Lipoprotein(a) variations between Chronic Coronary Syndrome and Acute Myocardial Infarction and their relation to the severity of coronary artery stenosis

doi:10.21203/rs.3.rs-2247410/v1

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Lipoprotein(a) variations between Chronic Coronary Syndrome and Acute Myocardial Infarction and their relation to the severity of coronary artery stenosis

https://doi.org/10.21203/rs.3.rs-2247410/v1

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Background

Lp(a) levels and the degree of coronary artery stenosis in patients with CAD at different times [e.g., acute myocardial infarction (AMI), chronic coronary syndrome (CCS)] are closely related to patients with coronary artery disease (CAD), but the differences in Lp(a) levels and the relationship between Lp(a) levels and the degree of coronary artery stenosis are unclear.

Methods

Based on the inclusion and exclusion criteria, we screened 217 patients with CCS and 141 patients with AMI. Their data were collected separately, including gender, age, marital status, hypertension, diabetes, smoking, drinking,troponin I, Creatine Kinase Isoenzyme(CKMB), Lp(a), apolipoprotein a [apo(a)],apolipoprotein b [apo(b)], LDL, HDL, TG, TC, D-dimer, fibrinogen, homocysteine, number of coronary artery lesions and the degree of stenosis,and echocardiography related indices.The correlation between Lp(a) level and the degree of coronary artery stenosis was tested by Spearman rank correlation, and the relationship between Lp(a) level and coronary artery obstruction was clarified using univarite and multivariate binary logistic regression analysis, and ROC curves were plotted to clarify the value of Lp(a) in predicting coronary artery obstruction and the cut-off value.

Results

In our study, the median Lp(a) concentration was significantly higher in AMI patients than CCS(336.0 vs 135.0 mg/L).Lp(a) was highly associated with the degree of coronary stenosis in patients with CCS(r = 0.811,p<0.001) and was not found in patients with AMI(r = 0.029, p > 0.05).Lp(a) was associated with coronary artery obstruction(define as coronary artery stenosis ≥ 50%) in a multivariate regression analysis compared to other factors(OR:1.024;95%CI:1.016–1.032).The receiver operating characteristic(ROC) curve shows that the area under curve(AUC) of lipoprotein(a) is 93.9%,and the cut-off value of Lp(a) for predicting coronary artery obstruction was 130 mg/L(sensitivity: 85.83% ,specificity: 88.46%).

Conclusions

Lp(a) levels were considerably greater in AMI patients compared to CCS patients, but they did not correlate with the severity of coronary artery stenosis in AMI patients. The level of coronary stenosis can be predicted by Lp(a). In patients with chronic coronary syndrome, Lp(a) > 130 mg/L indicates coronary artery stenosis > 50%.

Chronic Coronary Syndrome

Acute Myocardial Infarction

Lipoprotein(a)

severity of coronary stenosis

Chronic Coronary Syndromes (CCS) is a type of coronary artery disease (CAD), (with the exception of acute coronary thrombosis as the dominant clinical manifestation), characterized by a pathology of atherosclerotic plaque accumulation in epicardial arteries process [1]. This dynamic evolution can be improved by lifestyle, pharmacological and interventional treatments. Once these factors are poorly controlled it may evolve into an acute coronary event (e.g. Acute Myocardial Infraction (AMI)) that can endanger the patient's life.

Lipoprotein a,[Lp(a)] is mainly bound in the liver by Low Density Lipoprotein (LDL)-like particles, apolipoprotein a [apo(a)] and apolipoprotein b [apo(b)] and become [2]. Current studies have shown that polymorphisms in the LPA gene correlate with plasma Lp(a) levels [3], which are not affected by external factors (e.g., diet, environment, etc.) [4], and that it has properties that promote atherosclerosis, promote thrombosis, and is an independent risk factor for coronary heart disease [5].

In the last decades, several studies have shown that high Lp(a) levels are associated with poor prognosis in coronary artery disease [6-9], and a few studies have shown that Lp(a) is associated with coronary plaque progression [10]. The differences in Lp(a) levels between patients with chronic coronary syndrome and patients with acute myocardial infarction and the relationship between Lp(a) levels and the degree of coronary artery stenosis are unclear, so the aim of this study was to clarify the differences in Lp(a) levels between patients with chronic coronary syndrome and patients with acute myocardial infarction and the relationship between Lp(a) levels and the degree of coronary artery stenosis, and to clarify the Lp(a) prediction of coronary stenosis The value of Lp(a) to predict the degree of coronary stenosis.

