Frequently patients are found to have elevated troponin levels after noncardiac surgery, which carries a poor prognosis.1–3 However, this perioperative myocardial injury as determined by isolated troponin elevation is not synonymous with myocardial infarction (MI). In these studies, the incidence of diagnosed MI, according to the third universal definition,4 is not established but seems to be low (only 5%–30% of the patients with troponin elevation).a The optimal management of these patients is difficult because of a complete lack of information about the etiology of isolated postoperative troponin elevations.
The high sensitivity of current troponin assays detects ever-decreasing levels of troponin, making the clinical diagnosis of an MI without signs or symptoms of ischemia difficult. The problem is further compounded by the finding that up to 30% of nonsurgical patients suspected for a non-ST-elevation MI do not have significant coronary artery disease on invasive coronary angiography.5 Obviously, we cannot perform coronary angiography in all postsurgical patients with isolated troponin elevation. Irrespective of the feasibility and costs, the risk of bleeding complications early after surgery due to anticoagulation use during angiography makes the risk-benefit ratio seem unfavorable. In addition, numerous noncoronary factors, both cardiac and noncardiac, are known to result in troponin elevations (Fig. 1).
Troponin release and thus “myocardial injury” can be the result of noncoronary factors such as a high adrenergic drive, sepsis, inflammation, myocarditis, or right ventricular failure secondary from etiologies such as pulmonary embolism. These cannot be diagnosed simply by a troponin value nor should they be managed as an MI. Therefore, full knowledge of the pathophysiologic mechanisms involved is essential to tailor the management of patients with isolated troponin elevation. One can imagine that the treatment of patients with coronary artery disease is totally different from the treatment of patients with sepsis, inflammation, or pulmonary embolism. The impaired prognosis in combination with the current knowledge gap regarding the etiology of myocardial injury after surgery dictates that we follow a more pragmatic approach.
In this regard, Foucrier and colleagues, in this issue of the journal, are commended for their efforts to study the potential benefit of optimizing the medical treatment that targets a coronary artery etiology in patients with troponin elevation after vascular surgery.6 In this retrospective analysis of 667 consecutive major vascular surgical patients, 66 patients (10%) had postoperative troponin detected. The authors then analyzed the effect of starting anew or of increasing the dose of existing medications that are commonly prescribed to treat stable coronary artery disease according to established guideline recommendations for nonsurgical patients.7 A combination of 4 types of drugs for secondary prevention is proposed in these guidelines: antiplatelet agents, statins, β-blockers, and angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers. In the present analysis, 43 of the 66 patients with myocardial injury received this therapy, termed optimized medical therapy (OMT). Patients were followed for 1 year after surgery and evaluated for cardiovascular event-free survival. The results showed that patients with elevated troponin who received OMT had an almost 3-fold improvement in their survival at 1 year. The idea of OMT is appealing, particularly in vascular patients, because this population, for the most part, has established atherosclerosis, a high likelihood of coronary artery disease, and long-term morbidity.
We think it is important for readers to understand, however, that the troponin elevation seen in the present study may not have been due to a postoperative cardiac event. Foucrier et al.6 did not measure troponin levels prior to surgery. It has been shown that approximately 40% of high-cardiac-risk patients undergoing noncardiac surgery have elevated troponin as detected by high-sensitivity troponin T assays prior to surgery.8 This incidence of preexistent troponin elevation is much higher than the reported 10% elevations after surgery in the study of Foucrier et al.6 This could be explained by the use of a conventional troponin I assay instead of the newer and highly sensitive assays. Nevertheless, it can be expected that in the cohort of Foucrier et al.,6 some patients may have had elevated troponin prior to surgery. These patients with an already elevated troponin may show an additional rise after surgery, meaning new myocardial injury secondary to the surgical stress, or conversely show a stable but elevated troponin. The prognosis of patients with baseline elevation is poor, but a documented change in troponin after surgery might be worse compared with the prognosis of those without dynamic changes. This hypothesis too awaits further investigation. In the former group, more aggressive management may be required. This may also hold true for patients with the highest troponin elevations because their prognosis is worse than those with a subtle elevation.1–3
This report also indicates room to improve our preoperative care of high-cardiac-risk patients. Aspirin and statins are both effective in secondary cardiac prevention, and it was disappointing to see that, despite this knowledge, a majority of patients with known symptomatic atherosclerosis are not treated with either agent.7 Similar findings have been demonstrated in other observational series, pointing to the need for optimal cardiovascular risk management in all vascular patients.9 The randomized trials that have focused on preoperative cardiac risk reduction have, as yet, not modified outcomes. The failure of preoperative prophylactic treatment of patients with β-blockers and recently with aspirin was, however, not focused on secondary prevention; the studied therapies were started immediately prior to surgery. The failure of these agents to improve cardiac outcomes was based on safety issues, increased hypotension, and bleeding.10,11 There have been no studies that evaluate medically optimizing patients at high cardiac risk of perioperative MI prior to surgery.
Finally, as with all retrospective analyses, this analysis has several important limitations. This was a retrospective observation in a very small sample. The reason almost one-third of the patients with myocardial injury did not receive OMT is unstated or unknown. This could have led to residual confounding because it is conceivable that OMT was not initiated in patients experiencing anemia and/or hypotension, that is, in the population at the highest risk. Furthermore, it is unknown when the additional medication was started or when the dosages were escalated. There also is no mention of any harm secondary to these medication changes, and the study is underpowered to assess harms. One can imagine the risk of bleeding when starting aspirin in a very early phase after the operation.
OMT in patients with myocardial injury as detected by troponin elevation after vascular surgery remains an interesting hypothesis that now deserves to be tested prospectively to appropriately answer the question whether this therapy is beneficial. The design of such a trial should also take into account safety issues of additional medical treatment. As our patients become more complex, we must deal with the fact that our knowledge of patient characteristics is not accurate enough to reliably predict the risk of a perioperative MI on an individual level.12 It is conceivable that additional predictive information could be garnered with preoperative biomarkers such as troponin. However, most elective patients nowadays survive surgery utilizing modern anesthetic management and minimally invasive surgical techniques.13 The findings of Foucrier et al.6 offer hope that patients at risk for future major cardiovascular events can be identified by measuring troponin postoperatively and can be treated by focusing on the optimal cardiovascular disease management of those patients with postoperative elevated troponin.
Name: Hendrik M. Nathoe, MD, PhD.
Contribution: This author helped write the manuscript.
Attestation: Hendrik M. Nathoe approved the final manuscript.
Name: Wilton A. van Klei, MD, PhD.
Contribution: This author helped write the manuscript.
Attestation: Wilton A. van Klei approved the final manuscript.
Name: W. Scott Beattie, MD, PhD.
Contribution: This author helped write the manuscript.
Attestation: W. Scott Beattie approved the final manuscript.
This manuscript was handled by: Charles W. Hogue, Jr, MD.
a The incidence of MI was not stated in the VISION study.
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