Peak CRP Levels are Higher in Patients with ST Peak CRP Levels are Higher in Patients with ST Peak CRP Levels are Higher in Patients with ST Peak CRP Levels are Higher in Patients with ST Elevation Than NonElevation Than Non--ST Elevation ST Elevation

Acute Coronary SyndromeAcute Coronary SyndromeAcute Coronary SyndromeAcute Coronary Syndrome

Dr Syed Shahid HabibDr Mohammad Ibrahim Kurdi

Dr Zohair Al AseriKing Khalid University Hospital

King Saud University

INTRODUCTION• A large body of evidence suggests that inflammation

INTRODUCTIONA large body of evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis.

• The chronic inflammatory process can develop into an acute clinical event by the induction of plaque rupture, leading to acute coronary syndromes

• CRP levels increase after acute myocardial infarction (AMI) but their changes in the process of an acute ischemic attack has been studied mainly in patientsischemic attack has been studied mainly in patients with non-ST elevation AMI.

Libby. Circulation. 2002; 105 (9): 1135-43.Ercan E. Am Heart J. 2004; 147 (1): 54-7.

Trop T Trop T CKMBCKMB

ICAMICAMVCAMVCAM

E & P Selectin E & P Selectin Phospholipase A2Phospholipase A2 Adipose TissueAdipose Tissue

CRP is locally generated from CRP is locally generated from

CytokinesCytokines••ILIL--11ββ & IL& IL--66

••TNF TNF αα

y gy gEndothelium alsoEndothelium also

TNF TNF αα

CRPCRPFibrinogenFibrinogen

SAASAA

Ishikawa et al. Am J Ishikawa et al. Am J CardiolCardiol. 2004;93:611. 2004;93:611--4 .4 .Rader. NEJM. 2000; 343(16):1179Rader. NEJM. 2000; 343(16):1179

OBJECTIVEOBJECTIVE

T t d th diff iT t d th diff i h CRPh CRP l l il l iTo study the differences in To study the differences in hsCRPhsCRP levels in levels in patients with two clinical forms of ACS of patients with two clinical forms of ACS of

nonnon--ST elevation myocardial infarction ST elevation myocardial infarction yycompared to ST myocardial infarction. compared to ST myocardial infarction.

METHODSMETHODS

Recruited N = 94Recruited N = 94

FINALLY SELECTED = 89FINALLY SELECTED = 89FINALLY SELECTED = 89FINALLY SELECTED = 89

CONTROLCONTROLN=29 N=29

STEMISTEMIN=32N=32

NSTEMI NSTEMI N=28N=28

♂♂18 18 ♀♀ 11 11 ♂♂ 21 21 ♀♀7 7 ♂♂ 22 22 ♀♀10 10

HSHS CRP ATCRP AT BASELINEBASELINE PEAKPEAK ANDAND FOLLOW UPFOLLOW UPHSHS--CRP AT CRP AT BASELINEBASELINE PEAKPEAK AND AND FOLLOW UPFOLLOW UPLIPOPROTEIN(a)LIPOPROTEIN(a)

INCLUSION CRITERIAINCLUSION CRITERIAINCLUSION CRITERIAINCLUSION CRITERIA

NSTEMI: NSTEMI: Patients with NSTEMI were required to have angina-like chest pain at rest in the last 24 h lasting ≥ 5 min,

ith i t d ST t d i f ≥ 0 1 V i ≥ 2with associated ST-segment depression of ≥ 0.1 mV in ≥ 2 contiguous leads upon presentation

STEMI:STEMI: (1) ti h t i t tiSTEMI: STEMI: (1) continuous chest pain upon presentation, refractory to nitrates, and lasting ≥ 30 min; (2) ST-segment elevation of ≥ 0.2 mV in ≥ 2 contiguous precordial leads, or ≥ 0 1 mV in ≥ 2 contiguous limb leads or new (or presumably0.1 mV in ≥ 2 contiguous limb leads, or new (or presumably new) left bundle branch block on admission electrocardiogram; (3) presentation within the first 12 h from index pain.

EXCLUSION CRITERIAEXCLUSION CRITERIA(1) angina of secondary etiology

EXCLUSION CRITERIAEXCLUSION CRITERIA(1) angina of secondary etiology,

(2) recent surgery,

(3) active infection, or chronic inflammatory diseases

(4) significant hepatic or renal dysfunction, and

(5) malignancy, were not included as well as

(6) individuals with body temperature of >37.8° C at admission,

(7) coronary or cerebral event in that same period, those with

complete left bundle block, those with pacemaker rhythm, andcomplete left bundle block, those with pacemaker rhythm, and

those with serious aortic valve disease, obstructive hypertrophic

cardiomyopathy, and subjects who were critically ill or with

ongoing or recent (< 1 month) infectious diseases

HSCRP and HSCRP and LpLp(a) were (a) were measured by TIA on Hitachimeasured by TIA on Hitachi--measured by TIA on Hitachimeasured by TIA on Hitachi911 with kits manufactured 911 with kits manufactured by BIOKIT Spain a by BIOKIT Spain a St d di d ASt d di d AStandardized Assay.Standardized Assay.

