Is It Possible to Predict the Atherosclerosis in Aorta by the Patients Lipids Panel?

doi:10.21203/rs.3.rs-29282/v1

PDF

Research

Is It Possible to Predict the Atherosclerosis in Aorta by the Patients Lipids Panel?

https://doi.org/10.21203/rs.3.rs-29282/v1

This work is licensed under a CC BY 4.0 License

Version 1

posted 19 May, 2020

You are reading this latest preprint version

Background and Aim: Atherosclerosis is a chronic inflammatory event that characterized by stiffness and thickening of the vascular walls. In our daily practice, we assume the atherosclerotic potential of the patient by following the total cholesterol, HDL, LDL and triglyceride levels (Lipids panel). We aimed to understand the relation between the HDL, LDL, cholesterol levels and the atherosclerosis in large vascular structures such as ascending aorta.

Methods: We have searched for atherosclerosis in the aortic tissue samples with 48 patients. It is a study in which we examine the correlation of preoperative cholesterol values (HDL, LDL, triglyceride, total cholesterol) by dividing the patients into two groups according to the presence of plaque.

Results: 43 males (89.6%), and 5 females (10.4%) patients between 39 and 81 years of age were included in the study. There was no statistically significant difference between the patients' preoperative cardiovascular risk assessments. The free T3 values were within the normal range with of all patients, however there was a difference that patients in the non-atherosclerosis group have lower values. There was no statistically significant difference between two groups' HDL, LDL, total cholesterol, triglyceride parameters.

Conclusion: 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.

Cardiac & Cardiovascular Systems

Endocrinology & Metabolism

Lipoproteins

Atherosclerosis

LDL Cholesterol

There are many reasons among cardiovascular risk factors (CVRF), and the most important of these are diabetes mellitus (DM), smoking, high body mass index (BMI), high blood pressure and atherosclerosis.¹ The actual number of patients with atherosclerosis and cardiovascular disease is quite high, even if their cardiovascular risk are resulted low. Atherosclerosis remains as an important risk factor with coronary artery disease and peripheral vascular diseases in middle-age asymptomatic patient groups where there are no other risk factors mentioned.^2,3 In middle-age group patients with low CVRF, it is seen that if they are classified by coronary artery classification or carotid ultrasound, approximately 60% of them have subclinical atherosclerosis.⁴

Atherosclerosis is a chronic inflammatory event that characterized by stiffness and thickening of the vascular walls. Local vascular damage, inflammation and oxidative stress are the basis of its pathology. Vascular endothelial damage can be count as the first step of this process. Platelet and leukocyte adhesion and lipid accumulation occur in this damaged area. These adhesive cells release endothelial-induced growth factor and therefore cause smooth muscle cell proliferation.⁵ Atherosclerotic plaque has content rich in cholesterol and fatty acid. Besides, lipoproteins responsible with carrying cholesterol and fatty acid which makes it significantly important for plaque build-up. Relationship between atherosclerosis and low-density lipoproteins (LDL) was described in the study of Austin et al. for the first time.⁶ LDL is a cholesterol-rich triglyceride-poor molecule. Goldstein at al. defined the LDL receptors⁷, thus we now have more detailed information about LDL. It is known that there is an inverse proportional relationship between triglyceride and high density lipoprotein (HDL) levels. It is considered that HDL does its work by moving cholesterol in the opposite direction. Indeed, HDL reduces atherosclerotic plaque build-up by protecting the LDL from oxidation.⁸ Also, triglyceride (TG) has an effect on atherosclerosis independently from HDL and LDL. Increase in TG level causes a decrease in serum HDL level and an increase in LDL. Under normal circumstances, TG does not accumulate in the vascular wall normally, but it tends to pass to the sub-endothelial cavity through the damaged endothelium when TG-rich lipoprotein levels increase in blood. This pathologic accumulation increases oxidation and smooth muscle proliferation, and contributes to the formation of atheroma plaques. ⁹

In the light of these, in our daily practice, we assume the atherosclerotic potential of the patient by following the total cholesterol, HDL, LDL and triglyceride levels (Lipids panel). According to the patients’ laboratory results, we determine our anti-atherosclerotic treatment so as to reduce cardiovascular risk. 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.

