Biomarker Insights 2013:8 1–7

doi: 10.4137/BMI.S11015

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Biomarker Insights

O r I g I n A L r e S e A r c h

Biomarker Insights 2013:8 1

Lipid Profile of Patients with Acute Myocardial Infarction and its Correlation with Systemic Inflammation

haseeb A. Khan1, Abdullah S. Alhomida1 and Samia h. Sobki21Department of Biochemistry, college of Science, King Saud University, riyadh, Saudi Arabia. 2Division of clinical Biochemistry, Department of Pathology, Prince Sultan Military Medical city, riyadh, Saudi Arabia.corresponding author email: khan_haseeb@yahoo.com; haseeb@ksu.edu.sa

Abstract: The biomarker potential of using various lipids fractions for predicting risk of acute myocardial infarction (AMI) is ­controversial.­We­ therefore­compared­ the­ lipid­profiles,­ including­ serum­ total­ cholesterol­ (TC),­ low-density­ lipoprotein­cholesterol­(LDL),­ high-density­ lipoprotein­ cholesterol­ (HDL)­ and­ triglycerides­ (TG),­ in­ 67­AMI­ patients.­ Patients­ included­ 28­ STEMI­ (ST-­elevated­myocardial­infarction)­patients,­39­NSTEMI­(non-ST-elevated­myocardial­infarction)­patients­and­25­patients­with­chest­pain.­Control­group­included­54­age-­and­gender-matched­normal­subjects.­We­also­studied­the­correlation­between­lipid­profile­and­systemic­inflammation­in­these­subjects.­There­were­significant­decreases­in­TC,­LDL­and­HDL­levels­in­both­STEMI­and­NSTEMI­patients­as­compared­to­normal­subjects;­however,­patients­with­chest­pain­did­not­show­any­significant­change­in­these­lipids.­Serum­TG­levels­did­not­differ­significantly­among­the­study­groups.­There­were­significant­increases­in­serum­high-sensitive­C-reactive­protein­(hs-CRP)­levels­in­STEMI­and­NSTEMI­patients,­as­compared­to­control­group.­Serum­hs-CRP­showed­significant­inverse­correlation­with­HDL;­however,­hs-CRP­was­not­correlated­with­TC,­LDL,­and­TG.­In­conclusion,­our­findings­suggest­that­reduction­in­serum­TC­does­not­prevent­the­risk­of­AMI,­whereas­a­decrease­in­serum­HDL­and­increase­in­hs-CRP­strongly­predisposes­the­risky­individuals­to­an­AMI­event.­We­emphasize­the­importance­of­HDL­and­CRP­measurements­for­the­assessment­of­a­combined­lipid-inflammation­risk­factor­that­could­be­a­useful­predictor­of­high­risk­individuals,­as­well­as­a­prognostic­marker­in­AMI­patients.

Keywords:­acute­myocardial­infarction,­lipid­profile,­inflammation,­biomarker

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IntroductionThe pathogenesis of acute myocardial infarction (AMI)­ is­ multifactorial;­ however,­ several­ studies­have implicated impaired lipid metabolism as one of the crucial factors in the development of this disease. Kumar et al1­observed­significantly­higher­total­cho-lesterol­(TC)­and­triglyceride­(TG)­levels­and­lower­high-density­lipoprotein­cholesterol­(HDL)­levels­in­AMI­patients.­ In­ a­ series­ of­ 50­male­AMI­patients,­serum­ low-density­ lipoprotein­ cholesterol­ (LDL)­levels­ and­ the­ ratio­ of­ LDL­ to­ HDL­were­ not­ sig-nificantly­different­among­the­two­groups;­however,­serum­ HDL­ levels­ were­ significantly­ decreased­ in­AMI group.2­ The­ risk­ of­AMI­was­ associated­with­an­increase­in­LDL­and­a­decrease­in­HDL,­in­both­Asians­ and­ non-Asians.3­ Lower­ concentrations­ of­serum­HDL­and­higher­serum­TG­were­found­to­be­independent­ risk­ factors,­while­serum­LDL­was­not­associated­ with­AMI.4 Woo et al5 observed higher mean­TC,­LDL,­and­TG,­as­well­as­lower­mean­HDL­in­AMI­ patients;­ high­HDL­was­ among­ the­ protec-tive factors. Lehto et al6­did­not­find­any­difference­in­mean­serum­TC­levels­between­the­AMI­patients­and­controls,­whereas­mean­HDL­was­significantly­lower­in­ the­AMI­ group.­The­ cardiac­marker,­ troponin­T,­has­been­positively­correlated­with­TC,­LDL,­and­TG­and­negatively­correlated­with­HDL.7

