Skip to main content

Main menu

  • Online first
    • Online first
  • Current issue
    • Current issue
  • Archive
    • Archive
  • Submit a paper
    • Online submission site
    • Information for authors
  • About the journal
    • About the journal
    • Editorial board
    • Information for authors
    • FAQs
    • Thank you to our reviewers
      • Thank you to our reviewers
    • American Federation for Medical Research
  • Help
    • Contact us
    • Feedback form
    • Reprints
    • Permissions
    • Advertising
  • BMJ Journals

User menu

  • Login

Search

  • Advanced search
  • BMJ Journals
  • Login
  • Facebook
  • Twitter
JIM

Advanced Search

  • Online first
    • Online first
  • Current issue
    • Current issue
  • Archive
    • Archive
  • Submit a paper
    • Online submission site
    • Information for authors
  • About the journal
    • About the journal
    • Editorial board
    • Information for authors
    • FAQs
    • Thank you to our reviewers
    • American Federation for Medical Research
  • Help
    • Contact us
    • Feedback form
    • Reprints
    • Permissions
    • Advertising
Open Access

Circulating lipid and lipoprotein profiles and their correlation to cardiac function and cardiovascular outcomes in patients with acute myocardial infarction

Haoyu Wu, Chen Wang, Gulinigaer Tuerhongjiang, Xiangrui Qiao, Yiming Hua, Jianqing She, Zuyi Yuan
DOI: 10.1136/jim-2021-001803 Published 27 September 2021
Haoyu Wu
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Chen Wang
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Gulinigaer Tuerhongjiang
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Xiangrui Qiao
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yiming Hua
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jianqing She
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
2 Key Laboratory of Molecular Cardiology, Xi'an Jiaotong University, Xi'an, China
3 Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Ministry of Education, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Jianqing She
Zuyi Yuan
1 Department of Cardiovascular Medicine, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, China
2 Key Laboratory of Molecular Cardiology, Xi'an Jiaotong University, Xi'an, China
3 Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Ministry of Education, Xi'an, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • eLetters
  • Info & Metrics
  • PDF
Loading

Abstract

Recent studies showed that lipoproteins represent major risk factors, both positive and negative, for atherosclerotic cardiovascular disease. The aim of the present study was to describe the relationship between plasma lipid profile and cardiac function and cardiovascular outcomes in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). Two independent groups of subjects including a total of 797 patients diagnosed of AMI undergoing PCI admitted to the First Affiliated Hospital of Xi’an Jiaotong University were included in the present study. We performed a cross-sectional study for the correlation between plasma lipid profile and cardiac function based on the first group, including 503 patients with AMI. We further validated the correlation and did the follow-up of 2.4 years of major cardiovascular outcomes on the second group, including 294 patients with AMI. Our results showed that apolipoprotein A-I (ApoA-I) level was significantly reduced, and the high-density lipoprotein cholesterol (HDL-C):ApoA-I ratio was increased in the patients with lower LVEF or higher N-terminal pro-B-type natriuretic peptide levels compared with the control; there was a positive correlation between cardiac function and ApoA-I, and a negative correlation between cardiac function and the HDL-C:ApoA-I ratio. Meanwhile, multivariate Cox analysis showed that ApoA-I was independent predictors of major adverse cardiovascular events (MACEs). Kaplan-Meier survival analysis showed the ApoA-I levels exhibited a significant effect on predicting the incidence of MACEs. In sum, plasma ApoA-I level is positively associated with the cardiac function of patients with AMI after PCI, and ApoA-I is an independent indicator to predict the incidence of MACEs.

Significance of this study

What is already known about this subject?

  • The attack of acute myocardial infarction (AMI) is life-threatening, and long-term chronic ischemia of the myocardium will cause adverse clinical outcomes, such as ischemic heart failure as well as fatal arrythmia.

  • The abnormal lipid metabolism took a critical part in plaque formation and atherosclerosis in the development of AMI.

  • However, few studies were concerned about the relationship between whole lipid types and cardiac function, and the correlation of prognosis with lipid profile remains controversial due to the lack of long-term follow-up results.

What are the new findings?

  • In this study, we found that apolipoprotein A-I (ApoA-I) levels were significantly reduced, and the high-density lipoprotein cholesterol (HDL-C):apolipoprotein A-I (ApoA-I) ratio were increased in the patients with lower LVEF or higher N-terminal pro-B-type natriuretic peptide level.

  • The Pearson correlation analysis showed positive correlations between cardiac function and ApoA-I, and negative correlations between cardiac function and the HDL-C:ApoA-I ratio.

  • Moreover, ApoA-I levels exhibited a significant effect on predicting the incidence of major adverse cardiovascular events (MACEs).

How might these results change the focus of research or clinical practice?

  • The present study provides broad and straightforward support that ApoA-I should be introduced into clinical practice for the assessment of the cardiac function in patients with AMI undergoing percutaneous coronary intervention, and also predicts the incidence of MACEs.