Study Design

For 10 weeks starting in June 2019, we evaluated the patients who underwent coronary artery bypass grafting due to isolated coronary artery disease. Only elective cases with patients over 18 years of age were included in the study. Emergency cases and patients who had full arterial grafts were excluded from the study. HDL, LDL, triglyceride and total cholesterol levels were checked preoperatively. We have searched for atherosclerosis in the aortic tissue samples with 48 patients. It is a study in which we examine the correlation of preoperative cholesterol values (HDL, LDL, triglyceride, total cholesterol) by dividing the patients into two groups according to the presence of plaque.

Laboratory Evaluation

Venous 8 milliliters (ml) of blood was drew from each patient into tubes without anticoagulants. These blood samples were left for clot formation for 20 minutes before centrifugation for a minimum of 10 minutes at 4000 rpm within total 30 minutes. Total cholesterol, triglyceride, HDL-cholesterol (HDL-C) plasma concentrations of the serum samples were evaluated with enzymatic chemical cleaning method using Cobas 6000 (Roche Diagnostics GmbH, Mannheim, Germany). LDL cholesterol(LDL-C) values were calculated by the Friedewald formula. The threshold value for HDL-C is 45 mg / dl, 70 mg / dl for LDL-C (for high-risk patients), 200 mg / dl for triglyceride, 200 mg / dl for total cholesterol. Accepted values for LDL should be < 100 mg / dl in moderate risk group, and < 70 mg / dl for high risk groups. Since all of our patients were at high risk, our threshold value in LDL is also 70 mg / dl.

Sampling the ascending aortic tissue

The proximal anastomoses of saphenous vein grafts are performed on the aorta while coronary artery bypass grafting (CABG). We chose the correct region for anastomoses after manual examining the presence or absence of hard plaque in the aortic tissue. While aortic side or cross-clamping during the CABG, a small incision was made on the aorta using No: 11 scalpels. After that, aortic tissue samples were taken by using aortic punch (IBC Aortic Punch size: 4.0 mm / 4.4 mm ®) (Fig. 1)

Pathology Evaluation

The aortic tissue samples stored with gluteraldehyde solutions under sterile conditions and taken to the pathology laboratory. Tissue samples were processed by routine clinical laboratory methods, being fixed in 10% formaldehyde and embedded in paraffin wax. Tissue sections were cut, using a microtome, at 5 micrometer thickness, placed onto glass slides, and the sections were stained with hematoxylin and eosin(H&E) and examined under the light microscope. Histochemical evaluation was done with orcein.

Vascular atherosclerosis were classified as AHA lesion type I, II, III, IV,V or VI plaques by two independent reviewers blinded to histopathology.¹⁰ (Figure-2) (Table-1) In histopathologic examination, the evaluation of type 3,4,5 and 6 was considered significant in terms of atherosclerosis in our study and was selected into atherosclerosis group.

Type 1	Initial lesion (isolated macrophage foam cells)
Type 2a	type prone to progression of atherosclerosis (mainly intracellular lipid accumulation)
Type 2b	type resistant to progression of atherosclerosis
Type 3	Pre-Atheroma (type 2 + small extracellular lipids pool)
Type 4	Atheroma ( type 2 + core of extracellular lipid)
Type 5a	Fibro atheroma (lipid core + fibrotic layer or multiple lipid core)
Type 5b	Calcific lesion (fibrotic layer, mainly calcific)
Type 5c	Fibrotic lesion (fibrotic layer, mainly fibrotic)
Type 6	Lesion with surface defect, and/or hematoma-hemorrhage, and/or thrombotic deposit (surface defect, hematoma-hemorrhage, thrombus)

Table 1

Atherosclerotic Lesions in Histological Classification (Appearance With the Eyes)

Statistical Analysis

SPSS v21.0 and Microsoft Office Excel 2016 were used for data collection and analysis. Categorical variables are expressed in frequency (n) and percentage (%), while continuous variables were expressed as mean ± standard deviation and median (smallest-largest value). The suitability of the data to normal distribution was evaluated by the coefficient of variation, histogram curves and Shapiro Wilk Test. While chi-square test and fisher's exact test are used to evaluate the difference between groups for categorical variables; Independent groups t test was used if normal distribution conditions were provided in evaluating the difference between two independent groups for continuous variables. In cases where normal distribution conditions are not met, Mann Whitney U test was used. Statistical significance value was taken as p < 0.05 in the analyzes.

