Original Manuscripts

Angiology
1-5
Relationship Between C-Reactive Protein to ª The Author(s) 2021
Article reuse guidelines:
sagepub.com/journals-permissions
Albumin Ratio and Infarct-Related Artery DOI: 10.1177/00033197211024047
journals.sagepub.com/home/ang
Patency in Patients With ST-Segment
Elevation Myocardial Infarction

Kadriye Gayretli Yayla, MD1 , Cagri Yayla, MD2 ,

Mehmet Akif Erdol, MD2 , Mustafa Karanfil, MD2 ,
Ahmet Goktug Ertem, MD2 , and Adnan Burak Akcay, MD2

Abstract
The C-reactive protein to albumin ratio (CAR) is a predictive marker of systemic inflammatory state in atherosclerotic coronary
disease when compared with the predictive value of these 2 markers separately. We investigated the relationship between CAR
and infarct-related artery (IRA) patency in patients with ST-segment elevation myocardial infarction (STEMI). The study popu-
lation (n ¼ 1047) was divided into 2 groups according to IRA patency which was assessed by the Thrombolysis in Myocardial
Infarction (TIMI) flow grade. Nonpatent flow was defined as TIMI grade 0 (no-reflow), 1, and 2 flows, and normal flow was defined
as TIMI 3 flow. There was a significant positive correlation between CAR and SYNTAX score (r ¼ 0.312, P < .001) and a negative
correlation between CAR and TIMI grade flow (r ¼ 0.210, P < .001). At a cutoff level of 0.693, the CAR predicted TIMI
no-reflow with a sensitivity of 65.4% and a specificity of 65.5% (area under the curve: 0.670, 95% CI: 0.62-0.71, P < .001). Mul-
tivariate logistic regression analyses showed that CAR was an independent predictor of IRA patency (0.003 [0.001-0.029];
P < .001). A higher CAR is a significant and independent predictor of IRA patency in patients with STEMI.

Keywords
serum C-reactive protein to albumin ratio, myocardial infarction, infarct-related artery patency

Introduction
Early reperfusion is an important part of treating ST-segment
elevation myocardial infarction (STEMI) since early restora-
tion of coronary flow in an infarct-related artery (IRA)
improves ventricular function and decreases mortality.1 When
a patent IRA occurs before coronary intervention, this is asso-
ciated with reduced in-hospital mortality and preservation of
ventricular performance in patients with STEMI.2
The no-reflow phenomenon was first defined by Krug et al;
they found interstitial edema and red cell packing in capillaries
after temporary coronary occlusion.3 The no-reflow phenom-
enon is classified by the postintervention Thrombolysis in
Myocardial Infarction (TIMI) flow grade.4
Thrombus and fragile atheromatous plaque are present in
most patients with STEMI; this can result in distal emboliza-
tion and subsequent no-reflow during primary percutaneous
coronary intervention (PCI).5
Inflammation plays a central role in the development and
progression of atherosclerosis.6 C-reactive protein (CRP) is a
highly sensitive acute phase reactant produced rapidly and in
large quantities by the liver in response7,8 to inflammatory
cytokines such as interleukin (IL) 6. Albumin is a negative
acute phase protein, and a low serum albumin level is associ-
ated with the intensity of the infection-triggered inflammatory
response in critically ill patients.9 Recently, the CRP to albu-
min ratio (CAR) was shown to be a better predictor of the
systemic inflammatory state in atherosclerotic coronary dis-
eases when compared with the predictive value of these 2 mar-
kers separately.10-12 However, the relationship between the
serum CAR and patency of the IRA in patients with STEMI
is not yet defined. Therefore, we investigated the relationship
between CAR, the anatomical synergy between PCI with taxus
and cardiac surgery (SYNTAX) score, and IRA patency (using
1
Department of Cardiology, Dr. Abdurrahman Yurtaslan Ankara Onkoloji
Education and Research Hospital, University of Health Sciences, Ankara,
Turkey
2
Department of Cardiology, Ankara City Hospital, University of Health
Sciences, Ankara, Turkey
Corresponding Author:
Kadriye Gayretli Yayla, Department of Cardiology, Dr. Abdurrahman Yurtaslan
Ankara Onkoloji Education and Research Hospital, University of Health
Sciences, Ankara, Turkey.
