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

Makoto Suzuki, Itaru Takamisawa, Atsushi Seki, Tetsuya Tobaru, Fumiyasu Seike, Hideaki Shimizu, Morimasa Takayama

Department of Cardiology, Ehime Prefectural Central Hospital, Ehime, Japan.
Department of Cardiovascular Medicine, Sakakibara Heart Institute, Tokyo, Japan;.

DOI: 10.4236/health.2013.510222                

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.

Keywords

Cardiogenic Shock; Myocardial Infarction; Inflammation; Reperfusion; Acidosis

Conflicts of Interest

The authors declare no conflicts of interest.

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