| dc.description.abstract | Background: Myocardial injury affects up to one in three patients undergoing
non-cardiac surgery. However, very little is known about the underlying
pathophysiology. In the general population, patients with elevated resting heart
rate are at increased risk of cardiac events, mortality, heart failure and
autonomic dysfunction, while hypertension is a well described risk factor for
cardiovascular disease. I hypothesised that common abnormalities of heart rate
or blood pressure were associated with myocardial injury after non-cardiac
surgery.
Methods: This thesis comprises a series of secondary analyses of data from
five prospective multi-centre epidemiological studies of surgical patients. The
main outcome of interest was myocardial injury, defined using objective
measurement of cardiac troponin. I used logistic regression analysis to test for
association between exposures and outcomes.
Results: In a large international cohort, patients with high preoperative heart
rate had increased risk of myocardial injury and patients with very low
preoperative heart rate had reduced risk of myocardial injury. Patients with
elevated preoperative pulse pressure had increased risk of myocardial injury,
independent of existing hypertension or systolic blood pressure. High heart rate,
or high or low systolic blood pressure during surgery, was associated with
increased risk of myocardial injury. In a separate study, elevated preoperative
heart rate was associated with cardiopulmonary and autonomic dysfunction,
and reduced left ventricular stroke volume, suggestive of heart failure. Finally,
autonomic dysfunction, identified using cardiopulmonary exercise testing, was
associated with elevated preoperative heart rate, elevated plasma NT-Pro-BNP
(indicative of heart failure) and postoperative myocardial injury.
Conclusions: Elevated preoperative heart rate, autonomic dysfunction and
subclinical heart failure may be part of a common phenotype associated with
perioperative myocardial injury. Further research is needed to characterise the
pathological processes responsible for myocardial injury, and to identify
potential therapeutic targets. | en_US |