Introduction

Coronary artery disease (CAD) is the major cause of mortality and morbidity in China and worldwide. Despite the technological advancement and the increasing level of awareness,1 2 acute myocardial infarction (AMI) is still a life-threatening emergency, and long-term chronic ischemia of the myocardium will cause adverse clinical outcomes, such as ischemic heart failure as well as fatal arrythmia.3 Actually, the condition of patients with AMI who may have poor prognosis could be greatly improved by timely and appropriate interventions. Based on this, finding an efficient predictor related with cardiac function and cardiovascular outcomes is urgently needed.

Lipid abnormalities have been widely documented to be associated with higher cardiovascular disease (CVD) risk.4 Widely used clinical CVD risk calculators frequently include classical biochemistry measures of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), or a combination of these.5–7 However, the predictive value of non-traditional lipid risk factors has also gained increasing attention from researchers, including high-density lipoprotein cholesterol (HDL-C), non-HDL, apolipoprotein A-I (ApoA-I), etc.8 HDL-C was ascribed as ‘good’ cholesterol and negatively correlates to the risk of CVDs as proven by several clinical and animal studies.9–12 Non-HDL-C has been suggested as a pragmatic and cost-effective alternative to direct LDL-C measurement, also proven to be associated with increased CVD risk.13 ApoA-I is the principal protein component of HDL particles and is also of interest for its potential value for predicting CVD risks.14–16 Specifically, ApoA-I level is a consistent discriminator of atherosclerotic burden among patients with stable CAD.17 However, the correlation between ApoA-I and cardiac function, as well as long-term outcomes in patients with AMI undergoing percutaneous coronary intervention (PCI), remain underexplored.

With these considerations, our work was conducted to evaluate the lipid profile of patients with AMI after PCI and the relationship among dyslipidemia, cardiac function and long-term cardiovascular outcomes.

Materials and methods

Study population

This study enrolled two independent groups of subjects including a total of 797 patients diagnosed with AMI undergoing PCI, admitted to the First Affiliated Hospital of Xi’an Jiaotong University. We performed a cross-sectional study of the correlation between plasma lipid profile and cardiac function based on the first group including 503 patients with AMI admitted between January 2013 and December 2015. We further validated the correlation and did the follow-up of 2.4 years on the second group including 294 patients with AMI between January 2016 and December 2016; 28 (9.52%) patients were lost follow-up. AMI was defined based on the universal definition criteria by the joint European Society of Cardiology (ESC)/American College of Cardiology Foundation/American Heart Association/World Heart Federation Task Force.18 The exclusion criteria were (1) age<18 years, (2) pregnancy, (3) renal dysfunction (serum creatinine>133 μmol/L) or liver dysfunction (serum alanine transaminase>3 times the upper normal limit), and (4) malignant tumors. All patients received guideline-recommended therapy for AMI. The detailed demographic, clinical, drug, hematological, echocardiography and angiographic data were obtained from the hospital documentation.

The estimation of sample size was performed using G*Power software V.3.1.9.6.19 A sample size of 252 achieves 95% power to detect an effect size of 0.25 using F tests with a significance level of 0.05.

Lipid profile measures

Venous blood samples for lipidomic analyses were collected before coronary catheterization. The following laboratory assays were performed in the clinical laboratory department: TC and triglyceride (TG) were detected using detection kit from FUJIFILM via N-(3-sulfopropyl)- 3-methoxy-5-methylaniline (HMMPS) method; HDL-C and LDL-C were detected using detection kit via direct measurement method from FUJIFILM; ApoA-I, Apo B and Apo E were measured using a detection kit from SEKISUI by turbidimetric inhibition immunoassay. All laboratory assays were performed in duplicate and the results were averaged.

Other blood biochemical measures

Standard clinical biochemical and hematological measures were made by the local laboratory of the First Affiliated Hospital of Xi’an Jiaotong University. Serum was collected for analysis including liver, kidney and electrolytes (HITACHI 7180; HITACHI, Tokyo, Japan). Full blood samples were used to test the hematological parameters (KX 21 n analyzers; Sysmex, Kobe, Japan). After these tests, all samples were stored at −80°C for future analysis. The serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were detected as a batch analysis in a central laboratory by electrochemiluminescence immunoassay (Roche Diagnostics, Rotkreuz, Switzerland).

Evaluation of the echocardiography

Echocardiography was performed using Philips iE33 ultrasound system (Philips, Amsterdam, Netherlands) by experienced cardiologists of the First Affiliated Hospital of Xi’an Jiaotong University. The left ventricular ejection fraction (LVEF) value was uniformly measured by biplane Simpson rule.20

Assessment of outcomes

Patients in the follow-up cohort were followed up semiannually by clinic visits or by telephone interviews conducted by trained nurses or doctors. Major adverse cardiovascular event (MACE) is defined as the end point of this study, which referred to the composite of all-cause death, heart failure, non-fatal myocardial infarction (MI), and symptom-driven revascularization. The follow-up ended on June 31, 2018 or patient death.