The management of dyslipidemia after myocardial infarction­is­an­important­aspect­of­post-myocardial­infarction care.8 Using the bivariate and multivariate Cox­proportional­hazards­analysis­to­identify­indepen-dent­predictors­of­subsequent­major­adverse­coronary­events (hospitalization for AMI or acute coronary syndrome),­ it­was­ found­ that­HDL­predicted­major­adverse­ coronary­ events,­ which­ in­ turn­ provided­support­ for­ interventions­ targeting­HDL­ for­ cardio-vascular risk reduction.9­Another­ Cox­ proportional­hazards­model­ has­ revealed­ that­ plasma­HDL—but­not­ LDL—predicts­ the­ risk­ of­ recurrent­ cardiovas-cular­events­over­ the­ensuing­16­weeks.­Even­LDL­

reduction does not account for the clinical risk reduc-tion­with­atorvastatin­treatment­after­acute­coronary­syndrome­(ACS).10 Li et al11­have­shown­that­the­cases­with­ low­ HDL­ level­ had­ rates­ of­AMI­ events­ and­CHD­mortality­ similar­ to­ those­of­ the­entire­group,­including­hyperlipidemia.­However,­AMI­attacks­and­deaths­decreased­significantly­at­the­normal­and­high­HDL­levels,­indicating­that­protective­effect­of­HDL­against coronary artery disease is more prominent in people­with­low­lipid­level.

The above literature clearly indicates an important role­of­lipids­metabolism­in­AMI.­However,­the­bio-marker­value­of­various­components­of­lipids­profile­is­not­clear­due­to­conflicting­findings­in­various­­studies.­We­therefore­compared­the­lipid­profiles­of­AMI­and­chest­pain­patients­with­respect­to­normal­subjects.­In­addition,­we­also­studied­the­role­of­inflammation­in­AMI­and­evaluated­its­correlation­with­lipid­profiles.

Patients and MethodsThis­ prospective­ study­ was­ conducted­ on­ 67­AMI­patients­ and­ 25­ patients­ with­ chest­ pain­ admitted­to­ Prince­ Sultan­ Cardiac­ Center­ and­ King­ ­Khalid­University­Hospital,­Riyadh,­Saudi­Arabia.­The­AMI­patients­ were­ classified­ into­ STEMI­ (ST-elevated­myocardial­ infarction,­N­=­ 28)­ and­NSTEMI­ (non-ST-elevated­ myocardial­ infarction,­ N­ =­ 39).­ Mean­ages­ of­ STEMI,­ NSTEMI,­ and­ chest­ pain­ patients­were­56.21­±­12.65­years,­61.98­±­10.83­years,­and­53.83­±­13.75­years,­respectively­(Table 1). We also included­ 54­ age-­ and­ gender-matched­ controls­ for­comparison.

The diagnosis of myocardial infarction required the­ presence­ at­ least­ two­ of­ the­ following­ criteria:­(i) history of characteristic prolonged ($30­­minutes)­pain­ or­ discomfort,­ (ii)­ creatine­ kinase­ (CK)­ lev-els­ exceeding­ twice­ the­ upper­ limit­ of­ normal­ (or­CK—MB­$ 50%­of­total­CK);­(iii)­presence­of­new­Q­waves­or­new­abnormal­ST—T­features.12­Patients­with­ STEMI­ were­ classified­ on­ the­ basis­ of­ the­

Table 1. characteristics of subjects.

Age (y) Male/female ratio Smoking (%) BMI (kg/m2)control 54.85 ± 10.14 3.6 28 27.64 ± 3.78STeMI 56.21 ± 12.65 4.8 41 28.97 ± 4.80nSTeMI 61.98 ± 10.83 3.3 24 28.81 ± 5.04chest pain 53.83 ± 13.75 2.9 26 32.27 ± 9.63

