European Journal of Vascular & Endovascular Surgery
Volume 35, Issue 4 , Pages 413-419, April 2008

Perioperative Myocardial Injury after Elective Open Abdominal Aortic Aneurysm Repair Predicts Outcome

Cambridge Cardiovascular Unit, Addenbrooke's Hospital, Cambridge, UK

Accepted 7 October 2007. published online 06 December 2007.

Article Outline

Objective

Myocardial injury, detected by rises in cardiac troponin I (TnI), is common and associated with decreased survival following open AAA surgery. We examined the relationship between perioperative myocardial injury and postoperative outcome.

Design

Observational Cohort Study.

Methods

Forty-three consecutive patients who underwent elective open AAA repair were screened for perioperative myocardial injury or infarction using serial TnI measurements (taken on days 1, 3, and 7), ECG and clinical assessment. The primary outcome was survival free of cardiac failure, or myocardial infarction (MI) at follow-up.

Results

Twenty (47%) of the 43 patients had a TnI elevation. Of these, 11 (26%) patients met the criteria for MI. At a mean (±SD) follow-up of 1.5±0.8 years, 12 (28%) subjects had experienced at least one endpoint event. Survival free of cardiac failure or MI was 55% in patients who had TnI rises compared to 87% in those without (P=0.02). Logistic regression revealed that TnI elevation was an independent predictor of outcome with an odds ratio of 5.4 (95% CI 1.2–2.4, P=0.03).

Conclusion

Perioperative myocardial injury after elective open AAA repair predicts outcome after surgery. Routine TnI measurement should be considered in all patients, especially in those with high cardiovascular risk.

Keywords: Abdominal aortic aneurysm, Myocardial injury, Outcome

 

Patients undergoing major vascular surgery are at significant risk of developing postoperative myocardial complications, particularly myocardial infarction.1, 2 Stress, hemodynamic changes, and oxygen supply and demand mismatch frequently lead to cardiac ischemia in these patients.3 Identifying perioperative myocardial infraction is often difficult as chest pain is infrequent, ECG changes are often subtle and transient3 and CK-MB may be falsely elevated as a result of the operative procedure.4 Cardiac troponins are highly sensitive and specific biomarkers of myocardial injury which have improved the ability to diagnose perioperative myocardial infarction.3, 4, 5, 6

Subclinical myocardial injury after vascular surgery, detected by a rise in serum cardiac troponin, is common and associated with decreased survival.5, 7, 8, 9, 10, 11 Recent reports suggest that cardiac troponin I (TnI) is raised in nearly half of all patients undergoing emergency AAA repair for rupture,12, 13 and that these rises were also associated with decreased survival.13 In keeping with these findings, myocardial ischemia seen as significant ST segment depression on ECG has been shown in up to 40% of patients having elective AAA repair.14 Furthermore myocardial injury, detected by rises in TnI, have been described in 25–47% of elective AAA procedures.12, 15, 16 Recent reports suggest that myocardial injury may be less frequent after endovascular repair.15, 16 Thus, it is important to understand the prognostic implications of myocardial injury after elective open AAA repair. We examined the relationship between perioperative myocardial injury, detected by serum rises in TnI, and postoperative outcome at a mean of 1.5 years after operation.

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Methods 

This study represents a sub-group analysis of a randomized controlled trial approved by the Cambridge Research Ethics Committee.17 Each patient gave informed, written consent. Suitable patients were invited to participate in the trial at the time of scheduling for AAA repair.

Patients 

Forty-three control patients from a consecutive series of 86 enrolled in a randomized controlled trial17 who underwent elective AAA surgery were included in this observational cohort study. On informed consent to the study, baseline TnI levels were recorded. Subsequent blood specimens were analyzed on the morning of postoperative days 1, 3 and 7. Potential participants were excluded from analysis if they were more than 90 years of age; required concomitant procedures other than AAA repair; or had experienced an acute coronary syndrome or myocardial infraction within 3 months. Demographic and clinical variables were recorded and all patients risk stratified according to the prospectively validated physiological operative severity score for the enumeration of mortality and morbidity (POSSUM) risk stratification scoring system.18

Treatment and procedures 

Patients with cardiac symptoms were assessed by a cardiologist and referred for non-invasive stress testing as clinically mandated. Patients with unfavorable results or changes in symptoms were referred for coronary angiography. Subsequently revascularized patients were included in the analysis. Beta blockers were prescribed in the absence of contraindications preoperatively with dose titrated towards heart rate of 60.

