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2007, Number S4

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Arch Cardiol Mex 2007; 77 (S4)

Inflammation and plaque instability

Malpartida F, Vivancos R, Urbano C, Mora J

Language: Spanish
References: 30
Page: 16-22
PDF size: 179.07 Kb.


ABSTRACT

The mechanisms that regulate the stability of the atheroma plaque are a new focus of interest to understand the pathophysiology of acute coronary syndromes (ACS) and its therapy. Up to 75% of ACS are clinical expression of an unstable plaque rupture. The identification of unstable or so called vulnerable plaque (VP) became an interesting target, since they are the substrate of eventual future events. The VP determinant factors are: the size and consistence of lipid core, thickness of fibrous cap around this core, and the balance inflammation- reparation inside this cap. Inflammation plays a starring role in every single atherosclerosis stage. High sensitivity C - reactive protein (hs-CRP) is one of the most used markers of inflammation. We determined hs-CRP in 104 patients. The elevation of this marker was 5.85 mg/L in stable angina, 19.92 in non ST elevation ACS, and 50.41 mg/L in whom that presented ACS with ST elevation. (p ‹ 0.01). The majority of coronary occlusion occurs in previously non-significant (‹ 70%) angiographic stenosis. Therefore, the current challenge is to identify and treat VP using whether invasive or non-invasive methods. This lead to a new concept: the “vulnerable patient”. Using these new diagnostic techniques, along with the information obtained from clinical trials in course, we should be able to prevent future coronary events.


REFERENCES

  1. Fuster V, Fayad ZA, Badimon JJ: Acute coronary syndromes: Biology. Lancet 1999; 353 Suppl. 2: S115-S119.

  2. Davies MJ: The pathophysiology of acute coronary syndromes. Heart 2000; 83: 361-366.

  3. Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT: Macrophage infiltration in acute coronary syndromes: implications for plaque rupture. Circulation 1994; 90: 775-778.

  4. Falk E, Shah PK, Fuster V: Coronary plaque disruption. Circulation 1995; 92: 657-671.

  5. Muller JE, Abela GS, Nesto RW, Tofler GH: Triggers, acute risk factors and vulnerable plaques: The lexicon of a new frontier. JACC 1994; 23: 809-813.

  6. Virmani R, Burke AP, Farb A. Plaque rupture and plaque erosion. Thromb Haemost 1999; 82 Suppl. 1: 1-3.

  7. Fuster V, Badimon L, Badimon JJ, Chesebro JH: The pathogenesis of coronary artery disease and the acute coronary syndromes (2). NEJM 1992; 326: 310-318.

  8. Urbano C, Arias A, Esteban A, et al: Comparación de los niveles de proteína C reactiva en pacientes con angina estable e inestable. Rev Esp Cardiol 2004; 57 Supl 2: 70.

  9. Hamm CW: Developing role of biomarkers. World Congress of Cardiology 2006. Barcelona, 2-6 Septiembre.

  10. Koenig W: Lipoprotein-associated phospholipase A2: an overview of a novel cardiovascular risk marker. World Congress of Cardiology 2006. Barcelona, 2-6 Septiembre.

  11. Lupi E, Chuquiure E, Gaspar J, Férez SM: De la placa vulnerable solitaria, a la coronariopatía de múltiples vasos. De sus fundamentos, a las implicaciones terapéuticas modernas. Una realidad clínica en el espectro de los SICA. Arch Cardiol Mex 2006; 76 Supl.1: S6-S34.

  12. Ambrose JA, Tannenbaum MA, Applegate RJ, et al: Angiographic progression of coronary artery disease and the development of myocardial infarction. JACC 1988; 12: 56-62.

  13. Little WC, Constantinescu M, Applegate RJ, et al: Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? Circulation 1988; 78: 1157-1166.

  14. Nobuyosi M, Tanaka M, Nosaka H, et al: Progression of coronary atherosclerosis: is coronary spasm related to progression? JACC 1991; 18: 904-910.

  15. Giroud D, Li JM, Urban P, et al: Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography. Am J Cardiol 1992; 69: 729-732.

  16. Waters D, Lesperánce J, Francetich M, et al: A controlled clinical trial to assess the effect of a calcium channel blocker on the progression of coronary atherosclerosis. Circulation 1990; 82: 1940-1953.

  17. Leber AW, Knez A, von Ziegler F, et al: Quantification of obstructive and nonobstructive coronary lesions by 64-slice computed tomography: a comparative study with quantitative coronary angiography and intravascular ultrasound. JACC 2005; 46: 147-154.

  18. Blank A, Alexandrovicz G, Muchnik L, et al: Miniature self-contained NMR probe for clinical applications. Magn Reson Med 2005; 54: 105-112.

  19. Ohtani T, Ueda Y, Mizote I, et al: Number of yellow plaques detected in a coronary artery is associated with future risk of acute coronary syndrome. Detection of vulnerable patients by angioscopy. JACC 2006; 47: 2194-2200.

  20. Libby P, et al: Act local, act global: inflammation and the multiplicity of “vulnerable” coronary plaques. JACC 2005; 45: 1600-1602.

  21. Nair A, Kuban BD, Tuzcu EM, Schoenhagen P, Nissen SE, Vince DG: Coronary plaque classification with intravascular ultrasound radiofrequency data analysis. Circulation 2002; 106: 2200-2206.

  22. Murahige A, Hiro T, Fujii T, et al: Detection of lipid-laden atherosclerotic plaque by wavelet analysis of radiofrequency intravascular ultrasound signals: in vitro validation and preliminary in vivo application. JACC 2005; 45: 1954-1960.

  23. Kawasaki M, Sano K, Okubo M, et al: Volumetric quantitative analysis of tissue characteristics of coronary plaques after statin therapy using three-dimensional integrated backscatter intravascular ultrasound. JACC 2005; 45: 1946-1953.

  24. Verheye S, van Langenhove G, van Es GA, Serruys P: The percutaneous assessment of regional and acute coronary hot unstable plaques by thermographic evaluation (PARACHUTE) study: a prospective reproducibility and prognostic clinical study using thermography to predict future ischemic cardiac events. Int J Cardiovasc Intervent 2004; 6: 69-75.

  25. Schaar JA, Regar E, Mastik F, et al: Incidence of high-strain patterns in human coronary arteries: assessment with three-dimensional intravascular palpography and correlation with clinical presentation. Circulation 2004; 109: 2716-2719.

  26. Wilensky RL, Song HK, Ferrari VA: Role of magnetic resonance and intravascular magnetic resonance in the detection of vulnerable plaques. JACC 2006; 47 Suppl C: C48-C56.

  27. Mukai T, Nohara R, Ogawa M, et al: A catheter-based radiation detector for endovascular detection of atheromatous plaques. Eur J Nucl Med Mol Imaging 2004; 31: 1299-1303.

  28. Caplan JD, Waxman S, Nesto RW, Muller JE: Near-infrared spectroscopy for the detection of vulnerable coronary artery plaques. JACC 2006; 47 Suppl C: C92-C96.

  29. Wilson PW, D’Agostino RB, Levy D, et al: Prediction of coronary heart disease using risk factor categories. Circulation 1998; 97: 1837-1847.

  30. Braunwald E: Epilogue: what do clinicians expect from imagers? JACC 2006; 47 Suppl C: C101-103.




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