	No Atherosclerosis		Atherosclerosis		P value
	Mean ± std	Median	Mean ± std	Median
Age	64.91 ± 8.91	65(48–83)	59.50 ± 10.54	58.5(39–76)	0.076ǂ
Smooking (Pack-year)	27.44 ± 27.57	25(0-100)	21.57 ± 18.23	18.5(0–55)	0.755*
ECO (EF%)	52.53 ± 9.18	57.5(32–60)	55.07 ± 6.12	57.5(42–60)	0.535*
Ascending Aorta	35.35 ± 3.47	35(30–45)	35.07 ± 4.78	36(28–47)	0.820ǂ
BMI(Kg/m²)	26.88 ± 4.74	26.55(20.2–40.4)	27.47 ± 3.12	27.38(22.77–33.06)	0.460*
WBC	8.27 ± 2.32	8.15(4.6–14.6)	8.12 ± 2.35	7.9(5.1–13)	0.733*
Lymphocyte	1.99 ± 0.92	1.8(0.9–5.7)	2.21 ± 0.82	1.9(1.5–4.2)	0.270*
Neutrophils	5.30 ± 2.10	4.95(1.2–12.5)	5.43 ± 2.03	4.85(2.7–9.4)	0.981*
Hematocrit	38.49 ± 4.18	39.35(28.8–46.4)	37.35 ± 3.85	37.7(30.44–44.3)	0.383ǂ
Creatinine	0.91 ± 0.21	0.9(0.5–1.69)	0.90 ± 0.34	0.82(0.54–1.8)	0.266*
TSH	1.98 ± 1.87	1.55(0.03–10.47)	1.53 ± 0.75	1.59(0.7–3.53)	0.517*
Free T3	2.94 ± 0.38	2.97(2.03–3.58)	3.28 ± 0.54	3.3(2.22–4.45)	0.018ǂ
HbA1c(%)	5.4 ± 0,3	5.3 (5.0–5.8)	5.6 ± 0,2	5.4 (5.0–5.9)	0.518*
Total Cholesterol	173.91 ± 41.36	165(109–276)	156.79 ± 36.36	149(107–223)	0.186ǂ
HDL(mg/dl)	41.42 ± 12.53	40(21–80)	42.57 ± 15.41	36(22–67)	0.735*
LDL(mg/dl)	115.24 ± 40.44	109(59–210)	99.64 ± 29.95	99.5(53–143)	0.221*
Triglycerides(mg/dl)	167.61 ± 105.06	144(53–528)	148.21 ± 89.68	127(58–420)	0.537*
Albumin	4.20 ± 1.03	4.14(3.13–9.54)	4.25 ± 0.43	4.19(3.62–5.01)	0.266*
CRP	11.71 ± 17.48	4.5(0.5–63)	7.16 ± 6.06	7.4(1.1–22)	0.785*
Total Bilirubin	0.63 ± 0.29	0.57(0.23–1.42)	0.65 ± 0.35	0.53(0.28–1.36)	0.916*
Direct Bilirubin	0.22 ± 0.09	0.21(0.09–0.44)	0.26 ± 0.11	0.28(0.06–0.46)	0.226ǂ
(*: Chi-square test was applied. fisher exact test was performed. ECO: Echocardiography, BMI:Body mass index, WBC:white blood cell)

Table 2

Preoperative baseline values according to the presence of atherosclerotic plaque.

There were 48 cases in our study. All of these patients had an elective isolated CABG. And then, all of them were in the high-risk patient group according to the 2019 ESC / EAS dyslipidemia guidelines for the management of dyslipidemias. 43 males (89.6%), and 5 females (10.4%) patients between 39 and 81 years of age were included in the study. There was no statistically significant difference between the patients' preoperative cardiovascular risk assessments. (Table-2). The free T3 values were within the normal range with of all patients, however there was a difference that patients in the non-atherosclerosis group have lower values. There was no statistically significant difference between two groups' HDL, LDL, total cholesterol, triglyceride parameters. All other preoperative results are presented in Table-2. 9 (18.75%) patients have a two-vessels bypass, 26 (54.2%) of them three-vessels, 8 (16.7%) of them four-vessels, 5 (10, 4%) of them five-vessels bypass. We took tissue samples from one side or both sides of the ascending aorta. 40 tissue samples were taken from the right side of the ascending aorta, and 12 of them resulted in atherosclerosis group. Another 44 samples were taken from the left side, and 4 had atherosclerosis. With two patients, atherosclerosis was observed in both the left and right side of the aorta.

