1 Department of Anaesthesiology, 2 Department of Surgery and 3 Division of Cardiology, University Hospital Lausanne (CHUV), 46 Rue Bugnon, CH-1011 Lausanne, Switzerland*Corresponding author. E-mail: donat.spahn@chuv.hospvd.ch
This article is accompanied by Editorial II.
Accepted for publication: June 11, 2003
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Abstract |
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Br J Anaesth 2004; 92: 7437
Keywords: complications, coronary artery disease; heart, coronary revascularization; surgery, non-cardiac
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Introduction |
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In patients with severe CAD, percutaneous transluminal coronary angioplasty (PTCA) before surgery may reduce postoperative morbidity and mortality.13 The use of intracoronary stents has modified the situation. Kaluza and colleagues4 reported that PTCA with coronary stenting increased the risk of stent thrombosis and myocardial infarction if surgery was performed within 6 weeks. The new ACC/AHA guidelines propose a 46-week interval between PTCA with stenting and non-cardiac surgery "to allow 4 full weeks of dual antiplatelet therapy and re-endothelialization of the stent to be completed, or nearly so".5
We present a case of early non-cardiac surgery performed after coronary revascularization by balloon angioplasty and stenting, where the recommended delay was respected.
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Case report |
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Baseline ECG (Fig. 1A), bronchoscopy, spirometry and lung volumes were all within normal limits. Exercise testing confirmed ischaemic heart disease, with retrosternal pain accompanied by a 0.2 mV depression of the ST segments in leads V5 and V6 at 96% of the theoretical maximal heart rate. Coronary angiography showed severe two-vessel disease with 90% stenosis of the proximal and middle parts of the circumflex coronary artery (Cx), 75% stenoses of the proximal and middle parts of the left anterior descending coronary artery (LAD) and 95% stenosis of a diagonal branch of the LAD (Fig. 2). Left ventricular function was preserved, with an ejection fraction of 0.65. Both Cx and LAD were dilated and stented, with two stents in each of the coronary arteries (two Jomed stents in the Cx and two Velocity stents in the LAD) (Fig. 3). Since the diagonal branch was considered a minor coronary artery it was not dilated. The patient was treated with clopidogrel 75 mg day1 and aspirin 300 mg day1 for 4 weeks, followed by aspirin 300 mg day1 alone for 2 more weeks. Clopidogrel was stopped 2 weeks before surgery to allow the use of an epidural catheter and to reduce the risk of surgical haemorrhage.
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On arrival in the recovery room, the patient was in pain and epidural analgesia was given, with a total of 8 mg of i.v. morphine; labetalol 20 mg was given i.v. to suppress the responses to pain (arterial pressure 200/90 mm Hg, heart rate 116 beats min1), after which the patient became pain free and cardiovascular measures improved (arterial pressure 150/90 mm Hg, heart rate 76 beats min1). One h later, however, the patient developed sudden severe retrosternal pain and dyspnoea. Conventional ECG displayed Pardee curves up to 0.6 mV above baseline in leads V1V4 (Fig. 1B). The patient was given supplemental oxygen; acetylsalicic acid 500 mg, esmolol boluses up to 40 mg and morphine 8 mg were administered i.v. An infusion of nitroglycerine was started at 2 µg kg1 min1. Arterial pressure and heart rate remained stable at 140/80 mm Hg and 80 beats min1, respectively.
Emergency coronary angiography showed occlusion of the proximal LAD stent (Fig. 4) but there was no flow reduction in the Cx stents. After successful recanalization of the proximal LAD stent, several thrombi and a distal occlusion were found in the LAD (Fig. 5). Because of the risk of postoperative haemorrhage, intracoronary thrombolytic therapy was not given, nor treatment with a IIb-IIIa receptor inhibitor (abciximab).
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During the second night after surgery the patient developed left bundle branch block (Fig. 1D) and cardiac failure (arterial pressure 83/48 mm Hg, heart rate 105 beats min1, central venous pressure 16 cm H2O) with pulmonary oedema. Transthoracic ECG showed extensive anteroseptoapical akinesia and hypokinesia in the other segments of the left ventricle. Ejection fraction was estimated at 0.20. Troponin-I levels exceeded 100 µg litre1, confirming a large myocardial infarction.
