Abstract 5868: Intensive Coronary Inflammatory Storm and Myocardial Tissue-Level Reperfusion Injury in Patients With a Cardiogenic Shock Complicating ST-segment Elevation Myocardial Infarction
We investigated the characteristics of culprit coronary inflammation and the relation of those with myocardial tissue-level reperfusion in patients with a cardiogenic shock complicating anterior ST-segment elevation myocardial infarction (STEMI).
Methods The study subjects consisted of 14 consecutive Killip class IV patients (10 men, 69±12 years) and 18 well-matched baseline characteristics except Killip class (17 men, 64±9 years) with an early onset of a first anterior STEMI. When underwent emergent coronary angioplasty, aspirated culprit coronary thrombus and peripheral blood were sampled to measure coronary and systemic levels of high sensitive C-reactive protein (hs-CRP), interleukin (IL)-6, matrix metalloproteinase (MMP)-9 and angiotensin II. Myocardial tissue-level reperfusion injury was defined by the presence of both angiographic myocardial blush grade 0/1 and less than 50 % resolution of ST-segment elevation after angioplasty.
Results In-hospital mortality was 57 % with shock and 5 % without shock (p=0.003). Despite recanalization of culprit coronary lesions in all, myocardial tissue-level reperfusion injury was observed in 8 patients with shock and 3 without shock (57 vs. 17 %, p=0.026). Coronary levels of hs-CRP, IL-6 and angiotensin II except MMP-9 were extremely higher in patients with shock than without shock (hs-CRP, 9.2±6.9 vs. 1.7±2.1 mg/L, p=0.001, IL-6, 379±137 vs. 24±20 pg/mL, p=0.003, angiotensin II, 19±10 vs. 10±6 pg/mL, p=0.010, MMP-9, 176±128 vs. 132±144 ng/mL, p=0.406). Further coronary levels of angiotensin II showed a positive relation with hs-CRP (r=0.468, p=0.007) and IL-6 (r=0.757, p=0.001). Both IL-6 and angiotensin II revealed higher in coronary levels than in systemic levels. In a multivariate regression analysis, culprit coronary levels of angiotensin II were especially associated with myocardial tissue-level reperfusion injury (r=0.529, p=0.011).
Conclusions The presence of intensive culprit coronary inflammation may play a crucial role in the high incidence of myocardial tissue-level reperfusion injury in patients with a cardiogenic shock complicating STEMI.