Research Article | | Peer-Reviewed

Correlation Between Serum Apolipoprotein A and Clinical Outcome in Patients with Non-ischemic Heart Failure

Received: 4 January 2025     Accepted: 22 January 2025     Published: 10 February 2025
Views:       Downloads:
Abstract

Previous studies on the correlation between serum apolipoprotein A-I (apoA-I) and the severity of heart failure (HF) as well as short-term clinical outcomes in patients with heart failure due to non-ischemic cardiomyopathy (NICM) have been inconclusive. To address this, we aimed to determine the impact of apoA-I on the severity of heart failure and short-term clinical outcomes in patients with HF due to NICM. In this single-center, observational study, we recruited 154 patients with NICM heart failure (NYHA functional class II-IV) and 80 control patients with normal cardiac function. Baseline characteristics were collected during hospitalization, and follow-up records were obtained 6 months after discharge. Statistical analyses included Pearson’s chi-squared test and Spearman's correlation analysis, while the receiver operating characteristic (ROC) curve was used to discriminate patients with severe heart failure. Results showed that serum apoA-I levels were significantly lower in the heart failure group compared to controls and decreased with increasing cardiac function class. Additionally, serum apoA-I was positively correlated with left ventricular ejection fraction (LVEF) and negatively correlated with B-type natriuretic peptide (BNP) and cardiac function class. Patients who experienced clinical events within 6 months of discharge had significantly lower apoA-I concentrations compared to those without events. In conclusion, low serum apoA-I concentrations in patients with NICM and heart failure may be associated with more severe heart failure and a higher probability of recurrent clinical events in the short term.

Published in Cardiology and Cardiovascular Research (Volume 9, Issue 1)
DOI 10.11648/j.ccr.20250901.12
Page(s) 25-31
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2025. Published by Science Publishing Group

Keywords

Heart Failure, Apolipoprotein A-I, Heart Rate, Cardiac Function, Clinical Outcome