2.1 Study patients and design

The study was approved by the ethics committee of the First Affiliated Hospital of Nanchang University. 217 patients with CCS and 141 patients with AMI from January 1, 2021 to June 30, 2022 at the First Affiliated Hospital of Nanchang University were collected according to the nadir criteria, and the inclusion criteria were as follows.

CCS group: 1. age 18-85 years; 2. diagnosis in accordance with the 2019 ESC CCS diagnosis and management guidelines [1].

AMI group: 1. age 18-85 years; 2. diagnosis in accordance with the 2018 Fourth Universal Definition of Myocardial Infarction [11].

Exclusion criteria: (1) aortic disease (e.g., entrapment, calcification), cerebral infarction, pulmonary embolism (2) malignant arrhythmia (e.g., ventricular tachycardia, ventricular fibrillation) (3) familial hypercholesterolemia (4) acute pancreatitis, gastrointestinal bleeding, etc. (5) cancer and radiotherapy (6) hyperthyroidism or hypothyroidism (7) pregnancy or lactation (8) use of PCSK9 inhibitors (9) hepatic insufficiency (10) severe renal insufficiency (creatinine >265umol/L) (11) incomplete data

2.2 Data Collection

All data were collected from the inpatient electronic medical record system of the First Affiliated Hospital of Nanchang University.

Basic data: including name, gender, age, marital status, hypertension, diabetes, smoking, drinking, etc.

Laboratory data: All data were collected from the first test results of patients admitted to the hospital, including troponin I, Creatine Kinase Isoenzyme(CKMB), Lp(a), apo(a), apo(b), LDL, HDL, TG, TC, D-dimer, fibrinogen, homocysteine

Examination data: coronary angiography and echocardiography were included. Coronary angiography was performed independently by two doctors in all patients, and the number of coronary artery lesions and the degree of stenosis were recorded according to the intraoperative angiographic results (in case of multiple vessel lesions, the maximum degree of stenosis was taken for statistical analysis). Echocardiography was performed independently by one ultrasonographer, and the data included left ventricular ejection fraction(LVEF), left ventricular end-diastolic diameter(LVDD), left atrial diameters(LAD),left ventricular posterior wall thickness(LVPWT), Interventricular septal thickness(IVST), right ventricular internal diameter(RVD), right ventricular outflow tract(RVOT) and pulmonary artery diameter(PAD).

Statistical analysis

All data analysis was done using SPSS 26.0 and Excel 2019. Count data were expressed as percentages, comparisons were made using the chi-square test, and the normality test was performed using the K-S test for measurement data, and data obeying normal distribution were expressed as mean ± standard deviation(SD), and non-normal distribution was expressed as median (interquartile range).The t-test was used to analyze the normality data, and the Mann-Whitney test was used for non-normality data. Risk factors for coronary artery obstruction were analyzed by binary logistic regression, the predictive value of Lp(a) for coronary artery obstruction was analyzed by ROC, and the correlation analysis between Lp(a) and the degree of coronary artery stenosis was evaluated by non-parametric test (Spearman rank correlation), and P < 0.05 was statistically significant.

3.1 Characteristic of study groups

As show in Table 1,There was no significant difference between the two groups in gender, age, hypertension, diabetes, smoking and drinking (p > 0.05), but the number of married people was lower in the AMI group than in the CCS group (p = 0.001). There was no significant difference between the two groups in LDL, TG, TC, and left atrial diameters (p<0.05). For apo(a), apo(b), D-dimer, fibrinogen, and homocysteine, the AMI group was higher than the CCS group (p<0.05), and for LVEF, RVOT, and PAD, the CCS group was higher than the AMI group (p<0.05). The median (interquartile spacing) was not significantly different between the two groups on LVPWT and IVST although p < 0.05. Lp(a), CK-MB, troponin I, number of diseased vessels and degree of coronary stenosis were significantly higher in the AMI group than in the CCS group.