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­following­criteria:­(i)­continuous­chest­pain­upon­presen-tation,­refractory­to­nitrates,­and­lasting­$ 30­­minutes;­(ii)­ST-segment­elevation­of­$0.2­mV­in­$2­contigu-ous­precordial­leads,­or­$0.1­mV­in­$2­contiguous­limb­leads,­or­new­left­bundle­branch­block­on­admis-sion­ electrocardiogram;­ (iii)­ presentation­within­ the­first­12­hours­from­index­pain.­Patients­with­NSTEMI­were­required­to­have­angina-like­chest­pain­at­rest­in­the­last­24­hours­lasting­$ 5­minutes,­with­associated­ST­segment­depression­of­$0.1­mV­in­$2­contigu-ous leads upon presentation.13­The­patient­exclusion­criteria­ included­ recent­ surgery,­ active­ infection,­chronic­ inflammatory­ diseases,­ significant­ hepatic,­or renal dysfunction and malignancy. The protocol of this­study­was­approved­by­our­Institutional­Review­Board­ (IRB)­ for­ human­ studies­ and­ all­ the­ patients­signed informed consent.

Venous­blood­was­collected­after­overnight­fasting­from­ all­ the­ subjects­ in­ serum­ separator­Vaccutainer­tubes.­The­ levels­ of­ serum­ total­ cholesterol,­ lipopro-teins,­triglycerides,­and­hs-CRP­were­analyzed­using­an­Autoanalyzer­(Roche,­Germany).­The­data­were­evalu-ated­by­one-way­analysis­of­variance­(ANOVA)­followed­by­Dunnett’s­multiple­comparison­test­using­SPSS­sta-tistical­package­version­17.­Pearson’s­and­Spearman’s­tests­were­used­for­correlation­analysis­of­continuous­and categorical variables respectively. P values ,­0.05­were­considered­as­statistically­significant.

ResultsThe characteristics of patients and controls are sum-marized in Table 1. The family history of associated diseases­ was­ noted­ for­ hypertension­ (3/28­ STEMI,­1/39­ NSTEMI­ and­ 5/25­ chest­ pain)­ and­ CAD­ and­hypertension­(1­STEMI,­2­NSTEMI­and­2­chest­pain).­There­ were­ significant­ decreases­ in­ TC­ (ANOVA­F =­ 13.848,­P =­ 0.000),­ LDL­ (ANOVA­F­=­ 6.520,­P =­0.000),­and­HDL­(ANOVA­F­=­6.027,­P =­0.001)­levels­ in­ both­ STEMI­ and­ NSTEMI­ patients,­ as­

­compared­to­normal­subjects;­however,­patients­with­chest­pain­did­not­show­any­significant­change­in­these­lipids (Table­2­and­Fig.­1).­Serum­TG­levels­did­not­differ­significantly­among­STEMI,­NSTEMI,­or­chest­pain­patients,­as­compared­to­control­group­(ANOVA­F =­0.061,­P =­0.980)­(Table­2­and­Fig. 1). The com-monly­used­informative­lipids­ratios—including­TC/HDL,­LDL/HDL,­and­TG/HDL—did­not­differ­sig-nificantly­among­different­groups­(Fig.­2).

There­were­significant­increases­in­serum­hs-CRP­levels­in­STEMI­and­NSTEMI­patients­as­compared­to­control­group­(ANOVA­F­=­3.213,­P =­0.025)­(Fig.­3).­Serum­hs-CRP­showed­significant­inverse­correlation­with­HDL­(R­= −0.193,­P =­0.042).­However,­hs-CRP­was­not­correlated­with­TC­(R­= −0.010,­P =­0.910),­LDL­ (R­=­ 0.065,­P =­ 0.497)­ and­TG­ (R­= −0.031,­P =­0.733).

Age­was­significantly­and­inversely­correlated­with­TC­(R­= −0.144,­P =­0.025)­and­LDL­(R­= −0.164,­P =­ 0.015)­ and­ directly­ correlated­ with­ hs-CRP­(R­=­0.193,­P =­0.022)­(Table­3).­There­was­no­sig-nificant­ correlation­ between­ age­ and­HDL­ and­TG.­Body­mass­index,­gender,­and­smoking­did­not­show­any­ significant­ correlation­ with­ lipids­ or­ hs-CRP­(Table­3).­We­did­not­observe­any­significant­corre-lation­between­systolic­blood­pressure­and­ lipids­or­hs-CRP;­ however,­ diastolic­ blood­ pressure­ showed­significant­correlation­with­TC­(R­=­0.198,­P =­0.013)­and­LDL­(R­=­0.162,­P =­0.046)­but­not­with­HDL,­TG­or­hs-CRP­(Table­3).