Patients underwent elective open AAA repair using a standardized operating technique by one of three consultant vascular surgeons. Patients were induced with intravenous propofol, atracurium, and remifentanyl followed by maintenance with inhaled desflurane. All patents received systemic heparinization and perioperative beta-blockers titrated to a target heart rate of 60.

Post-operatively all patients received patient-controlled intravenous morphine and/or bupivicaine and fentanyl epidural analgesia. Patients with evidence of myocardial infarction in-hospital were subsequently managed by conventional medical treatment including antiplatelet agents, beta-blockers, angiotensin converting enzyme inhibitors (or angiotensin receptor blockers) and cholesterol lowering drugs in the absence of any contra-indications.

Outcomes 

The primary outcome was the combined endpoint of death, myocardial infarction or congestive cardiac failure. Follow-up was performed by review of case notes, death certificates, autopsy reports and structured telephone interview of all patients at the completion of study enrollment.

In hospital, myocardial injury was defined as peak serum level>0.54ng/mL in keeping with published reports correlating this level with cardiac morbidity and mortality,7 and myocardial infarction according to the revised ACC/AHA guidelines (TnI elevation>1.5ng/mL with at least one of the following: typical ischemic symptoms, ECG changes indicative of ischemia, or new pathological Q-waves).19 The TnI cutoff for this definition was established in keeping with published reports correlating this level with clinical myocardial infarction.11 TnI was measured using an automated immunoflourescence detector (Dade Behring, Milton Keynes, UK). All patients were monitored for ischemia for 48 hours after surgery using Holter electrocardiograms (Lifecard CF, Del Mar Reynolds, Hertford, UK) and screened using computerized ST-segment analysis (Pathfinder, Del Mar Reynolds, Hertford, UK).3 ST-deviations, ≥0.2mV in one lead or ≥0.1mV in two contiguous leads lasting more than 10mins, were reviewed by a consultant cardiologist (DPD). Each patient's number of events and longest and cumulative ischemia duration was recorded. In addition daily 12 lead ECGs were performed each morning perioperatively. Cardiac failure was defined as dyspnea either at rest or with minimal activity, paroxysmal nocturnal dyspnea, and edema, either pulmonary or peripheral. In hospital following daily examination, patients with clinical evidence of fluid overload or new pulmonary congestion on chest radiograph were classified as cardiac failure. In the event of patients reporting myocardial infarction or congestive cardiac failure at follow-up, confirmation was sought from the patient's primary care physician.

Statistical methods 

Descriptive variables are presented as means with standard deviations (SD), or medians with interquartile ranges (IQR), and compared with the t-test or Mann Whitney test respectively. Estimations of precision are to be presented with 95% confidence intervals. Categorical data and frequencies are expressed as percentage and compared with chi-square or Fisher's exact test where appropriate. Conventional levels of significance (α of 0.05) were applied throughout. Logistic regression was performed to identify risk factors for postoperative outcomes. Statistical analysis was undertaken using SPSS for windows version 11.0 (Chicago, Illinois, USA) and S Plus version 6 (Seattle, Washington, USA).

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Results 

Of the 43 patients, 11 patients (27%) were referred for noninvasive stress testing following cardiology consultation, all of whom had a history of cardiac symptoms (exertional chest pain or dyspnea). Of these three underwent coronary angiography and 8 non-invasive stress testing. Three patients subsequently underwent revascularization by percutaneous coronary intervention. These were the only patients revascularized within three to six months of AAA surgery. The remaining 8 patients were treated medically, predominantly through increaseing pre-existing anti-anginal medication dosages. Seven patients had previous revascularization greater than 6 months prior to referral for AAA surgery.

Twenty patients (47%) had postoperative myocardial injury. The majority of peak TnI measurements occurred on postoperative days 1 (40%) and 3 (35%). Patients who suffered myocardial injury were significantly more likely to have a history of angina, hypercholesterolemia, higher Canadian Classification Angina scores, and suffered a previous myocardial infarction at baseline (Table 1). The operative characteristics of the two groups were similar with regards to aneurysm size, aortic cross-clamp time and total operative time, however patients who had myocardial injury had significantly higher physiological risk scores (Table 2). Median time to event was 138 days (IQR 93) in the myocardial injury group compared to 160 days (IQR 140) in the Tn negative group (P=0.39) Of the 20 patients who had myocardial injury, 11 (55%) suffered a myocardial infarction in hospital. All 11 had raised TnI levels and diagnostic ECGs in the absence of chest pain. Two patients died in hospital as a consequence.