Table1：Characteristics of participants
Characteristics	CCS（n=217）	AMI（n=141）	Total（n=358）	P
Age,yeas	62.35±10.332	63.79±12.404	62.92±11.199	0.232
Male	150（69.1%）	104（73.8%）	254（70.9%）	0.345
Married	211（92.7%）	125（88.7%）	336（93.9%）	0.001*
Hypertension	108（49.8%）	73（51.8%）	181（50.6%）	0.711
Diabetes	26（12.0%）	20（14.2%）	46（12.8%）	0.543
Smokers	80（36.9%）	57（40.4%）	137（38.3%）	0.498
Drinkers	47（21.7%）	23（16.3%）	70（19.6%）	0.213
Lp(a),mg/L	115.0（58.0,254.5）	336.0(218.05,547.55)	196.0（88.0,380.6）	＜0.001**
CK-MB,U/L	15.5（12.7,18.9）	41.0（24.0,92.0）	18.5（14.0,32.2）	＜0.001**
Troponin I,ug/L	0.01（0.01,0.01）	0.68（0.18，2.28）	0.01（0.01,0.42）	＜0.001**
LDL,mmol/L	2.34（1.82,2.82）	2.42（1.81,2.89）	2.36（1.82,2.84）	0.361
HDL,mmol/L	1.09（0.92,1.33）	1.00（0.87,1.18）	1.05（0.89,1.24）	0.001*
apo(a),g/L	0.99（0.91,1.13）	1.08（0.94,1.23）	1.02（0.92,1.19）	0.04*
apo(b),g/L	0.73（0.60,0.85）	0.85（0.71,1.02）	0.75（0.64,0.91）	＜0.001**
TG,mmol/L	1.23（0.90,1.84）	1.23（0.97，1.81）	1.23（0.93,1.83）	0.58
TC,mmol/L	4.02（3.44,4.56）	4.13（3.50,4.76）	4.04（3.47,4.58）	0.327
D-dimer,mg/L FEU	0.25（0.18,0.43）	0.37（0.19,0.78）	0.29（0.18,0.51）	0.002*
Fibrinogen,g/L	2.84（2.40,3.30）	3.60（2.98,4.54）	3.10（2.50,3.84）	＜0.001**
Creatinine,umol/L	71.7（57.9,83.8）	81.8（67.7,102.1）	75.25（62.02,89.05）	＜0.001**
Homocysteine,umol/L	11.4（9.5,13.8）	13.2（10.9,17.6）	12.2（10.0,14.9）	＜0.001**
LVEF,%	63（60,65）	56（52,59）	60（56,65）	＜0.001**
LVDD,mm	46（43,49）	46（44,50）	46（43,49）	0.101
LAD,mm	33（30,36）	33（30,37）	33（30,36）	0.969
LVPWT,mm	10（9,10）	10（9,10）	10（9,10）	0.006*
IVST,mm	10（9,10）	10（9,10）	10（9,10）	0.005*
RVD,mm	22（20,24）	21（20,23）	22（20,23）	0.01*
ROVT,mm	28（26,30）	27（25,29）	28（25,29）	0.001*
PAD,mm	22（20,23）	21（20,22）	21（20,22）	0.001*
Single vessel disease	126（58.1%）	17（12.1%）	143（39.9%）	＜0.001**
CAND,%	50（30,70）	95（95,100）	80（40,95）	＜0.001**

Lp(a):Lipoprotein a;CK-MB:Creatine Kinase MB Isoenzyme;LDL:Low density lipoprotein;HDL:High density lipoprotein;apo(a):apolipoprotein a;apo(b):apolipoprotein b;TG:triglyceride;TC:Total cholesterol;LVEF:Left ventricular ejection fraction;LVDD:Left ventricular end diastolic diameter;LAD:Left atrial diameter;LVPWT:Left ventricular posterior wall thickness;IVST:Interventricular septal thickness;RVD:Right ventricular diameter;ROVT:Right ventricular outflow tract;PAD:Pulmonary arterial diameter;CAND:Coronary artery narrow degree *:p＜0.05；**：p＜0.001

3.2 Correlation analysis of Lp(a) and the degree of coronary artery stenosis

Lipoprotein a levels and the degree of coronary artery stenosis in both groups are shown in Figure 1

From Figure 1, we can see that the Lp(a) level and the degree of coronary stenosis were significantly higher in the AMI group than in the CCS group.Therefore, we analyzed the correlation between Lp(a) levels and the degree of coronary artery stenosis.As show in Table 2，We could learn that Lp(a) levels were significantly correlated with the degree of coronary stenosis in patients in the CCS group and overall (r_c=0.811,r_t =0.735,,P<0.001), but they were not correlated in the AMI group.

