ AHA) guidelines set a value of <70 mg/dl as the therapeutic target for LDL-C for high-risk patients such as those with ACS. However, most randomized controlled clinical trials have compared statin with placebo or compared a high dose of statin with a standard dose of statin. In other words, the statin dosage was fixed, and the study design did not allow for the adjustment of the administered dose toward the therapeutic ypercholesterolemia, particularly an increase in the low-density lipoprotein cholesterol (LDL-C) level, has been established as one of the most important risk factors for coronary artery disease (CAD). Statins revolutionized the treatment of hypercholesterolemia, and many clinical trials have shown that LDL-C-lowering therapy with statins (hydrophilic or lipophilic) can significantly reduce the incidence of CAD in both primary and secondary prevention.1 These beneficial effects of statins are mainly related to the magnitude of LDL-C level reduction, although statins also have anti-inflammatory and anti-oxidant pleiotropic effects. Moreover, a recent study reported that statin therapy improved mortality rates in patients with heart failure.2 However, a low LDL-C level is associated with poor prognosis in patients with acute coronary syndrome (ACS) and heart failure.3–5 This is called the “cholesterol paradox”.

Low-Density Lipoprotein Cholesterol Level and Statin Therapy in Patients With Acute Myocardial Infarction (Cholesterol Paradox)