Table I: Clinical characteristics of ACS patients pwith STEMI compared to NSTEMI.

ControlControl NSTEMINSTEMI STEMISTEMI

NN 2929 2828 3232

Gender M/FGender M/F 18/1118/11 2121//77 2222//1010

AgeAge 5454..62 62 ±± 1010..6060 5959..22 22 ±± 1313..1212 5555..57 57 ±± 1111..4444

BMIBMI 2626..12 12 ±± 66..0808 2525..24 24 ±± 77..4444 2929..23 23 ±± 44..7373****

BP SystolicBP Systolic 129129..93 93 ±± 1919..0707 136136..37 37 ±± 2323..6868** 130130..41 41 ±± 1616..8888

BP DiastolicBP Diastolic 7575..83 83 ±± 1212..2626 7979..56 56 ±± 1818..3232 7676..72 72 ±± 1111..8484

Data is expressed as Mean ± SD* 0 05 STEMI & C t l*p<0.05 versus STEMI & Control**p<0.01 versus NSTEMI & Control

T bl I Li id d L ( ) P fil ACS ti tTable I: Lipid and Lp(a) Profile ACS patients with STEMI compared to NSTEMI.

TC TC mmolmmol/L/L 4.38 4.38 ±± 0.500.50 44..49 49 ±± 11..6666 44..22 22 ±± 11..3737

TG l/LTG l/L 1 111 11 ±± 0 490 49 22 0202 ±± 11 6262 11 7777 ±± 00 8484TG mmol/LTG mmol/L 1.11 1.11 ±± 0.490.49 22..02 02 ±± 11..6262 11..77 77 ±± 00..8484

LDL mmol/LLDL mmol/L 2.71 2.71 ±± 0.530.53 22..72 72 ±± 11..3131 22..69 69 ±± 11..0303

HDL mmol/LHDL mmol/L 1.07 1.07 ±± 0.320.32 00..69 69 ±± 00..3030 00..70 70 ±± 00..2020

Lp(a) mg/dlLp(a) mg/dl 14.5714.57±± 11.81##11.81## 3131..92 92 ±± 3737..3434 2222..05 05 ±± 1818..6666

Systolic blood pressure (SBP), Diastolic Blood pressure (DBP), Total cholesterol (TC), Triglycerides (TG), Low density Lipoprotein (LDL) and High density lipoprotein (HDL) and Lipoprotein(a) [Lp(a)].Differences were studied by Kruskal Wallis test for Lp(a) and ANOVA for otherDifferences were studied by Kruskal–Wallis -test for Lp(a) and ANOVA for other parameters.## p<0.01 versus NSTEMI & STEMI

T bl I Li id d L ( ) P fil ACS ti tTable I: Lipid and Lp(a) Profile ACS patients with STEMI compared to NSTEMI.

Cardiac EnzymesCardiac Enzymes IU/LIU/L NSTEMINSTEMI STEMISTEMI

Troponin TTroponin T 0.95 0.95 ±± 1.511.51 2.61 2.61 ±± 2.762.76

CKMBCKMB 111.75 111.75 ±± 44.3344.33 205.39 205.39 ±± 152.15*152.15*

ASTAST 38.00 38.00 ±± 31.1331.13 95.00 95.00 ±± 72.66*72.66*

LDHLDH 188.38 188.38 ±± 92.6392.63 309.00 309.00 ±± 213.02213.02

Creatine kinase myocardial bound (CKMB), Aspartate aminotransferase (AST), Lactate dehydrogenase (LDH)Differences were studied by Mann–Whitney -testData is expressed as Mean ± SD*p<0.05 versus NSTEMI

Figure 1 - Comparison of mean CRP levels at baseline, peak and at 4-6 weeks of follow up in all ACS, NSTEMI and STEMI patients

DISCUSSIONDISCUSSION• In our study, the difference in CRP levels was significant between

DISCUSSIONDISCUSSIONSTEMI and NSTEMI patients at peak levels only. This suggests that it might be influenced by the degree of early myocardial tissue necrosis. Therefore, this variation in CRP kinetics should be taken into consideration when designing future studies.into consideration when designing future studies.

• The higher the maximum CRP recorded, the more severe the infarction suffered, the greater the likelihood of ventricular remodeling, the lower the ejection fraction, and the greater the riskremodeling, the lower the ejection fraction, and the greater the risk of heart failure, heart rupture, and death.

• The results of the present study expand upon previous reports that demonstrated non-significant differences in CRP levels at baselinedemonstrated non significant differences in CRP levels at baseline in patients with acute coronary syndromes, which tended to be higher in successive samples.

Sánchez PL . Rev Esp Cardiol. 2006; 59 (5): 441-7 Brunetti ND. Int J Cardiol. 2006; 109 (2): 248-56.Auer J. Jpn Heart J. 2002; 43 (6): 607-19

Conclusions

• STEMI patients have significantly higher peak CRP levels compared to NSTEMI patientsCRP levels compared to NSTEMI patients.

• These data suggest that inflammatory processes play an independent role in theprocesses play an independent role in the pathogenesis of myocardial infarction.

• CRP assessment may assist in risk ystratification after myocardial infarction.

THANKS