TY - JOUR
T1 - Selenoprotein P in Myocardial Infarction with Cardiogenic Shock
AU - Büttner, Petra
AU - Obradovic, Danilo
AU - Wunderlich, Sebastian
AU - Feistritzer, Hans-Josef
AU - Holzwirth, Erik
AU - Lauten, Philipp
AU - Fuernau, Georg
AU - de Waha-Thiele, Suzanne
AU - Desch, Steffen
AU - Thiele, Holger
PY - 2019/3/1
Y1 - 2019/3/1
N2 - BACKGROUND:
Reperfusion strategies in acute myocardial infarction (AMI) may result in ischemia reperfusion injury characterized by increased oxidative stress, inflammation and ultimately death of myocardial tissue which may be of particular importance in infarct-related cardiogenic shock (CS). Many anti-oxidative and immune regulatory processes depend on selenium which in large proportions is bound to circulating selenoprotein P (SelP). Individual SelP patterns may therefore be associated with inflammatory response and possibly mortality in patients with CS post AMI.
METHODS:
In the randomized Intra-Aortic Balloon Pump in cardiogenic Shock II (IABP-SHOCK II)-trial, 600 patients with CS complicating AMI were assigned to therapy with or without IABP. In a predefined biomarker substudy of 147 patients, we analyzed SelP levels 1 and 3 days following randomization. Samples were compared to healthy controls and associations with the unspecific inflammatory marker C-reactive protein (CRP) were analyzed.
RESULTS:
Compared with controls SelP levels in patients with infarct-related CS were markedly higher (2.7-fold at day 1 and 5.7-fold at day 3 following AMI, all p < 0.001). Thirty-day mortality was significantly higher in patients with SelP levels above the 75th percentile at day 3 following AMI (26% vs. 46%, p = 0.045). SelP was significantly proportionally correlated with CRP 1 (R = 0.762, p < 0.0001) and 3 days (R = 0.777 p < 0.0001) following AMI.
CONCLUSIONS:
SelP levels are significantly increased post AMI with CS. Higher SelP levels are associated with increased CRP levels indicative for inflammatory processes. Future studies should focus on the characterization of SelP profiles following AMI and the identification of pathomechanisms affected by SelP.
AB - BACKGROUND:
Reperfusion strategies in acute myocardial infarction (AMI) may result in ischemia reperfusion injury characterized by increased oxidative stress, inflammation and ultimately death of myocardial tissue which may be of particular importance in infarct-related cardiogenic shock (CS). Many anti-oxidative and immune regulatory processes depend on selenium which in large proportions is bound to circulating selenoprotein P (SelP). Individual SelP patterns may therefore be associated with inflammatory response and possibly mortality in patients with CS post AMI.
METHODS:
In the randomized Intra-Aortic Balloon Pump in cardiogenic Shock II (IABP-SHOCK II)-trial, 600 patients with CS complicating AMI were assigned to therapy with or without IABP. In a predefined biomarker substudy of 147 patients, we analyzed SelP levels 1 and 3 days following randomization. Samples were compared to healthy controls and associations with the unspecific inflammatory marker C-reactive protein (CRP) were analyzed.
RESULTS:
Compared with controls SelP levels in patients with infarct-related CS were markedly higher (2.7-fold at day 1 and 5.7-fold at day 3 following AMI, all p < 0.001). Thirty-day mortality was significantly higher in patients with SelP levels above the 75th percentile at day 3 following AMI (26% vs. 46%, p = 0.045). SelP was significantly proportionally correlated with CRP 1 (R = 0.762, p < 0.0001) and 3 days (R = 0.777 p < 0.0001) following AMI.
CONCLUSIONS:
SelP levels are significantly increased post AMI with CS. Higher SelP levels are associated with increased CRP levels indicative for inflammatory processes. Future studies should focus on the characterization of SelP profiles following AMI and the identification of pathomechanisms affected by SelP.
UR - https://www.ncbi.nlm.nih.gov/pubmed/30889044
UR - http://www.mendeley.com/research/selenoprotein-p-myocardial-infarction-cardiogenic-shock
U2 - 10.1097/SHK.0000000000001342
DO - 10.1097/SHK.0000000000001342
M3 - Journal articles
SN - 1073-2322
SP - 1
JO - Shock
JF - Shock
ER -