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. 2006 Dec 5;25(3):112–116. doi: 10.1002/clc.4960250306

Plasma C‐reactive protein predicts left ventricular remodeling and function after a first acute anterior wall myocardial infarction treated with coronary angioplasty: Comparison with brain natriuretic peptide

Itsuro Morishima 1,✉, Takahito Sone 1, Hideyuki Tsuboi 1, Junichiro Kondo 1, Hiroaki Mukawa 1, Hiroki Kamiya 2, Nobuyuki Hieda 3, Kenji Okumura 2
PMCID: PMC6654268  PMID: 11890369

Abstract

Background: C‐reactive protein (CRP) directly participates in the myocardial injury of acute myocardial infarction (MI). Although high plasma CRP levels in the acute phase strongly indicate a poor early clinical outcome of patients with MI, the impact of CRP levels on late left ventricular (LV) function and remodeling, which are closely associated with long‐term prognosis, remains unknown.

Hypothesis: Acute plasma CRP levels may predict late LV function and remodeling after MI.

Methods: We prospectively studied 12 consecutive patients with a first acute anterior MI recanalized by angioplasty. We measured plasma CRP levels on Days 0, 1, 2, 3, 4, and 7, and calculated the area under the curve (AUC). We also measured plasma brain natriuretic peptide (BNP) levels on Day 3 as the referential indicator of LV dysfunction and late LV remodeling. Late LV indices were independently assessed on a left ventriculogram obtained at 5.3 months to estimate the extent of LV remodeling.

Results: Plasma CRP reached its peak at Day 2.8 (8.68 ± 4.57 mg/dl). On linear regression analysis, the AUC of CRP (35.21 ± 19.33 mg/dl X day) correlated positively with BNP (316.5 ±418.6 pg/ml) (r = 0.646, p = 0.023). The AUC of CRP, peak CRP, and BNP correlated significantly with late LV indices. Among these, the AUC of CRP showed the best correlation with end‐diastolic volume index (r = 0.765, p = 0.004), end‐systolic volume index (r = 0.907, p < 0.001), and ejection fraction (r = −0.862, p<0.001).

Conclusions: Patients with high plasma CRP levels may be at risk for late LV dysfunction and remodeling; theoretically, their longterm prognosis may be poor. Measuring plasma CRP levels may provide valuable information for long‐term risk stratification after MI.

Keywords: acute myocardial infarction, brain natriuretic peptide, C‐reactive protein, left ventricular remodeling

