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ABSTRACT
Aims
Out of 50 patients 44% were in Anterior MI, 36% in Inferior MI, 20% as
NSTEMI. Patients had Canadian Cardiac Society (CCS) II/III angina in 50% and
shortness of breath (NYHA III/IV ) in 44 % cases. Among them with AMI showed
clinical signs of HF (Killip class >1) during the week of study. 8 cases (16%)
presented with cardiogenic shock. Patients with HF were older (mean age), more
frequently were female (%) and had diabetes (%), and had a higher heart
rate(mean) and a smaller LVEF (%) than patients without HF. It was observed tht
in 3rd group of CRP value had more in-hospital mortalities (%) &
complications(%).
CONCLUSION:
High C-reactive protein (CRP) levels have been associated with higher mortality
rate in patients with acute myocardial infarction (AMI)
Introduction
Coronary angiogram fails to show the active dynamic changes that occurred
within vary short period of ischaemic pain. CRP is the marker of that events
and could be used for targeting high risk group for urgent coronary interventions .
The aim of this study was to test the hypothesis that there is a relationship
between high CRP levels and complications progression during the first week of
hospitalization for AMI, and that high CRP level is associated with death and ln-
hospital mortality after AMI.
Methods
The patients were followed daily for MACE. CRP serum were obtained during
the 3rd/4th day of hospitalization. The criteria for AMI diagnosis were based on
fulfillment of at least 2 of the following: central chest pain lasting >30 minutes,
typical changes in serum enzymes (total creatine kinase [CK], CK-MB, Troponin
I), typical electrocardiogram changes with occurrence of pathological Q waves
and/or localized ST-T changes in at least 2 contiguous leads.[16]
CRP Measurement
In all patients, venous blood was drawn on the , third/4th day, for measurement
of CRP. . Venous blood samples were put in ice and centrifuged within 20
minutes at 4°C, and the plasma was stored at -20°C until assayed (storage time
<1 month). CRP was measured at the University of Padova by means of the
nephelometric method with particle-bound goat antihuman CRP (Beckman
Instruments, Inc, Fullerton, Calif) and expressed as mg/L. The lower limit of the
measurements range of the assay was 1 mg/L.[17]
Literature Review
Statistical Analysis
Statistical analysis was made using Systat 7.0 for Windows package (SPSS Inc,
Evanston, Ill) and JMP 4.0 for Windows (SAS Institute Inc, Cary, NC).
Results
Of the 50 patients included in the study, all had evidence of AMI on the basis of
the aforementioned criteria. The other 30 subjects of MI were used as a control .
The 2 groups were balanced for age and sex. Nitrates, antiplatelets, and
anticoagulants were more frequently used in the patients with AMI
CRP value
CRP Value
Sex
Age
Types of MI
Types of MI %
Ant (MI) 22(44%)
Inf ( MI) 18(36%)
NSTEMI 10(20%)
Clinical Presentations
30%
25%
20%
15%
Series1
10%
5%
0%
1 2 3
25%
0%
1
R/F:
Name of Disease N (%)
DM 22(80 %)
HTN 11( 40%)
Dyslipidaemia 12 (50%)
F/H 8(30%)
smoking 10 (38 %)
MACE
Name N (%)
Death 1(%)
LVF 20(%)
Cardiogenic shock 8 (%)
Arrhythmia(Brady/ Tachy ) 7(%)
Angina 8 (%)
Others 1 (%)
CRP and HF
Among the patients with AMI, 26 (%) showed clinical signs of HF (Killip class >1)
during the week of study, patients with HF were older, more frequently were
female and had diabetes, and had a higher heart rate and a smaller LVEF than
patients without HF. Time to presentation from onset of symptoms to coronary
care unit, and peak CK-MB did not differ between the 2 groups. Third-day CRP
data were considered for the analyses.
Discussion
The patients were divided into 3 l groups- Group I, Group II, Group-III on the
basis of CRP value . Among 50 patients, 16 patients were in Group I , 24 patients
were in Group II, 10 patients in Group III . Out of 50 patients 36 (%) were males
& 14 (%) were females having a male: female Ratio of. Avanzas et al (2004)
studied on similar sample size (55 patients). The mean age of the study
population was , 48.0 ± 9.8 years respectively ,which is quite similar to the
mean age group of the study by Ben-Hamda et al (2004). Symptoms severity
were noted in the form of CCS and NYHA . 25 (%) were in CCS II/III, and 32
out of 50 (%) presented with HF symptoms NYHA II-IV .
