{"id":54218,"date":"2023-12-31T10:08:15","date_gmt":"2023-12-31T10:08:15","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=54218"},"modified":"2024-01-05T07:59:40","modified_gmt":"2024-01-05T07:59:40","slug":"diagnostic-value-of-crp-h-fabp-pct-lp-pla2-and-cytokines-in-stable-angina","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol16no4\/diagnostic-value-of-crp-h-fabp-pct-lp-pla2-and-cytokines-in-stable-angina\/","title":{"rendered":"Diagnostic Value of CRP, H-FABP, PCT, Lp-PLA2 and Cytokines in Stable Angina"},"content":{"rendered":"\n

Introduction<\/strong><\/p>\n\n\n\n

Coronary artery disease  (CAD) \nis a significant cause of worldwide \nmortality and morbidity, with an incidence of one in every 6 deaths in\nWestern countries 1<\/sup>. In the past, coronary heart disease showed high\nincidence in older ages 2<\/sup>. However, nowadays, de to accelerated lifestyle\nchanges, economic stresses, and other factors, the incidence of coronary heart\ndisease has increased  in middle-aged\nadults 3<\/sup>.<\/p>\n\n\n\n

In\nstable angina, increased oxygen demand occurs only with physical exertion. Increased myocardial\noxygen demand from exercise is due to increases of heart rate and blood\npressure, as well as increased the contractility of the myocardium, among other\nfactors 4<\/sup>.<\/sup><\/p>\n\n\n\n

Many biochemical markers are\nsensitive and specific for myocardial ischemia and can be easily and rapidly\nmeasured in serum 5<\/sup>.  Elevated\nlevels of CK-MB activities, Trop I, and MYO are routinely used in early\ndiagnosis of acute coronary syndrome 6<\/sup>. <\/p>\n\n\n\n

Heart-fatty acid binding protein (H-FABP)\ncould be an important biomarker for the early diagnosis of coronary\nsyndrome  according to many recent\ninvestigations. FABPs are relatively low molecular weight cytoplasmic proteins\nthat are prominent in tissues with high metabolism of fatty acid, such as the\nheart 7<\/sup>.<\/p>\n\n\n\n

Different cardiac diseases,\nincluding coronary syndrome and atherosclerosis, are associated with elevation\nof serum proinflammatory cytokines and CRP 8-13<\/sup>. Furthermore, lipoprotein-associated\nphospholipase A2 (Lp-PLA2) has been considered as one of the  inflammatory biomarker of many cardiovascular\ndiseases 7<\/sup>. Procalcitonin (PCT) is also implicated as an\ninflammatory marker of early atherosclerosis 14<\/sup>.<\/p>\n\n\n\n

The current study aims to investigate\nthe diagnostic values of additional biomarkers in stable angina. The establishment of new diagnostic\ntests will enhance the diagnostic abilities to facilitate fast decision making\nin emergency units.<\/p>\n\n\n\n

Methods<\/strong><\/p>\n\n\n\n

Patients and exclusion criteria<\/strong><\/p>\n\n\n\n

The current study was performed on 86\npatients complaining  stable angina, at\nNasiriyah Heart Center from October 2021 to October  2022.  Eighty-six,\nhealthy subjects (age-matched) were taken as  a control group.  Patients with  unstable angina,  myocardial infarction, and any other heart\ndisease, and those on statins therapy\nwere not included in the study, to avoid interference with the studied parameters.\n<\/p>\n\n\n\n

Methods<\/strong><\/p>\n\n\n\n

Blood samples were drawn in the\nemergency department. Serum CRP hs, H-FABP, CK-MB, Trop I, MYO, Lp-PLA2 and PCT\nwere determined by electro-chemiluminescence immunoassay (Nipigon Health Corp.,\nCanada).   Blood sugar (Randox,\nUnited Kingdom) and\nserum total cholesterol,  triglycerides (Biolabo \/France),  LDL, VLDL and HDL (Cobas \/Germany) were determined using Cobas\nC311 photometric assays. Serum IL-6 was determined\nby electro-chemiluminescence immunoassay (ECL, Canada) and serum IL-9, IL-1\u03b2\nand TNF-\u03b1 were assayed by ELISA (Wuhan Fine Biotech Co., Ltd., China),\naccording to operational manuals.<\/p>\n\n\n\n

Ethical\napproval<\/strong><\/strong><\/p>\n\n\n\n

The ethical committee at Thi-Qar\nHealth Directorate has approved the research, and informed consent was taken\nfrom all participants.<\/p>\n\n\n\n