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References

  • 1. Entman ML, Michael L, Rossen RD, Dreyer WJ, Anderson DC, Taylor AA, Smith CW: Inflammation in the course of early my‐ocardial ischemia. FASEB J 1991; 5: 2529–2537 [DOI] [PubMed] [Google Scholar]
  • 2. Neumann F‐J, Ott I, Gawaz M, Richardt G, Holzapfel H, Jochum M, Schömig A: Cardiac release of cytokines and inflammatory responses in acute myocardial infarction. Circulation 1995; 92: 748–755 [DOI] [PubMed] [Google Scholar]
  • 3. Gauldie J, Richards C, Northemann W, Fey G, Baumann H: IFN beta 2/BSF2/IL‐6 is the monocyte‐derived HSF that regulates receptor‐specific acute phase gene regulation in hepatocytes. Ann NY Acad Sci 1989; 557: 46–59 [PubMed] [Google Scholar]
  • 4. De Beer FC, Hind CRK, Fox KM, Allan RM, Maseri A, Pepys MB: Measurement of serum C‐reactive protein concentration in myocardial ischaemia and infarction. Br Heart J 1982; 47: 239–243 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Pietilä K, Harmoinen A, Pöyhönen L, Koskinen M, Heikkilä J, Ruosteenoja R: Intraveous streptokinase treatment and serum C‐reactive protein in patients with acute myocardial infarction. Br Heart J 1987; 58: 225–229 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6. Pietilä K, Harmoinen A, Teppo AM: Acute phase reaction, infarct size and in‐hospital morbidity in myocardial infarction patients treated with streptokinase or recombinant tissue type plasminogen activator. Ann Med 1991; 23: 529–535 [DOI] [PubMed] [Google Scholar]
  • 7. Pietilä K, Harmoinen A, Hermens W, Simoons ML, van de Werf F, Verstraete M: Serum C‐reactive protein and infarct size in myocardial infarct patients with a closed versus an open infarct‐related coronary artery after thrombolytic therapy. Eur Heart J 1993; 14: 915–919 [DOI] [PubMed] [Google Scholar]
  • 8. Ueda S, Ikeda U, Yamamoto K, Takahashi M, Nishinaga M, Nago N, Shimada K: C‐reactive protein as a predictor of cardiac rupture after acute myocardial infarction. Am Heart J 1996; 131: 857–860 [DOI] [PubMed] [Google Scholar]
  • 9. Griselli M, Herbert J, Hutchinson WL, Taylor KM, Sohail M, Krausz T, Pepys MB: C‐reactive protein and complement are important mediators of tissue damage in acute myocardial infarction. J Exp Med 1999; 190: 1733–1739 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Lagrand WK, Niessen HW, Wolbink GJ, Jaspars LH, Visser CA, Verheugt FW, Meijer CJ, Hack CE: C‐reactive protein colocalizes with complement in human hearts during acute myocardial infarction. Circulation 1997; 95: 97–103 [DOI] [PubMed] [Google Scholar]
  • 11. Pietilä KO, Harmoinen AP, Jokiniitty J, Pasternack AI: Serum C‐reactive protein concentration in acute myocardial infarction and its relationship to mortality during 24 months of follow‐up in patients under thrombolytic treatment. Eur Heart J 1996; 17: 1345–1349 [DOI] [PubMed] [Google Scholar]
  • 12. Tommasi S, Carluccio E, Bentivoglio M, Buccolieri M, Mariotti M, Politano M, Corea L: C‐reactive protein as a marker for cardiac ischemic events in the year after a first, uncomplicated myocardial infarction. Am J Cardiol 1999; 83: 1595–1599 [DOI] [PubMed] [Google Scholar]
  • 13. Nikfardjam M, Müllner M, Schreiber W, Oschatz E, Exner M, Domanovits H, Laggner AN, Huber K: The association between C‐reactive protein on admission and mortality in patients with acute myocardial infarction. J Intern Med 2000; 247: 341–345 [DOI] [PubMed] [Google Scholar]
  • 14. Pfeffer MA, Braunwald E: Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation 1990; 81: 1161–1172 [DOI] [PubMed] [Google Scholar]
  • 15. St John Sutton M, Pfeffer MA, Moye L, Plappert T, Rouleau JL, Lamas G, Rouleau J, Parker JO, Arnold MO, Sussex B, Braunwald E: Cardiovascular death and left ventricular remodeling two years after myocardial infarction: Baseline predictors and impact of long‐term use of captopril: Information from the Survival and Ventricular Enlargement (SAVE) trial. Circulation 1997; 96: 3294–3299 [DOI] [PubMed] [Google Scholar]
  • 16. Sutton MG, Sharpe N: Left ventricular remodeling after myocardial infarction: Pathophysiology and therapy. Circulation 2000; 101: 2981–2988 [DOI] [PubMed] [Google Scholar]
  • 17. Motwani JG, McAlpine H, Kennedy N, Struthers AD: Plasma brain natriuretic peptide as an indicator for angiotensin‐converting‐enzyme inhibition after myocardial infarction. Lancet 1993; 341: 1109–1113 [DOI] [PubMed] [Google Scholar]
  • 18. Sumida H, Yasue H, Yoshimura M, Okumura K, Ogawa H, Kugiyama K, Matsuyama K, Kikuta K, Morita E, Nakao K: Comparison of secretion pattern between A‐type and B‐type natriuretic peptides in patients with old myocardial infarction. J Am Coll Cardiol 1995; 25: 1105–1110 [DOI] [PubMed] [Google Scholar]
  • 19. Omland T, Aakvaag A, Bonarjee VV, Caidahl K, Lie RT, Nilsen DW, Sundsfjord JA, Dickstein K: Plasma brain natriuretic peptide as an indicator of left ventricular systolic function and long‐term survival after acute myocardial infarction. Comparison with plasma atrial natriuretic peptide and N‐terminal proatrial natriuretic pep‐tide. Circulation 1996; 93: 1963–1969 [DOI] [PubMed] [Google Scholar]
  • 20. Darbar D, Davidson NC, Gillespie N, Choy AM, Lang CC, Shyr Y, McNeill GP, Pringle TH, Struthers AD: Diagnostic value of B‐type natriuretic peptide concentrations in patients with acute myocardial infarction. Am J Cardiol 1996; 78: 284–287 [DOI] [PubMed] [Google Scholar]
  • 21. Richards AM, Nicholls MG, Yandle TG, Ikram H, Espiner EA, Turner JG, Buttimore RC, Lainchbury JG, Elliott JM, Frampton C, Crozier IG, Smyth DW: Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction. The Christchurch Cardioendocrine Research Group. Heart 1999; 81: 114–120 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22. Nagaya N, Nishikimi T, Goto Y, Miyao Y, Kobayashi Y, Morii I, Daikoku S, Matsumoto T, Miyazaki S, Matsuoka H, Takishita S, Kangawa K, Matsuo H, Nonogi H: Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J 1998; 135: 21–28 [DOI] [PubMed] [Google Scholar]
  • 23. Nagaya N, Goto Y, Nishikimi T, Uematsu M, Miyao Y, Kobayashi Y, Miyazaki S, Hamada S, Kuribayashi S, Takamiya M, Matsuo H, Kangawa K, Nonogi H: Sustained elevation of plasma brain natriuretic peptide levels associated with progressive ventricular remodeling after acute myocardial infarction. Clin Sci 1999; 96: 129–136 [PubMed] [Google Scholar]
  • 24. Tsuji T, Imagawa K, Masuda H, Haraikawa M, Shibata K, Kono M, Inouye K, Uchida K: Stabilization of human brain natriuretic pep‐tide in blood samples (letter). Clin Chem 1994; 40: 672–673 [PubMed] [Google Scholar]
  • 25. Liuzzo G, Biasucci LM, Gallimore JR, Caligiuri G, Buffon A, Rebuzzi AG, Pepys MB, Maseri A: Enhanced inflammatory response in patients with preinfarction unstable angina. J Am Coll Cardiol 1999; 34: 1696–1703 [DOI] [PubMed] [Google Scholar]
  • 26. Pfeffer MA: Left ventricular remodeling after acute myocardial infarction. Ann Rev Med 1995; 46: 455–466 [DOI] [PubMed] [Google Scholar]

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