Share This Article:

Clinical evidence of exaggerated inflammation in patients with a cardiogenic shock complicating ST-segment elevation myocardial infarction

Abstract Full-Text HTML Download Download as PDF (Size:151KB) PP. 1648-1653
DOI: 10.4236/health.2013.510222    2,734 Downloads   3,692 Views   Citations

ABSTRACT

We characterized the degree of systemic and coronary inflammation and the impact of those on clinical state in patients with a cardiogenic shock complicating first anterior ST-segment elevation myocardial infarction (STEMI). Methods: We recruited 14 consecutive patients with cardiogenic shock (10 men, 69 ± 12 years) and 18 well-matched baseline characteristics without shock (17 men, 64 ± 9 years) undergoing percutaneous coronary intervention (PCI) for an early phase of a first anterior STEMI in whom plasma level of cardiac enzyme was less elevated. We measured systemic and coronary levels of C-reactive protein, interleukin-6, and angiotensin II, and evaluated the relation of those to myocardial tissue-level reperfusion using both angiographic myocardial blush grade from 0 to 3, with the highest grade indicating normal myocardial perfusion, and a resolution of the sum of ST-segment elevation in 12-lead electrocardiogram. Results: In-hospital mortality was 57% in patients with cardiogenic shock and 6% without shock (p = 0.005). Coronary levels of C-reactive protein (9.2 ± 6.9 vs. 1.7 ± 2.1 mg/L, p = 0.001), interleukin-6 (379 ± 137 vs. 24 ± 20 pg/mL, p = 0.003), and angiotensin II (19 ± 10 vs. 10 ± 6 pg/mL, p = 0.010) were extremely higher in patients with shock than without shock. Interleukin-6 and angiotensin II, but not C-reactive protein, revealed higher in coronary levels than in systemic levels. The presence of both myocardial blush grade < 3 and ST-segment resolution < 50%, indicating failed myocardial tissue-level reperfusion, was found in 8 patients with shock and 3 without shock (57% vs. 17%, p = 0.026). A multivariate regression analysis showed culprit coronary levels of angiotensin II as a special association with failed myocardial tissue-level reperfusion (p = 0.012). Conclusions: The exaggerated systemic and coronary inflammation, presumably associated with myocardial mal-reperfusion, was presented in patients with a cardiogenic shock complicating first anterior STEMI.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

Suzuki, M. , Takamisawa, I. , Seki, A. , Tobaru, T. , Seike, F. , Shimizu, H. and Takayama, M. (2013) Clinical evidence of exaggerated inflammation in patients with a cardiogenic shock complicating ST-segment elevation myocardial infarction. Health, 5, 1648-1653. doi: 10.4236/health.2013.510222.