DiscussionOur­results­showed­significant­decreases­in­TC,­LDL,­and­HDL­levels­ in­AMI­patients­ (Table­2).­ ­Gorecki­et al14­ observed­ higher­ levels­ of­ TC­ and­ LDL­ in­patients­with­complicated­versus­those­with­uncompli-cated­clinical­course­of­infarction,­suggesting­higher­levels­of­ these­biomarkers­during­ the­first­24­hours­of AMI have a strong negative prognostic value.

Table 2. Lipid profiles of control and patient groups.

Tc LDL HDL TGcontrol 5.185 ± 0.136 3.298 ± 0.161 1.194 ± 0.052 1.422 ± 0.127STeMI 3.769 ± 0.203** 2.418 ± 0.237* 0.896 ± 0.050** 1.399 ± 0.160nSTeMI 3.901 ± 0.184** 2.336 ± 0.125* 0.921 ± 0.049** 1.476 ± 0.183chest pain 4.767 ± 0.267 2.973 ± 0.231 1.058 ± 0.071 1.491 ± 0.173

Notes: Values are mean ± SeM, mmol/l. *P , 0.01 and **P , 0.001 versus control group using Dunnett’s multiple comparison test.

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Akosah et al15 reported acceptable or optimal LDL levels­ in­ a­ series­ of­ 183­young­ adults­ experiencing­AMI.­Gaziano­et­al8­found­that­the­mean­TC­and­LDL­levels­were­significantly­lower­while­in-hospital­than­levels­2­ to­3­months­ later;­however,­ from­a­ ­clinical­

­perspective,­ in-hospital­ levels­ can­ be­ used­ to­ guide­decisions­regarding­lipid-lowering­therapy,­which­can­begin­ in­ the­ immediate­ post-MI­ setting.­ In­ a­ series­of­34­AMI­patients,­on­the­first­day­after­admission­there­were­ significant­decreases­ in­TC­ (14.1%)­and­

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Figure 1. Box plots showing lipid profile (TC, LDL, HDL and TG) in normal subjects and patients with AMI (STEMI and NSTEMI) and chest pain. Notes: Values are median 25%–75% interquartile; outliers and extremes are shown as filled circles and stars respectively. The P values are against control group using Dunnett’s test.

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Figure 3. Serum hs-crP in different groups. Note: *P , 0.05 versus control group using Dunnett’s test.

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Figure 2. ratios of Tc, LDL and Tg to hDL in controls and different patient groups.

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Table 3. correlations between subjects’ characteristics and biochemical parameters.

Tc LDL HDL TG hs-CRPAge r = −0.144 r = −0.164 r = −0.071 r = −0.034 r = 0.193

P = 0.025* P = 0.015* P = 0.293 P = 0.596 P = 0.022*gender r = −0.029 r = −0.108 r = −0.008 r = −0.043 r = 0.071

P = 0.657 P = 0.105 P = 0.909 P = 0.501 P = 0.401Smoking r = 0.076 r = 0.019 r = −0.028 r = 0.108 r = 0.135

P = 0.370 P = 0.808 P = 0.727 P = 0.163 P = 0.231BMI r = −0.034 r = −0.097 r = 0.035 r = 0.012 r = −0.072

P = 0.644 P = 0.202 P = 0.645 P = 0.876 P = 0.505BP (systolic) r = 0.133 r = 0.095 r = 0.116 r = −0.011 r = −0.175

P = 0.095 P = 0.242 P = 0.154 P = 0.895 P = 0.185BP (diastolic) r = 0.198 r = 0.162 r = 0.158 r = 0.024 r = −0.230

P = 0.013* P = 0.046* P = 0.052 P = 0.766 P = 0.079

Note: *Statistically significant.

LDL­ (14.4%),­ as­ well­ as­ insignificant­ decreases­ in­HDL­(9.3%)­and­TG­(19.5%).16­On­the­basis­of­lipid­profile­data­of­97­patients­with­NSTEMI­and­unsta-ble­angina,­it­has­been­concluded­that­HDL­level­(as­opposed­to­LDL­and­TG)­adds­prognostic­value­to­the­prediction­of­in-hospital­recurrent­events­during­non-ST-elevation­ acute­ coronary­ syndromes.17­Rosoklija­et al18­have­ followed-up­ the­HDL­cholesterol­ levels­in­ STEMI­ patients­ from­ 24­ hours­ to­ 3­months­ and­concluded that the optimal times for determining the HDL­level­are­the­first­24­hours­of­the­actual­event;­this­is­due­to­the­fact­that­in­the­first­24­hours­there­is­ a­ relevant­ decrease­ of­ the­HDL­ cholesterol­ level­in the blood. The cause of reduced serum lipids in AMI patients in our study is not clear. It could be related­ to­dietary­modifications­or­due­ to­metabolic­changes­during­acute­crisis.­Nevertheless,­ the­ lipids­data negate the general conception that dietary lipids restrictions may prevent the risk of AMI.