Table 2.Correlation of Lp(a) with the degree of coronary stenosis
Groups	r	P
CCS	0.811	＜0.001
AMI	0.029	0.729
Total	0.735	＜0.001

*:p＜0.05；**:p＜0.001

3.3 Risk factors for coronary artery obstruction

We further divided all patients into obstructive and non-obstructive according to the degree of coronary stenosis ≥50%, and included gender, age, marital status, hypertension, diabetes, smoking, drinking, Lp(a), CK-MB, HDL,LDL, apo(a),apo(b) ,D-dimer,fibrinogen,creatinine,and troponin I in the univariate binary logistic regression analysis of coronary artery obstruction.

Table 3.Univariate binary logistic regression analysis of coronary obstruction
Variables	OR	95%CI	P
Gender	1.277	0.779-2.092	0.332
Age	1.036	1.015-1.058	0.001*
Marital status	9.283	1.032-69.942	0.032*
Smoking	0.802	0.498-1.291	0.363
Drinking	1.591	0.918-2.758	0.098
Hypertension	0.869	0.551-1.373	0.548
Diabetes	0.262	0.101-0.684	0.006*
Lp（a）	1.026	1.020-1.033	＜0.001**
CK-MB	1.087	1.050-1.126	＜0.001**
Troponin I	7.45E+73	1.575E+10-3.524E+137	0.023*
HDL	0.604	0.313-1.164	0.132
LDL	1.191	0.904-1.569	0.213
Apo(a)	1.958	0.628-6.109	0.247
Apo(b)	9.772	3.167-30.155	＜0.001**
D-dimer	5.446	2.190-13.544	＜0.001**
Fibrinogen	1.458	1.135-1.873	0.003*
Creatinine	1.025	1.013-1.038	＜0.001**
Homocysteine	1.025	0.991-1.061	0.153
LVEF	0.866	0.826-0.909	＜0.001*
ROVT	0.92	0.860-0.985	0.017*
RVD	1.004	0.977-1.031	0.787
LVPWT	1.184	0.983-1.426	0.075
IVST	1.069	0.921-1.240	0.383

Lp(a):Lipoprotein a;CK-MB:Creatine Kinase MB Isoenzyme;LDL:Low density lipoprotein;HDL:High density lipoprotein;apo(a):apolipoprotein a;apo(b):apolipoprotein b;LVEF:Left ventricular ejection fraction;ROVT:Right ventricular outflow tract;RVD:Right ventricular diameter;Left ventricular posterior wall thickness;IVST:Interventricular septal thickness;OR:Odds Ratio CI:Confidence interval ; *:p＜0.05；**:p＜0.001

From Table 3, it is known that Lp(a), age,diabetes, marital status, apo(b),CK-MB, troponin I,D-dimer,fibrinogen,creatinine,LVEF and ROVT are risk factors for coronary artery obstruction.The above risk factors were further included in the multivariate binary logistic regression analysis, and it could be known that Lp(a) (OR：1.024,95%CI:1.016-1.032,p < 0.001) and diabetes (OR:0.159;95%CI:0.039-0.65,p < 0.05) were independent risk factors for coronary artery obstruction.The results are shown in Table 4.

Table 4.Multivariate binary logistic regression analysis of coronary obstruction
Variables	OR	95%CI	P
Age	1.038	0.99-1.088	0.119
Marital status	1.01	0.056-18.214	0.995
Diabetes	0.159	0.039-0.65	0.01*
Lp（a）	1.024	1.016-1.032	＜0.001**
CK-MB	1.035	0.967-1.108	0.322
Troponin I	1.200E+35	0-1.229E+103	0.312
Apo(b)	1.107	0.144-8.523	0.992
D-dimer	2.857	0.97-8.418	0.057
Fibrinogen	1.005	0.759-1.331	0.974
Creatinine	1.002	0.979-1.026	0.836
LVEF	1.022	0.942-1.108	0.604
ROVT	0.879	0.772-1.001	0.052

Lp(a):Lipoprotein a;CK-MB:Creatine Kinase MB Isoenzyme;apo(b):apolipoprotein b;LVEF:Left ventricular ejection fraction;ROVT:Right ventricular outflow tract;OR:Odds Ratio;CI:Confidence interval ; *:p＜0.05；**:p＜0.001

3.4 The value of Lp(a) in predicting coronary artery obstruction

Using Lp(a) as the test variable and coronary artery obstruction as the status variable, ROC curves were plotted to determine the cut-off value of Lp(a). The results showed in Figure 2,and the area under the curve (AUC) was 0.939 (95% CI: 0.916-0.962,p＜0.001), and the optimal cut-off value of Lp(a) for predicting coronary obstruction was determined to be 130 mg/L(sensitivity: 85.83% ,specificity: 88.46%) by calculating the Youden index.