Statistical analysis<\/strong><\/p>\n\n\n\n

The significant variations between groups were assayed\nusing the Student t-test (SPSS, version 26).  Proportions were analyzed by\nChi-square. If\nthe p-value is 0.05 or less, the differences were considered significant.<\/p>\n\n\n\n

Results<\/strong><\/p>\n\n\n\n

Characteristics\nof patients<\/strong><\/p>\n\n\n\n

Eighty\nsix patients with stable angina and eighty-six  healthy subjects were studied in this research.\nThe patient’s mean age was 44.0\u00b110.9 years and the healthy\nsubjects mean age was 41.9\u00b110.1 years (P = 0.192). Among\nthe patients, 47(54.65%)\nwere males and 39 (45.35%) were females and among the healthy subjects, 73(84.88%)\nwere males and 13(15.12%) were females (P<0.001).\nAmong the patients and control groups, 39 (45.35%) and  40 (46.51%) respectively were smokers (P = 0.823).\nThere was no significant variation in the frequency of\noverweight\n[41 (47.67%) vs 37 (43.02%), P = 0.080] and obesity [28 (32.56%) vs 19 (22.10%),\nP = 0.080] between patients and the control group respectively. However, the\ngroup of patients with stable angina showed more frequent occurrence of hypertension\n[27 (31.40%) vs 1 (1.16%), P < 0.001] and diabetes [39 (45.35%)  vs 1 (1.16%), P < 0.001] compared to the  healthy control (Table 1). <\/p>\n\n\n\n

Biomarkers in stable angina<\/strong><\/p>\n\n\n\n

Table 2 showed that the level of troponin I\nwas not significantly changed (0.0210\u00b10.0034 vs 0.0200\u00b10.0038 ng\/ml, P = 0.054)\nin stable angina. However, in comparison with the healthy control, the  stable angina patients showed a significant elevation\nof serum CK-MB level (3.02\u00b11.46 vs 2.15\u00b11.91 ng\/ml, P < 0.001), myoglobin (62.02\u00b18.40\nvs 49.40\u00b16.00 ng\/ml, P < 0.01), hsCRP (28.90\u00b15.50 vs 7.35\u00b13.51 nmol\/l, P < 0.01), Lp-PLA2 (127.6\u00b119.2 vs 105.0\u00b122.7\nng\/ml, P < 0.01), H-FABP) 6.59\u00b12.71 vs 4.90\u00b11.43, ng\/ml, P < 0.001)  and PCT\n(0.056\u00b10.05 vs 0.026\u00b10.02 ng\/ml, P < 0.01). <\/p>\n\n\n\n

Lipid\nprofile in stable angina<\/strong><\/p>\n\n\n\n

As\nshown in Table 3, the  stable angina\npatients exhibited significantly higher serum level of total cholesterol\n(171.1\u00b124.5 vs 161.2\u00b125.1 mg\/dl, P < 0.05), triglycerides (184.7\u00b137.7 vs 131.8\u00b127.3, mg\/dl, P <\n0.001), LDL cholesterol (90.7\u00b18.5 vs 79.5\u00b128.5 mg\/dl, P < 0.05), and VLDL\ncholesterol (38.3\u00b114.5 vs 27.1\u00b111.3 mg\/dl, P < 0.01), with a significant\ndecline in serum HDL cholesterol (36.0\u00b110.2 vs 43.0\u00b19.2 mg\/dl, P < 0.01). <\/p>\n\n\n\n

Cytokines\nin stable angina  <\/strong><\/p>\n\n\n\n

In comparison with healthy control group, the\npatients with stable angina showed significantly elevated serum levels of IL1\u03b2\n(11.5\u00b13.6 vs 4.6\u00b13.2 nmol\/l, P < 0.001), IL-6 (7.9\u00b16.8 vs 4.3\u00b12.2 Pg\/ml, P <\n0.001), IL-9 (3.7\u00b12.5 vs 2.5\u00b11.6 pg\/ml, P < 0.01) and  TNF-\u03b1 (5.2\u00b14.6  vs 2.6\u00b11.7 ng\/ml, P < 0.001) (Table 4). <\/p>\n\n\n\n

Table 1: The characteristics of patients with stable angina in comparison with healthy control group. <\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