1. Introduction
Heart failure (HF) is the final stage in the development of various cardiovascular diseases . It is a group of syndromes in which various structural and/or functional heart diseases lead to impaired ventricular filling and/or ejection function. In this stage, the cardiac output cannot meet the metabolic needs of body's tissues, with clinical manifestations of pulmonary and/or body circulation stasis and insufficient blood perfusion to organs and tissues . HF has typical symptoms (e.g. shortness of breath, ankle edema and fatigue) and signs (increased jugular venous pressure, fine rales in the lungs, displaced apical pulses). It is a worldwide health problem with a high morbidity and mortality rate and a trend towards younger population . Apolipoprotein A (apoA) is the major structural protein of high-density lipoprotein (HDL-C), of which apoA-I and apoA- II account for about 90% of the protein . The ratio of apoA -I to apoA- II is about 3:1 . Since apoA- I catalyzes lecithin-cholesterolacyltransferase (LCAT) to transport excess cholesterol esters from tissues to the liver for disposal, apoA-I has tissue lipid scavenging and anti-atherosclerotic effects . Therefore, apoA-I and apoB have also been used as risk factors to predict coronary heart disease . It has been demonstrated that low concentrations of serum apoA-I may affect the development and prognosis of coronary artery disease . In patients with chronic heart failure, it has been found that low total serum cholesterol may be associated with poor prognosis. However, few studies have been conducted to assess the severity and prognosis of apoA-I in Chinese patients with chronic heart failure, especially those with non-ischemic heart failure. The aim of this study was to investigate the correlation between serum apoA-I concentrations and the severity as well as clinical outcome of heart failure patients with non-ischemic cardiomyopathy (NICM).
2. Methods
2.1. Study Population and Data Collection
Between July 2018 and July 2021, one hundred and fifty-four patients with chronic heart failure who were hospitalized in the Department of Cardiology, the First Hospital Affiliated to Soochow University were enrolled, and the diagnostic criteria were referred to the guidelines for the diagnosis and management of heart failure published by the European Society of Cardiology (ESC) in 2012 and graded according to the New York Heart Association (NYHA) cardiac function classification. Patients with ischemic cardiomyopathy, pulmonary embolism, myocarditis, autoimmune diseases, and primary diseases with severe pulmonary, hepatic, renal, hematologic, connective tissue, and neoplastic complications were excluded. All subjects were followed up to 6 months after hospital discharge until the first of the following clinical events occurred: all-cause death and rehospitalization due to heart failure exacerbation.
2.2. Clinical Assessment
All subjects were recorded age, sex, height, weight, calculated body mass index BMI (weight (kg) / height2 (m2)) and other general information. The history of hypertensive disease, diabetes mellitus, atrial fibrillation and smoking were also recorded. In each group, 5 ml of fasting elbow venous blood was collected in the early morning of the second day of admission and sent to the laboratory for the determination of glutamyl aminotransferase (ALT), glutamic aminotransferase (AST), creatinine (Cr), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A (apo-A), and superoxide dismutase (hs-CRP). Sensitive C-reactive protein (hs-CRP) and other biochemical indexes were used to calculate creatinine clearance (CrCl) according to the Cockcroft-Gault formula, CrCl = (140-age) × body weight (Kg) / (0.818 × creatinine (umol/L)) in male patients; CrCl = (140-age) × body weight (Kg) × 0.85 / (0.818×creatinine (umol/L)). 3 ml of venous blood was collected and placed in anticoagulation tubes containing ethylenediaminetetraacetic acid (EDTA) and sent to the laboratory. B-type amino-terminal natriuretic peptidogen (BNP) was measured by electrochemiluminescence immunoassay on a Roche Elecsys E170 automatic immunoassay analyzer. The included patients underwent cardiac ultrasound (GE VIVIDi/VIVIq color echocardiograph, USA) in the cardiac ultrasound room on the second day after admission, and left ventricular ejection fraction (LVEF) was recorded. This cardiac echocardiography was conducted by an echocardiographer who was not involved in the study. The ethical approval for this study was obtained from the Ethics Committees of the First Affiliated Hospital of Soochow University. The ethics code for this study is SS2018072.
2.3. Statistical Analysis
All data were processed using SPSS 26.0 statistical software. The measurement data were expressed as mean ± standard deviation (x̄±SD). One-way ANOVA followed by Bonferroni, Tukey, or Games-Howell post hoc test (dependent on the result of Levene’s test to determine the equality of variances) was used to examine the effect of cardiac function. Pearson's correlation analysis and Spearman's correlation analysis were used for correlation analysis, while the results of individual tests were plotted as receiver operating characteristic curve (ROC), and the area under the curve (AUC) was calculated. A value of p < 0.05 (two-sided) was considered to be statistically significant.
3. Results
3.1. Comparison of Clinical Characteristics Between Control Group and NICM Heart Failure Patients with Cardiac Function Class II-IV (NYHA)
In total, 154 patients with chronic heart failure were enrolled, including 108 males and 46 females with a mean age of 63.79 ± 11.25 years. The control group consisted of 80 individuals with normal heart function, including 41 males and 39 females, with a mean age of 60.31 ± 8.75 years. The patients were divided into four groups (80 control, 18 class II, 49 class III, and 87 class IV) according to the NYHA classification of heart failure severity, and the comparison between the groups is shown in Table 1. Clinical characteristics such as age, sex, BMI, incidence of diabetes, incidence of atrial fibrillation, smoking rate, systolic and diastolic blood pressure were not significantly different between the groups. There was no significant difference in the etiology of heart failure in the heart failure group, but with the increase of NYHA classification, the heart rate of patients gradually increased, and the difference of heart rate among the groups was statistically significant. The biochemical parameters of total cholesterol (TC), triglycerides (TG), low-density cholesterol (LDL-C), high-density cholesterol (HDL-C), apolipoprotein B (apoB), lipoprotein a (LP(a)), creatinine content (Cr), creatinine clearance (CrCl), and hypersensitive C-reactive protein (Hs-CRP) were not significantly different among the three groups in heart failure. However, the concentration of apolipoprotein A-I (apoA-I) decreased gradually with increasing NYHA classification (p<0.05). With increasing severity of heart failure, BNP gradually increased and LVEF values gradually decreased (p<0.05).
Table 1. Comparison of characteristics in patients with heart failure of different cardiac function grades.