Statistical analysis

All statistical analyses were performed by SPSS V.22.0 for Windows. Data were presented as frequencies and percentages for categorical variables, as mean±SD for normally distributed continuous variables and median (with 25th and 75th percentiles) for non-normally distributed continuous variables. The Kolmogorov-Smirnov test was used to assess normal distribution of quantitative variables. Simple t-test was used to compare continuous variables which are in normal distribution. Kruskal-Wallis test was used to compare continuous variables which do not conform to the normal distribution. χ2 test was used to compare categorical variables. To describe the relationship between plasma lipid profile and cardiac function, patients were divided into subgroups according to the baseline LVEF levels and the NT-proBNP level. The cut-off point of LVEF was defined based on the 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failures, which represent varying degrees of cardiac function (<40%, 40%–50%, and >50%). To limit the influence of extreme observations, NT-proBNP was natural logarithmically transformed to obtain log NT-proBNP. Then patients were grouped according to the tertiles of baseline log NT-proBNP level. Simple linear analysis was used to calculate the correlation between plasma lipid profile and cardiac function. Univariate and multivariate survival analyses involving Cox regression analysis were constructed to calculate HRs and 95% CIs for MACEs. The multivariable Cox models were adjusted by age, sex, height, weight, creatinine, LVEF, and NT-proBNP. To assess the prognostic value of the ApoA-I level, Kaplan-Meier survival curves were used and compared by log-rank test. All probability values were two-tailed. A p value of <0.05 was considered statistically significant.

Results

Baseline characteristics of the first group

A total of 503 patients with a diagnosis of AMI after PCI were enrolled in the first group. The patients were grouped according to the baseline LVEF levels (<40%, 40%–50%, and >50%). Baseline characteristics of patients in different LVEF subgroups are shown in table 1. Compared with the patients in the group with higher levels of LVEF, the patients with lower levels of LVEF showed a higher level of heart rate (84.43±19.92 vs 72.86±12.26, p<0.001). In addition, the patients with lower levels of LVEF had significantly lower levels of ApoA-I level (1.02±0.24 vs 1.11±0.19, p<0.05) in the plasma. Furthermore, no differences were found in other lipids levels among different LVEF groups, such as TG, TC, LDL-C, HDL-C, non-HDL, the HDL-C:LDL- C ratio and the HDL-C:ApoA-I ratio. No differences in other risk factors were found between different LVEF level groups, such as age, gender, alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine, and blood urea nitrogen (BUN).

View this table:
  • View inline
  • View popup
Table 1

Baseline characteristics of the first group

As shown in table 1, the patients were grouped according to the baseline NT-proBNP level, which was transformed by natural logarithm (<6.82, 6.82–9.06, and >9.06). We found that the patients with higher levels of log NT-proBNP also had significantly higher levels of weight, heart rate, ALT, AST, creatine and the HDL-C:LDL- C ratio but lower TG and ApoA-I level in the plasma.

Correlation between lipid and lipoprotein profiles and cardiac function in patients with AMI in the first group

As shown in table 2, Pearson correlation analysis also showed a significantly positive correlation between ApoA-I level and LVEF (r=0.165, p<0.001) but a significantly negative correlation between plasma ApoA-I level and log NT-proBNP (r=−0.181, p<0.001). Interestingly, the HDL-C:ApoA-I ratio was positively correlated with the log NT-proBNP level (r=0.14, p<0.05), and the TG level was negatively correlated with the log NT-proBNP level (r=−0.171, p<0.05).

View this table:
  • View inline
  • View popup
Table 2

Correlation between serum lipid profile and cardiac function in patients with acute myocardial infarction in the first group

Baseline characteristics of the second group

A total of 294 patients with a diagnosis of AMI after PCI were enrolled in the validation cohort. The patients were also grouped according to the baseline LVEF level (<40%, 40%–50%, and >50%) and the log NT-proBNP level (<7.51, 7.51–9.58, and >9.58). Compared with patients in the group with the highest level of LVEF, the patients in the group with lower levels of LVEF had a higher level of heart rate (80.13±17.96 vs 69.05±11.45, p<0.001) and lower levels of ApoA-I level (1.00±0.23 vs 1.08±0.18, p=0.175) (table 3). In addition, the patients with lower levels of LVEF had significantly higher levels of AST, BUN, creatine and UA. We found the same results in the different log NT-proBNP level group analysis. Interestingly, the patients with higher levels of log NT-proBNP also had significantly lower levels of ApoA-I but higher levels of HDL-C:ApoA-I ratio (table 3).

View this table:
  • View inline
  • View popup
Table 3

Baseline characteristics of the second group

Correlation between plasma lipid profile and cardiac function in patients with AMI in the second group

As shown in table 4, Pearson correlation analysis also showed a significantly positive correlation between ApoA-I level and LVEF (r=0.165, p<0.05) but a significantly negative correlation between ApoA-I level and log NT-proBNP (r=−0.23, p<0.001). Interestingly, the HDL-C:ApoA-I ratio was positively correlated to the log NT-proBNP level (r=0.14, p<0.05), and the TG level was negatively correlated to the log NT-proBNP level (r=−0.175, p<0.05).