In spite of increased anticoagulant therapy (heparin titrated to aPTT of 4555 s), dobutamine 8 µg kg1 min1 and norepinephrine 0.4 µg kg1 min1, the patients clinical status deteriorated, with tachypnoea (24 bpm) and tachycardia (131 beats min1). Arterial pressure was 101/58 mm Hg. A pulmonary artery catheter showed pulmonary hypertension (39/24 mm Hg) and increased pulmonary capillary wedge pressure (mean 21 mm Hg). Cardiac index was 2.17 litre min1 m2. In view of the patients advanced age, the extent of myocardial infarction, the severe left ventricular dysfunction and the poor prognosis of the malignant lung disease (T1N1M0), haemodynamic and respiratory support was not increased and the patient died in asystole on the fourth day after surgery.
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Discussion |
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Recent research has focused on the long-term consequences of endothelial injury and its inflammatory reaction, leading to neointimal hyperplasia and late in-stent stenosis.13 This occurs in 1530% of patients within months of intracoronary stenting and requires reintervention. New anti-inflammatory and antimitogen drugs, as well as new techniques such as intracoronary radiation, are being tested, with contradictory results.14 Stent technology is also advancing, and new types of intracoronary stents are being used, including the cytostatic eluting stents. Designed to prevent neointimal hyperplasia in the stents lumen, these stents effectively inhibit cellular proliferation on the stent wall, delaying intimal healing and increasing fibrinogen deposition.15 Patients treated with such stents will need longer dual antiplatelet therapy. The consequences of these new stents for a patient having surgery are unclear.
Compared with simple balloon angioplasty, the intracoronary stent offers better short- and long-term outcome in patients not having surgery.16 For surgical patients, PTCA with balloon dilation may reduce the risk of perioperative cardiac complications.2 3 17 No studies, however, have compared preoperative PTCA with and without stenting. Recent reports of adverse outcomes4 18 and the present case suggest that non-cardiac surgery soon after coronary stenting is associated with a major risk of postoperative myocardial ischaemia, even if the recommended interval of 6 weeks is respected. There are no prospective randomized trials defining the minimum safe delay between PTCA with stenting and subsequent surgery. Therefore, treatment has to be guided by basic science and observational studies. A 3-month delay between PTCA with stenting and any surgical intervention has been recently recommended to minimize the risk of in-stent thrombosis.19 However, in the case described here, the pulmonary lesion turned out to be a potentially operable lung cancer, and a 3-month delay after coronary revascularization may have been difficult to justify because of the risk of tumour progression. Comparing the images of the pre- and postoperative coronarographies we can also see that the high-grade stenosis of the diagonal branch remained unchanged throughout the perioperative period. Although it is a critical stenosis, it can be considered as a stable coronary lesion because it has an intact endothelium. An incompletely re-endothelialized stent, on the other hand, is an unstable coronary lesion and should be treated as such (i.e. with aggressive antiplatelet therapy). We stopped clopidogrel 2 weeks before the operation, as recommended5 to prevent surgical haemorrhage and to allow placement of an epidural catheter. However, 6 weeks may not be long enough for re-endothelialization to be completed. In retrospect, continuation of clopidogrel until the day of surgery, forgoing the advantages of epidural analgesia and accepting an increased risk of bleeding, might have been a better choice.
What alternative strategies exist for the perioperative management of such patients? First, aggressive haemodynamic management with perioperative ß-blockade without PTCA or stenting may be considered. This approach has been advocated by six publications summing a total of 502 patients receiving perioperative ß-blockade. Only three of these studies were randomized (201 ß-block patients in total) and only two were outcome studies (158 ß-block patients vs 154 controls). These studies found that perioperative ß-blockade reduced cardiac morbidity and mortality in high-risk patients.19 20 Second, if PTCA with stenting is performed before surgery, surgery should be postponed for as long as possible and antiplatelet therapy should be continued in the perioperative period. If this is inappropriate and coronary intervention is indicated, we suggest a two-step procedure: if surgery cannot be postponed for 3 months, preoperative revascularization could be limited to a balloon angioplasty without stenting. Once the patient has recovered from the non-cardiac operation, a definitive PTCA with stenting could then be done. Because intracoronary stenting has better short- and long-term results compared with angioplasty without stenting, and because no clinical data are available comparing the two techniques in a perioperative setting, cardiologists may be reluctant to apply this latter approach. Even if preoperative coronary revascularization, with or without stenting, is performed, these patients should still be considered as high risk and could benefit from perioperative ß-blockade.
In conclusion, we describe a fatal myocardial infarction in a patient with CAD who had major surgery for malignant disease after coronary revascularization with PTCA and stenting 6 weeks before this surgery. The AHA/ACC guidelines recommend a 46-week interval between coronary stenting and major non-cardiac surgery but this case illustrates that a risk continues after this interval and that additional aggressive antiplatelet therapy and haemodynamic protective measures, such as ß-blockade and optimal pain control, are needed.
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