Cardiac Function Classification (NYHA)

control (N=80)

Grade II (N=18)

Grade III (N=49)

Grade IV (N=87)

P value

Age

60.31±8.75

63.67±12.12

64.33±9.96

63.52±11.86

>0.05

Male (%)

41(51.25%)

10(55.56%)

34(69.39%)

64(73.56%)

>0.05

BMI

23.79±2.51

23.95±3.09

24.36±3.36

23.82±4.35

>0.05

Diabetes (%)

7(8.75%)

2(11.11%)

9(18.37%)

14(16.09%)

>0.05

AF (%)

3(3.75%)

2(11.11%)

18(36.73%)

28(32.18%)

>0.05

Smoking (%)

18(22.50%)

8(44.44%)

14(28.57%)

29(33.33%)

>0.05

SP (mmHg)

124.89±14.81

138.72±32.16

125.76±24.12

118.48±21.52

>0.05

DP (mmHg)

77.75±8.47

83.72±20.55

76.00±14.73

74.66±13.95

>0.05

HR (bpm)

73.63±10.67

76.56±13.29

79.61±24.48

85.45±19.67

<0.05

Etiology

Dilated cardiomyopathy (%)

11 (61.11%)

22 (44.90%)

58 (66.67%)

Hypertension (%)

4 (22.22%)

22 (44.90%)

17 (19.54%)

>0.05

Heart Valve (%)

3 (16.67%)

5 (10.20%)

12 (13.79%)

TC (mmol/L)

4.42±0.73

4.23±0.75

3.85±1.22

3.72±1.03

>0.05

TG (mmol/L)

1.59±0.88

1.40±0.69

1.32±0.95

1.08±0.58

>0.05

LDL-C (mmol/L)

2.63±0.64

2.59±0.61

2.28±0.84

2.33±0.84

>0.05

HDL-C (mmol/L)

1.17±0.27

1.05±0.20

1.03±0.37

0.95±0.30

>0.05

ApoAI (g/L)

1.32±0.27

1.21±0.15

1.15±0.23

1.02±0.19

<0.05

ApoB (g/L)

0.89±0.19

0.88±0.17

0.85±0.22

0.84±0.28

>0.05

LP(a) (mg/L)

171.51±196.79

149.19±123.91

107.52±82.11

155.56±228.75

>0.05

ApoAI/ApoB

1.56±0.39

1.44±0.41

1.43±0.38

1.35±0.38

>0.05

Cr (umol/L)

63.38±13.25

81.35±17.35

85.55±28.32

96.22±39.43

>0.05

CrCl (ml/min)

97.26±22.58

75.75±23.98

71.57±30.58

69.74±31.15

>0.05

BNP (pg/ml)

50.12±30.99

1741.37±1509.41

3079.44±2626.87

7401.92±7671.88

<0.05

LVEF (%)

66.39±51.21

43.22±15.20

39.33±17.95

31.94±12.10

<0.05

HsCRP (mg/L)

