Myocardial injury and systemic fibrinolysis in patients undergoing repair of ruptured abdominal aortic aneurysm: a preliminary report

Abstract

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.