Parameters<\/strong><\/p>\n<\/td>\n

\n

Control Group<\/strong><\/p>\n<\/td>\n

\n

Patients Group<\/strong><\/p>\n<\/td>\n

\n

P. value<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Patient number<\/strong><\/p>\n<\/td>\n

\n

86<\/strong><\/p>\n<\/td>\n

\n

86<\/strong><\/p>\n<\/td>\n

\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Age (yrs)<\/p>\n<\/td>\n

\n

41.9\u00b110.1<\/p>\n<\/td>\n

\n

44.0\u00b110.9<\/p>\n<\/td>\n

\n

 NS<\/p>\n<\/td>\n<\/tr>\n

\n

Gender<\/p>\n<\/td>\n

\n

Male<\/p>\n<\/td>\n

\n

73 (84.88%)<\/p>\n<\/td>\n

\n

47 (54.65%)<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

Female<\/p>\n<\/td>\n

\n

13 (15.12%)<\/p>\n<\/td>\n

\n

39 (45.35%)<\/p>\n<\/td>\n<\/tr>\n

\n

Smoking<\/p>\n<\/td>\n

\n

40 (46.51%)<\/p>\n<\/td>\n

\n

39 (45.35%)<\/p>\n<\/td>\n

\n

NS<\/p>\n<\/td>\n<\/tr>\n

\n

Hypertension<\/p>\n<\/td>\n

\n

1 (1.16%)<\/p>\n<\/td>\n

\n

27 (31.40%)<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

Obesity<\/p>\n<\/td>\n

\n

Normal weight<\/p>\n

(18.5 \u2013 24.9) Kg\/m2<\/sup><\/p>\n<\/td>\n

\n

30 (34.88%)<\/p>\n<\/td>\n

\n

17(19.77%)<\/p>\n<\/td>\n

\n

 NS<\/p>\n<\/td>\n<\/tr>\n

\n

Overweight<\/p>\n

(25.0 \u2013 29.9) Kg\/m2<\/sup><\/p>\n<\/td>\n

\n

37 (43.02%)<\/p>\n<\/td>\n

\n

41 (47.67%)<\/p>\n<\/td>\n<\/tr>\n

\n

Obese, \u226530 Kg\/m2<\/sup><\/p>\n<\/td>\n

\n

19 (22.10%)<\/p>\n<\/td>\n

\n

28 (32.56%)<\/p>\n<\/td>\n<\/tr>\n

\n

Diabetic<\/p>\n<\/td>\n

\n

1 (1.16%)<\/p>\n<\/td>\n

\n

39 (45.35%)<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

NS: non-significant<\/p>\n\n\n

Table 2: Serum biochemical markers levels in  stable angina  in comparison with the healthy control group. <\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

Serum biochemical markers<\/strong><\/p>\n<\/td>\n

\n

Control Group<\/strong><\/p>\n<\/td>\n

\n

Patients Group<\/strong><\/p>\n<\/td>\n

\n

P. value<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

hsCRP (nmol\/l(<\/p>\n<\/td>\n

\n

7.35\u00b13.51<\/p>\n<\/td>\n

\n

28.90\u00b15.50<\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n

\n

H-FABP )ng\/ml (<\/p>\n<\/td>\n

\n

4.90\u00b11.43<\/p>\n<\/td>\n

\n

6.59\u00b12.71<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

CK-MB) ng\/ml(<\/p>\n<\/td>\n

\n

2.15\u00b11.91<\/p>\n<\/td>\n

\n

3.02\u00b11.46<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

Trop I (ng\/ml (<\/p>\n<\/td>\n

\n

0.0200\u00b10.0038<\/p>\n<\/td>\n

\n

0.0210\u00b10.0034<\/p>\n<\/td>\n

\n

 (NS)<\/p>\n<\/td>\n<\/tr>\n

\n

MYO) ng\/ml (<\/p>\n<\/td>\n

\n

49.40\u00b16.00<\/p>\n<\/td>\n

\n

62.02\u00b18.40<\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n

\n

Lp-PLA2 )ng\/ml (<\/p>\n<\/td>\n

\n

105.0\u00b122.7<\/p>\n<\/td>\n

\n

127.6\u00b119.2<\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n

\n

PCT (ng\/ml (<\/p>\n<\/td>\n

\n

0.026\u00b10.02<\/p>\n<\/td>\n

\n

0.056\u00b10.05<\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

CK-MB: Creatine kinase,  H-FABP: heart type fatty acid binding protein,  hsCRP: High sensitive C reactive protein,  Lp-PLA2: Lipoprotein-associated phospholipase A2,  MYO: Myoglobin,  NS: non-significant, PCT: Procalcitonin, Trop I: Troponin I,<\/p>\n\n\n