1.78±2.07

4.73±3.92

4.93±4.90

6.19±5.15

>0.05

Table 1. BMI, Body Mass Index; AF, atrial fibrillation; SP, systolic pressure; DP, diastolic pressure; HR, heart rate; TC, serum total cholesterol; TG, serum triglycerides; LDL-C, serum low-density cholesterol; HDL-C, serum high-density cholesterol; LVEF, left ventricular ejection fraction; Cr, serum creatinine; CrCl, creatinine clearance; BNP, B-type amino-terminal natriuretic peptidogen; CRP, C-reactive protein.
3.2. Correlation Analysis of Serum apoA-I Concentration with LVEF Value, BNP, and Cardiac Function Classification
Pearson and Spearman correlation analyses showed a positive correlation between serum apo-A and LVEF values (r=0.470, p<0.001); a negative correlation with BNP (r=-0.382, p<0.001); and a negative correlation with NYHA classification (r=-0.598, p<0.001) (Figure 1-Figure 3).
Figure 1. Correlation analysis of serum apoA-I concentration with BNP.
Figure 2. Correlation analysis of serum apoA-I concentration with LVEF value.
Figure 3. Correlation analysis of serum apoA-I concentration with cardiac function classification.
3.3. ROC Curve of Serum apoA-I Concentration to Evaluate the Severity of Heart Failure
Figure 4. ROC curve of serum apoA-I concentration to evaluate the severity of heart failure.
According to NYHA classification, those with NYHA class IV were regarded as patients with severe heart failure, and the ROC curve was drawn to evaluate the reflection of apoA-I on the severity of chronic heart failure. The calculated AUC was 0.815, indicating that serum apoA-I concentration has a potential diagnostic value for the severity of clinical symptoms in patients with non-ischemic heart failure, and when apoA-I was 118.5 mg/dl, the sensitivity was 85.1% and the specificity was 64.6% (see Figure 4).
3.4. Serum apoA-I Concentrations in Patients with Different Short-term Prognosis
At the follow-up within 6 months of discharge, 21 (13.63%) patients had a clinical event, 17 patients were readmitted for worsening heart failure symptoms, 3 patients died due to cardiac death, and 1 patient died from other causes (Table 2). apoA-I concentrations were statistically lower in patients in the group with clinical events compared with those in the group without clinical events (Figure 5, p<0.05).
Table 2. Follow-up of patients with different cardiac function classifications at 6 months.

Grade II (N=18)

Grade III (N=49)

Grade IV (N=87)

Re-hospitalization due to worsening heart failure symptoms

1 (5.56%)

4 (8.16%)

12 (13.79%)

Death

pump Failure

0 (0.00%)

0 (0.00%)

2 (2.30%)

sudden death

0 (0.00%)

0 (0.00%)

1 (1.15%)

other causes

0 (0.00%)

0 (0.00%)

1 (1.15%)

