Apolipoproteins and lipid indices in patients with multiple coronary occlusions.

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V. R. Bhagwat andN. T. Venugqnl

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BIOMEDICITTEVol.33 No.1: (January-March) 2013

Contents

with age and gender: Ahospital based studySuprita Gupta, Rakesh Kumar Gupta, Amar Nath Thahr and Amit Kumar Patel

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www. bio me d.icin e onlin e. or g Biomedicine - YoL 33 No. 1: 2013

Biomedicine: 2013; 33(1): 90-96

Apolipoproteins and Hpid indices in,patients with multiple coronary occlusionsV R Bhagwatr and N T Venugopaf

1. Professor and Head, Dep of Biochemisfry, SBH Golrt. Medical College, Dhule - 424 002 (Maharashtra),India

2. Assistant Professor, Dept of Biochemistry, DYPatil Medical College, Kolhapur (Maharashtra),India

(Received: 74.01.2013 Revised: 27.02.2013 Accepted: 22.02.2013)

Corresponding AuthorDr. V. R Bhagwat. Email: [email protected] Mobile: +91-9422238523

AbstractBackground and obiectives: Dyslipidemia is a most common finding in patients with cardiovascular abnormalities in India.The sensitivity and specificity in prediction of coronary artery disease ls variable among biochemical markers. Assessment ofriskforcoronery artery disease involving apolipoproteins isvery much essential forlndian patienb.Meterid end Methods: This is a case control study done in 31 patients with angiographically conffrmed multiple coronarTocclusions. Conventional as well as novel lipid prolile involving apolipoproteins A1, B end Lipoprotein{a) serum levels weremeasured by immuno-turbidimetric assay in the patients along with 13 normat control subjects.Results: Totilcholectcmlendtotdtriglyceridelevels ere found to be higher, However, they do notcorrelatewith the degree ofoon nfiy occJurion in tlc ptfomtr. Indircct mrrkers such as LDL:HDL ratio do not truly reflect the severity of coronaryethercsclemir. ApoB v.lrcs rrc pntrd witt tte degree of coronary occlusions and therefore indicate increased risk ofcorenaryrftetydiseuc.Elemtedlp(e)lwelrintrepdienbporitivelycorreletewithseverityofcoronaryocclusion.Conclusion: Thc AI:LDL ntio is beilner-tten A1:B rrtio in tcms of sensitivity for coronarT artery disease risk straffication.Lp(a) seemsto be moresensifive indicetorthen apoB. Lp(a) appears to be a primary riskfactorwhen the total cholesterol orLDL is marginally elevated.Keywords:Apolipoprotein-Al,Apolipoprotein-BrLipoprtein(a), SerumlipldsrCoronaryocclusion

Introduction explain the risk of CAD adequately and havelimitations (6 & 7). It is now gradually replaced bynovel lipid markers such as apolipoproteins, due toseveral advantages (7,8 &9).

Apolipoprotein A1 (apoAl) is increasinglyrecognized as anti-atherogenic as it is inherentlyinvolved in reverse cholesterol transport (10 &11).Apolipoprotein B (apoB) is atherogenic, being a

major protein of LDL, which is the predominantcirculating atherogenic lipid particle (11). Inaddition to these, a yarrarlt hybrid lipoprotein-a [Lp(a)l is known to play key role in athero-thrombosisleading to CAD (12). Several reports publishedrecently indicate variable paffern of these novelmarkers forlndians (1 ,6,8 & 9). Inview ofthese, thisstudy was undertaken to assess these markers forpossible association with lipid indices,apolipoproteins and severity ofcoronary occlusion inangrographically confirmed p atients .

mong the cardiovascular diseases (CVD),coronary artery disease (CAD) is theleading cause of mortality in the modern

times. It is reported that South Asians have higherprevalence of CVD and are more prone to CADcomparedto otherregions ofthe world (1,2& 3).Themortality rates from CAD among south Asians arereported to be 2-3 times higher than for Caucasians,irrespective of gender, religron, social class, dietaryhabits or country of residence Q & 3). CAD isresponsible for more than 40-50 o/o of all deaths inIndia (3). The risk asses$ne,nt of multi-factorialdisease likeCAD is rather difficult due to complexinteractions of several factors. However, riskstratification' is possible with the aid of severalbiochemical markers (1, 4 & 5). Monitoring ofpatients using classical lipid markers such as Totalcholesteroi (TC), Triglycerides (TG), High densirylipoprotein (HDL), Low density lipoprotein (LDL)was much popular in the past, however they do not

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Material and Methods

Study desiggr: This is a studywith case control designinvolving ffend analysis. The study was initiated afterclearance from the institutional ethical cornmittee.The subjects were enrolled in the sfidy afterobtaining infonrred consent from the concernedindividual subjects.