Table 1. Patient demographics and co-morbidities
TnI positiveTnI negativeP
Sample size2023
Median age, years (IQR)76 (10)76 (9)0.84
Males, n (%)18 (90)22 (96)0.46

Cardiac risk factors, n (%)
History of angina9 (45)2 (9)0.006
History of hypertension14 (70)12 (52)0.95
History of diabetes mellitus2 (10)1 (5)0.47
History of smoking14 (70)16 (70)0.98
History of hypercholesterolemia12 (60)7 (30)0.05

Medical History
Angina CCS, (IQR)0 (0–1)0 (0–0)0.03
NYHA score, (IQR)1 (1–2)1 (1–2)0.72
Previous myocardial infraction, (%)10 (60)3 (25)0.03
Previous coronary revascularization, (%)5 (25)2 (9)0.43
Cardiac failure, (%)1 (5)0 (0)0.91
Left ventricular function, (IQR)2 (1)1 (1)0.06
Renal impairment∗ (%)1 (5)1 (4)0.91
GFR, mL/min (SD)58 (20)65 (27)0.30

Cardiac medications, (%)
Beta-blocker10 (45)7 (30)0.32
Calcium channel antagonist6 (30)6 (30)0.97
ACE or AIIR inhibitor10 (50)5 (32)0.24
Nitrate3 (15)4 (17)0.83
Statin10 (50)8 (35)0.31
Antiplatelet14 (70)10 (44)0.08
Anticoagulant1 (4)1 (5)0.92

IQR, Inter-quartile range; CCS, Canadian Classification Score; NYHA, New York Heart Association; CABG, Coronary Artery Bypass Grafting; GFR, Glomerular Filtration Rate; ACE, Angiotensin Converting Enzyme; AIIR, Angiotensin II Receptor.

∗Renal impairment was defined as peak serum creatinine>177μmol/L (2.0mg/dL) according to guidelines for risk stratification in patients undergoing major vascular surgery and noncardiac surgery.2

Table 2. Operative characteristics and postoperative outcomes
TnI positiveTnI negativeP
Median AAA diameter, cm (IQR)6.7 (1.8)6.5 (1.5)0.25
Median ASA score (IQR)3 (0)3 (0)0.59
Median POSSUM Physiology Score, (IQR)24 (9)19 (8)0.02
Median POSSUM Operative Score, (IQR)20 (3)20 (4)0.72
Supra-renal clamp, n (%)3 (15)2 (9)0.52
Median blood loss, mL (IQR)1250 (1025)1450 (1178)0.34
Median cross-clamp time, mins (IQR)55 (29)59 (22)0.35
Median operating time, mins (IQR)190 (42)190 (87)1.0
ICU admission∗, n (%)13 (65)8 (35)0.05
Postoperative stay, days (IQR)12 (7)9 (9)0.13

AAA, Abdominal Aortic Aneurysm Repair, IQR, Inter-quartile range; ASA, American Society of Anesthesiologists; POSSUM, physiological operative severity score for the enumeration of mortality and morbidity, ICU, Intensive Care Unit; SD, Standard Deviation.

∗Patients were routinely monitored in the operating room recovery for 24 hours postoperatively. Transfer to the ICU was based on postoperative recovery.

Mean (± SD) follow-up was 571±291 days. One patient refused follow-up. During the follow-up period, 12 (28%) subjects experienced at least one endpoint event. Four (9%) patients died, 6 (14%) suffered a myocardial infarction, and 2 (5%) developed congestive cardiac failure (Table 3). Of the 4 deaths, 2 were in patients with myocardial injury (P=0.83). Of the 6 myocardial infarctions, 5 were in patients with myocardial injury (P=0.05). Four of these events were reinfarctions. Both of the patients who developed cardiac failure had perioperative myocardial injury (P=0.12). Event free survival was 72% overall, 55% in patients who suffered myocardial injury compared to 87% in those without elevations in TnI (P=0.02) (Table 3). Logistic regression analysis revealed that myocardial injury was an independent predictor of outcome with an odds ratio of 5.4 (95% confidence interval 1.2–24, P=0.03) (Table 4). Furthermore, patients with myocardial injury, were significantly more likely to be admitted to the intensive care unit postoperatively (P=0.05), although total hospital stay was not significantly different between the two groups (Table 2).