Figure 5. Comparison of apoA-I levels in patients without and with clinical events.
4. Discussion
High-density lipoprotein cholesterol (HDL-C) and its major protein component, apolipoprotein A-I (apoA-I), have been extensively studied for their roles in cardiovascular health and disease . Our study found that serum apoA-I levels were significantly lower in patients with non-ischemic cardiomyopathy (NICM) heart failure compared to controls, and these levels decreased further with increasing NYHA functional class. This observation is consistent with previous studies that have demonstrated a strong correlation between low apoA-I levels and poor prognosis in heart failure patients .
Several studies have investigated the role of apoA-I in both ischemic and non-ischemic heart failure. For example, apoA-I levels were significantly lower in patients with ischemic heart failure compared to non-ischemic heart failure, suggesting that the pathophysiological mechanisms underlying these two conditions may differ . Our findings in NICM patients align with these observations, highlighting the potential role of apoA-I in reflecting disease severity and prognosis.
The differences in apoA-I levels between ischemic and non-ischemic heart failure may be attributed to distinct underlying mechanisms. Ischemic heart failure is often associated with coronary artery disease, where atherosclerosis plays a significant role. ApoA-I, with its anti-inflammatory and anti-atherosclerotic properties, may be more directly involved in the pathogenesis of ischemic heart failure . In contrast, non-ischemic cardiomyopathy may involve more diverse etiologies, such as genetic factors, infections, or autoimmune diseases, which may influence apoA-I levels differently .
Our study also examined the relationship between apoA-I and apoB levels. Previous research has shown that the apoA-I/apoB ratio can be a powerful predictor of cardiovascular risk . We found that while apoA-I levels were significantly associated with heart failure severity and clinical outcomes, apoB levels did not show similar correlations. This suggests that apoA-I may be a more sensitive biomarker for assessing disease progression in heart failure patients.
The significant correlation between apoA-I levels and heart failure severity highlights its potential as a biomarker for monitoring disease progression and predicting short-term outcomes . Future studies should aim to validate these findings in larger cohorts and explore the role of apoA-I in different types of heart failure. Additionally, interventions targeting apoA-I, such as lifestyle modifications or pharmacological treatments, may be investigated to improve outcomes in heart failure patients . The significant variation in heart rate between groups in our study reflects the body's compensatory response to worsening cardiac function. This finding highlights the importance of considering heart rate as a clinical marker of heart failure severity and prognosis. In future studies, interventions aimed at managing heart rate (e.g., beta-blockers) may be further explored to improve outcomes in patients with advanced heart failure.
In conclusion, our study provides valuable insights into the role of apoA-I in non-ischemic heart failure. By comparing our findings with similar studies and discussing the potential mechanisms underlying the observed correlations, we hope to contribute to a better understanding of the pathophysiology of heart failure and the development of more effective diagnostic and therapeutic strategies.
Abbreviations

HF

Heart Failure

NICM

Non-ischemic Cardiomyopathy

NYHA

New York Heart Association

LVEF

Left Ventricular Ejection Fraction

BNP

B-type Natriuretic Peptide

HDL-C

High-Density Lipoprotein Cholesterol

apoA-I

Apolipoprotein A-I

apoB

Apolipoprotein B

LP(a)