Selection of patients: 44'patients were selected fromthe cardiology OPD when first cardiac event wasreporrted. Their age ranged between 42-80 years. The .

recruited patimts were exalr-rined clinically bycardiologists and were advised for plannedangiogaphy. The angiogram film was interpreted byinterventional radiologist Based on the radiologicalfindings and number of blocks in the coronaxyvessels, the patients were categorized into fourgroups. Group I included 13 normal healthy controls

NIIC) with no abnormalities in the coronary vessels,Group II comprised of 12 pattents with single blochGroup III had l0 patients with two blocks ufojleGroup tvhad 9 patrents withthree blocks in coronaryvessels. The age matched NHC group had normalfindings, no history of angina or' any cardiovasculardisorders. These were vohurteers selected from thehospital staff after detailed clinical and laboratoryinvestigations. AIso they were free from metabolicdisorders like diabetes, liver or renal diseases. The)rwere not non smokers, non alcoholic nor did theyhave anlx addictions to dnrgs.

Sample processing: \hnous blood samples werecollected when the first cardiac event was reportod,byphlebotorlry- avoiding venous stasis. 5 ml ofurholeblood was transferred to plain and EDTAbulbs. After20-30 minutos, it was centrifuged at 4000 rpm forabout 15 minutes. Upper clear serum was separatedand stored in dry bulbs atT-;&oC until analysis on thesarne day as far as possible.

Lipid profile analysis: The classical lipid profileincluded serum levels ofTG, TC, IIDL and LDL. TGand TC were measwedby enryatrc methods usrqgcou mercially available single reagent end-pointassay kits from Eli-T€ch, SEPPIM, ffid France (13).The TG assay has within-rf,trn CV of 1.5 % and

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V; RBhagwat and N. TVeiagopal Apohpoprotcins........". oeclusions

between-run CV of 3.6 %urhile the TC assay has 0.89/o and 3.1 % respectively. IlDl-cholesterol (IIDLc)was estimated by immuno-turbidimteric as$ay usingready-to-use reagents from Accurex Biomedicals,Mumbai (14). The precision ofthe assay was within-nm CV of 1.1 % and between-rurr CV of 4.2 ya.

LDlcholesterol (LDLo) was calculated usingFriedwald's equation (15), when TG is below 400mg1dl. All the values were e.xpressed in md/dl.

Assay of apolipoptoteins: The novel lipid profileincluded apoAl, apoB and Lp(a). The lipoproteinmeasurement was based on the turbidimetricimmunoassay. Latex particles coated with antibodiesfor specific apolproteins when mixed with sanrplecontaining the apoproteins produces agglutination,which is measured in BT- 2000 analy zer(manufactured b Biotechnicon Instnrments, USA),A set of two reagents required for single test each furapoAl, apoB and Lp(a) were procured fromSPINREACT, Santa Coloma, Spain (16). Theprocedure was carried out in accordance with themanufacturer's suggestions. All the values wereexpressed as mg/dl. The lipid indices (TC:LDL&,LDLc:HDLc, Al lB, B :A1, A I :HDI* and Al :LDLc)were calculated as ratio ofthe individual values.

Statistical Analysis: The statistical calculationsincluded arithmefic as well as geometric mean,standard deviation (SD) of samples from the meanvalues. Student 't' test was done for testing equahryof means of two samples. Trend analysis of the lipidindices across the groups was also done usingstatistical tool ofl\flicrosoft Office Excel 2007 .

Results

The pattem of classical hpid profile assessed in thepatients included in the study is given in Tbble l.Mean values of TG 0ro not much variable in thepatient goups except in the last group IV which washigher by about 18. L% more than the confiol group.None of the subject has TG level above 400 mg/di.TC shour increasing tnend across the goups. It wassignificrmfly higher by 5l.3Yo in group IV than theconfiols (P<).005). Similarly LDLc level washighest (55.87yo) in gr,oup IV (P<0.001). HDLcwas

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V RBhagwat and N. TVenugopal fitolipoproteins .......... occlusions

Table 1 Classical Lipid Profile in CAD

92

Parameters Group-I (NHC) Group-II Group-III @ouble Group-fyn = 13 (Single block) block) n:10 (Ttiple

n = 12 block) n:9TG (mgldl) 133.4+32.0 141.2+45.6 149.9+s9.9 163.5+63.0

(0.176) (0.ss) (1.101)

