Clinical evidence of exaggerated inflammation in patients with a cardiogenic shock complicating ST-segment elevation myocardial infarction
- 1 Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;
- 2 Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;
- 3 Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;
- 4 Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;
- 5 Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;
- 6 Department of Cardiology, Ehime Prefectural Central Hospital, Ehime, Japan
- 7 Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;
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 angiogra phic 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-lev el reperfusion (p = 0.012). Concl usions: The exaggerated systemic and coronary inflammation, presumably associated with myocardial mal-reperfusion, was presented in patients with a cardiogenic shock complicating first anterior STEMI.
- 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
- 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.
- 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
- 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
- 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
- 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.
- 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
- 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
- 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
- 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