Email: kgyayla@gmail.com
2 Angiology XX(X)

the TIMI flow grade) in patients with STEMI before coronary defined means + SD, and categorical variables were expressed as
intervention and PCI. percentages. The Kolmogorov-Smirnov test was used to test nor-
mality of distribution. Categorical variables were compared with
the w2 test, and continuous variables were compared with the
Methods Student t test or Mann-Whitney U test. Receiver operating char-
acteristic curve analysis was used to define the optimum cutoff
Coronary angiographies were reviewed between February 2015
level of CAR to predict the TIMI no-reflow. Logistic regression
and October 2019. A total of 1216 consecutive patients with
analysis was used to determine the odds ratios and 95% CI of
STEMI undergoing primary PCI within 12 hours from symptom
possible confounding factors in IRA patency. Possible confound-
onset were evaluated. After exclusion of patients, 1047 patients
ing factors were tested in a univariate regression model, and con-
were included for this study. Exclusion criteria were severe founders with a P < .1 were tested in multivariate analysis.
valve disease, malignancy, renal or hepatic dysfunction, acute
A 2-sided P < .05 was considered significant.
or chronic infection, hematologic disease, chronic obstructive
lung disease, atrial fibrillation, cerebrovascular disease, periph-
eral artery disease, stroke, or intestinal diseases. ST-segment Results
elevation myocardial infarction was defined as an increase in
A total of 1047 patients were enrolled in the present study.
troponin I >1 ng/mL with a new ST elevation measured from the
There were 879 patients in the occluded group and 168 patients
J point in 2 contiguous leads with at least 0.2 mV in leads V1,
in the patent group, with a mean age of 56.6 + 11.4 years;
V2, and V3 or at least 0.1 mV in the remaining leads during the 23.3% were female. Baseline characteristics are shown in
first 12 hours after the onset ofsymptoms.13 Baseline clinical
Table 1. There were no statistically significant differences
demographic characteristics were reviewed. The study was
among the groups in means of age, gender, rate of hyperten-
approved by the local ethics committee.
sion, diabetes mellitus, smoking, glucose, creatinine, aspartate
Venous blood was drawn from an antecubital vein on admis-
aminotransferase, alanine aminotransferase, alkaline phospha-
sion. A Coulter Counter LH Series (Beckman Coulter Inc) was
tase, gamma glutamyl transferase, international normalized
used for complete blood count analysis. The neutrophil to lym-
ratio, lipid variables, hemoglobin, and white blood cell and
phocyte ratio (NLR) was calculated as the total neutrophil
platelet counts. The majority (82.6%) of patients had TIMI
counts divided by those of lymphocytes using the same blood 0 flow in the occluded IRA group before PCI.
samples drawn on admission.14 Troponin I levels were mea-
Left ventricular EF was lower in the occluded group than in
sured with a Beckman Image 800 analyzer. The albumin and
the patent group (41.5% + 5.7% vs 52.3% + 4.6%; P ¼ .043).
CRP levels were measured using a Roche Diagnostics Cobas
The NLR was significantly higher in the occluded group than
8000 c502 analyzer. The CAR was calculated as the ratio of
the patent group (2.3 [1.5-3.7] vs 1.9 [1.4-3.9]; P ¼ .034).
CRP to the albumin level multiplied by 100. Transthoracic
There was a significant positive correlation between the
echocardiography was performed for each patient immediately
CAR and SYNTAX score (r ¼ 0.312, P < .001) and a negative
after primary PCI in the intensive cardiac care unit (Vivid 7 GE
correlation between the CAR and TIMI grade flow
Medical System).The ejection fraction (EF) was calculated (r ¼ 0.210, P < .001). Also, the NLR was positively corre-
using the modified Simpson method.
lated with the CAR (r ¼ 0.077, P ¼ .013; Table 2).