TC (mg/dl) 149.4+32.7 148.8 L23.8 177.6+52.4 L226.0+58.2(0.0s3) (1.4e3) (3.s77)

LDLc (me/dl) 98.8 + 38.0 104.0 + 18.3 109.5 +32.9 o154.0 +26.3(0.441) (0.722) (4.027)

HDLc (me/dl) 42.7 +6.6 *36.2*7.9 #34.8+7.8 L32.9+7.5(2.223) (2.s72) (3.163)

Figures are Mean + SD; Figures in parenthesis are the 't'values;#P<0.02, *P<0.05, AP<0.005, oP<0.001 cfNHC

Table 2 Novel Lipid Profile in CAI)

Parameters Group-I (NHC) Group-II Group-III @ouble Group-fVn:13 (Single block) block) n: 10 (tiple

n:12 block)n=9apoAl (mg/dD 146.9t39.6 130.1133.2 125.8+26.4 110.0 +47.5

(1.rs2) (t.s2e) (l.els)apo B (me/dD 84.5 +27.3 101.1 + 15.5 #111.0 + 17.4 o154.0 +22.1

(r.887) (2.831) (6s7e)Lp(a) (mg/dD 17.0+12.9 21.0*20.8 #76.2 + 63.0 *80.7 +78.2

(0.s72) (2.e2s) (2.421)

Lp(a) GM ll.8s 21.24 s4.87 60.6

Range 1.07 - 44.9 26.3 - 180.8 30.8 - 199.3 18 - 212.1

Figures are Mean + SD; GM: Geometric mean;

Figures in parenthesis are the't'values;#P<0.01, *P<0.05, oP<0.001 cfNHC

significantly lower in all the patient groups (Table 1). values show elevated trend across the groups (Fig I )

Table 2 show the novel lipid profile found in the Highestvaluewas2l2'3ingrouprv'

subjects under the study. The apoAl show declining The lipid ratios or indices, when calculated by takingfrend in the mean values across the patient groups. It individual values are shown in the Table 3. It is seen

was not statistically significant. The apoB values, on from the values that the TC:HDLc, LDLc:HDLc andthe contast, show increasing trend in the patients B:Al ratiosshowaincreasingfendwhileAl:LDlc(Table2).ItwassignificantlyhigheringrouplVby and A1:B ratio show decreasing trend across the82.2% compared to the confrol group (P<0.001). groups. The A1:HDLc ratio did not show anyLp(a) values were highly variable. The arithmetic significantvariationsacrossthepatientgroups(Tablemean values are masked by high SD values 3). The Al:B and B:Al ratios reflect the frend ofindicating skewed distribution. The geometric mean apoB values however, they were statistically not

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significant. The decreasing trend in the A1:LDLc is

significantly noticeable (Fig 2).

180

160

tlo

olDoactmboE80c360

o

20

0

IrpoAl IrPoB +Lph)Apolipoproteins in the Subjects s

80

70

60

sF=T40-

30

20

t0

0

Fig I The bars are the mean values of apoAl and apoB whereas circles are the

Geometric mean of Lp(a) in each group.

The line indicates the trend in the values relative to each group.

Lipid Indices in the Subiects{_TC/HDLc LDtc/HDL3 *rler AvBolrB/A1 -1-1{HD[c {-AUl-DLc

6

5.5

5

{54

35

3

25

2

i5I

05

0

Fig 2 The chart shows mean values of each lipidindex for each group and the line

shows the trend and not the longifudinal change of the group.

V R. Bhagwat and N. T Venugopal Apolipoproteins.......... occlusions

Discussion

The results ofthe present study indicate dyslipidemiain angiographically confirmed patients with multiplecoronary occlusions. The findings, in genetal, agree

with those reported by others (4,5 & 8). It is true thatconventional or classical lipid profile do not giveadequate information regarding risk of CAD. This isobvious from the results. TC and TG levels are

higher; however, they do not correlate with thedegree ofcoronary occlusion in the patients. Even thelipid index such as LDLc:HDLI ratio does not fiulyreflect the severity of coronary atherosclerosis whichis an indirect measure of CAD risk. This studyobserved some relationship of TC:HDLc ratio withcoronary occlusion. The increasing trend in the indexis almost due to increasing trend in the TC values.

