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 el 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.
Highlights
A presence of cardiogenic shock remains serious limitations to achieve the rewarding clinical benefits in patients with a ST-segment elevation myocardial infarction (STEMI) regardless of the early prompt reperfusion by percutaneous coronary intervention (PCI) [1,2] Because progressive and excessive systemic as well as myocardial tissue-level mal-perfusion may play a crucial role in the pathogenesis of cardiogenic shock [3], we postulated adequate systemic and myocardial tissue-level reperfusion as the key issue to provide great advantages in patients treated with PCI for a cardiogenic shock complicating STEMI
We found a critical role of systemic inflammation in the mechanisms of cardio-renal syndrome linked with fatal clinical outcomes in patients with a STEMI [6]
Suzuki et al / Health 5 (2013) 1648-1653 outcomes in a STEMI, we investigated our hypothesis that a great exaggeration of systemic and coronary inflammation may be presented in the setting of a cardiogenic shock complicating STEMI, and those inflammations may play a role in the pathogenesis of mal-reperfusion in patients treated with PCI for a cardiogenic shock complicating STEMI
Summary
A presence of cardiogenic shock remains serious limitations to achieve the rewarding clinical benefits in patients with a ST-segment elevation myocardial infarction (STEMI) regardless of the early prompt reperfusion by percutaneous coronary intervention (PCI) [1,2] Because progressive and excessive systemic as well as myocardial tissue-level mal-perfusion may play a crucial role in the pathogenesis of cardiogenic shock [3], we postulated adequate systemic and myocardial tissue-level reperfusion as the key issue to provide great advantages in patients treated with PCI for a cardiogenic shock complicating STEMI.Reperfusion of a severely ischemic myocardium might result in lethal reperfusion injury, possibly arising from inflammatory reactions in patients with a STEMI [4,5]. We found a critical role of systemic inflammation in the mechanisms of cardio-renal syndrome linked with fatal clinical outcomes in patients with a STEMI [6]. In view of those relations of inflammation to clinical OPEN ACCESS. M. Suzuki et al / Health 5 (2013) 1648-1653 outcomes in a STEMI, we investigated our hypothesis that a great exaggeration of systemic and coronary inflammation may be presented in the setting of a cardiogenic shock complicating STEMI, and those inflammations may play a role in the pathogenesis of mal-reperfusion in patients treated with PCI for a cardiogenic shock complicating STEMI.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