Lipoprotein A

Cr

Creatinine

CrCl

Creatinine Clearance

Hs-CRP

Hypersensitive C-Reactive Protein

TC

Total Cholesterol

TG

Triglyceride

LDL-C

Low-Density Lipoprotein Cholesterol

ROC

Receiver Operating Characteristic

AUC

Area Under the Curve

ESC

European Society of Cardiology

LCAT

Lecithin-Cholesterol Acyltransferase

AF

Atrial Fibrillation

SP

Systolic Pressure

DP

Diastolic Pressure

HR

Heart Rate

Author Contributions
Chiqian Ma: Conceptualization, Data curation, Formal Analysis, Investigation, Methodology, Writing – original draft
Licong Chen: Data curation, Investigation, Methodology, Software
Shikun Sun: Project administration, Resources
Xiaodong Qian: Resources, Validation
Yiren Qin: Conceptualization, Supervision, Writing – original draft, Writing – review & editing
Ethics Approval
The Ethics Committees of the First Affiliated Hospital of Soochow University approved this study. The participants provided their written informed consent to participate in this study.
Funding
This work was supported by the Suzhou Science and Technology Projects under grant SS202072, SKY2021065.
Data Availability Statement
Data that support the findings of this study are available from the corresponding author upon reasonable request.
Conflicts of Interest
The authors declare that they have no conflict of interest.
References
[1] Petrie MC, Verma S, Docherty KF, Inzucchi SE, Anand I, Belohlavek J, Bohm M, Chiang CE, Chopra VK, de Boer RA et al: Effect of Dapagliflozin on Worsening Heart Failure and Cardiovascular Death in Patients With Heart Failure With and Without Diabetes. JAMA 2020, 323(14): 1353-1368.
[2] Yin J, Lu X, Qian Z, Xu W, Zhou X: New insights into the pathogenesis and treatment of sarcopenia in chronic heart failure. Theranostics 2019, 9(14): 4019-4029.
[3] Pinsky MR: The right ventricle: interaction with the pulmonary circulation. Crit Care 2016, 20: 266.
[4] Kraigher-Krainer E, Shah AM, Gupta DK, Santos A, Claggett B, Pieske B, Zile MR, Voors AA, Lefkowitz MP, Packer M et al: Impaired systolic function by strain imaging in heart failure with preserved ejection fraction. J Am Coll Cardiol 2014, 63(5): 447-456.
[5] Aaron CP, Hoffman EA, Lima JAC, Kawut SM, Bertoni AG, Vogel-Claussen J, Habibi M, Hueper K, Jacobs DR, Jr., Kalhan R et al: Pulmonary vascular volume, impaired left ventricular filling and dyspnea: The MESA Lung Study. PLoS One 2017, 12(4): e0176180.
[6] Liu L, Eisen HJ: Epidemiology of heart failure and scope of the problem. Cardiol Clin 2014, 32(1): 1-8, vii.
[7] Wong CM, Hawkins NM, Petrie MC, Jhund PS, Gardner RS, Ariti CA, Poppe KK, Earle N, Whalley GA, Squire IB et al: Heart failure in younger patients: the Meta-analysis Global Group in Chronic Heart Failure (MAGGIC). Eur Heart J 2014, 35(39): 2714-2721.
[8] Segrest JP, Li L, Anantharamaiah GM, Harvey SC, Liadaki KN, Zannis V: Structure and function of apolipoprotein A-I and high-density lipoprotein. Curr Opin Lipidol 2000, 11(2): 105-115.
[9] Melchior JT, Street SE, Vaisar T, Hart R, Jerome J, Kuklenyik Z, Clouet-Foraison N, Thornock C, Bedi S, Shah AS et al: Apolipoprotein A-I modulates HDL particle size in the absence of apolipoprotein A-II. J Lipid Res 2021, 62: 100099.