High­ serum­ levels­ of­ HDL­ are­ associated­ with­reduced risk for the development of atherosclerotic disease.­HDL­particles­are­believed­to­be­antiathero-genic,­ secondary­ to­ their­ capacity­ to­ drive­ reverse­cholesterol­ transport­ and­ antagonize­ pathways­of­ inflammation,­ thrombosis,­ and­ oxidation.­ The­majority­ of­ patients­ in­ both­ the­ primary­ and­ sec-ondary­ prevention­ settings­ continue­ to­ ­experience­­significant­ ­residual­ risk­ for­ acute­ cardiovascular­events,­ even­ when­ their­ LDL­ cholesterol­ is­ low-ered aggressively via a combination of lifestyle modification­ and­ pharmacologic­ intervention.19 Al Aqeel et al20­ have­ observed­ that­ HDL­ appears­ to­

be the main lipid risk factor in patients presenting with­AMI­ in­Kuwaiti­ patients,­ suggesting­ that­pri-mary prevention strategies should focus on treat-ment­ modalities­ that­ increase­ HDL.­ In­ an­ in-vivo­mouse­ model­ of­ myocardial­ ischemia/reperfusion,­it­has­been­observed­that­HDL­and­its­sphingolipid­component,­ sphingosine-1-phosphate,­ dramatically­attenuated­the­infarct­size,­suggesting­a­rapid­thera-peutic­elevation­of­plasma­HDL­levels­may­be­ben-eficial­ in­ patients­ at­ high­ risk­ of­ acute­myocardial­ischemia.21 There is an increased focus on targeting and­treating­low­serum­levels­of­HDL­in­an­effort­to­further­reduce­risk­for­cardiovascular­events,­includ-ing myocardial infarction.19

In­our­study,­none­of­the­lipids­ratios­were­found­to­be informative in prediction of AMI (Fig.­2).­On­the­contrary,­LDL/HDL­ratio­has­been­suggested­to­be­an­independent predictor for AMI in the Japanese rural population.22­Goswami­et­al23 have suggested that the apo-B/apo-AI­ratio­is­a­better­discriminator­of­CAD­risk­in­the­atherosclerosis-prone­population­than­any­of­ the­conventional­ lipid­ ratios­ such­as­TC/HDL­or­LDL/HDL.­ Karthikeyan­ et­ al3 have also found the strongest­ association­ occurs­ between­ApoB/ApoA1­and the risk of AMI. McQueen et al24 have observed the­ highest­ population-attributable­ risk­ (PAR)­ with­the­ ratio­ of­ ApoB/ApoA1­ (54%)­ compared­ to­ the­PAR­associated­with­ the­ ratios­of­LDL/HDL­(37%)­and­TC/HDL­(32%).

We­ observed­ significant­ increase­ in­ hs-CRP­levels in AMI patients (Fig.­ 3),­which­ is­ in­ agree-ment­with­earlier­reports.25–27­hs-CRP­is­a­sensitive­

