TY - JOUR
T1 - Myocardial injury and systemic fibrinolysis in patients undergoing repair of ruptured abdominal aortic aneurysm: a preliminary report
AU - Haggart, Paul
AU - Adam, Donald
AU - Ludman, Peter
AU - Bradbury, Andrew
PY - 2001/6/1
Y1 - 2001/6/1
N2 - Background: ruptured abdominal aortic aneurysm (AAA) is associated with inhibition of systemic fibrinolysis. Hypofibrinolysis is a risk-factor for ischaemic myocardial injury, one of the commonest complications of ruptured AAA repair. Cardiac troponin I (cTnI) is one of the most sensitive and specific marker of myocardial injury currently available.
Objective: to examine, for the first time, the relationship between fibrinolytic activity and myocardial injury in patients operated for ruptured AAA.
Methods: twenty patients (18 men and 2 women of median age 74, range 65-86 years) undergoing repair of ruptured AAA were prospectively studied. Plasma tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) activity were measured pre-operatively, immediately before and five minutes following aortic clamp release. Serum cTnI was measured pre-operatively, 6 and 24 h following clamp release.
Results: cTnI was detectable at one or more sample points in 13 (65%) patients, and in 7 out of 8 patients who suffered major cardiac complications. There was a significant negative correlation between pre-operative t-PA activity and cTnI before operation (r = -0.55, p = 0.01) and 6 h (r = -0.51, p = 0.02) after clamp release. There was a significant positive correlation between pre-operative PAI activity and cTnI before operation (r = +0.50, p = 0.03), 6 h (r = +0.47, p = 0.04) and 24 h (r = +0.50, p = 0.03) after clamp release. There was no correlation between pre- and intra-operative hypotension or blood transfusion requirement and cTnI release.
Conclusions: hypofibrinolysis during ruptured AAA repair is associated with the development of peri-operative myocardial injury. The causal mechanisms underlying this state are not clear but treatment of this prothrombotic/hypofibrinolytic diathesis may help to limit myocardial cell necrosis.
AB - Background: ruptured abdominal aortic aneurysm (AAA) is associated with inhibition of systemic fibrinolysis. Hypofibrinolysis is a risk-factor for ischaemic myocardial injury, one of the commonest complications of ruptured AAA repair. Cardiac troponin I (cTnI) is one of the most sensitive and specific marker of myocardial injury currently available.
Objective: to examine, for the first time, the relationship between fibrinolytic activity and myocardial injury in patients operated for ruptured AAA.
Methods: twenty patients (18 men and 2 women of median age 74, range 65-86 years) undergoing repair of ruptured AAA were prospectively studied. Plasma tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) activity were measured pre-operatively, immediately before and five minutes following aortic clamp release. Serum cTnI was measured pre-operatively, 6 and 24 h following clamp release.
Results: cTnI was detectable at one or more sample points in 13 (65%) patients, and in 7 out of 8 patients who suffered major cardiac complications. There was a significant negative correlation between pre-operative t-PA activity and cTnI before operation (r = -0.55, p = 0.01) and 6 h (r = -0.51, p = 0.02) after clamp release. There was a significant positive correlation between pre-operative PAI activity and cTnI before operation (r = +0.50, p = 0.03), 6 h (r = +0.47, p = 0.04) and 24 h (r = +0.50, p = 0.03) after clamp release. There was no correlation between pre- and intra-operative hypotension or blood transfusion requirement and cTnI release.
Conclusions: hypofibrinolysis during ruptured AAA repair is associated with the development of peri-operative myocardial injury. The causal mechanisms underlying this state are not clear but treatment of this prothrombotic/hypofibrinolytic diathesis may help to limit myocardial cell necrosis.
KW - troponin
KW - post-operative myocardial infarction
KW - aortic allaneurysm
UR - http://www.scopus.com/inward/record.url?scp=0034947213&partnerID=8YFLogxK
U2 - 10.1053/ejvs.2001.1367
DO - 10.1053/ejvs.2001.1367
M3 - Article
VL - 21
SP - 529
EP - 534
JO - European Journal of Vascular Surgery
JF - European Journal of Vascular Surgery
IS - 6
ER -