View this table:
  • View inline
  • View popup
Table 4

Correlation between serum lipid profile and cardiac function in patients with acute myocardial infarction in the second group

ApoA-I level as an independent predictor of MACE occurrence

During the median of 28.57 months of follow-up period, 76 (25.90%) patients experienced MACEs. Kaplan-Meier curves were used to illustrate the survival free from adverse events in different ApoA-I level groups in patients with AMI undergoing PCI, as shown in figure 1. Overall, patients with lower ApoA-I levels had a significantly worse outcome of survival free from MACEs during the follow-up period. Kaplan-Meier survival analysis demonstrated that lower admission ApoA-I level was significantly associated with MACE occurrence (p<0.001, log-rank test).

Figure 1
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 1

Kaplan-Meier analysis of MACEs based on the ApoA-I levels. The 294 patients were divided by tertiles of the ApoA-I levels: 0.99, 0.99–1.14, and >1.14 g/L. Risk of a MACE increased with decreasing tertile of the ApoA-I levels (log-rank test 33.354, p<0.001). ApoA-I, apolipoprotein A-I; MACE, major adverse cardiovascular event.

We then used Cox regression model for further analysis as shown in table 5. In univariate Cox analysis, we found that the lower ApoA-I level was significantly associated with an increased risk of MACEs in patients with AMI undergoing PCI (HR 2.294, 95% CI 1.239 to 4.248; p=0.008) over a median of 2.4 years of follow-up. This relationship remained significant in multivariate Cox analysis (HR 3.411, 95% CI 1.373 to 8.665; p=0.008) after adjustment for age, sex, height, weight, creatinine, LVEF, and NT-proBNP.

View this table:
  • View inline
  • View popup
Table 5

Univariate and multivariate Cox analysis for MACEs in the second group

Discussion

CVD, especially AMI, is still the leading cause of death in China and worldwide, and its morbidity and mortality have continued to increase in recent years.1 2 Despite advances in therapeutic strategies for AMI, patients remain at a high risk of MACEs, particularly in the immediate weeks to months after the event.21 Dyslipoproteinemia is common in patients with AMI and usually predicts recurrent cardiovascular events.22 23 In the present study, we assessed the relationship between circulating lipid and lipoprotein profiles to the cardiac function and cardiology outcomes in patients with AMI undergoing PCI. Our results showed that ApoA-I levels were significantly reduced, and the HDL-C:ApoA-I ratios were increased in the patients with lower LVEF or higher NT-proBNP levels; there were positive correlations between cardiac function and ApoA-I, and negative correlations between cardiac function and the HDL-C:ApoA-I ratio. The ApoA-I levels exhibited a significant effect on predicting the incidence of MACEs.

The major novelty is that in the present study, we have demonstrated the utility of ApoA-I for predicting future adverse cardiovascular events in patients with AMI undergoing PCI from two clinical groups. Findings from the Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) study concur that levels of ApoA-I were higher compared with their CAD population without heart failure among patients with new-onset heart failure.24 A large cohort of Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) study proved that higher baseline HDL and ApoA-I were associated with a better prognosis; particularly, ApoA-I was more predictive than LDL or HDL.25 Moreover, a cross-sectional study of 199 patients with stable CAD also found that ApoA-I levels increased with increasing NYHA class.24 In our study, we have identified the correlation between ApoA-I and the cardiac function of patients with AMI after PCI. The cardiac function is strongly associated with the changes in lipid profile, with positive correlations between cardiac function and ApoA-I, and negative correlations between cardiac function and the HDL-C:ApoA-I ratio.

Furthermore, ApoA-I is an independent indicator to predict the incidence of MACEs. It is identified that ApoA-I is a key functional apolipoprotein component of HDL particles and plays a central role in cholesterol efflux, and has also been of interest for predicting CVD risks.26 27 In agreement with our results, the Apo-I Event Reducing in Ischemic Syndromes-I (AEGIS-I) trial, a phase IIb trial of patients with recent MI, found that a reconstituted ApoA-I (CSL112) was developed to enhance cholesterol efflux capacity. Notably, CSL112 was safe and confirmed its potential to remove cholesterol from atherosclerotic plaques.28–30 A meta-analysis proved that incident CVD events occurred more frequently in those subjects with lower ApoA-I, and ApoA-I had the strongest (inverse) associations with risk of fatal CVD.31 32 A case–control study found that ApoA-I was inversely related to mortality: for each 1 SD increase of ApoA-I, 31% and 33% decreases in all-cause and cardiovascular mortality were recorded.33 So far, ApoA-I has been little used in epidemiological studies. Furthermore, ApoA-I measurement is much less influenced than HDL-C by intravascular enzymes and lipid transfer proteins, which participate in HDL remodeling. Thus, ApoA-I measurement may improve assessment of cardiovascular risk.34

In this study, we evaluated the circulating levels of TG, TC, HDL, LDL, non-HDL, ApoA-I, etc. It is interesting that only ApoA-I showed its correlation to cardiac function. Theoretically, there are several reasons. First, HDL protects against atherosclerosis through multiple mechanisms, including amelioration of endothelial dysfunction, removal of excess cholesterol from macrophages, as well as antioxidative, anti-inflammatory, and antiapoptotic effects. ApoA-I is the primary functional apolipoprotein component of HDL, which plays pivotal roles in the reverse cholesterol transport pathways by modulating HDL-C formation, stabilization, binding to the hepatic scavenger receptors, and activating lecithin cholesterol acyl transferase. Therefore, the oxidation of particular residues on ApoA-I creates a dysfunctional HDL particle that is associated with an increased incidence of cardiovascular events.9 10 35 36 Our data provide evidence that ApoA-I could be introduced into clinical practice for assessing the cardiac function of patients with AMI undergoing PCI and for predicting the incidence of MACEs.

