This website is intended for healthcare professionals only.

Hospital Healthcare Europe
Hospital Pharmacy Europe     Newsletter    Login            

Myocardial revascularisation

Charles Pirlet
University Hospital (CHU) of Liege, Belgium

Dr William Wijns
Cardiovascular Center, OLV Ziekenhuis, Aalst, Belgium

Professor Philippe Kolh
Cardiovascular Surgery Department, University Hospital (CHU) of Liege, Belgium

Coronary artery disease (CAD) can be managed by optimal medical therapy and/or mechanical revascularisation, either by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).

In the setting of evolving drugs, techniques and evidence regarding these therapeutic options, the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) have published a guidelines document1,2 establishing indications for revascularisation and the appropriate modalities of achieving it.

In the spirit of co-operation between cardiologists and cardiac surgeons, new concepts were coined. The creation of a ‘heart team’, comprising at least an interventional cardiologist, a non-interventional cardiologist and a cardiac surgeon, is a recommended approach to multidisciplinary decision- making. Indications for ‘ad hoc PCI’ where the therapeutic procedure is performed during the diagnostic angiogram are defined by an institutional protocol that accounts for the clinical conditions, the severity and urgency of the presentation and local experience.

In the current context of transparency requirements and patient rights, a special emphasis was placed on the need for objective patient information and formal patient consent.

Before revascularisation is considered, significant stenoses and their repercussions in terms of ischaemia will have to be identified. Coronary angiography is recommended when the possibility of ischaemic heart disease is evaluated as highly probable (>90%). For intermediate situations (10%–90%), functional tests such as stress echocardiography and nuclear imaging are recommended because the presence of ischaemia is correlated to adverse events,3-6 not the presence of coronary stenoses.

In patients with a low risk profile, coronary CT may be used to rule out CAD, as its negative predictive value is high.7,8 Fractional flow reserve (FFR) tests that are performed during invasive angiography or prior to PCI have proven to be useful to evaluate the functional consequences of a stenosis9-11 when functional work-up was not done prior to the angiogram.

Interventional management, whether it is percutaneous or surgical, depends on the clinical presentation – stable coronary artery disease, non-ST elevation acute coronary syndrome and ST elevation myocardial infarction. Moreover, related clinical conditions – such as diabetes, heart failure, renal insufficiency, associated vascular disease, previous revascularisation – also have an impact.

Stable coronary artery disease
Evidence shows that CABG compared to optimal medical therapy (OMT), at the price of a highly invasive procedure, reduces mortality in certain anatomical presentations of CAD deemed to be at a particular high risk.12 These situations include three-vessel disease, left main (LM) involvement and, to some extent, lesions on the proximal left anterior descending (LAD) artery. A large area of ischaemia, as defined by more than 10% of the left ventricle (LV), also carries a poor prognosis and revascularisation is beneficial.3

PCI has failed to show a decrease in mortality, although current evidence only pertains to more moderate CAD than the situations described above.13 However, PCI has been proven to alleviate symptoms caused by CAD. The value of historical trials is difficult to evaluate as OMT, PCI and CABG are constantly improving.

A novel trial, the SYNTAX trial,14 comparing CABG versus PCI with paclitaxel-eluting stents in patients with three-vessel and/or left main disease concluded that CABG remains the standard of care for these anatomical situations. Indeed, PCI failed to reach the non-inferiority criteria, as there was a difference in combined major adverse cardiac or cerebral events largely due to repeat revascularisation in the PCI group.

However, hypothesis-generating analysis of predefined subgroups shows that certain populations do not benefit from CABG compared to PCI. Coronary angiograms were attributed a purely angiographic score, the SYNTAX score, that estimates the severity of CAD. There was no benefit of CABG compared to PCI in patients with threevessel disease whose SYNTAX scores were inferior to 23 and in patients with LM involvement with SYNTAX scores lower than 32.

On this basis, indications for revascularisation were defined on grounds of prognosis and symptoms in patients with significant coronary stenoses (>90% or FFR <0,80 for 50%–90% stenoses). The decision to perform PCI or CABG then depends on the anatomical situation and the SYNTAX score.

Significant stenoses on the left main or the proximal LAD, two- or three-vessel disease with LV dysfunction and large areas of ischaemia represent indications for revascularisation for prognosis. Symptom relief through revascularisation of significantly stenotic arteries will be sought in patients with angina refractory to OMT or heart failure symptoms (provided that those stenotic arteries supply an ischaemic and viable territory of more than 10% of the LV).

PCI will be preferred in single- and two-vessel disease without involvement of the LAD. In all the other situations, CABG is the gold standard. Nevertheless, PCI should be considered in single- and two-vessel disease with involvement of the LAD, in three-vessel disease with a SYNTAX score inferior to 23 and in isolated ostial or shaft lesions of the LM. PCI may be considered in isolated bifurcation lesions on the LM and in LM disease associated with two- or three-vessel disease with a SYNTAX score less than 33.

