Association between early postoperative coagulation activation and peri‐operative myocardial ischaemia in patients undergoing vascular surgery

Abstract

SummaryWe investigated the association of peri-operative myocardial ischaemia with activation of coagulation and endogenous fibrinolysis in patients undergoing vascular surgery. In 50 patients, continuous Holter monitoring was performed to assess peri-operative myocardial ischaemia and 12-lead electrocardiography was recorded preoperatively and 72 h postoperatively to assess myocardial infarction. Serial blood samples were drawn peri-operatively to determine the concentrations of fibrin monomers (for activation of coagulation), D-dimer (for endogenous fibrinolysis) and cardiac troponin T and I. Patients with myocardial ischaemia showed higher concentrations of fibrin monomers at 48 h, and higher concentrations of D-dimer preoperatively and at 24 and 48 h postoperatively. In patients with peri-operative myocardial ischaemia, strong positive correlations were observed between fibrin monomer and D-dimer concentrations at 15 min and 4 h postoperatively, and cardiac troponins at 15 min and at 4, 24, 48 and 72 h postoperatively. Early postoperative activation of coagulation and fibrinolysis is associated with peri-operative myocardial cell damage among patients who are at risk for, or have a history of, coronary artery disease plus peri-operative myocardial ischaemia. Episodes of peri-operative myocardial ischaemia occur in 18-74% of noncardiac surgery patients with, or at risk of, coronary artery disease [1]. Early postoperative myocardial ischaemia is the single most important predictor of adverse cardiac outcome and is associated with a nine-fold increase in the odds of having cardiac death, nonfatal myocardial infarction or unstable angina [1,2]. Myocardial ischaemia is induced by an increase in myocardial oxygen demand and ⁄ or by a decrease in supply. The latter may be due to activation of platelets and blood coagulation with subsequent formation of intracoronary fibrin and microthrombosis [3][4][5][6]. In nonsurgical patients with an unstable pattern of angina, a temporal relationship exists between systemic thrombin activity and ST segment shifts [7,8]. Because it is well known that major surgery, especially vascular, causes systemic coagulation activation [9][10][11][12][13][14][15][16][17][18], peri-operative hypercoagulation might be associated with peri-operative myocardial ischaemia and subsequent myocardial cell damage. To prevent ischaemic cardiac complications, early administration of antiplatelet therapy (aspirin) after coronary bypass surgery has been investigated, showing reduced rates of ischaemic events not only involving the heart, but also the brain, kidneys and gastrointestinal tract [3]. We designed the present study to investigate the peri-operative time course of serum levels of fibrin monomers and D-dimer, sensitive markers of coagulation and endogenous fibrinolysis, in patients undergoing noncardiac surgery. The

The implications of serum enzymes and coagulation activities in postinfarction myocardial

“…A high concentration of fibrinogen was associated with nonpatency infarct related coronary artery [35]. Although it is believed that early postoperative activation of coagulation and fibrinolysis is associated with perioperative myocardial cell damage [36], the findings of our study and of others [37] have led us to believe that fibrinogen has a weak link to the prediction of myocardial damage associated with cardiovascular events.…”

Infections of respiratory or abdominal origin in ICU patients: what are the differences?

“…Moreover, although the assumed Glasgow coma score is supposed to be used for the SOFA score, it is possible that neurological dysfunction may have been overestimated in sedated patients. The association between abdominal infections and coagulation failure may be related to the fact that more patients with abdominal infections had septic shock, which frequently provokes coagulation abnormalities [24], or by the fact that most of these patients were postoperative, as surgery may be associated with altered coagulation [25,26]. However, all these suggestions remain speculative as our study design does not allow us to determine the reasons underlying these associations.…”

The pathophysiology of peri‐operative myocardial infarction

“…Although, surgical post‐mortem studies have shown few thrombi in patients without evidence of plaque rupture, there is evidence to suggest that thrombolysis occurs in a number of patients before death [51]. In vascular surgical patients, a positive correlation between myocardial ischaemia and a marker of fibrinolysis has been shown as early as 15 min to 4 h postoperatively ( r = 0.59–0.78, p < 0.002) [52]. In patients without myocardial ischaemia it appears that markers of fibrinolysis may be evident later, possibly after 24 h postoperatively [53].…”