Among the important risk factors of CAD, 39% patients were smoker, 40%
patients were hypertensive, 80% patients were diabetic, 50% patients were
dyslipidaemic and 30% had family history of IHD . There was no difference
observed among four groups of patients in terms of risk factor profile. This is also
shown by Siddique et al (2003).
With incresing anginal pain ,ECG changes were more frequent in class III and IV
in which 62 % showed < 1 mm deprssion , and 24 % with > 1 mm . GUSTO IIb
study and TIMI III Registry of ACS patients showed presence of ST segment
deviation > 0.5 mm confers a worse prognosis .
To our knowledge, the present study is one of the first to highlight the
relationship between baseline CRP and occurrence of heart failure in the first few
days after AMI. Our data showed that CRP soon after admission was higher in
patients with AMI with clinical signs of HF compared to those in Killip class 1.
These data suggest that CRP may predict the risk of HF or may play a direct role
in augmenting microvascular inflammatory response after ischemic insult.[22] In
other words, the marked CRP rise in patients with AMI with HF at entry or in
those who developed HF in the subsequent days may not only be an
epiphenomenon but may represent a pathogenic process that leads to
myocardial damage and left ventricular dysfunction.[22, 23] Previous data indicate
that CRP may induce complement activation, and a pathogenetic role of
complement activation that may lead to maladaptive cardiac remodeling has
been described in acute ischemic left ventricular damage.[24, 25]
CRP and In hospital MACE :
Thus, CRP can be used as a new and even simpler tool for risk stratification and
CRP can be used as a marker to identify those subsets of patients with MI who
may need to undergo invasive strategies on priority basis .
Conclusions
CRP are simple, affordable and widely available test which can be easily done in
each and every patient admitted to hospital and CRP can be used as a new and
even simpler tool for risk stratification in MI . More over, coronary angiogram
fails to show the active dynamic changes that occurred within vary short
ischaemic pain periods . CRP is the marker of that events and could be used for
targeting high risk group for urgent coronary interventions .
Limitations of the Study
Several limitations of our study should be mentioned. We are aware that the cut-
off values for CRP prediction of events were based on a statistical test and not
on prospective data. Only longitudinal studies in larger groups will confirm the
validity of our cut-offs.
Address of Correspondence:
3. Fuster V, Moreno PR, Fayad ZA, Corti R, Badimon JJ. Atherothrombosis and
high-risk plaque: part I: evolving concepts. J Am Coll Cardiol 2005;46:937–954.
5. Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, Liu K, Shea S,
Szklo M, Bluemke DA, O’Leary DH, Tracy R, Watson K, Wong ND, Kronmal RA.
Coronary calcium as a predictor of coronary events in four racial or ethnic
groups. N Engl J Med 2008;358:1336–1345.
6. Rittersma SZ, van der Wal AC, Koch KT, Piek JJ, Henriques JP, Mulder KJ,
Ploegmakers JP, Meesterman M, de Winter RJ. Plaque instability frequently
occurs days or weeks before occlusive coronary thrombosis: a pathological
thrombectomy study in primary percutaneous coronary intervention. Circulation
2005;111:1160–1165.
7. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N
Engl J Med 2005;352:1685–1695.
9. Lee KW, Lip GY, Tayebjee M, Foster W, Blann AD. Circulating endothelial
cells, von Willebrand factor, interleukin-6, and prognosis in patients with acute
coronary syndromes. Blood 2005;105:526–532.
12. Keeley EC, Boura JA, Grines CL. Comparison of primary and facilitated
percutaneous coronary interventions for ST-elevation myocardial infarction:
quantitative review of randomised trials. Lancet 2006;367:579–588.
15. Armstrong PW, Granger CB, Adams PX, Hamm C, Holmes D Jr, O’Neill WW,
Todaro TG, Vahanian A, Van de Werf F. Pexelizumab for acute ST-elevation
myocardial infarction in patients undergoing primary percutaneous coronary
intervention: a randomized controlled trial. JAMA 2007;297:43–51.
17. Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F,
Avezum A, Goodman SG, Flather MD, Anderson FA Jr, Granger CB. Prediction
of risk of death and myocardial infarction in the six months after presentation
with acute coronary syndrome: prospective multinational observational study
(GRACE). BMJ 2006;333:1091–1094.