Coronary angiography was performed using the Judkins tech-
Using a cutoff level of 0.693, the CAR predicted TIMI no-
nique. Each coronary artery was displayed in at least 2 different
reflow with a sensitivity of 65.4% and a specificity of 65.5% (area
planes. Angiograms and TIMI scale and SYNTAX scores were
under the curve: 0.670, 95% CI: 0.62-0.71, P < .001; Figure 1).
assessed by at least 2 experienced interventional cardiologists
In univariate logistic regression analysis, CAR and SYN-
who did not have knowledge of the clinical data. Before coronary
TAX score were significantly associated with IRA patency.
intervention and PCI, TIMI flow grade was documented for each
Multivariate logistic regression analyses showed that the
patient. Patients divided into 2 groups according to the TIMI CAR was an independent predictor of IRA patency (0.003
scale.15 Nonpatent flow was defined as TIMI grade 0 (no-reflow),
[0.001-0.029]; P < .001; Table 3).
1, and 2 flows, and normal flow was defined as TIMI 3 flow
grade.16-19 Patients with TIMI flow grade 0 to 2 were included
in the occluded group, and patients with TIMI 3 flow grade were Discussion
included in the patent group. For TIMI scores, interobserver and
We assessed the relationship between the CAR and IRA
intraobserver coefficients of variation were 2.5% and 2.0%,
patency in patients with STEMI, and we found that the CAR
respectively. The SYNTAX score was calculated using the site
is an independent predictor of IRA patency in these patients.
“http://www.syntaxscore.com.” Interobserver and intraobserver Plaque rupture is the trigger event in the development of
coefficients of variation were 2.6% and 2.2%, respectively.
STEMI. Thrombus blocks a coronary artery and stops the blood
flow to myocardial tissue resulting in myocardial injury.20 Ster-
Statistical Analysis ile inflammation, elevated concentrations of inflammatory
All analyses were conducted using the SPSS 21.0 Statistical Pack- cytokines, platelet activation, and leukocytosis are recognized
age Program for Windows (SPSS Inc). Continuous variables were in acute myocardial infarction.20 Mast cells and macrophages,
Gayretli Yayla et al 3

Table 1. Baseline Characteristics and Laboratory Parameters of the Table 2. Correlations Between CAR and SYNTAX Score and TIMI
Study Groups (n ¼ 1047). Flow.

Infarct-related artery Variables r P

Occluded group Patent group
Parameters (n ¼ 879) (n ¼ 168) P TIMI flow 0.210 <.001
SYNTAX score 0.312 <.001
Age, years 56.6 + 11.4 56.4 + 11.4 .866 NLR 0.077 .013
Female, n (%) 204 (23.2) 40 (23.8) .866
Hypertension, n (%) 444 (50.5) 81 (48.2) .585 Abbreviations: CAR, C-reactive protein to albumin ratio; NLR, neutrophil to
lymphocyte ratio; TIMI, thrombolysis in myocardial infarction.
Diabetes mellitus, n (%) 165 (18.7) 21 (12.5) .066
Smoking, n (%) 570 (64.8) 104 (61.9) .466
LVEF, % 41.5 + 5.7 52.3 + 4.6 .043
Infarct-related artery, .093
n (%)
LAD 351 (39.9) 66 (39.3)
LCX 174 (19.8) 45 (26.8)
RCA 354 (40.3) 57 (33.9)
TIMI flow in IRA, n (%) <.001
0 726 (82.6)
I 60 (6.8)
II 93 (10.6)
III 168 (100)
Glucose, mg/dL 114 + 45 112 + 41 .506
Creatinine, mg/dL 0.93 + 0.22 0.91 + 0.20 .172
ALT, IU/L 24 + 12 23 + 14 .292
AST, IU/L 23 + 10 22 + 12 .215
GGT, IU/L 26 + 13 27 + 11 .470
ALP, IU/L 106 + 41 109 + 39 .333
INR 0.69 + 0.11 0.71 + 0.10 .907
Albumin, g/dL 4.3 + 0.4 4.5 + 0.3 <.001
Total cholesterol, 184 + 42 182 + 44 .509
mg/dL
LDL-C, mg/dL 111 + 35 110 + 35 .891
HDL-C, mg/dL 41 + 10 41 + 11 .701
Triglycerides, mg/dL 141 (105-207) 141 (107-207) .985 Figure 1. The receiver operating characteristic (ROC) curve analysis
Hemoglobin, g/dL 14.7 + 1.5 14.9 + 1.4 .207 of C-reactive protein to albumin ratio for the prediction of the
WBC,103/mm3 10.3 + 3.6 9.9 + 3.8 .170 thrombolysis in myocardial infarction (TIMI) no-reflow.