Acute coronary syndromes
The immediate objective of acute coronary syndrome (ACS) management is treatment of the culprit artery within adequate delays.15,16 Other lesions will be re-evaluated as in stable CAD. In cardiogenic shock, however, PCI of all major stenotic arteries is warranted.17

Risk stratification is the first step in the management of non-ST elevation ACS (NSTE-ACS). Very high-risk situations require emergency PCI as soon as possible. High-risk patients should be treated within 24 hours. Low-risk groups can be evaluated by functional imaging and, if positive, PCI should be done within 72 hours.

Primary PCI within two hours from the first medical contact is the gold standard for ST elevation myocardial infarction (STEMI).18-20 This delay should be reduced to 90 minutes in patients younger than 75 years of age presenting with large anterior STEMI with recent onset of symptoms.

If PCI is not available in this delay, thrombolysis should be performed.21 In the case of thrombolysis, routine PCI within 24 hours is mandatory.22,23 If thrombolysis fails, the patient should undergo emergency rescue PCI.24,25

CABG has shown increased mortality if performed early after STEMI. Therefore, PCI is the preferred approach. However, if anatomy is unfavourable for PCI or PCI fails, CABG will be indicated after three to seven days.26 Large ischaemic areas, persistent pain, life-threatening arrhythmia or haemodynamic instability (despite IABP) will precipitate emergency CABG.

Emergency cardiac surgery is the only vali- dated treatment of mechanical complications of myocardial infarction (papillary muscle rupture or ventricular septal defect).

Related conditions
Diabetes: Diabetic patients seem to benefit more from CABG than non-diabetic patients.27-30 Drugeluting stents (DES) are recommended in diabetic patients when PCI is performed.31

Patients requiring valve surgery: If cardiac surgery is necessary for an aortic or mitral valve indication, CABG should be performed concomitantly if coronary artery diameter stenosis ≥70%.32

Heart failure: In the presence of viable myocardium in the territory of the target area, CABG is the preferred mode of revascularisation.33,34 Surgical ventricular reconstruction in association with CABG may be considered in selected patients, although this technique showed no increase in survival. 35

Repeat revascularisation: When revascularisation fails, whether it is in the acute setting or at a later stage, PCI should be performed. After CABG, PCI of the native arteries and arterial grafts is safer than PCI of saphenous venous grafts and anastomotic sites.

Associated carotid disease: There is no consensus as to the timing of revascularisation when there are indications for carotid endarterectomy and myocardial revascularisation. Clinical presentation will usually dictate management.

Technical aspects of CABG
Arterial grafts remain the most significant improvement in CABG, especially with internal thoracic arteries;36-40 they should be harvested whenever possible.

Off-pump techniques and minimisation of aortic manipulation seem to minimise the incidence of peri-operative CVA.41,42

Technical aspects of PCI
Drug-eluting stents (DES) are recommended in stable CAD, especially for lesions on the LM, bifurcation lesions and lesions with narrow diameters. With dual anti-platelet therapy (DAPT), there are no differences in mortality between DES and bare metal stents (BMS), but the rate of in-stent restenosis is significantly reduced with DES.43,44

BMS will be favoured when DAPT is or likely to become problematic. Patients who are under long term anticoagulation, who are allergic to acetylsalicylic acid or thienopyridines, or who are suspected of having poor compliance would probably fare better with a BMS. BMS will also be preferred if non-elective surgery is planned in the short term, if there is an increased risk of bleeding and when medical history is difficult to gather, for example in emergency situations.

Some particular situations are worthy of mention: chronic total occlusions and occluded venous grafts. Chronic total occlusions may be treated when the vessel supplies a viable territory45 but these complicated procedures should be performed in specialised facilities by experienced operators. Occluded venous grafts are at risk of distal embolisation of thrombi. Distal protective devices reduce this complication.46,47

Other considerations include vascular access via the radial artery to reduce the risk of bleeding and systematic manual thrombo-aspiration during STEMI.48

New techniques such as the use of drug-eluting balloons to treat in-stent restenosis appear to be promising.49,50

Antithrombotic therapy
Anticoagulation is recommended in ACS and during catheterisation. Alongside unfractionated heparin (UFH), other molecules have been validated: low molecular-weight heparin (LMWH), bivalirudin and fondaparinux. LMWH is considered to be equivalent to UFH and both are viable options in all situations. Bivalirudin can be used in high-risk ACS including STEMI,51,52 whereas fondaparinux may be considered in lower-risk ACS, due to its lower bleeding risk.53

Acetylsalicylic acid is recommended for life when CAD is diagnosed.54 DAPT is recommended for 12 months after an ACS, for six to 12 months after a DES and for a month after a BMS. Clopidogrel is still a valid option, but, for STEMI, other agents such as prasugrel55 or ticagrelor56 should be preferred.

Glycoprotein IIb-IIIa inhibitors are now restricted to use in the catheter lab in ACS with high thrombotic burden.57,58

Conclusion
These guidelines discuss the respective roles of PCI and CABG, allowing cardiologists and surgeons to co-operate more efficiently. However, a sizeable proportion of recommendations are based solely on expert opinion. Therefore, significant research remains to better define the role of new therapies, techniques and devices.