		No Atherosclerosis		Atherosclerosis
		n	%	n	%	p value
Gender	Male	31	72.09	12	27.91	0.621ǂ
	Female	3	60	2	40
Diabetes Mellitus	(-)	18	66.67	9	33.33	0.471*
	(+)	16	76.19	5	23.81
Hypertension	(-)	13	68.42	6	31.58	0.766*
	(+)	21	72.41	8	27.59
Total Cholesterol	< 200 mg/dl	24	66.67	12	33.33	0.336*
	> 200 mg/dl	9	81.82	2	18.18
HDL Cholesterol	> 45 mg/dl	10	71.43	4	28.57	0.906*
	< 45 mg/dl	23	69.7	10	30.3
LDL Cholesterol	< 70 mg/dl	13	65	7	35	0.501*
	> 70 mg/dl	20	74.07	7	25.93
Triglycerides	< 200 mg/dl	24	66.67	12	33.33	0.336*
	> 200 mg/dl	9	81.82	2	18.18
(*:Chi-square test was applied. ǂ:Fisher exact test was performed.)

Table 3

Comparison of Risk Classes and HDL, LDL, Total Cholesterol, Triglyceride according to the 2019 ESC/EAS dyslipidemia guidelines for the management of dyslipidemias.

There was no statistically significant difference between two groups in favor of cardiovascular risk factors. 19 patients were using statin due to hyperlipidemia history. 4 of them were in the atherosclerosis group and there was no statistically significant difference in both groups. There was no statistically significant difference in the presence of atherosclerosis in any lipid panel (HDL-C, LDL-C, Total cholesterol and triglyceride) (Table-3)

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.

Acknowledgements:

There is no acknowledgements.

Ethics Committee Approval:

Ethics committee approval was received at Istanbul University-Cerrahpasa at 21.05.2019(committee number:59491012-604.01.02)

Informed Consent:

Informed consent was obtained from the participants.

Financial Disclosure and Funding

The authors have not declared financial support.

Conflict of Interest:

No conflict of interest was declared by the authors.

Availability of data and material:

Due to the legal system in our country and the law of protection of personal data, we cannot share patient data in detail.

Competing interests:

No competing of interest was declared by the authors.

Authors' contributions:

All authors read and approved the final manuscript

1. Wilson,P.W.etal.1998.Predictionofcoronaryheartdisease using risk factor categories. Circulation. 97: 1837–1847. 
2. Yusuf S, Rangarajan S, Teo K, et al. Cardiovas. cular risk and events in 17 low. , middle. , and high. income countries. N Engl J Med 2014;371:818–27.
3. Silverman MG, Blaha MJ, Krumholz HM, et al. Impact of coronary artery calcium on coronary heart disease events in individuals at the extremes of traditional risk factor burden: the Multi. Ethnic Study of Atherosclerosis. Eur Heart J 2014;35: 2232–41.
4. Fernandez. Friera L, Penalvo JL, Fernandez. Ortiz A, et al. Prevalence, vascular distribution, and multiterritorial extent of subclinical athero. sclerosis in a middle. aged cohort: the PESA (Progression of Early Subclinical Atherosclerosis) study. Circulation 2015;131:2104–13.
5. Mayo clinic Cardiology review Joseph G. Murphy , MD. The Endothelium Second Edition.2001; 99. 106  
6. Austin MA, Kraus RM. LDL density and atherosclerosis. JAMA 1995; 373: 115.  
7. Goldstein JL, Brown MS. The LDL receptor. Atherioscler Thromb Vasc Biol 2009; 29: 431. 8.
8. Kontush A, Chapman MJ. Antiatherogenic function of HDL particle subpopulations: focus on antioxidative activities. Curr Opin Lipidol 2010; 21: 312. 8.
9. Ravi GR, Pradeepa R, Mohan V. Hypertriglyceridemia and coronary artery disease. an update. Indian Heart J 2004;56:21. 6.
10. Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association be. tween low. density. lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6:e010401.
11. Ference BA, Ginsberg HN, Graham I, et al. Low. density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Soci. ety Consensus Panel. Eur Heart J 2017;38:2459–72.
12. Jarcho JA, Keaney JF Jr. Proof that lower is better–LDL cholesterol and IMPROVE. IT. N Engl J Med 2015;372:2448–50.
13. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT).JAMA. 1986;256:2823. 2828.
14. MRC/BHF Heart Protection Study Investigators. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high. risk individuals: a randomised placebo. controlled trial. Lancet. 2002; 360:7. 22.
15. Downs JR, Clearfield M, Weis S, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. AirForce/Texas Coronary Atherosclerosis Prevention Study. JAMA. 1998;279:1615. 1622.
16. Long. Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339: 1349. 1357.
17. Nissen SE , Tuzcu EM, Schoenhagen P. Statin therapy, LDL cholesterol, C. reactive protein, and coronary artery disease. N Engl J Med. 2005 Jan 6;352(1):29. 38.
18. PJ. Barter , G Brandrup. Wognsen ,MK. Palmer. Effect of statins on HDL. C: a complex process unrelated to changes in LDL. C: analysis of the VOYAGER Database. Journal of Lipid Research Volume 51, 2010.
19. Brunzell JD, Davidson M, Furberg CD, et al. Lipoprotein management in pati. ents with cardiometabolic risk: consen. sus conference report from the American Diabetes Association and the American College of Cardiology Foun. dation. J Am Coll Cardiol 2008;51: 1512. 24.
20. Srinivasan SR, Myers L, Berenson GS. Distribution and correlates of non. high. density lipoprotein cholesterol in child. ren: The Bogalusa Heart Study. Pediatrics 2002;110:29.
21. Smets EML, Pequeriaux NCV, Blaton V, Goldschmidt HMJ. Analytical Perfor. mance of a Direct Assay for LDL. Cho. lesterol. Clin Chem Lab Med 2001;39: 270. 80.
22. Esteban. Salan M, Guimon. Bardesi A, De La Vuida. Unzueta J, et al. Analytical and Clinical Evaluation of Two Homoge. nous Assays for LDL. cholesterol in Hyperlipidemic Patients. Clin Chem 2000;46:1121. 31.
23. Youn YJ, Lee NS, Kim JY, Lee JW, Sung JK, Ahn SG, et al. Normative values and correlates of mean common carotid intima. media thickness in the Korean rural middle. aged population: the Atherosclerosis RIsk of Rural Areas in Korea General Population (ARIRANG) study. J Korean Med Sci 2011; 26: 365. 71.
24. L Fernández. Friera, V Fuster, B López. Melgar et al. Normal LDL. Cholesterol Levels Are Associated With Subclinical Atherosclerosis in the Absence of Risk Factors. JACC Vol. 70, No. 24, 2017 December 19, 2017:2979–91. 
25. Xing FY, Neeland IJ, Gore MO, et al. Associa. tion of prediabetes by fasting glucose and/or haemoglobin A1c levels with subclinical athero. sclerosis and impaired renal function: observations from the Dallas Heart Study. Diab Vasc Dis Res 2014;11:11–8.
26. Sander D, Schulze. Horn C, Bickel H, Gnahn H, Bartels E, Conrad B. Combined effects of hemoglobin A1c and C. reactive protein on the pro. gression of subclinical carotid atherosclerosis: the INVADE study. Stroke 2006;37:351–7.
27. J.M. Alegret , L. Masana, N. Martinez. Micaelo et al. LDL cholesterol and apolipoprotein B are associated with ascending aorta dilatation in bicuspid aortic valve patients. Q J Med 2015; 108:795–801.

PDF

Version 1

posted 19 May, 2020

You are reading this latest preprint version

Is It Possible to Predict the Atherosclerosis in Aorta by the Patients Lipids Panel?

Status:

Version 1

Abstract

Figures

Introduction

Methods And Materials

Study Design

Laboratory Evaluation

Sampling the ascending aortic tissue

Pathology Evaluation

Statistical Analysis

Results:

Discussion

Declarations

Acknowledgements:

Ethics Committee Approval:

Informed Consent:

Financial Disclosure and Funding

Conflict of Interest:

Availability of data and material:

Competing interests:

Authors' contributions:

References

Status:

Version 1