Neutrophils, 103/mm3 6.7 + 3.1 5.8 + 2.9 .038
Lymphocytes,103/mm3 2.5 (2.1-2.8) 2.7 (1.8-2.6) .047
Platelets, 103/mm3 266 + 72 270 + 67 .555 Table 3. Univariate and Multivariate Logistic Regression Analysis for
Troponin I, ng/mL 1.2 (0.2-8.9) 0.5 (0.1-4.0) .023 Assessment of Predictors of Infarct-Related Artery Patency.
NLR 2.3 (1.5-3.7) 1.9 (1.4-3.9) .034
CRP, mg/dL 4.9 (3.0-9.4) 3.0 (2.1-4.9) <.001 Univariable Multivariable
SYNTAX score 12 (5-23) 7 (4-18) .012 Variables OR (95% CI) P OR (95% CI) P
CAR 0.11 (0.06-0.22) 0.06 (0.04-0.10) <.001 NLR 0.955 (0.900-1.013) .126 - -
Data are given as mean + SD, n (%), or median (interquartile range). LVEF 1.003 (0.987-1.019) .109 - -
Abbreviations: ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, CAR 0.003 (0.001-0.023) <.001 0.003 (0.001-0.029) <.001
aspartate aminotransferase; CAR, C-reactive protein to albumin ratio; CRP, C- SYNTAX 0.976 (0.958-0.994) .009 0.994 (0.975-1.014) .569
reactive protein; GGT, gamma glutamyl transferase; HDL-C, high-density lipo- score
protein cholesterol; INR, international normalized ratio; IRA, infarct-related
artery; LAD, left anterior descending; LDL-C, low-density lipoprotein choles- Abbreviations: CAR, C-reactive protein to albumin ratio; LVEF, left ventricular
terol; LVEF, left ventricular ejection fraction; LCX, left circumflex; NLR, neu- ejection fraction; NLR, neutrophil to lymphocyte ratio; OR, odds ratio.
trophil to lymphocyte ratio; RCA, right coronary artery; TIMI, Thrombolysis in
Myocardial Infarction; WBC, white blood cell.
Lai et al evaluated the association between the characteris-
tics of coronary atherosclerotic plaques and inflammatory
which are involved in atherosclerotic plaque formation, gener- biomarkers; they found that the mean concentrations of high-
ate pro-inflammatory cytokines, such as tumor necrosis factor sensitivity CRP and IL-6 were significantly higher in the soft,
alpha, interferon gamma, IL-1, and IL-6. Furthermore, mast mixed, and hard plaque groups compared with controls.22
cells deliver angiogenic and pro-inflammatory mediators, such Kaminska et al observed that CRP, IL-6, and white blood cells
as histamine, arachidonic acid metabolites, proteolytic as inflammation biomarkers can be useful indicators of the
enzymes, and platelet activating factor.21 presence of coronary artery disease.23 Several studies have
4 Angiology XX(X)
shown that the CRP level at admission is related to increased
short- and long-term major adverse cardiac events (MACEs) in
patients with acute coronary syndrome (ACS) treated with
PCI.24-27 In patients with ACS, the relationship between CRP
and cardiovascular outcomes remains uncertain. A high level
of CRP may be an indicator of a greater burden of myocardial
ischemia and tissue damage.28
Coronary flow is an independent predictor of worse outcomes
in patients with STEMI.29 Stone et al found better outcomes
relating the incidence of heart failure, preservation of EF, and
clinical end point at 6 months in patients exhibiting IRA TIMI
flow grade 3 compared with those with TIMI grades 0 to 2.1 Early
reperfusion with higher level TIMI flow was specified to be an
independent predictor of in-hospital and mid-term mortality and a
powerful predictor of favorable clinical outcome.15,30
Serum albumin has been considered as a biomarker of pro-
tein synthesis, immunocompetence status, and nutritional sta-
tus.31 However, low serum albumin levels are also related to
consistent systemic inflammation, and evidence shows that
serum albumin has a limited role as a marker of nutritional
status.31 Albumin decreased conversion of arachidonic acid
to thromboxane A2 and increased conversion of endoperoxides
to prostaglandin D2.32 Low serum albumin level is related to
higher blood viscosity, platelet aggregation, damaged endothe-
lial function, and platelet-induced lumen narrowing in the cor-
