Reply to “Small Dense Low-Density Lipoprotein Could Be Used as a Therapeutic Marker for Treatment in Patients With Acute Coronary Syndrome”

We thank Yildirim and colleagues ¹ for their interest on our article ² and their insightful comments. We agree with them about the potential limitations of measuring small-dense low-density lipoprotein (sdLDL) in patients with acute coronary syndrome (ACS). In our study, we found that baseline concentrations of sdLDL were significantly higher in patients presenting with ACS in comparison with healthy controls, whereas low-density lipoprotein cholesterol and total cholesterol levels were comparable between patients with coronary artery disease and controls. We further observed that in the next 24 hours following the onset of ACS, the sdLDL levels decreased in patients with ACS, although this did not attain significance nor did the changes in sdLDL values differ significantly between patients with myocardial infarction and patients with unstable angina. As we mentioned in the main article, the first blood sample was collected after patient admission and diagnosis of ACS. All the patients were treated with heparin following the diagnosis of ACS. The second blood sample was collected 24 hours after admission.

We knew that heparin can affect the patients’ levels of lipid profile as reported previously ³ but it was not ethically appropriate to randomize patients to a non-heparin arm. Miida et al ³ also mentioned in their study that heparin affects the lipoprotein concentration in a dose-dependent manner. Although, it was not the purpose of the main article; we reanalyzed the data to look at sdLDL levels based on heparin treatment received. For various reasons, about 40% of the patients in the ACS group did not undergo any invasive procedure such as angiography or coronary angioplasty. Thus, we divided the patients with ACS into 2 groups, those who underwent coronary intervention (n = 122) and those who did not (n = 82). In this regard, the changes in sdLDL (first sample − second sample sdLDL concentrations) were calculated in patients without any procedure (1.38 ± 0.18 mg/dL) and in patients who underwent angiography or coronary intervention (1.78 ± 0.21 mg/dL), and then compared these values, but the analyses failed to show any significant difference (P = .0.899). Both the groups of patients received heparin, while the patients with coronary angiography received much higher levels of heparin because of catheterization procedure, but the changes in sdLDL levels were not significantly different between the 2 groups, indicating that heparin administration does not have a significant effect on sdLDL levels in this group of patients. We have to mention that this was not the main purpose of our study, and thus this result should be further studied. If this result (heparin may not affect sdLDL concentrations) was confirmed by future studies that would be very interesting as Miida ³ recommend avoiding analysis of routine lipoprotein profiles after coronary angiography and angioplasty, but using sdLDL, we can monitor the changes in lipoproteins more accurately.

Ultimately, our results indicate higher levels of sdLDL in patients with ACS than healthy participants, and the changes in sdLDL levels were not significantly different between the first and second blood samples. The use of sdLDL in routine clinical practice should be further studied to determine the actual role of sdLDL in the patient’s treatment. In regard to the use of sdLDL in routine clinical practice, we think that some issues such as the importance of size or sdLDL concentrations should be addressed first during the treatment of patients with cardiovascular disease and the effect of reducing sdLDL levels by the treatment on cardiac events.