Table 3. Major adverse outcomes after open AAA repair after discharge
TnI positiveTnI negativeP value
Sample size2023
Myocardial infarction, n (%)5 (25)1 (4)0.05
Cardiac failure, n (%)2 (10)00.12
Death, n (%)2 (10)2 (9)0.83
∗Composite, n (%)9 (45)3 (13)0.02

∗Composite defined as death, congestive cardiac failure, or myocardial infarction; only one event for each patient was counted.

Table 4. Logistic regression analysis of predictors of outcome in patients undergoing elective open abdominal aortic aneurysm repair
Univariable Predictors of Outcome
VariableOR95% CIP
TnI elevation5.41.2–240.03
Age, per year1.00.91–1.10.71
Previous myocardial infarction1.50.36–6.30.58
Angina0.950.16–5.80.96
NYHA III/IV2.30.64–8.40.20
Diabetes mellitus6.00.49–730.16
Hypertension1.90.46–7.50.37
Smoking0.330.13–1.40.13
Hypercholesterolemia1.10.29–4.40.83
ECG abnormalities∗1.20.33–1.20.11
Antiplatelet therapy0.720.19–2.80.63
POSSUM risk score, per unit1.10.96–1.20.18
Total operative time, per min1.00.99–1.00.25
Total cross-clamp time, per min0.980.92–1.00.49
Aneurysm size, per cm0.730.38–1.40.36

OR, odds ratio; CI, confidence intervals; NYHA, New York Heart Association; POSSUM, physiological operative severity score for the enumeration of mortality and morbidity.

∗ECGs were screened for AV block, uncontrolled SVT, pathological Q waves, LVH, LBBB, and ST-T wave abnormalities.

Renal injury, a consequence of hemodynamic changes following application of the aortic cross-clamp and ischemia-reperfusion injury following its release, is also a common cause of morbidity and mortality following elective AAA repair.20, 21 Importantly, the incidence of renal impairment and glomerular filtration rate were similar between the two groups (Table 1). Furthermore, both the incidence of new renal impairment and change from baseline glomerular filtration rate were not different between the myocardial injury and Tn negative groups (Table 5), excluding the potentially confounding effect that myocardial injury was simply a marker of renal impairment.

Table 5. Incidence of postoperative renal impairment and GFR change from baseline
TnI positiveTnI negativeP value
Renal Impairment
Day 1 – New renal impairment, n (%)3 (15)9 (39)0.08
Day 1 – GFR, mL/min (SEM)−8 (3)−9 (7)0.84
Day 3 – New renal impairment, n (%)0 (0)4 (17)0.05
Day 3 – GFR, mL/min (SEM)−4 (4)−5 (8)0.63
Day 7 – New renal impairment, n (%)0 (0)0 (0)N/A
Day 7 – GFR, mL/min (SEM)1 (3)−2 (5)0.30

GFR, Glomerular Filtration Rate.

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Discussion 

In this observational cohort study, we investigated the prognostic implications of serum TnI elevations after elective open AAA repair. We observed, first, that patients with myocardial injury were higher risk patients and were significantly more likely to have risk factors for cardiovascular disease. Second, over half of patients with myocardial injury suffered a myocardial infarction according to ACC/AHA guidelines. Finally, at a mean follow-up of 1.5 years, survival free of cardiac failure or myocardial infarction was significantly lower in patients with perioperative myocardial injury. Logistic regression analysis revealed that myocardial injury was an independent predictor of outcome.

Following elective AAA repair the commonest cause for perioperative death is cardiac-related.22, 23 Significant coronary artery disease is present in half to two-thirds of these patients.24, 25 Cross-clamping of the abdominal aorta leads to a sudden increase in afterload and subsequent subendocardial ischemia3, 26, 27 which rarely presents with chest pain.4 The emergence of highly sensitive markers of myocardial damage such as TnI and T have revealed that myocardial necrosis is common. In magnetic resonance studies TnI rises correlate with new myocardial hyperenhancement representative of ischemia.28 In patients with a ruptured AAA, the incidence of TnI elevation has been reported between 46-58%.12, 13 Recently, it was shown that elevations in this cardiac marker, in the presence or absence of overt cardiac dysfunction, were associated with perioperative death.13 However, in addition to cardiovascular co-morbidity, these patients suffer ischemic stress as a result of massive hemorrhage and transfusion. To determine the prognostic implications of myocardial injury after elective open AAA repair we performed a prospective observational cohort study and found, at a mean follow-up of 1.5 years, survival free of cardiac failure or myocardial infarction was 32% lower in patients with TnI elevations. These findings support previous studies which show myocardial injury is prognostic in both vascular surgery patients5, 7, 8, 9, 10, 11 and non-cardiac surgery patients.29, 30