[10] De Oliveira e Silva ER, Kong M, Han Z, Starr C, Kass EM, Juo SH, Foster D, Dansky HM, Merkel M, Cundey K et al: Metabolic and genetic determinants of HDL metabolism and hepatic lipase activity in normolipidemic females. J Lipid Res 1999, 40(7): 1211-1221.
[11] Pussinen PJ, Jauhiainen M, Ehnholm C: ApoA-II/apoA-I molar ratio in the HDL particle influences phospholipid transfer protein-mediated HDL interconversion. J Lipid Res 1997, 38(1): 12-21.
[12] Millar JS, Cuchel M: ApoA-I-Directed Therapies for the Management of Atherosclerosis. Curr Atheroscler Rep 2015, 17(10): 60.
[13] Walldius G, Jungner I, Aastveit AH, Holme I, Furberg CD, Sniderman AD: The apoB/apoA-I ratio is better than the cholesterol ratios to estimate the balance between plasma proatherogenic and antiatherogenic lipoproteins and to predict coronary risk. Clin Chem Lab Med 2004, 42(12): 1355-1363.
[14] Fernandez ML, Webb D: The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk. J Am Coll Nutr 2008, 27(1): 1-5.
[15] Srinivasan SR, Berenson GS: Serum apolipoproteins A-I and B as markers of coronary artery disease risk in early life: the Bogalusa Heart Study. Clin Chem 1995, 41(1): 159-164.
[16] Rubenfire M, Brook RD: HDL cholesterol and cardiovascular outcomes: what is the evidence? Curr Cardiol Rep 2013, 15(4): 349.
[17] Barter P: HDL-C: role as a risk modifier. Atheroscler Suppl 2011, 12(3): 267-270.
[18] Van Lenten BJ, Hama SY, de Beer FC, Stafforini DM, McIntyre TM, Prescott SM, La Du BN, Fogelman AM, Navab M: Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J Clin Invest 1995, 96(6): 2758-2767.
[19] Zhang Y, Zanotti I, Reilly MP, Glick JM, Rothblat GH, Rader DJ: Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation 2003, 108(6): 661-663.
[20] Georgila K, Vyrla D, Drakos E: Apolipoprotein A-I (ApoA-I), Immunity, Inflammation and Cancer. Cancers (Basel) 2019, 11(8).
[21] Chiesa G, Sirtori CR: Recombinant apolipoprotein A-I (Milano): a novel agent for the induction of regression of atherosclerotic plaques. Ann Med 2003, 35(4): 267-273.
[22] Karjalainen MK, Holmes MV, Wang Q, Anufrieva O, Kahonen M, Lehtimaki T, Havulinna AS, Kristiansson K, Salomaa V, Perola M et al: Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study. Atherosclerosis 2020, 299: 56-63.
[23] Banos-Gonzalez MA, Pena-Duque MA, Angles-Cano E, Martinez-Rios MA, Bahena A, Valente-Acosta B, Cardoso-Saldana G, Angulo-Ortiz J, de la Pena-Diaz A: Apo(a) phenotyping and long-term prognosis for coronary artery disease. Clin Biochem 2010, 43(7-8): 640-644.
[24] Sun L, Guo M, Xu C, Qiao X, Hua Y, Tuerhongjiang G, Lou B, Li R, Bai X, Zhou J et al: HDL-C/apoA-I Ratio Is Associated with the Severity of Coronary Artery Stenosis in Diabetic Patients with Acute Coronary Syndrome. Dis Markers 2021, 2021: 6689056.
[25] Voigt A, Rahnefeld A, Kloetzel PM, Kruger E: Cytokine-induced oxidative stress in cardiac inflammation and heart failure-how the ubiquitin proteasome system targets this vicious cycle. Front Physiol 2013, 4: 42.
[26] Ayoub KF, Pothineni NVK, Rutland J, Ding Z, Mehta JL: Immunity, Inflammation, and Oxidative Stress in Heart Failure: Emerging Molecular Targets. Cardiovasc Drugs Ther 2017, 31(5-6): 593-608.
Cite This Article
  • APA Style