Limitations

The present study had several limitations. First, this was a single-center study restricted to Chinese patients with AMI after PCI. As mentioned previously, caution should be exercised when generalizing our findings to other ethnic groups, and further studies involving different ethnic groups are needed to support our findings. Moreover, we did not collect any data whether the patients had taken any medication (particularly lipid-lowering medication) during the 2.4 years of follow-up and, if they were (which is most likely), which medication and in what doses.

Conclusion

In summary, our results demonstrate that ApoA-I levels were significantly reduced, and the HDL-C:ApoA-I ratios were increased in the patients with lower LVEF or higher NT-proBNP level compared with the control. Pearson correlation analysis further showed positive correlations between cardiac function and ApoA-I and negative correlations between cardiac function and the HDL-C:ApoA-I ratio. In addition, the ApoA-I levels exhibited a significant effect on predicting the incidence of MACEs. Therefore, the ApoA-I level was positively associated with the cardiac function of patients with AMI after PCI, and ApoA-I is an independent indicator to predict the incidence of MACEs.

Data availability statement

The datasets used and/or analyzed during the present study are available from the corresponding author on reasonable request.

Ethics statements

Patient consent for publication

Not required.

Ethics approval

Ethical approval was obtained from the ethics committee of the First Affiliated hospital of Xi’an Jiaotong University. Written informed consent was obtained from all study subjects. All steps of the study conformed to the Helsinki Declaration.

Footnotes

  • HW and CW contributed equally.

  • Contributors JS and ZY designed the study. HW, CW, SQ, YH and JS collected the data. HW and CW analyzed the data. JS and HW wrote the paper.

  • Funding This study was supported by National Natural Science Foundation of China (81500219, 81400302, and 81570406), the Natural Science Foundation of Shaanxi province (2018KW067, 2017JM8016, and 2016SF217), and the Fundamental Research Funds for the Central Universities in China (1191329724 and 191329849), the Clinical Research Award of the First Affiliated Hospital of Xi'an Jiaotong University, China (No. XJTU1AF-CRF-2018–025).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, an indication of whether changes were made, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