18. Le May MR, So DY, Dionne R, Glover CA, Froeschl MP, Wells GA, Davies
RF, Sherrard HL, Maloney J, Marquis JF, O’Brien ER, Trickett J, Poirier P, Ryan
SC,Ha A, Joseph PG, Labinaz M. A citywide protocol for primary PCI in ST-
segment elevation myocardial infarction. N Engl J Med 2008;358:231–240.
20. Lee KL, Woodlief LH, Topol EJ, Weaver WD, Betriu A, Col J, Simoons M,
Aylward P, Van de Werf F, Califf RM. Predictors of 30-day mortality in the
era of reperfusion for acute myocardial infarction. Results from an international
trial of 41,021 patients. GUSTO-I Investigators. Circulation 1995;91:1659–1668.
21. Morrow DA, Antman EM, Charlesworth A, Cairns R, Murphy SA, de Lemos
JA, Giugliano RP, McCabe CH, Braunwald E. TIMI risk score for ST-elevation
myocardial infarction: a convenient, bedside, clinical score for risk assessment at
presentation: an intravenous nPA for treatment of infarcting myocardium early
II trial substudy. Circulation 2000;102:2031–2037.
24. Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, Abramsky SJ,
Forman S, Ruzyllo W, Maggioni AP, White H, Sadowski Z, Carvalho AC,
Rankin JM, Renkin JP, Steg PG, Mascette AM, Sopko G, Pfisterer ME, Leor J,
Fridrich V, Mark DB, Knatterud GL. Coronary intervention for persistent occlusion
after myocardial infarction. N Engl J Med 2006;355:2395–2407.
25. Menon V, Pearte CA, Buller CE, Steg PG, Forman SA, White HD, Marino P,
Katritsis DG, Caramori P, Lasevitch R, Loboz-Grudzien K, Zurakowski A,
Lamas GA, Hochman JS. Lack of benefit from percutaneous intervention of
persistently occluded infarct arteries after the acute phase of myocardial
infarction is time independent: insights from Occluded Artery Trial. Eur Heart J
2008, in press.
26. Silber S, Albertsson P, Avile´s FF, Camici PG, Colombo A, Hamm C,
Jørgensen E, Marco J, Nordrehaug JE, Ruzyllo W, Urban P, Stone GW, Wijns
W; Task Force for Percutaneous Coronary Interventions of the European Society
of Cardiology. Guidelines for percutaneous coronary interventions. The Task
Force for Percutaneous Coronary Interventions of the European Society of
Cardiology. Eur Heart J 2005;26:804–647.
27. Canto JG, Every NR, Magid DJ, Rogers WJ, Malmgren JA, Frederick PD,
French WJ, Tiefenbrunn AJ, Misra VK, Kiefe CI, Barron HV. The volume of
primary angioplasty procedures and survival after acute myocardial infarction.
National Registry of Myocardial Infarction 2 Investigators. N Engl J Med 2000;
342:1573–1580.
29. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous
thrombolytic therapy for acute myocardial infarction: a quantitative review of 23
randomised trials. Lancet 2003;361:13–20.
30. Grines CL, Cox DA, Stone GW, Garcia E, Mattos LA, Giambartolomei A,
Brodie BR, Madonna O, Eijgelshoven M, Lansky AJ, O’Neill WW, Morice MC.
Coronary angioplasty with or without stent implantation for acute myocardial
infarction. Stent Primary Angioplasty in Myocardial Infarction Study Group.
N Engl J Med 1999;341:1949–1956.
31. Stone GW, Grines CL, Cox DA, Garcia E, Tcheng JE, Griffin JJ, Guagliumi
G, Stuckey T, Turco M, Carroll JD, Rutherford BD, Lansky AJ. Comparison of
angioplasty with stenting, with or without abciximab, in acute myocardial
infarction.N Engl J Med 2002;346:957–966.
33. Laarman GJ, Suttorp MJ, Dirksen MT, van Heerebeek L, Kiemeneij F,
Slagboom T, van der Wieken LR, Tijssen JG, Rensing BJ, Patterson M.
Paclitaxel-eluting versus uncoated stents in primary percutaneous coronary
intervention. N Engl J Med 2006;355:1105–1113.