SummaryWe investigated the use of measurements of serum concentrations of the cardiac proteins troponins I and T as biochemical markers of myocardial cell damage in 80 patients undergoing vascular or major orthopaedic surgery. Holter electrocardiographic monitoring was carried out before surgery and for 3 days after surgery. Blood samples for troponins I and T and creatine kinase-MB isoenzyme were taken on each of these 4 days. Outcome was assessed at 3 months using a patient questionnaire, general practitioner follow-up and case notes review. Silent postoperative myocardial ischaemia was detected in 21 patients; increases in troponins I and T and creatine kinase-MB occurred in four, six and 17 of these patients, respectively. Eight patients suffered major postoperative complications (cardiac death, myocardial ischaemia, congestive cardiac failure, unstable angina and cerebrovascular accident) and 21 minor complications (poorly controlled hypertension needing increased or new additional treatment, palpitations, increased tiredness or shortness of breath in the absence of known respiratory disease). There were no associations between postoperative ischaemia and cardiac protein concentrations. The relative odds for the associations of major adverse outcome at 3 months after surgery and postoperative ischaemia or increased serum concentrations of the three proteins were 5.39 [95% confidence intervals 1.16±27.67] for postoperative ischaemia; 5.64 [1.07±31.00] for creatine kinase-MB isoenzyme; 17.00 [2.20±116.54] for troponin T and 13.20 [1.12±135.00] for troponin I. We found troponin T to be the only prospective marker for both major and minor cardiovascular complications (relative odds 10.65 [1.26±252.88]).
SummaryTwo hundred and seventy-five non-cardiac surgical patients were recruited to determine risk factors associated with the development of postoperative cardiovascular complications during the first year after surgery. Patients underwent ambulatory electrocardiography pre-and postoperatively. There were 34 adverse events over the whole study period. Twenty-four occurred within 6 months and the remaining 10 occurred between 6 and 12 months postoperatively. Silent myocardial ischaemia was associated with adverse outcome over both the first 6 months [OR 4.44 . None of these was a useful predictor of long-term outcome (between 6 and 12 months postsurgery). These results are at variance with other published data, but we conclude that monitoring for peri-operative silent myocardial ischaemia does not aid the prediction of longterm cardiovascular complications.
We have studied core temperature changes occurring during induction of general anaesthesia and surgery in 18 patients undergoing elective aortic aneurysm repair. In the operating theatre, all patients were warmed with a forced-air warmer and a warming mattress, and received warmed (37 degrees C) intravenous fluids. Despite this, mean (SD) [range] core temperatures in the anaesthetic room decreased by 1.5 (0.3)[1.1-2.2] degrees C, while intravascular lines, epidural and urinary catheters were inserted before the introduction of warming methods in theatre. In one-third of patients, the core temperature was still below 36 degrees C at the end of surgery. The overall temperature decrease correlated significantly with the duration of time between induction of general anaesthesia and surgical incision (R2 = 0.6912), when the patients were not being warmed. Hypothermia may thus be prevented by minimising the period that the patient is anaesthetised without being warmed. Vascular lines, urinary and epidural catheters should be inserted before the induction of general anaesthesia or, alternatively, warming methods should be introduced in the anaesthetic room.
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