References

  1. ↵
    1. Virani SS ,
    2. Alonso A ,
    3. Benjamin EJ , et al
    . Heart disease and stroke statistics-2020 update: a report from the American Heart Association. Circulation 2020;141:e139–596.doi:10.1161/CIR.0000000000000757 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31992061
    OpenUrlCrossRefPubMed
  2. ↵
    1. Timmis A ,
    2. Townsend N ,
    3. Gale CP , et al
    . European Society of Cardiology: cardiovascular disease statistics 2019. Eur Heart J 2020;41:12–85.doi:10.1093/eurheartj/ehz859 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31820000
    OpenUrlCrossRefPubMed
  3. ↵
    1. Roth GA ,
    2. Johnson C ,
    3. Abajobir A , et al
    . Global, regional, and national burden of cardiovascular diseases for 10 causes, 1990 to 2015. J Am Coll Cardiol 2017;70:1–25.doi:10.1016/j.jacc.2017.04.052 pmid:http://www.ncbi.nlm.nih.gov/pubmed/28527533
    OpenUrlFREE Full Text
  4. ↵
    1. Reiner Željko
    . Hypertriglyceridaemia and risk of coronary artery disease. Nat Rev Cardiol 2017;14:401–11.doi:10.1038/nrcardio.2017.31 pmid:http://www.ncbi.nlm.nih.gov/pubmed/28300080
    OpenUrlPubMed
  5. ↵
    1. Arnett DK ,
    2. Blumenthal RS ,
    3. Albert MA , et al
    . 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease: Executive summary: a report of the American College of Cardiology/American heart association Task force on clinical practice guidelines. Circulation 2019;140:e563–95.doi:10.1161/CIR.0000000000000677 pmid:http://www.ncbi.nlm.nih.gov/pubmed/30879339
    OpenUrlPubMed
  6. ↵
    1. Arsenault BJ ,
    2. Boekholdt SM ,
    3. Kastelein JJP
    . Lipid parameters for measuring risk of cardiovascular disease. Nat Rev Cardiol 2011;8:197–206.doi:10.1038/nrcardio.2010.223 pmid:http://www.ncbi.nlm.nih.gov/pubmed/21283149
    OpenUrlCrossRefPubMed
  7. ↵
    1. Mach F ,
    2. Baigent C ,
    3. Catapano AL , et al
    . 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J 2020;41:111–88.doi:10.1093/eurheartj/ehz455 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31504418
    OpenUrlCrossRefPubMed
  8. ↵
    1. Chapman MJ ,
    2. Ginsberg HN ,
    3. Amarenco P , et al
    . Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur Heart J 2011;32:1345–61.doi:10.1093/eurheartj/ehr112 pmid:http://www.ncbi.nlm.nih.gov/pubmed/21531743
    OpenUrlCrossRefPubMedWeb of Science
  9. ↵
    1. Ouimet M ,
    2. Barrett TJ ,
    3. Fisher EA
    . HDL and reverse cholesterol transport. Circ Res 2019;124:1505–18.doi:10.1161/CIRCRESAHA.119.312617 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31071007
    OpenUrlCrossRefPubMed
  10. ↵
    1. Rosenson RS ,
    2. Brewer HB ,
    3. Ansell BJ , et al
    . Dysfunctional HDL and atherosclerotic cardiovascular disease. Nat Rev Cardiol 2016;13:48–60.doi:10.1038/nrcardio.2015.124 pmid:http://www.ncbi.nlm.nih.gov/pubmed/26323267
    OpenUrlPubMed
  11. ↵
    1. Ferrari R ,
    2. Aguiar C ,
    3. Alegria E , et al
    . Current practice in identifying and treating cardiovascular risk, with a focus on residual risk associated with atherogenic dyslipidaemia. Eur Heart J Suppl 2016;18:C2–12.doi:10.1093/eurheartj/suw009 pmid:http://www.ncbi.nlm.nih.gov/pubmed/28533705
    OpenUrlCrossRefPubMed
  12. ↵
    1. Catapano AL ,
    2. Graham I ,
    3. De Backer G , et al
    . 2016 ESC/EAS guidelines for the management of Dyslipidaemias. Eur Heart J 2016;37:2999–3058.doi:10.1093/eurheartj/ehw272 pmid:http://www.ncbi.nlm.nih.gov/pubmed/27567407
    OpenUrlCrossRefPubMed
  13. ↵
    1. Langlois MR ,
    2. Chapman MJ ,
    3. Cobbaert C , et al
    . Quantifying atherogenic lipoproteins: current and future challenges in the era of personalized medicine and very low concentrations of LDL cholesterol. A consensus statement from EAS and EFLM. Clin Chem 2018;64:1006–33.doi:10.1373/clinchem.2018.287037 pmid:http://www.ncbi.nlm.nih.gov/pubmed/29760220
    OpenUrlAbstract/FREE Full Text
  14. ↵
    1. Barrett TJ ,
    2. Distel E ,
    3. Murphy AJ , et al
    . Apolipoprotein AI) promotes atherosclerosis regression in diabetic mice by suppressing myelopoiesis and plaque inflammation. Circulation 2019;140:1170–84.doi:10.1161/CIRCULATIONAHA.119.039476 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31567014
    OpenUrlCrossRefPubMed
  15. ↵
    1. Henson D ,
    2. Tahhan AS ,
    3. Nardo D , et al
    . Association between ApoA-I (apolipoprotein A-I) immune complexes and adverse cardiovascular Events-Brief report. Arterioscler Thromb Vasc Biol 2019;39:1884–92.doi:10.1161/ATVBAHA.119.312964 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31315438
    OpenUrlPubMed
  16. ↵
    1. Karthikeyan G ,
    2. Teo KK ,
    3. Islam S , et al
    . Lipid profile, plasma apolipoproteins, and risk of a first myocardial infarction among Asians: an analysis from the INTERHEART study. J Am Coll Cardiol 2009;53:244–53.doi:10.1016/j.jacc.2008.09.041 pmid:http://www.ncbi.nlm.nih.gov/pubmed/19147041
    OpenUrlFREE Full Text
  17. ↵
    1. Patel JV ,
    2. Abraheem A ,
    3. Creamer J , et al
    . Apolipoproteins in the discrimination of atherosclerotic burden and cardiac function in patients with stable coronary artery disease. Eur J Heart Fail 2010;12:254–9.doi:10.1093/eurjhf/hfp202 pmid:http://www.ncbi.nlm.nih.gov/pubmed/20089519
    OpenUrlCrossRefPubMed
  18. ↵
    1. Thygesen K ,
    2. Alpert JS ,
    3. White HD , et al
    . Universal definition of myocardial infarction. Eur Heart J 2007;28:2525–38.doi:10.1093/eurheartj/ehm355 pmid:http://www.ncbi.nlm.nih.gov/pubmed/17951287
    OpenUrlCrossRefPubMedWeb of Science
  19. ↵
    1. Faul F ,
    2. Erdfelder E ,
    3. Buchner A , et al
    . Statistical power analyses using G*Power 3.1: tests for correlation and regression analyses. Behav Res Methods 2009;41:1149–60.doi:10.3758/BRM.41.4.1149 pmid:http://www.ncbi.nlm.nih.gov/pubmed/19897823
    OpenUrlCrossRefPubMedWeb of Science
  20. ↵
    1. Prakash AM ,
    2. Sun Y ,
    3. Chiaramida SA , et al