Table 3: Lipid profile and blood sugar in  stable angina  in comparison with the healthy control group.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n
\n

Parameters<\/strong><\/p>\n<\/td>\n

\n

Control Group<\/strong><\/p>\n<\/td>\n

\n

Patients Group<\/strong><\/p>\n<\/td>\n

\n

P. value<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Triglycerides (mg\/dl)<\/p>\n<\/td>\n

\n

131.8\u00b127.3<\/p>\n<\/td>\n

\n

184.7\u00b137.7      <\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

Total cholesterol (mg\/dl)<\/p>\n<\/td>\n

\n

161.2\u00b125.1<\/p>\n<\/td>\n

\n

171.1\u00b124.5     <\/p>\n<\/td>\n

\n

 < 0.05<\/p>\n<\/td>\n<\/tr>\n

\n

HDL (mg\/dl)<\/p>\n<\/td>\n

\n

43.0\u00b19.2<\/p>\n<\/td>\n

\n

36.0\u00b110.2   <\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n

\n

LDL (mg\/dl)<\/p>\n<\/td>\n

\n

79.5\u00b128.5<\/p>\n<\/td>\n

\n

90.7\u00b18.5<\/p>\n<\/td>\n

\n

 < 0.05<\/p>\n<\/td>\n<\/tr>\n

\n

VLDL (mg\/dl)<\/p>\n<\/td>\n

\n

27.1\u00b111.3<\/p>\n<\/td>\n

\n

38.3\u00b114.5<\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n\n\n

Table 4: Serum cytokines levels in  stable angina  in comparison with the healthy control group.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n
\n

Parameters<\/strong><\/p>\n<\/td>\n

\n

Control Group<\/strong><\/p>\n<\/td>\n

\n

Patients Group<\/strong><\/p>\n<\/td>\n

\n

P. value<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

IL-6  (Pg\/ml)<\/p>\n<\/td>\n

\n

4.3\u00b12.2<\/p>\n<\/td>\n

\n

7.9\u00b16.8<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

IL-9  (Pg\/ml)<\/p>\n<\/td>\n

\n

2.5\u00b11.6<\/p>\n<\/td>\n

\n

3.7\u00b12.5<\/p>\n<\/td>\n

\n

<0.01<\/p>\n<\/td>\n<\/tr>\n

\n

IL1\u03b2 (nmol\/l)<\/p>\n<\/td>\n

\n

4.6\u00b13.2<\/p>\n<\/td>\n

\n

11.5\u00b13.6<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n

\n

TNF-\u03b1) ng\/ml(<\/p>\n<\/td>\n

\n

2.6\u00b11.7<\/p>\n<\/td>\n

\n

5.2\u00b14.6<\/p>\n<\/td>\n

\n

<0.001<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n\n\n

Discussion<\/strong><\/p>\n\n\n\n

Coronary artery disease  is a significant cause of worldwide  mortality and morbidity. Patients with stable\nCAD can have an unexpected clinical course, therefore, additional diagnostic\nand predictive biomarkers are still required 15<\/sup>.<\/p>\n\n\n\n

Our results showed a slight\nnonsignificant elevation in serum Troponin I level  in patients with stable angina.  Previous studies have also, recorded a slight\nincrease in  serum troponin I level in\npatients with stable angina. The elevation was positively correlated with the\nextension and severity of atherosclerosis. The necrosis of cardiomyocytes was\nunlikely to be the main cause of the increased levels 16-17<\/sup>. Patients of\nstable angina with elevated troponin levels\nshowed  poor long-term prognoses,\nwith higher earlier heart failure and sudden death 18<\/sup>.<\/p>\n\n\n\n

In our study, patients\nwith ischemic heart diseases also showed significant elevation of the serum levels\nof CK-MB and MYO. Increased serum level of CK-MB in stable angina was also\nrecorded by many authors. Furthermore, readmission and mortality, were more\nfrequently occurred in patients with high CK-MB 19-21<\/sup>.<\/p>\n\n\n\n

Myoglobin was also moderately increased\nin stable angina 22<\/sup>.  However,\nmyoglobin is useful for early exclusion of myocardial infarction, but is less\nuseful when blood sample was taken later.  Therefore, the elevation of serum myoglobin must\nbe used with other assessments to aid in the diagnosis 23-24<\/sup>.<\/sup><\/p>\n\n\n\n