    Ma, C., Chen, L., Sun, S., Qian, X., Qin, Y. (2025). Correlation Between Serum Apolipoprotein A and Clinical Outcome in Patients with Non-ischemic Heart Failure. Cardiology and Cardiovascular Research, 9(1), 25-31. https://doi.org/10.11648/j.ccr.20250901.12

    Copy | Download

    ACS Style

    Ma, C.; Chen, L.; Sun, S.; Qian, X.; Qin, Y. Correlation Between Serum Apolipoprotein A and Clinical Outcome in Patients with Non-ischemic Heart Failure. Cardiol. Cardiovasc. Res. 2025, 9(1), 25-31. doi: 10.11648/j.ccr.20250901.12

    Copy | Download

    AMA Style

    Ma C, Chen L, Sun S, Qian X, Qin Y. Correlation Between Serum Apolipoprotein A and Clinical Outcome in Patients with Non-ischemic Heart Failure. Cardiol Cardiovasc Res. 2025;9(1):25-31. doi: 10.11648/j.ccr.20250901.12

    Copy | Download

  • @article{10.11648/j.ccr.20250901.12,
      author = {Chiqian Ma and Licong Chen and Shikun Sun and Xiaodong Qian and Yiren Qin},
      title = {Correlation Between Serum Apolipoprotein A and Clinical Outcome in Patients with Non-ischemic Heart Failure},
      journal = {Cardiology and Cardiovascular Research},
      volume = {9},
      number = {1},
      pages = {25-31},
      doi = {10.11648/j.ccr.20250901.12},
      url = {https://doi.org/10.11648/j.ccr.20250901.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ccr.20250901.12},
      abstract = {Previous studies on the correlation between serum apolipoprotein A-I (apoA-I) and the severity of heart failure (HF) as well as short-term clinical outcomes in patients with heart failure due to non-ischemic cardiomyopathy (NICM) have been inconclusive. To address this, we aimed to determine the impact of apoA-I on the severity of heart failure and short-term clinical outcomes in patients with HF due to NICM. In this single-center, observational study, we recruited 154 patients with NICM heart failure (NYHA functional class II-IV) and 80 control patients with normal cardiac function. Baseline characteristics were collected during hospitalization, and follow-up records were obtained 6 months after discharge. Statistical analyses included Pearson’s chi-squared test and Spearman's correlation analysis, while the receiver operating characteristic (ROC) curve was used to discriminate patients with severe heart failure. Results showed that serum apoA-I levels were significantly lower in the heart failure group compared to controls and decreased with increasing cardiac function class. Additionally, serum apoA-I was positively correlated with left ventricular ejection fraction (LVEF) and negatively correlated with B-type natriuretic peptide (BNP) and cardiac function class. Patients who experienced clinical events within 6 months of discharge had significantly lower apoA-I concentrations compared to those without events. In conclusion, low serum apoA-I concentrations in patients with NICM and heart failure may be associated with more severe heart failure and a higher probability of recurrent clinical events in the short term.},
     year = {2025}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Correlation Between Serum Apolipoprotein A and Clinical Outcome in Patients with Non-ischemic Heart Failure
    AU  - Chiqian Ma
    AU  - Licong Chen
    AU  - Shikun Sun
    AU  - Xiaodong Qian
    AU  - Yiren Qin
    Y1  - 2025/02/10
    PY  - 2025
    N1  - https://doi.org/10.11648/j.ccr.20250901.12
    DO  - 10.11648/j.ccr.20250901.12
    T2  - Cardiology and Cardiovascular Research
    JF  - Cardiology and Cardiovascular Research
    JO  - Cardiology and Cardiovascular Research
    SP  - 25
    EP  - 31
    PB  - Science Publishing Group
    SN  - 2578-8914
    UR  - https://doi.org/10.11648/j.ccr.20250901.12
    AB  - Previous studies on the correlation between serum apolipoprotein A-I (apoA-I) and the severity of heart failure (HF) as well as short-term clinical outcomes in patients with heart failure due to non-ischemic cardiomyopathy (NICM) have been inconclusive. To address this, we aimed to determine the impact of apoA-I on the severity of heart failure and short-term clinical outcomes in patients with HF due to NICM. In this single-center, observational study, we recruited 154 patients with NICM heart failure (NYHA functional class II-IV) and 80 control patients with normal cardiac function. Baseline characteristics were collected during hospitalization, and follow-up records were obtained 6 months after discharge. Statistical analyses included Pearson’s chi-squared test and Spearman's correlation analysis, while the receiver operating characteristic (ROC) curve was used to discriminate patients with severe heart failure. Results showed that serum apoA-I levels were significantly lower in the heart failure group compared to controls and decreased with increasing cardiac function class. Additionally, serum apoA-I was positively correlated with left ventricular ejection fraction (LVEF) and negatively correlated with B-type natriuretic peptide (BNP) and cardiac function class. Patients who experienced clinical events within 6 months of discharge had significantly lower apoA-I concentrations compared to those without events. In conclusion, low serum apoA-I concentrations in patients with NICM and heart failure may be associated with more severe heart failure and a higher probability of recurrent clinical events in the short term.
    VL  - 9
    IS  - 1
    ER  - 

    Copy | Download

Author Information
  • The Department of Cardiology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China

  • The Department of Neurology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China

  • The Department of Cardiology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China

  • The Department of Cardiology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China

  • The Department of Neurology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China

  • Abstract
  • Keywords
  • Document Sections

    1. 1. Introduction
    2. 2. Methods
    3. 3. Results
    4. 4. Discussion
    Show Full Outline
  • Abbreviations
  • Author Contributions
  • Ethics Approval
  • Funding
  • Data Availability Statement
  • Conflicts of Interest
  • References
  • Cite This Article
  • Author Information