Reference
1. Kolh P et al. Eur J Cardiothorac Surg 2010; 38 Suppl:S1-S52.
2. Wijns W et al. Eur Heart J 2010; 31(20):2501- 2555.
3. Davies RF et al. Circulation 1997; 95(8):2037- 2043.
4. Jahnke C et al. Circulation 2007; 115(13):1769- 1776.
5. Metz LD et al. J Am Coll Cardiol 2007; 49(2):227-237.
6. Mowatt G et al. Nucl Med Commun 2005; 26(3):217-229.
7. Meijboom WB et al. J Am Coll Cardiol 2008; 52(25):2135-2144.
8. Mowatt G et al. Heart 2008;94(11):1386-1393.
9. Botman KJ et al. Catheter Cardiovasc Interv 2004;63(2):184-191.
10. Pijls NH et al. J Am Coll Cardiol 2007;49(21):2105-2111.
11. Tonino PA et al. N Engl J Med 2009;360(3):213- 224.
12. Yusuf S et al. Lancet 1994;344(8922):563-570.
13. Boden WE et al. N Engl J Med 2007;356(15):1503-1516.
14. Serruys PW et al. N Engl J Med 2009;360(10):961-972.
15. Di Mario C et al. Int J Cardiovasc Intervent 2004;6(3-4):128-133.
16. Ijsselmuiden AJ et al. Am Heart J 2004;148(3):467-474.
17. Hochman JS et al. N Engl J Med 1999;341(9):625-634.
18. Boersma E. Does time matter? Eur Heart J 2006;27(7):779-788.
19. Nallamothu B et al. Heart 2007;93(12):1552- 1555.
20. Van De Werf F et al. Eur Heart J 2008;29(23):2909-2945.
21. Bonnefoy E et al. Eur Heart J 2009;30(13):1598- 1606.
22. Cantor WJ et al. N Engl J Med 2009;360(26):2705-2718.
23. Fernandez-Aviles F et al. Lancet 2004;364(9439):1045-1053.
24. Gershlick AH et al. N Engl J Med 2005;353(26):2758-2768.
25. Wijeysundera HC et al. J Am Coll Cardiol 2007;49(4):422-430.
26, Weiss ES et al. J Thorac Cardiovasc Surg 2008;135(3):503-511.
27. Hannan EL et al. N Engl J Med 2008;358(4):331- 341.
28. Hlatky MA et al. Lancet 2009;373(9670):1190- 1197.
29. Locker C et al. Ann Thorac Surg 2004;78(2):471- 475.
30. Sedlis SP et al. J Am Coll Cardiol 2002;40(9):1555-1566.
31. Stettler C et al. BMJ 2008; 337:a1331.
32. Vahanian A et al. Eur Heart J 2007;28(2):230- 268.
33. Allman KC et al. J Am Coll Cardiol 2002;39(7):1151-1158.
34. Smith PK et al. Ann Thorac Surg 2006;82(4):1420-1428.
35. Jones RH et al. N Engl J Med 2009;360(17):1705- 1717.
36. Loop FD et al. N Engl J Med 1986;314(1):1-6.
37. Lytle BW et al. Ann Thorac Surg 2004;78(6):2005-2012.
38. Sabik JF (III) et al. Ann Thorac Surg 2005;79(2):544-551.
39. Sabik JF (III) et al. J Thorac Cardiovasc Surg 2006;131(1):90-98.
40. Taggart DP et al. Lancet 2001;358(9285):870- 875.
41. Sedrakyan A et al. Stroke 2006;37(11):2759- 2769.
42. Shroyer AL et al. N Engl J Med 2009;361(19):1827-1837.
43. Kirtane AJ et al. Circulation 2009;119(25):3198- 3206.
44. Stettler C et al. Lancet 2007; 370(9591):937-948.
45. Hannan EL et al. Circulation 2006; 113(20):2406-2412.
46. Baim DS et al. Circulation 2002;105(11):1285- 1290.
47. Stone GW et al. Circulation 2009;119(5):680- 686.
48. Svilaas T et al. N Engl J Med 2008;358(6):557- 567.
49. Scheller B et al. N Engl J Med 2006;355(20):2113-2124.
50. Unverdorben M et al. Circulation 2009;119(23):2986-2994.
51. Stone GW. Lancet 2007; 369(9565):907-919.
52. Stone GW et al. N Engl J Med 2008;358(21):2218-2230.
53. Mehta SR et al. J Am Coll Cardiol 2007;50(18):1742-1751.
54. Collaborative meta-analysis of randomised trials. BMJ 2002;324(7329):71-86.
55. Wiviott SD et al. N Engl J Med 2007;357(20):2001-2015.
56. Wallentin L et al. N Engl J Med 2009;361(11):1045-1057.
57. Ellis SG et al. N Engl J Med 2008;358(21):2205- 2217.
58. Giugliano RP et al. N Engl J Med 2009;360(21):2176-2190.

x