Patients with myocardial injury had significantly higher physiological risk scores and more cardiovascular risk factors. These findings highlight the importance of using preoperative cardiac risk evaluation and longer term cardiology follow-up in these patients. In light of a recent large randomized controlled trial which determined that routine coronary artery revascularization before elective AAA surgery failed to significantly alter long-term outcome,31 the need to identify patients at risk of cardiac morbidity and mortality remains paramount. Markers of myocardial injury, such as TnI, may be able to identify such patients. In our study, of the 6 patients with follow-up myocardial infarctions, 5 were in patients with myocardial injury, four of which were reinfarctions. In the nine patients who had perioperative myocardial injury and a subsequent endpoint event at follow-up, the median TnI level was 4.78 (IQR 0.61–23.64). These patients may benefit from optimization of cardioprotective medical therapies associated with survival benefits such as aspirin, beta-blockers, angiotensin converting enzyme inhibitors and statins.32

It would appear initially that the 47% incidence of Tn elevation compared to that reported in the literature is high. Critically, most previous studies investigating the prognostic implications of Tn elevation after myocardial injury have been for major vascular surgery, which includes infrainguinal bypass surgery, as opposed to specifically AAA repair. In these studies the incidence is reported to be between 10–23%.5, 8, 9, 10, 31, 33 However, cross-clamping of the abdominal aorta for AAA repair leads to a markedly different physiological and hemodynamic response to cross clamping the iliac artery for infrainguinal revascularisation procedures.34 In studies looking directly at AAA repair Haggart and collegues found myocardial damage, as assessed by cardiac troponin I elevation, complicated 58% of emergency and 30% of elective AAA repairs. Abraham and collegues15 reported a 25% incidence of troponin elevation on a single recording 24 hours following AAA repair. Recently, Schouten and collegues showed Tn elevations in 47% of patients with >3 cardiovascular risk factors undergoing conventional open AAA repair.16 In the face of other trials describing myocardial ischemia seen as significant ST segment depression on ECG in 30-40% of patients having elective AAA repair,14, 35 the authors believe that in the face of increasingly sensitive Tn assays, that the incidence of myocardial injury in these high risk patients is accurate.

In keeping with previous reports showing underutilization of cardiac medical therapy among patients undergoing AAA repair,36 in our study population, more than half of patients undergoing surgery were not treated with these drugs preoperatively. The authors are unable to confirm how the present findings on postoperative outcome would be affected by increased utilization of cardiac medications. However, in keeping with previous reports it is likely that optimization of medical therapy would have reduced perioperative events. Nevertheless, the authors believe that the findings of the present study are valuable as they highlight that postoperative outcome is worse in those patients with perioperative troponin elevation, irrespective of there medical and operative risk. When patients who had myocardial injury and subsequently suffered an event were compared to patients with myocardial injury who remained free from subsequent events, we found no significant differences in baseline or operative characteristics (data not shown). These findings indicate that events in patients with myocardial injury were not simply a reflection of increased preoperative cardiovascular/operative risk, but were related to postoperative myocardial injury.

Determining the prognostic implications of raised TnI levels after elective open AAA repair has become particularly important in the face of new data showing that endovascular therapy attenuates myocardial injury. Abraham and colleagues reported an 18% absolute risk reduction in the incidence of raised troponin, despite a 19% higher rate of preoperative myocardial infarction. Similarly, Schouten and co-workers showed a benefit favoring endovascular repair in reducing cardiovascular outcomes.16, 37 Despite this finding, the incidence of long-term cardiac mortality was similar in both groups. These findings suggest the possibility that the surgical stress of aortic clamping and subsequent hemodynamic instability in elective open surgery simply unveil cardiovascular disease in the perioperative period which may remain masked in patients who undergo endovascular repair.

In conclusion, we have demonstrated that elevation in TnI after elective open AAA repair predicts outcome 1.5 years after surgery. Techniques to reduce myocardial injury may be able to improve morbidity and mortality after AAA repair. Furthermore, patients with TnI elevations were significantly higher risk and had a higher incidence of cardiovascular risk factors. Routine TnI measurement should be considered in all patients at high cardiovascular risk to allow appropriate follow-up and optimization of medical therapy.

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PII: S1078-5884(07)00659-4

doi:10.1016/j.ejvs.2007.10.007

European Journal of Vascular & Endovascular Surgery
Volume 35, Issue 4 , Pages 413-419, April 2008

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