References

[1] Babaev, A., Frederick, P.D., Pasta, D.J., Every, N., Sichrovsky, T., Hochman, J.S. and NRMI Investigators. (2005) Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA, 294, 448-454.
http://dx.doi.org/10.1001/jama.294.4.448
[2] Suzuki, M., Fujita, S., Seike, F., Enomoto, D. and Honda, K. (2013) Wide QRS Complex and myocardial tissue-level reperfusion in cardiogenic shock complicating ST-segment elevation myocardial infarction. Gazzetta Medica Italiana, 172, 137-143.
[3] Reynold, H.R. and Hochman, J.S. (2008) Cardiogenic shock: Current concepts and improving outcomes. Circulation, 117, 686-697.
http://dx.doi.org/10.1161/CIRCULATIONAHA.106.613596
[4] Suzuki, M., Sakaue, T., Tanaka, M., Hirose, E., Saeki, H., Matsunaka, T., Hiramatsu, S. and Kazatani, Y. (2006) Association between right bundle branch block and impaired myocardial tissue-level reperfusion in patients with acute myocardial infarction. Journal of the American College of Cardiology, 47, 2122-2124.
http://dx.doi.org/10.1016/j.jacc.2006.02.034
[5] Suzuki, M., Shimizu, H., Miyoshi, A., Takagi, Y., Sato, S. and Nakamura, Y. (2011) Association of coronary inflammation and angiotensin II with impaired microvascular reperfusion in patients with ST-segment elevation myocardial infarction. International Journal of Cardiology, 146, 254-256.
http://dx.doi.org/10.1016/j.ijcard.2010.10.067
[6] Suzuki, M., Seike, F., Miyoshi, A., Shimizu, H., Takagi, Y., Sato, S. and Honda, K. (2013) Critical role of systemic inflammation in patients with ST-segment elevation myocardial infarction complicated with renal dysfunction. International Journal of Cardiology, Epub ahead of print.
[7] Suzuki, M., Inaba, S., Nagai, T., Tatsuno, H. and Kazatani, Y. (2003) Relation of C-reactive protein and interleukin-6 to culprit coronary artery plaque size in patients with acute myocardial infarction. American Journal of Cardiology, 91, 331-333.
http://dx.doi.org/10.1016/S0002-9149(02)03162-4
[8] Suzuki, M., Saito, M., Nagai, T., Saeki, H. and Kazatani, Y. (2006) Systemic versus coronary levels of inflammation in acute coronary syndromes. Angiology, 57, 459-463.
http://dx.doi.org/10.1177/0003319706290742
[9] The TIMI Study Group (1985) The Thrombolysis in Myocardial Infarction (TIMI) trial: Phase I findings. The New England Journal of Medicine, 312, 932-936.
http://dx.doi.org/10.1056/NEJM198504043121437
[10] Rentrop, K.P., Cohen, M., Blanke, H. and Phillips, R.A. (1985) Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. Journal of the American College of Cardiology, 5, 587-592.
http://dx.doi.org/10.1016/S0735-1097(85)80380-6
[11] Poli, A., Fetiveau, R., Vandoni, P., del Rosso, G., D’Urbano, M., Seveso, G., Cafiero, F. and De Servi, S. (2002) Integrated analysis of myocardial blush and ST-segment elevation recovery after successful primary angioplasty. Real-time grading of microvascular reperfusion and prediction of early and late recovery of left ventricular function. Circulation, 106, 313-318.
http://dx.doi.org/10.1161/01.CIR.0000022691.71708.94
[12] Suzuki, M. (2012) Acute coronary syndromes as autoinflammatory disorders. Current Pharmaceutical Design, 18, 4370-4384.
http://dx.doi.org/10.2174/138161212802481228
[13] Trevani, A.S., Andonegui, G., Giordano, M., Lopez, D.H., Gamberale, R., Minucchi, F. and Geffner, J.R. (1999) Extracellular acidification induces human neutrophil activetion. Journal of Immunology, 162, 4849-4857.
[14] Carbonell, T., Ródenas, J., Alfaro, V., Mitjavila, M.T. and Palacios, L. (2002) Extracellular pH affects inflammatory cell production of superoxide and nitric oxide. Journal of Physiology and Biochemistry, 58, 115-120.
http://dx.doi.org/10.1007/BF03179847
[15] Yellon, D.M. and Hausenloy, D.J. (2007) Myocardial reperfusion injury. The New England Journal of Medicine, 357, 1121-1135.
http://dx.doi.org/10.1056/NEJMra071667
[16] Zhang, Q., Raoof, M., Chen, Y., Sumi, Y., Sursal, T., Junger, W., Brohi, K., Itagaki, K. and Hauser, C.J. (2010) Circulating mitochondrial DAMPs cause inflammatory response to injury. Nature, 464, 104-107.
http://dx.doi.org/10.1038/nature08780
[17] Thiele, H., Sick, P., Boudriot, E., Diederich, K.W., Hambrecht, R., Niebauer, J. and Schuler, G. (2005) Randomized comparison of intra-aortic balloon support with a percutaneous left ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock. European Heart Journal, 26, 1276-1283. http://dx.doi.org/10.1093/eurheartj/ehi161
[18] Thiele, H., Zeymer, U., Neumann, F.J., Ferenc, M., Olbrich, H.G., Hausleiter, J., Richardt, G., Hennersdorf, M., Empen, K., Fuernau, G., Desch, S., Eitel, I., Hambrecht, R., Fuhrmann, J., Bohm, M., Ebelt, H., Schneider, S., Schuler, G., Werdan, K. and IABP-SHOCK II Trial Investigators (2012) Intraaortic balloon support for myocardial infarction with cardiogenic shock. The New England Journal of Medicine, 367, 1287-1296.
http://dx.doi.org/10.1056/NEJMoa1208410
[19] Adrogue, H.J. and Madias, N.E. (1998) Management of life-threatening acid-base disorders. First of two parts. The New England Journal of Medicine, 338, 26-34.
http://dx.doi.org/10.1056/NEJM199801013380106

  
comments powered by Disqus

Copyright © 2018 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.