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How to Prevent Perioperative Myocardial Injury: the Conundrum Continues
JianZhong Sun, MD, PhD; David Maguire, MD, Joseph Seltzer, MD, Zvi Grunwald, MD
Department of Anesthesiology, Jefferson Medical College, Thomas Jefferson University.
Philadelphia, PA, USA
Introduction
Perioperative myocardial injury (PMI), including myocardial ischemia, cardiac dysfunction,
cardiac arrhythmias, myocardial infarction and cardiac arrest continues to be a major challenge to
perioperative physicians because of its clinical and economic impact. Despite extensive clinical
and basic research, the mechanisms responsible for PMI remain enigmatic. Currently, the
predominant theories are that PMI may be caused by prolonged stress-induced myocardial
ischemia or atherosclerotic plaques rupture or a combination of two. Clinically perioperative
myocardial ischemia and infarction may present differently, pathologically they are all secondary
to alterations of coronary plaque morphology and function or/and the loss balance between
myocardial oxygen supply and demand. The potential triggers for PMI include extreme surgical
stress, catecholamine release and inflammatory reaction. Our recent study demonstrated that
catecholamine stimulation can aggravate myocardial injury by provoking inflammatory reaction
and increasing myocardial apoptosis [1].
Clinical strategies to prevent PMI have been evolving greatly. In 1977 Goldman and colleagues
pioneered the concept of a risk index to account for the multifactorial nature of contributors to
risk for cardiac morbidity [2], which has led to the landmark development in perioperative
medicine, i.e., the ACC/AHA guidelines for perioperative cardiovascular evaluation for
noncardiac surgery in 1996 and an update in 2002 [3]. However, due to the poor positive
predictive value of non-invasive cardiac stress tests, the controversy about benefit of coronary
revascularization before non-cardiac surgery and the considerable risk of coronary angiography
and coronary revascularization in high-risk patients, perioperative physicians have been
continuously searching for alternative approaches to prevent/reduce perioperative cardiac
complications. In 1996, Mangano et al performed a randomized clinical trial to investigate the
effect of β-blocker, atenolol, on patient outcomes and concluded that in patients with risk for
coronary artery disease (CAD) who must undergo noncardiac surgery, treatment with atenolol
during hospitalization can reduce mortality and the incidence of cardiovascular complications for
as long as two years after surgery. In 2003, Poldermans et al provided evidence in a case-
controlled study that statin use reduces perioperative mortality in patients undergoing major
vascular surgery. These significant developments in perioperative medical therapy have shifted
interest of perioperative cardiac care greatly, from risk stratification and potential coronary
revascularization to risk modification with β-blockers or/and statins. Nevertheless, the debate and
controversy exist in almost every aspect of clinical strategies to prevent PMI.
Cardiac risk assessment
1. ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery
can help to stratify cardiac risk and it focused on preoperative testing to identify patients with
significant CAD and subsequent coronary revascularization [3]. The guidelines are currently
中華麻醉在線 http://www.csaol.cn 2007年9月
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playing a major role in the field of perioperative medicine. However, the Guidelines rely on
predominantly observational data and expert opinion because there were no randomized trials
to support the process.
2. Lee revised cardiac risk index, including high risk surgical procedure, history of CAD, history
of CHF, history of CVA, preoperative insulin treatment and serum creatinine over 2.0mg/dl is
a practical clinical risk index that physicians can use to facilitate risk estimation [4].
Perioperative monitoring
1. Le Manach et al proposed a different approach: monitoring perioperative cardiac troponin I
(cTnI) concentrations and early institution of treatment for those patients with increased cTnI
before it leads to irreversible necrosis. In their study, intense postoperative cTnI surveillance
revealed two types of PMI according to time of appearance and rate of increase in cTnI: acute
(24hr)
increase of cTnI may lead to prolonged myocardial ischemia for later events [5].
2. In the patients with cardiac surgery, Croal et al found that cTnI levels measured 24 hours after
cardiac surgery predict short-, medium-, and long-term mortality and remain independently
predictive when adjusted for all other potentially confounding variables, including operation
complexity [6].
Prophylactic coronary revascularization
ACC/AHA guidelines recommend coronary revascularization only for subgroups of high-risk
patients with unstable cardiac symptoms or those for whom coronary artery revascularization
offers a long-term benefit.
1. Coronary artery bypass graft (CABG) before noncardiac surgery: Eagle et al have shown that
among 1961 patients undergoing higher-risk surgery (involving the thorax, abdomen,
vasculature, and head and neck), prior CABG was associated with fewer postoperative deaths
and myocardial infarctions compared with medically managed CAD. Prior CABG was most
protective in patients with advanced angina and/or multivessel CAD [7].
2. Coronary revascularization before vascular surgery: However, in Coronary Artery
Revascularization Prophylaxis trial, McFalls et al found that coronary artery revascularization
(CABG or PCI) before elective vascular surgery in patients with stable CAD does not
significantly alter the long-term outcome (survival rates) when compared to medical therapy
and therefore coronary revascularization before elective vascular surgery among patients with
stable cardiac symptoms cannot be recommended [8].
3. CABG vs. percutaneous coronary intervention (PCI) before vascular surgery: In the report by
Ward et al [9], among patients receiving multivessel coronary artery revascularization as
prophylaxis for elective vascular surgery, patients having a CABG had fewer myocardial
infarctions and tended to spend less time in the hospital after the vascular operation than
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patients having a PCI. More complete revascularization was accounted for the intergroup
differences.
4. CABG vs. coronary angioplasty before noncardiac surgery: In a randomized study, Hassan et
al found that rates of myocardial infarction and death after noncardiac surgery are similarly
low after CABG or coronary angioplasty in patients with stable and multivessel CAD [10].
Percutaneous transluminal coronary angioplasty (PTCA) in surgical patients
1. Brief history of PTCA: PTCA was introduced by Gruntzing in 1977. In 1986, Puel and Sigwart
deployed the first coronary stent to act as a scaffold to prevent vessel closure and to reduce
the incidence of angiographic restenosis. By 1999, stenting composed 84.2% of all PCI.
There are two types of stent: bare metal stents (BMS) and drug-eluting stents (DES,
introduced in 2001). At present, 90% of all stents placed in the US and Europe are DES.
Despite the enthusiasm that resulted with the advent of DES, incomplete endothelialization
and stent thrombosis continue to plague these devices. Initial animal studies demonstrated
complete endothelialization with BMS at 28 days, whereas DES uniformly showed
incomplete healing at 180 days.
2. PTCA and surgical complications: In 2000, Kaluza et al [11] first reported on 40 patients treated
with BMS who underwent noncardiac surgery within
[1]
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