Our results also revealed that the\nserum level of  hs-CRP was elevated significantly\nin patients with stable angina. The previous studies mentioned that\ninflammation played an essential  roles\nin atherogenesis initiation and progression. \nAlthough hs-CRP  was elevated in stable angina, but its level\nwas significantly less than the level recorded in patients with acute\nmyocardial infarction 25-26<\/sup>.Increased hs-CRP level was proportional\n to the necrotic core in the culprit\nlesion, the length of the lesion was positively correlated\nwith the hs-CRP level.  In stable angina, elevation of hs-CRP\nreflected the inflammatory severity of the atherosclerotic plaque 27<\/sup>.<\/p>\n\n\n\n

H-FABP was also significantly elevated in\nstable angina in the current research. In studying the value of H-FABP in diagnosis\nand prognosis in a multicenter, prospective study carried out on patients with stable coronary artery disease, it appeared that H-FABP was a potential\nprognostic biomarker for future outcomes. \nMany studies reported that high H-FABP increased the hospital\nreadmission and mortality 28-32<\/sup>. <\/p>\n\n\n\n

According to our results, the patients with\nstable angina also showed significantly increased serum Lp-PLA2 levels. Many\nprevious studies revealed that its level was significantly increased in stable\nangina. Several evidences\nsuggested the Lp-PLA2 promoted atherosclerosis by several pathways 33-35<\/sup>.\nHigher level of Lp-PLA2 in stable angina was associated with poor\nintracoronary function (coronary arteriosclerosis, vasoconstriction, and poor\noutflow). Lp-PLA2 is an important factor linked between inflammatory changes\nand endothelial dysfunction, which enhances \nthe development of CAD. These studies recommended the use of Lp-PLA2 as\na useful tool for assessing the level of risk in CAD 36-39<\/sup>.<\/p>\n\n\n\n

We also recorded that procalcitonin\n(PCT) was significantly elevated in stable angina. PCT is the precursor of the\nhormone calcitonin, it was a biomarker utilized in the diagnosis of sepsis. It\nindicated the severity of bacterial infection when it progressed into sepsis,\nits high level was correlated with high mortality 40-41<\/sup>.  The impact of PCT in cardiovascular diseases\nwas also studied, it appeared that in patients with CAD, the extent of\natherosclerosis and its adverse outcome were positively correlated with PCT\nlevels 42-44<\/sup>. <\/sup>The high level of  PCT within 48 hours post-admission reflected\nan inflammatory condition that associated with increased early and six-month\nmortality 14<\/sup>.<\/sup><\/p>\n\n\n\n

Recent\nresearches showed that the atherosclerosis is an\ninflammatory disease. Inflammatory\ncytokines were participated in its  initiation and progression, and their serum\nlevels strongly predict coronary artery disease 45-47<\/sup>.<\/p>\n\n\n\n

Our study revealed that IL-6 was significantly elevated in\nstable angina, many previous studies recorded that serum IL-6 levels were elevated\nsignificantly in patients with stable angina in comparison with control 48-51<\/sup>.\nThe\nIL-6 genetic deficiency enhanced atherosclerotic plaques induced by pathogen\nand\/or diet 52<\/sup>.  While, the lipids and other vascular risk were\nbeneficially modified with the clinical using of tocilizumab, the IL-6 receptors\nblocker 53<\/sup>.  <\/sup>IL-6,\nwhich is largely produced by mononuclear cells, and may affected the initiation\nand development of coronary artery disease via a number of mechanisms. It\nincreased blood viscosity, platelet counts and accelerated fibrinogen\ndeposition 54<\/sup>.<\/p>\n\n\n\n

The\ncurrent study also showed that the serum TNF-\u03b1\nlevel was increased significantly in stable angina compared with control.  The same results were previously recorded by many\nauthors 55-56<\/sup>.  <\/sup>In\natherosclerosis, Th cells secrete large amounts of TNF-\u03b1  and promoted the progression of\natherosclerosis and plaque enlargement 57<\/sup>. Many  TNF-\u03b1 inhibitors suppressed the development\nof  atherosclerosis 58<\/sup>. <\/p>\n\n\n\n