It is also known that classical lipid markers such as

TC, TG are affected by several factors like diet,fasting and others. They are not sensitive enough inpredicting future cardiac events. Apolipoproteinshave been considered as more stable risk factors andrelatively unaffected by common factors unlikeclassical lipid markers (8). The pattern of the novelmarkers such as apoAl, apoB and Lp(a) in this studyshow distinct changes with closer association to thedegree of coronary atherosclerosis. ApoAl is themajor protein accounting for 70% all protein contentof HDL. It is well known that apoAl plays pivotalrole in reverse cholesterol transport as ligand,receptor and enryme activator (10). It is reported thatmore than 40% of myoc ardial infarction patients

Table 3 Lipid indices in the subjects.

Parameters Group-I (NHC)n:L3

Group-II(Single block)n:12

Group-III @ouble Group-fVblock)n:10 (Ttiple

block) n :9TC/HDLc ratio

LDLctHDLc ratio

A1/B ratio

B/Al ratio

A1 IHDLc ratio

A1 tLDLc ratio

3.59 + I .01

2.33 + 0.89

1.49 + 0.65

0.72 + 0.38

3.54 + 0.I71.52 + 0.28

4.29 +0.943.07 + 0 .99

1.58 + 0.53

0.73 + 0.18

3.59 + 0.20

#1.25 + 0.21

o5.07 + 0.81

#3.12 + 0.58

1.22 + 0.45

0.94 + 0.36

3.61 + 0.20

al.04 + 0.39

o5.81 + 0.75

o3.96 + 0.85

1.04 + 0.58

0.96 + 0253.&+029oo.7l + 0-34

Figures are mean + SD; #P<0.02, AP<0.005, oP<0.001 cf NHC

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V R. Bhagwat and N. T Venugopal Apolipoproteins .......... occhtsions

have low HDL and apoAl levels withangrographically assessed C A n 07).The apoAl has strong anti-atherogenic role. Variousmechanisms have been proposed to elucidate thisrole. Of these, one proposed antioxidant mechanismis the destnrction of oxidized LDL via HDLassociated paraoxonase- 1 and acetyl hydrolaseenzymes (18). However, it is reported that HDLappears to be selective target for myeloperoxidaseeatalyzed oxidation in patients with CAD (19). ThusIIDL is not only antioxidant but paradoxically appearto be pro-oxidant in ischemic heart disease (IHD)patients (3 ,6,20,2I &22),promoting LDL oxidationand monocyte chemotactic activity in the humanartery wall (23).Therefore, it is logical to assume thatthis pro-inflammatory dysfunctional HDLaccumulates oxidants that inhibit the antioxidantenzymes of HDL which in turn render apoAl unableto promote reverse cholesterol transport leading toatherosclerosis. Therefore, assessing CAD risk byHDL is no longer reliable and needs to be revised.This study finds a decreasing trend in A1:LDLoindex. This is due to the relative changes in the A1and LDLc values. The higher LDLc and lower A1values decreased the index in multiple occlusiongnoups. This has relevance to the risk of CAD andmaybe considered as potential predictor ofCAD.Although various factors such as diet, exercise,alcohol, smokitrg, hormones and certain dnrgs cansigpificantly influence the levels ofHDL and apoAl.Seve,ral family and twin studies have demonstrated astrong genetic heritability accounting for up to 66 %ofthe variability of HDL and apoAl levels (24). Thestrmg and positive correlation of plasma apoAl andHDL levels suggest that apoAl gene polymorphismmay be linked to the dysfuirctional HDL and geneticprodisposition to CAD in south Asians and Indians(24). Hence it is worthwhile to design systematic,&borate studies to pinpoint the increased risk ofCAD at moderate low or even nonnal levels of HDLcapoAl inlndians.

The ryoB is atherogenic as it is the major protein ofLDL. Ihere is abundance of evidence from caseffiol reports to support the role of apoB as anfpumt risk factor of IHD (6, 11 & 23).AfryUlmbased study indicated that elevated apoB

ffiinanlineorg

levels strongly associate with increased relative riskof IHD (23). The present results indicate that apoBhas a strong as soci ation with coron aryatherosclerosis. The mean levels of apoB are parallelwith the degree of coronary occlusions and thereforeindicate increased risk of CAD. This finding mayhave valuable implication in the management ofpatients from therapeutic point of view. Since it isreported that intensive lipid lowering therapytargeted to patients with elevated apoB levels notonly diminished the rate of progression of CAD butalso induced a net regression of angiographicallydetermined coronary lesions (25).