onary arteries.32 Oduncu et al examined the prognostic utility
of albumin in STEMI and showed that low serum albumin level
was an independent predictor of long-term mortality and devel-
opment of advanced heart failure.33 Kurtul et al showed that the
admission serum albumin level was inversely related to CAD
severity in patients with ACS.34
It has been suggested that the CAR is more consistent with
prognosis than CRP or albumin levels alone.24 Several studies
reported a relationship between CAR and atherosclerotic cor-
onary diseases.10,11,35 Acet et al found that the combination of
CAR and The Global Registry of Acute Coronary Events score
was an independent predictor of short-term MACEs in STEMI
patients undergoing primary PCI.27 Kalyoncuoglu and Durmus
showed that CAR is also useful for predicting the severity of
CAD in non-STEMI patients.36
In light of these results, it is reasonable to predict an associa-
tion between CAR and coronary flow in patients with STEMI. In
our study, we demonstrated that CAR was significantly higher in
patients with an occluded IRA. We showed that a higher CAR can
be a predictive marker of coronary flow in patients with STEMI.
Further studies are required to clarify whether a higher CAR is a
predictor of IRA in patients with STEMI.
This study has some limitations. First, it was a retrospective
study. So, it could not strictly control for confounding factors,
including undocumented history of medication, nutritional sta-
tus related to the level of serum albumin, and comorbidities.
Secondly, as this study was conducted in a single center, the
number of deceased patients was relatively small. Using a spot
laboratory value rather than values at a time interval is another
limitation of this study. We also did not evaluate other cyto-
kines or inflammatory markers.
In conclusion, we demonstrated a significant relationship
between the CAR and the degree of myocardial perfusion in
patients with STEMI. The CAR was an independent predictor
of an occluded IRA in patients who had undergone PCI for
STEMI. The CAR can be relatively easily calculated, so it can
be useful in daily clinical practice. Pharmacological intracor-
onary therapies may be considered primarily in patients with a
high CAR, although there is no strong evidence that this can
reduce the incidence of no-reflow during the procedure. In
addition, a different approach in terms of the duration of anti-
aggregant and anticoagulant treatment may be considered in
these patients. In order for these recommendations to reach a
level of evidence, large, prospective data will be needed..
Authors’ Note
All authors made substantial contributions to (1) conception and
design, or acquisition of data, or analysis and interpretation of data,
(2) drafting the article or revising it critically for important intellectual
content, and (3) final approval of the version to be published.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
ORCID iDs
Kadriye Gayretli Yayla https://orcid.org/0000-0002-0664-9164
Cagri Yayla https://orcid.org/0000-0002-5302-4052
Mehmet Akif Erdol https://orcid.org/0000-0002-2721-440X
Mustafa Karanfil https://orcid.org/0000-0002-5401-1149
Ahmet Goktug Ertem https://orcid.org/0000-0002-6963-6213
References
1. Stone GW, Cox D, Garcia E, et al. Normal flow (TIMI-3) before
mechanical reperfusion therapy is an independent determinant of
survival in acute myocardial infarction: analysis from the primary
angioplasty in myocardial infarction trials. Circulation. 2001;104:
636-41.
2. Brodie BR, Stuckey TD, Hansen C, Muncy D. Benefit of coronary
reperfusion before intervention on outcomes after primary angio-
plasty for acute myocardial infarction. Am J Cardiol. 2000;85:13-8.
3. Krug A, Du Mesnil de R, Korb G. Blood supply of the myocardium
after temporary coronary occlusion. Circ Res. 1966;19:57-62.