    . Quantitative assessment of pericardial effusion volume by two-dimensional echocardiography. J Am Soc Echocardiogr 2003;16:147–53.doi:10.1067/mje.2003.35 pmid:http://www.ncbi.nlm.nih.gov/pubmed/12574741
    OpenUrlPubMed
  21. ↵
    1. Fox KAA ,
    2. Dabbous OH ,
    3. Goldberg RJ , et al
    . Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE). BMJ 2006;333:1091. doi:10.1136/bmj.38985.646481.55 pmid:http://www.ncbi.nlm.nih.gov/pubmed/17032691
    OpenUrlAbstract/FREE Full Text
  22. ↵
    1. Winter M-P ,
    2. Wiesbauer F ,
    3. Blessberger H , et al
    . Lipid profile and long-term outcome in premature myocardial infarction. Eur J Clin Invest 2018;48:e13008. doi:10.1111/eci.13008 pmid:http://www.ncbi.nlm.nih.gov/pubmed/30062727
    OpenUrlPubMed
  23. ↵
    1. Welsh C ,
    2. Celis-Morales CA ,
    3. Brown R , et al
    . Comparison of conventional lipoprotein tests and apolipoproteins in the prediction of cardiovascular disease. Circulation 2019;140:542–52.doi:10.1161/CIRCULATIONAHA.119.041149 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31216866
    OpenUrlPubMed
  24. ↵
    1. Holme I ,
    2. Strandberg TE ,
    3. Faergeman O , et al
    . Congestive heart failure is associated with lipoprotein components in statin-treated patients with coronary heart disease insights from the incremental decrease in end points through aggressive lipid lowering trial (ideal). Atherosclerosis 2009;205:522–7.doi:10.1016/j.atherosclerosis.2009.01.023 pmid:http://www.ncbi.nlm.nih.gov/pubmed/19327776
    OpenUrlCrossRefPubMedWeb of Science
  25. ↵
    1. Wedel H ,
    2. McMurray JJV ,
    3. Lindberg M , et al
    . Predictors of fatal and non-fatal outcomes in the controlled rosuvastatin multinational trial in heart failure (CORONA): incremental value of apolipoprotein A-1, high-sensitivity C-reactive peptide and N-terminal pro B-type natriuretic peptide. Eur J Heart Fail 2009;11:281–91.doi:10.1093/eurjhf/hfn046 pmid:http://www.ncbi.nlm.nih.gov/pubmed/19168876
    OpenUrlCrossRefPubMedWeb of Science
  26. ↵
    1. Prats-Uribe A ,
    2. Sayols-Baixeras S ,
    3. Fernández-Sanlés A , et al
    . High-density lipoprotein characteristics and coronary artery disease: a Mendelian randomization study. Metabolism 2020;112:154351.doi:10.1016/j.metabol.2020.154351 pmid:http://www.ncbi.nlm.nih.gov/pubmed/32891675
    OpenUrlPubMed
  27. ↵
    1. Meikle PJ ,
    2. Formosa MF ,
    3. Mellett NA , et al
    . HDL phospholipids, but not cholesterol distinguish acute coronary syndrome from stable coronary artery disease. J Am Heart Assoc 2019;8:e011792. doi:10.1161/JAHA.118.011792 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31131674
    OpenUrlPubMed
  28. ↵
    1. Capodanno D ,
    2. Mehran R ,
    3. Gibson CM , et al
    . CSL112, a reconstituted, infusible, plasma-derived apolipoprotein A-I: safety and tolerability profiles and implications for management in patients with myocardial infarction. Expert Opin Investig Drugs 2018;27:997–1005.doi:10.1080/13543784.2018.1543399 pmid:http://www.ncbi.nlm.nih.gov/pubmed/30376729
    OpenUrlPubMed
  29. ↵
    1. Gibson CM ,
    2. Korjian S ,
    3. Tricoci P , et al
    . Rationale and design of Apo-I event reduction in ischemic syndromes I (AEGIS-I): a phase 2B, randomized, placebo-controlled, dose-ranging trial to investigate the safety and tolerability of CSL112, a reconstituted, infusible, human apoA-I, after acute myocardial infarction. Am Heart J 2016;180:22–8.doi:10.1016/j.ahj.2016.06.017 pmid:http://www.ncbi.nlm.nih.gov/pubmed/27659879
    OpenUrlPubMed
  30. ↵
    1. Michael Gibson C ,
    2. Korjian S ,
    3. Tricoci P , et al
    . Safety and tolerability of CSL112, a reconstituted, Infusible, plasma-derived apolipoprotein A-I, after acute myocardial infarction: the AEGIS-I trial (ApoA-I event reducing in ischemic syndromes I). Circulation 2016;134:1918–30.doi:10.1161/CIRCULATIONAHA.116.025687 pmid:http://www.ncbi.nlm.nih.gov/pubmed/27881559
    OpenUrlAbstract/FREE Full Text
  31. ↵
    1. Boekholdt SM ,
    2. Arsenault BJ ,
    3. Hovingh GK , et al
    . Levels and changes of HDL cholesterol and apolipoprotein A-I in relation to risk of cardiovascular events among statin-treated patients: a meta-analysis. Circulation 2013;128:1504–12.doi:10.1161/CIRCULATIONAHA.113.002670 pmid:http://www.ncbi.nlm.nih.gov/pubmed/23965489
    OpenUrlAbstract/FREE Full Text
  32. ↵
    1. Mora S ,
    2. Glynn RJ ,
    3. Ridker PM
    . High-density lipoprotein cholesterol, size, particle number, and residual vascular risk after potent statin therapy. Circulation 2013;128:1189–97.doi:10.1161/CIRCULATIONAHA.113.002671 pmid:http://www.ncbi.nlm.nih.gov/pubmed/24002795
    OpenUrlAbstract/FREE Full Text
  33. ↵
    1. Duparc T ,
    2. Ruidavets J-B ,
    3. Genoux A , et al
    . Serum level of HDL particles are independently associated with long-term prognosis in patients with coronary artery disease: the genes study. Sci Rep 2020;10:8138. doi:10.1038/s41598-020-65100-2 pmid:http://www.ncbi.nlm.nih.gov/pubmed/32424189
    OpenUrlPubMed
  34. ↵
    1. Sandhu PK ,
    2. Musaad SMA ,
    3. Remaley AT , et al
    . Lipoprotein biomarkers and risk of cardiovascular disease: a laboratory medicine best practices (LMBP) systematic review. J Appl Lab Med 2016;1:214–29.doi:10.1373/jalm.2016.021006 pmid:http://www.ncbi.nlm.nih.gov/pubmed/27840858
    OpenUrlAbstract/FREE Full Text
  35. ↵
    1. Javaheri A ,
    2. Rader DJ
    . Apolipoprotein A-I and cholesterol efflux: the good, the bad, and the modified. Circ Res 2014;114:1681–3.doi:10.1161/CIRCRESAHA.114.303974 pmid:http://www.ncbi.nlm.nih.gov/pubmed/24855198
    OpenUrlFREE Full Text
  36. ↵
    1. Rosenson RS ,
    2. Brewer HB ,
    3. Rader DJ
    . Lipoproteins as biomarkers and therapeutic targets in the setting of acute coronary syndrome. Circ Res 2014;114:1880–9.doi:10.1161/CIRCRESAHA.114.302805 pmid:http://www.ncbi.nlm.nih.gov/pubmed/24902972
    OpenUrlAbstract/FREE Full Text
PreviousNext
Back to top
Vol 69 Issue 7 Table of Contents
Journal of Investigative Medicine: 69 (7)
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
  • AFMR Highlights
  • Front Matter (PDF)
Email