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marker­of­inflammation­and­a­potential­independent­predictor of cardiovascular disease as it may play a­ role­ in­ the­development­of­atherosclerosis;­ addi-tionally,­it­also­adversely­affects­mortality.28­Suzuki­et al29 have found nearly equivalent systemic and coronary­ levels­ of­ hs-CRP­ in­AMI­ patients.­ They­also­ observed­ a­ positive­ correlation­ between­ sys-temic­hs-CRP­and­coronary­plaque­area,­suggesting­an­ important­ link­ between­ systemic­ and­ coronary­levels­of­ ­inflammation.­Their­observations­are­also­associated­ with­ vulnerable­ coronary­ morphology­in the development of acute coronary syndromes.29 Higher­ baseline­ hs-CRP­ level­ showed­ significant­association­with­12-month­all-cause­mortality,­inde-pendent­of­other­prognostic­markers,­in­overweight­or obese AMI patients.30­The­findings­of­a­cross­sec-tional­study­of­188­patients­with­STEMI­suggested­that­plasma­hs-CRP­could­be­useful­ for­prediction­of development of heart failure in AMI patients.31 Elevated­ serum­ hs-CRP­ levels­ in­ patients­ with­AMI ,­6­hours­may­portend­vulnerable­plaque­rup-ture.32­The­patients­with­persistent,­severe,­treatment-unresponsive unstable­angina­(UA)­had­significantly­higher­CRP­levels­and­a­higher­incidence­of­clinical­events­than­patients­with­treatment-responsive­UA,­suggesting an important prognostic value of plasma CRP.33­However,­ there­was­no­correlation­between­plasma­ CRP­ and­ TC­ or­ HDL­ in­ UA­ patients.33 A significant­inverse­correlation­between­hs-CRP­and­HDL­(but­not­with­other­lipid­fractions),­as­observed­in­our­study,­indicates­the­co-existence­of­inflamma-tion and impaired lipid metabolism in AMI patients. The­ correlation­ data­ showed­ that­ serum­HDL­was­not­ affected­ by­ age,­ gender,­ BMI,­ smoking,­ and­blood pressure (Table­3).­Although­the­levels­of­hs-CRP­were­directly­correlated­with­age,­hs-CRP­was­not­influenced­by­gender,­BMI,­smoking,­and­blood­pressure (Table­3).

ConclusionOur­findings­suggest­that­reduction­in­serum­choles-terol­does­not­prevent­the­risk­of­AMI.­There­was­a­significant­increase­in­systemic­inflammation­in­AMI­patients,­ inversely­correlated­with­HDL­levels,­ sug-gesting­an­important­role­of­inflammatory­mediators­in­AMI.­Thus,­a­decrease­in­serum­HDL­and­increase­in­hs-CRP­strongly­predispose­ the­ risky­ individuals­to the event of AMI. We emphasize the importance

of­HDL­and­hs-CRP­measurements­in­the­assessment­of­a­combined­lipido-inflammatory­risk­factor­for­the­screening of high risk individuals and the prognosis of AMI.

AcknowledgmentsThis­study­was­supported­by­the­National­Plan­for­Sci-ence­and­Technology­(NPST)­Program­by­King­Saud­University­ Project­ Number­ 08-BIO571-02.­ We­ are­thankful­to­Dr.­Shahid­Habib­and­Dr.­­Abdulrahman­Al­Moghairy­for­their­clinical­observations.­We­would­also­like­to­acknowledge­the­technical­assistance­of­Adnan­Ali Khan and the nursing staff of the King Khalid ­University­ Hospital­ and­ the­ Prince­ Sultan­ Cardiac­­Center­(Riyadh)­for­sample­collection­and­patient­care.

Author ContributionsConceived­ and­ designed­ the­ experiments:­ HAK,­ASA,­SHS.­Analyzed­the­data:­HAK.­Wrote­the­first­draft­ of­ the­ manuscript:­ HAK.­ Contributed­ to­ the­writing­of­ the­manuscript:­HAK,­ASA,­SHS.­Agree­with­ manuscript­ results­ and­ conclusions:­ HAK,­ASA,­SHS.­Jointly­developed­the­structure­and­argu-ments­ for­ the­ paper:­HAK,­ASA,­SHS.­Made­ criti-cal­revisions­and­approved­final­version:­HAK,­ASA,­SHS.­All­authors­reviewed­and­approved­of­the­final­manuscript.

FundingA­ grant­ from­ National­ Plan­ for­ Science­ and­ Tech-nology­ (NPST)­ Program­ by­ King­ Saud­ University­Project­Number­08-BIO571-02.

Competing InterestsAuthor(s)­disclose­no­potential­conflicts­of­interest.

Disclosures and EthicsAs a requirement of publication author(s) have pro-vided­to­the­publisher­signed­confirmation­of­compli-ance­with­legal­and­ethical­obligations­including­but­not­limited­to­the­following:­authorship­and­contribu-torship,­conflicts­of­interest,­privacy­and­confidential-ity­and­(where­applicable)­protection­of­human­and­animal­research­subjects.­The­authors­have­read­and­confirmed­ their­ agreement­with­ the­ ICMJE­ author-ship­and­conflict­of­interest­criteria.­The­authors­have­also­confirmed­that­this­article­is­unique­and­not­under­consideration­or­published­ in­any­other­publication,­

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and that they have permission from rights holders to reproduce any copyrighted material. Any disclo-sures­are­made­in­this­section.­The­external­blind­peer­reviewers­report­no­conflicts­of­interest.

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