4. Group TS. The Thrombolysis in Myocardial Infarction (TIMI)
trial. phase I findings. N Engl J Med. 1985;312:932-6.
5. Celik T, Balta S, Mikhailidis DP, et al. The Relation Between
No-Reflow Phenomenon and Complete Blood Count Parameters.
Angiology. 2017;68:381-8.
6. Spagnoli LG, Bonanno E, Sangiorgi G, Mauriello A. Role of
inflammation in atherosclerosis. J Nucl Med. 2007;48:1800-15.
7. Pepys MB, Baltz ML. Acute phase proteins with special reference
to C-reactive protein and related proteins (pentaxins) and serum
amyloid A protein. Adv Immunol. 1983;34:141-212.
Gayretli Yayla et al
8. Wilson AM, Swan JD, Ding H, et al. Widespread vascular pro-
duction of C-reactive protein (CRP) and a relationship between
serum CRP, plaque CRP and intimal hypertrophy. Atherosclero-
sis. 2007;191:175-81.
9. Ritchie RF, Palomaki GE, Neveux LM, Navolotskaia O, Ledue
TB, Craig WY. Reference distributions for the negative acute-
phase serum proteins, albumin, transferrin and transthyretin:
a practical, simple and clinically relevant approach in a large
cohort. J Clin Lab Anal. 1999;13:273-9.
10. Rencuzogullari I, Karabag Y, Cagdas M, et al. Assessment of the
relationship between preprocedural C-reactive protein/albumin
ratio and stent restenosis in patients with ST-segment elevation
myocardial infarction. Rev Port Cardiol. 2019;38:269-77.
11. Cagdas M, Rencuzogullari I, Karakoyun S, et al. Assessment of
Relationship Between C-Reactive Protein to Albumin Ratio and
Coronary Artery Disease Severity in Patients With Acute Coron-
ary Syndrome. Angiology. 2019;70:361-8.
12. Yayla C, Gayretli Yayla K. C-Reactive Protein to Albumin Ratio
in Patients With Saphenous Vein Graft Disease. Angiology. 2021:
3319721998863.
13. Myocardial infarction redefined–a consensus document of The
Joint European Society of Cardiology/American College of Car-
diology Committee for the redefinition of myocardial infarction.
Eur Heart J. 2000;21:1502-13.
14. Balta S, Ozturk C, Balta I, et al. The Neutrophil-Lymphocyte
Ratio and Inflammation. Angiology. 2016;67:298-9.
15. Mehta RH, Harjai KJ, Cox D, et al. Clinical and angiographic
correlates and outcomes of suboptimal coronary flow inpatients
with acute myocardial infarction undergoing primary percuta-
neous coronary intervention. J Am Coll Cardiol. 2003;42:1739-46.
16. Nunez J, Nunez E, Bodi V, et al. Usefulness of the neutrophil to
lymphocyte ratio in predicting long-term mortality in ST segment
elevation myocardial infarction. Am J Cardiol. 2008;101:747-52.
17. Akpek M, Kaya MG, Uyarel H, et al. The association of serum
uric acid levels on coronary flow in patients with STEMI under-
going primary PCI. Atherosclerosis. 2011;219:334-41.
18. Dogan M, Akyel A, Bilgin M, et al. Can Admission Neutrophil to
Lymphocyte Ratio Predict Infarct-Related Artery Patency in
ST-Segment Elevation Myocardial Infarction. Clin Appl Thromb
Hemost. 2013.
19. Celik T, Balta S, Ozturk C, et al. Predictors of No-Reflow Phe-
nomenon in Young Patients With Acute ST-Segment Elevation
Myocardial Infarction Undergoing Primary Percutaneous
Coronary Intervention. Angiology. 2016;67:683-9.
20. Scheen AJ. [From atherosclerosis to atherothrombosis: from a
silent chronic pathology to an acute critical event]. Rev Med
Liege. 2018;73:224-8.
21. Spinas E, Kritas SK, Saggini A, et al. Role of mast cells in ather-
osclerosis: a classical inflammatory disease. Int J Immunopathol
Pharmacol. 2014;27:517-21.
