According to the LDL-C hypothesis, LDL-C is a causative factor in atherosclerosis. Although the hypothesis is generally accepted, controversy continues about its validality.10–11 Evidences supporting this hypothesis emerge from experimental models, epidemiological cohorts, and cholesterol-lowering (mainly statin-based) clinical studies.12 However, the remaining conflicts should be considered.
Many studies have shown us that there is an important link between LDL-C and atherosclerotic cardiovascular disease.13 Therefore, we consider the LDL values as we are choosing the adequate treatment. Many clinical trials recommend statin therapy to manage LDL levels. 14–17 We also aim to maintain the HDL in adequately higher levels. In fact, since rosuvastatin and simvastatin are thought to have the effect on increasing HDL-C, we also prefer these statins in our patient groups.18 Therefore, that it is important to determine which of these laboratory parameters play a role in the process of artery atherosclerosis. In this study, we aimed to understand the relation between the HDL, LDL, cholesterol levels and the atherosclerosis in large vascular structures such as ascending aorta.
American Diabetes Association (ADA) and the American College of Cardiology (ACC) arrived at a consensus and published that non-HDL-K is a better indicator for identifying patients with high cardio-metabolic risk factors.19 Srinivasan et al. reported that non-HDL-K levels may be useful for the determination of lipoprotein-related risks.20 In our study, we investigated LDL and HDL values during the follow-up periods. 7 of 27 patients with LDL > 100 mg/dl and 10 of 33 patients with HDL < 45 mg/dl were in the atherosclerosis group but there was no statistically significant difference in these groups. The non-HDL-C which was used in the Srinivasan et al. study was not used in our study. There might be a statistically difference between the atherosclerosis and the non-atherosclerosis group, if it was used. In subsequent studies, non-HDL-C will be used along with the other lipid markers. Despite the importance of LDL-C, it may not be that cost-effective. There are many studies investigating for an easy and reliable methodology for its routine use.21 Since it is affordable and easy to use, Friedewald Formula (FF) is an easy and widely used method. However, while using this formula, if triglyceride is over 400 mg / dl, it causes the very low density lipoprotein (VLDL) to be over calculated and the LDL to be under calculated. This miscalculation raises doubts about if LDL is truly related with atherosclerosis. In our study, there were 1 patient with triglyceride over 400 in the atherosclerosis group and 2 patients in the non-atherosclerosis, which was not statistically significant.
Youn et al. examined the carotid intima media layers thickness in 1700 subjects and it appeared to be associated with increased body mass index (BMI) and high LDL cholesterol in healthy individuals.23 The LDL value was 113.1 ± 31.9 mg/dl in the male patients and 117.3 ± 32.2 mg/dl in the female. In our study, LDL mean ± std value was 99.64 ± 29.95 mg/dl in the group with atherosclerosis and 115.24 ± 40.44 mg/dl in non-atherosclerosis. No statistically significant difference was found between both LDL and BMI values and presence of atherosclerosis. (p: 0.221)
In a PESA study with 1779 subjects by L.Fernández-Friera et al.24, patients were examined by Doppler USG or CT. More than 0.5 mm thickening in the intima media or 1.5 mm intima thickness towards the lumen in the carotid arteries or infrarenal aorta was considered as atherosclerosis. BMI was 24.5 ± 3.3 kg/m2 in the non-atherosclerosis group and 25.3 ± 3.4 kg/m2 in the group with atherosclerosis. There was no statistical difference. Total cholesterol values were 187.0 ± 24.4 mg/dl in the non-atherosclerosis group and 194.6 ± 22.9 mg/dl in the group with atherosclerosis. The LDL was 125.7 ± 20.1 mg/dl versus 117.4 ± 21.7 mg/dl. The HDL value was 53.5 ± 10.1 mg/dl versus 55.4 ± 10.6 mg/dl. The triglyceride was 63 (50–83) mg/dl versus 68 (53–92) mg/dl. In our study, the triglyceride was 167.61 ± 105.06 mg/dl in the non-atherosclerosis group, while it was 148.21 ± 89.68 mg/dl in atherosclerosis group. Total cholesterol was 173.91 ± 41.36 mg/dl versus 156.79 ± 36.36 mg/dl. LDL value was 115.24 ± 40.44 mg/dl in the non-atherosclerosis group and it was 99.64 ± 29.95 mg/dl in the atherosclerosis group. HDL was 41.42 ± 12.53 mg/dl versus 42.57 ± 15.41 mg/dl. In our study, no statistically significant difference was found.
There are studies showing that there is a relationship between HbA1c and subclinical atherosclerosis. In 2,340 non-diabetic individuals, higher HbA1c concentrations (between 5.7% and 6.4%) were associated with increased carotid intima-media thickness.25 In an another prospective series (n = 2.652) with non-diabetic patients, HbA1c which in the near-highest level (> 5.7%) was associated with progression of both carotid intima-media thickness and cardiovascular events.26 In our study, the HbA1c was 5.4 ± 0.3 in the group without atherosclerosis and 5.6 ± 0.2 in the group with atherosclerosis. No statistically significant difference was found.
In a study with 91 patients, the relationship between LDL-K and ascending aorta was examined. LDL-K was observed to have a linear relationship with the ascending aorta diameter which was measured as 40.5 ± 7.3 mm. In our study, it was measured as 35.35 ± 3.47 mm in the group without atherosclerosis and 35.07 ± 4.78 mm in the group with atherosclerosis. However, it was not statistically significant.
The shortcomings of our study are; insufficient number of patients and taking tissue samples from plaque free areas of ascending aorta, as its required in CABG procedure. Therefore, since this region (calcific/fibrotic plaque) is avoided, the plaque load may be considered less.
As a result, in our study, no significant difference was found between HDL-C, LDL-C, triglyceride, total cholesterol values and the pathological process of aortic atherosclerosis. As a result of this study, we believe that it was necessary to correct the error margins of these parameters. In addition, it required the need for a clearer laboratory parameter to demonstrate atherosclerosis.