Thank you for your interest in spreading the word on JIM.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Circulating lipid and lipoprotein profiles and their correlation to cardiac function and cardiovascular outcomes in patients with acute myocardial infarction
(Your Name) has sent you a message from JIM
(Your Name) thought you would like to see the JIM web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
Alerts
Sign In to Email Alerts with your Email Address
Citation Tools
Circulating lipid and lipoprotein profiles and their correlation to cardiac function and cardiovascular outcomes in patients with acute myocardial infarction
Haoyu Wu, Chen Wang, Gulinigaer Tuerhongjiang, Xiangrui Qiao, Yiming Hua, Jianqing She, Zuyi Yuan
Journal of Investigative Medicine Oct 2021, 69 (7) 1310-1317; DOI: 10.1136/jim-2021-001803

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Cite This
  • APA
  • Chicago
  • Endnote
  • MLA
Loading
Circulating lipid and lipoprotein profiles and their correlation to cardiac function and cardiovascular outcomes in patients with acute myocardial infarction
Haoyu Wu, Chen Wang, Gulinigaer Tuerhongjiang, Xiangrui Qiao, Yiming Hua, Jianqing She, Zuyi Yuan
Journal of Investigative Medicine Oct 2021, 69 (7) 1310-1317; DOI: 10.1136/jim-2021-001803
Download PDF

Share
Circulating lipid and lipoprotein profiles and their correlation to cardiac function and cardiovascular outcomes in patients with acute myocardial infarction
Haoyu Wu, Chen Wang, Gulinigaer Tuerhongjiang, Xiangrui Qiao, Yiming Hua, Jianqing She, Zuyi Yuan
Journal of Investigative Medicine Oct 2021, 69 (7) 1310-1317; DOI: 10.1136/jim-2021-001803
Reddit logo Twitter logo Facebook logo Mendeley logo
Respond to this article
  • Tweet Widget
  • Facebook Like
  • Google Plus One
  • Article
    • Abstract
    • Introduction
    • Materials and methods
    • Results
    • Discussion
    • Limitations
    • Conclusion
    • Data availability statement
    • Ethics statements
    • Footnotes
    • References
  • Figures & Data
  • eLetters
  • Info & Metrics
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • Opium may affect coronary artery disease by inducing inflammation but not through the expression of CD9, CD36, and CD68
  • Bronchodilatory effect of higenamine as antiallergic asthma treatment
  • Evaluating reporting of patient-reported outcomes in randomized controlled trials regarding inflammatory bowel disease: a methodological study
Show more Original research

Similar Articles

 

CONTENT

  • Latest content
  • Current issue
  • Archive
  • Sign up for email alerts
  • RSS

JOURNAL

  • About the journal
  • Editorial board
  • Subscribe
  • Thank you to our reviewers
  • American Federation for Medical Research

AUTHORS

  • Information for authors
  • Submit a paper
  • Track your article
  • Open Access at BMJ

HELP

  • Contact us
  • Reprints
  • Permissions
  • Advertising
  • Feedback form

© 2023 American Federation for Medical Research