Past studies have shown that Lp(a) is associated with CAD, aortic stenosis, heart failure and stroke [5]. Whereas the development of CAD is a dynamic process [1], little attention has been paid to the changes in Lp(a) levels at different times. One study showed that elevated Lp(a) levels were associated with CD14, CD16 monocyte reduction and coronary atherosclerosis, but the study inclusion population did not include patients with acute coronary events [12]. In the last decades, coronary heart disease remains the leading cause of death worldwide [13]. Sufficient attention has been paid to the prevention of coronary heart disease, which can be effectively reduced by improving lifestyle and medications [14]. In patients with chronic coronary syndromes, it is difficult to predict the occurrence of acute coronary events (e.g., acute myocardial infarction). One can only know the degree of coronary artery stenosis by coronary angiography or coronary computed tomography angiography [15].

Lp(a) has proatherogenic and thrombogenic effects and has been shown to be associated with CAD [5,17]. lp(a) is not influenced by lifestyle (e.g., smoking, alcohol consumption, etc.) and its levels are associated with the LPA gene [3]. A prospective study showed that plasma Lp(a) levels were significantly higher in blacks than in whites, suggesting that Lp(a) levels differ between ethnic groups [18]. Statins are not effective in reducing Lp(a) levels [19], with the exception of PCSK9 inhibitors [20].In this study, we did not state the patients' medication status because they were screened at the time of inclusion. Also, Lp(a) levels are influenced by liver function [21]. Therefore, all of these possible factors were included as exclusion criteria in our study.

Our study showed that Lp(a) levels were significantly higher in the AMI group than in the CCS group (p<0.001). In CCS patients, Lp(a) levels were significantly correlated with the degree of coronary artery stenosis in patients with CCS(r=0.811, p<0.001), but there was no correlation between them in the AMI group (r=0.029, p>0.05), and this difference needs further study. Logistic regression analysis clarified that Lp(a) was an independent risk factor for coronary artery obstruction(OR:1.024;95%CI:1.016-1.032), and ROC curve analysis determined that Lp(a) predicted coronary artery obstruction at 130 mg/L (sensitivity 85.83%, specificity 88.46%), which provides a reference for predicting the degree of coronary stenosis and the control target of Lp(a) in CCS patients and enables timely intervention in CCS patients the progression of coronary atherosclerosis and prevent acute coronary events.

Lp(a) levels were significantly higher in patients with AMI than in patients with CCS , but Lp(a) levels correlated with the degree of coronary artery stenosis only in patients with CCS and not in AMI. In patients with chronic coronary syndrome, Lp(a) >130 mg/L suggests coronary artery stenosis >50%.

Ethical Approval and Consent to Participate：

The study was approved by the ethics committee of the First Affiliated Hospital of Nanchang University.We certify that all procedures used in this study adhere to the Declaration of Helsinki and that patients' informed consent was obtained before any data were collected.

Competing interests:

The authors declare that they have NO affiliation with or involvement in any organization or entity with any financial interest in the subject matter or materials discussed in this manuscript.

Author’s contributions：

HongwenZhu and ZhengzhongZheng contributed to the design and implementation of the research,Hongwen Zhu is responsible for collecting data, statistical analysis and writing the first draft,Zhenzhong Zheng guided the work and provided assistance throughout the process.

Funding

The study was supported by grant 20202ACBL206002 from the Foundation of Natural Science Foundation of Jiangxi Province, China.

Availability of data and materials:

The data used in this study can be obtained from the corresponding author upon reasonable request.

Consent for Publication：

All authors gave their consent for publication.

Acknowledgement：

Many thanks to Prof. Zheng for his mentoring and to our institute for assisting with the research.

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No competing interests reported.

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Lipoprotein(a) variations between Chronic Coronary Syndrome and Acute Myocardial Infarction and their relation to the severity of coronary artery stenosis

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