Lp(a) is a hybrid lipoprotein composed of apo(a) andapoB100, joined by a disulphide linkage (12). C-terminal of apo(a) consists of single copy of peptidesequence homologous to plasminogen (Kringle-V)as well as proteinase domain. However, this domainis inactive unlike plasmin (26). It is believed thatLp(a) could promote CVD in two ways. Its apo(a)moiety could promote thrombosis while its LDLcomponent promotes atherosclerosis. It is reportedthat Lp(a) competitively inhibits plaminogenreceptors on cell strface in-vitro (z7).Hence it ispossible that Lp(a) may act as competitive inhibitorofplasmin andprevent in - vivo fibrinolysis.

Present results show a very high degree ofvariabilityin serum levels of Lp(a) as seen from the high SDvalues. The distribution of Lp(a) value is skewed.Hence geometric mean was calculated instead ofarithmetic mean. The results strongly point out thatelevated Lp(a) in the patients positively correlatewith severity of coronary occlusion (Fig 2).lt seems

to be more sensitive indicator than apoB. In otherwords, the degree of coronary vessel blocks indicatesseverity of atherosclerosis which is the indirectmeasure of CAD risk. Therefore, Lp(a) appears to bea primary risk factor when the TC or LDL ismarginally elevated.

The high degree of variability in Lp(a) could be dueto variation in the apo(a) size. It is believed that morethan 90% ofthe Lp(a) is under genetic control(26).Itis reported that small sized apo(a) isoforms areassociated with coronary heart disease in overweightsubjects (9). Therefore, charactenzation of apo(a)phenotype might serve as a reliable marker in

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assessment of CAD risk. There is strong evidencethat Lp(a) and apo(a) size is ethnic dependant (9 &26). This partly explains why south Asians andIndians have high susceptibilrty to CVD. Hence moreextensive and comprehensive studies are warrantedto reveal the genetic basis and heightenedsusceptibility for CAD in Indianpopulation.

The analysis of novel lipid indices in the patientsshow that A1:LDLc ratio is marginally better thanA1:B ratio as the SD values are small, showingnarow deviations from the mean values. This indexindicates the atherogenic burden. The differences inthe A1:B index may not be clinically significant inpredicting the risk of future CAD. The reason couldbe that the changes in homeostasis of apoAl andapoB may not be balanced without changing theratio. The differences in the synthesis, secretion andcatabolism may not be much different for the twoapoproteins. However, with the available knowledgeon the metabolism of these apolipoproteins, itappears that A1:LDLc ratio is better than A1:B ratiointerms ofsensitivity for CAD risk stratification.

It is imperative to state the limitations of the study.Few confounders such as pre-medication, clusteringof associated sub-clinical illnesses like hypertension,insulin resistance and others were not taken intoaccount. In addition to these, small sample size foreach group may bias the results. In view of these,additional population based studies are clearlywarranted to justiff the use of novel lipids andindices for CAD risk stratification in Indian

, population.

Conclusion

The results ofthe present study indicate dyslipidemiain the patients with multiple coronary occlusions. TCand TG levels are higher; however, they do notcorrelatewith the degree of coronary occlusion in thepatients. The lipid index such as LDLc:HDLc doesnot reflect the severity of corolary atherosclerosis.ApoB values are parallel with the degree of coronaryocclusions and therefore indicate increased risk ofCAD. This finding has important implication in themanagement of patients from therapeutic point ofview. The A1:LDLc ratio is better than A1:B ratio interms of sensitivity for CAD risk stratification.Elevated Lp(a) levels in the patients positively

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V R Bhagwat and N. T Venugopal Apolipoproteins.......... occlusions

correlated with severity of coronary occlusion. Itseems to be more sensitive indicatorthan apoB. Lp(a)appears to be a primary risk factor when the TC orLDL is marginally elevated. It is imperative thatadditional population based studies are clearlywarranted to justiff the use of novel lipids andindices for CAD risk stratification in Indianpopulation.

C omp etin g interest disclosure

No competing interest existed or none detected. Noprofes sional confl icts exist.

Acknowledgment:

Authors wish to gratefully acknowledge the clinicalhelp rendered by DrAshok Bhupali,Dr C.V. Patil, DrG.V. Patil, Dr S.R. Patil, Dr Vinod Wagle andtechnical help supported by Dr R.S. Patil, NIr. SudhirSase and Ms Vaishali Rokade in analyzingthe bloodsamples.

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wwtttbioffiorg Biomedicine - VoL 33; No.I: 2013

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