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Strategies to Reduce Cardiac Risk in Noncardiac Surgery: Where Are We in 2005?

Fleisher, Lee A. M.D.

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CARDIOVASCULAR morbidity and mortality after noncardiac surgery continues to be an area of active investigative interest because of its clinical and economic impact.1 With the aging of the population, increasing numbers of patients present to surgery with complex comorbidities. Preoperative cardiovascular evaluation has been an area of intense interest and has led to the development of several sets of guidelines.2,3 These guidelines initially focused on the extensive identification of the presence and extent of coronary artery disease in patients with known or major risk factors. More recently, the focus has shifted to randomized trials that have addressed the issue of interventions to reduce this risk.1 Yet inherent in any approach to reduction in cardiovascular complications after noncardiac surgery is the need to understand the pathophysiology of perioperative cardiovascular morbidity.4 In this issue of Anesthesiology, Le Manach et al.5 add to the available knowledge on the subject and propose an additional approach to reduction of perioperative cardiac morbidity through the use of monitoring.
Le Manach et al. studied 1,152 consecutive patients who underwent abdominal infrarenal aortic surgery and identified four patterns of cardiac troponin I (cTnI) release after surgery. One group did not have any abnormal concentrations, whereas a second group had only mild increases of cTnI. It is interesting to note that two groups demonstrated increases of cTnI consistent with a perioperative myocardial infarction (PMI). One demonstrated acute (< 24 h) and early increases of cTnI above threshold, and the other demonstrated prolonged low levels of cTnI release, followed by a delayed (> 24 h) increase of cTnI. The authors suggest that these two different patterns represent two distinct pathophysiologies: acute coronary occlusion for early morbidity and prolonged myocardial ischemia for late events. Although the separation of these two patterns is clearly arbitrary, as highlighted in the limitations section of the article, there is some basis for these processes in the literature.
Given the available evidence, it is plausible that the authors have identified two distinct types of PMI. However, an early pattern of cTnI increase was seen in 38% of the study cohort (21 of 55 patients). Previous studies have demonstrated that virtually all events are preceded by prolonged ischemia (with either a cumulative duration of > 2 h or a single episode of > 30 min), suggesting that the incidence of PMI secondary to coronary occlusion may be lower than 38%.6,7 Similarly, most PMIs are not associated with Q waves, and the fatality rate has decreased in recent years, further supporting the idea that many of these early PMIs may not be due to acute coronary occlusion.6,7
One of the first publications describing the pathogenesis of cardiovascular risk in noncardiac surgery was published in the 1940s, in which coronary artery thrombosis was shown in an autopsy series.8 The presence of acute coronary thrombosis in the intraoperative and postoperative period in patients who sustain major or fatal cardiac events has been confirmed in a subsequent autopsy series by Dawood et al.9 Cohen and Aretz10 identified 26 cases of fatal postoperative myocardial infarction with coronary arteries available from autopsy. Coronary plaque rupture was associated with almost half of the fatal postoperative myocardial infarction cases. Ellis et al.11 performed a case–control study of 63 patients who had sustained a nonfatal myocardial infarction after undergoing major vascular surgery and who had undergone previous cardiac catheterization. They found that acute complete coronary thrombosis, which preoperatively served viable myocardium and nonobstructive lesions, was the most common cause of perioperative myocardial infarction or death.
An alternative mechanism for the genesis of acute myocardial infarction is secondary to supply:demand mismatches superimposed on a high-grade or critical coronary stenosis. Multiple investigators have demonstrated the association between perioperative tachycardia and myocardial infarction, as well as the benefits of perioperative β-blocker therapy titrated to control heart rate.12–15 The importance of hemodynamics has been further supported by several clinical investigations, which demonstrated a relation between prolonged ST-segment changes, particularly ST-segment depression, and subsequent cardiovascular morbidity.6,7 Additional etiologies have included cold-induced stress and anemia.16,17
How then do we use this information? Clearly, any approach to the reduction of perioperative cardiac morbidity must incorporate the multifactorial pathogenesis of PMI into a multimodal approach to reduction of morbidity. Therefore, no single approach may be successful. Several medical therapies have demonstrated promise in reducing but not eliminating PMI.1 Despite several randomized trials suggesting that perioperative β-blockade significantly reduces PMI, two recent investigations suggest that β-blocker therapy is not as effective as originally suggested.13,14,18,19 Those studies in which β blockade is titrated to control heart rate demonstrated the best efficacy, supporting the importance of controlling tachycardia and minimizing the probability of prolonged ischemia. Perioperative statin therapy has been shown to reduce PMI in a case–control trial and a randomized trial.20,21 The benefits of this agent most likely reflect the stabilization of coronary plaques, consistent with the proposed pathogenesis of early PMI. A recent large-scale randomized trial of preoperative coronary revascularization compared to medical therapy in major vascular surgery patients was unable to demonstrate different survival rates at an average of 2.7 yr postoperatively, which further supports the lack of a simple approach to this problem.22
As old and new agents continue to be evaluated as means of reducing PMI, Le Manach et al. propose a different approach: monitoring perioperative cTnI concentrations and early institution of treatment for those patients with increased cTnI before it leads to irreversible necrosis. Further research is required to determine whether early and aggressive antiischemic therapy in patients who have cTnI concentrations above threshold (> 1.5 ng/ml) will lead to reduced morbidity and whether the increased cost of monitoring is worth any potential reduction in morbidity. A great deal of research has been targeted to develop strategies to reduce PMI in noncardiac surgery. Although we are beginning to develop some answers, we still have much to learn.
Lee A. Fleisher, M.D.,
Department of Anesthesia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. fleishel@uphs.upenn.edu
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References

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