22. Lai CL, Ji YR, Liu XH, Xing JP, Zhao JQ. Relationship between
coronary atherosclerosis plaque characteristics and high sensitiv-
ity C-reactive proteins, interleukin-6. Chin Med J (Engl). 2011;
124:2452-6.
23. Kaminska J, Koper OM, Siedlecka-Czykier E, Matowicka-Karna
J, Bychowski J, Kemona H. The utility of inflammation and
5
platelet biomarkers in patients with acute coronary syndromes.
Saudi J Biol Sci. 2018;25:1263-71.
24. Wang W, Ren D, Wang CS, Li T, Yao HC, Ma SJ. Prognostic
efficacy of high-sensitivity C-reactive protein to albumin ratio in
patients with acute coronary syndrome. Biomark Med. 2019;13:
811-20.
25. Hartford M, Wiklund O, Mattsson Hulten L, et al. C-reactive
protein, interleukin-6, secretory phospholipase A2 group IIA and
intercellular adhesion molecule-1 in the prediction of late out-
come events after acute coronary syndromes. J Intern Med.
2007;262:526-36.
26. Zairis MN, Adamopoulou EN, Manousakis SJ, et al. The impact
of hs C-reactive protein and other inflammatory biomarkers on
long-term cardiovascular mortality in patients with acute coron-
ary syndromes. Atherosclerosis. 2007;194:397-402.
27. Acet H, Guzel T, Aslan B, Isik MA, Ertas F, Catalkaya S. Predic-
tive Value of C-Reactive Protein to Albumin Ratio in ST-Segment
Elevation Myocardial Infarction Patients Treated With Primary
Percutaneous Coronary Intervention. Angiology. 2021;72:244-51.
28. Heeschen C, Hamm CW, Bruemmer J, Simoons ML. Predictive
value of C-reactive protein and troponin T in patients with
unstable angina: a comparative analysis. CAPTURE Investiga-
tors. Chimeric c7E3 AntiPlatelet Therapy in Unstable angina
REfractory to standard treatment trial. J Am Coll Cardiol. 2000;
35:1535-42.
29. Lamas GA, Flaker GC, Mitchell G, et al. Effect of infarct artery
patency on prognosis after acute myocardial infarction. The Sur-
vival and Ventricular Enlargement Investigators. Circulation.
1995;92:1101-9.
30. Cura FA, L’Allier PL, Kapadia SR, et al. Predictors and prognosis
of suboptimal coronary blood flow after primary coronary angio-
plasty in patients with acute myocardial infarction. Am J Cardiol.
2001;88:124-8.
31. Mukai H, Villafuerte H, Qureshi AR, Lindholm B, Stenvinkel P.
Serum albumin, inflammation, and nutrition in end-stage renal
disease: C-reactive protein is needed for optimal assessment.
Semin Dial. 2018;31:435-9.
32. Mikhailidis DP, Ganotakis ES. Plasma albumin and platelet func-
tion: relevance to atherogenesis and thrombosis. Platelets. 1996;7:
125-37.
33. Oduncu V, Erkol A, Karabay CY, et al. The prognostic value of
serum albumin levels on admission in patients with acute ST-
segment elevation myocardial infarction undergoing a primary per-
cutaneous coronary intervention. Coron Artery Dis. 2013;24:88-94.
34. Kurtul A, Murat SN, Yarlioglues M, et al. Usefulness of Serum
Albumin Concentration to Predict High Coronary SYNTAX
Score and In-Hospital Mortality in Patients With Acute Coronary
Syndrome. Angiology. 2016;67:34-40.
35. Karabag Y, Cagdas M, Rencuzogullari I, et al. Relationship
between C-reactive protein/albumin ratio and coronary artery dis-
ease severity in patients with stable angina pectoris. J Clin Lab
Anal. 2018;32:e22457.
36. Kalyoncuoglu M, Durmus G. Relationship between C-reactive
protein-to-albumin ratio and the extent of coronary artery disease
in patients with non-ST-elevated myocardial infarction.
Coron Artery Dis. 2020;31:130-6.