The significant elevation of IL-1\u03b2\nin our study was in agreement with many previous studies 51, 59-60<\/sup>. IL-1\u03b2\nis released during ischemia and triggered neutrophil infiltration into the\nmyocardium. After reperfusion, under the synergistic action of IL-1\u03b2 with other\ncytokines and complements, neutrophils are subsequently activated and interact\nwith endothelial cells, generating reactive oxygen species (ROS) and\naggravating myocardial injury 61<\/sup>.The\nischemic damage was followed by remodeling and healing process that was\ncharacterized by a potent inflammatory response. In injured tissue, the\ninflammatory response was amplified by cryopyrininflammasome. Caspase-1,\ncleaves pro-IL-1\u03b2 once the inflammasome has been triggered by injury.\nFurthermore, leukocyte chemotaxis was induced by IL-1\u03b2  in injured myocardium and promoted chemokine\nand cytokine  production, and enhanced\nthe inflammatory response 62<\/sup>. <\/sup><\/p>\n\n\n\n

The serum IL-9 level was also\nsignificantly increased in stable angina in the current study. Elevation of\nplasma IL-9 has been recorded in ischemic heart diseases and acute ischemic\nstroke 63-64<\/sup>-64]. It was also increased significantly in coronary\natherosclerosis, with elevation of the  IL-9R expression and IL-9 level in the\natherosclerotic plaques 65<\/sup>.It was one of cytokines which involved\nin the pathophysiology of atherosclerosis. Treatment with IL-9 exacerbates\natherosclerosis, while, neutralization of IL-9 prevents atherosclerosis\ndevelopment. IL-9 enhances VCAM-1 expression in aortic endothelial cells through\na STAT3-dependent pathway, while,   neutralization of VCAM-1 protected from the increasing\nof plaque size induced by IL-9 66<\/sup>. <\/p>\n\n\n\n

In general, elevation of the serum\ncytokines may reflect the severity of inflammation in atheroseclerosis, it represented part of the pathogenesis of unstable\nangina and is positively correlated with the course of clinical and\nhemodynamically significant coronary artery disease 49-50, 67<\/sup>. <\/p>\n\n\n\n

Conclusions<\/strong><\/p>\n\n\n\n

Early diagnosis remains the main\nprinciples in the treatment of stable angina.\nThis study aims to investigate the benefit \nof additional biochemical markers in diagnosis  of stable angina pectoris. The study\nrevealed that hs-CRP, H-FABP, PCT, Lp-PLA2 and cytokines are sensitive, and can serve as diagnosis indicators of stable\nangina pectoris.  The elevation of some\ncytokines in patients of  stable angina\nmay open the door for subsequent studies to investigate the participation of cytokines  in pathogenicity of the disease, and to study\ntheir suppression as a new therapeutic approach.<\/p>\n\n\n\n

Acknowledgements<\/strong><\/p>\n\n\n\n

Wethank the dean and the staff of postgraduate department, Faculty of Medicine, Sousse, Tunisia.We thank the patients who participate in this research. We appreciate the efforts of the staff of Nasiriyah Heart Center.<\/p>\n\n\n\n

Conflict of Interest <\/strong><\/p>\n\n\n\n

There is no conflict of interest<\/p>\n\n\n\n

Funding<\/strong> Sources<\/strong><\/p>\n\n\n\n

The authors declare that they do not received  financial support from any source.<\/p>\n\n\n\n

References<\/strong><\/p>\n\n\n\n

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    Abbreviations<\/strong><\/p>\n\n\n\n

    CK-MB: Creatine kinase, CRP hs: High\nsensitive C reactive protein,  cTnI: Cardiac Troponin I,  HDL-C: high\ndensity lipoprotein cholesterol, H-FABP: heart type fatty acid binding\nprotein,  IL6:  Interleukin 6, LDL-C: low density lipoprotein\ncholesterol, Lp-PLA2: Lipoprotein-associated phospholipase A2, MI: Myocardial\ninfarction,  MYO: Myoglobin, PCT:\nProcalcitonin, BS: blood sugar, TC: total cholesterol, TG: triglycerides,\nVLDL-C: very low density lipoprotein cholesterol. <\/p>\n","protected":false},"excerpt":{"rendered":"

    Introduction Coronary artery disease  (CAD)  is a significant cause of […]<\/p>\n","protected":false},"author":15,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[111],"tags":[],"class_list":["post-54218","post","type-post","status-publish","format-standard","hentry","category-vol16no4"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/54218","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/15"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=54218"}],"version-history":[{"count":5,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/54218\/revisions"}],"predecessor-version":[{"id":55180,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/54218\/revisions\/55180"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=54218"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=54218"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=54218"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}