Percutaneous coronary intervention in saphenous vein graft disease

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Chapter 25 Percutaneous coronary intervention in saphenous vein graft disease

AZFAR G. ZAMAN, JAGATH. HERATH

KEY POINTS

Long term outcome of CABG is limited by occlusive atherothrombotic disease of vein grafts in up to 50% of patients after ten years.

Repeat surgical intervention carries a high risk of morbidity and mortality.

PCI should be the preferred first route of revascularization in patients with previous CABG.

Stent placement in vein grafts is associated with a high (up to 20%) risk of distal embolisation and consequent complications.

Routine use of embolic protection devices significantly reduces procedural complications during vein graft PCI and where anatomy permits, their use is mandatory.

Three types of embolic protection devices are available: distal occlusion, proximal occlusion and distal filter. The type to use is determined by lesion location in the vein graft.

The routine use of glycoprotein IIb/IIIa inhibitors is not recommended for vein graft PCI. Some evidence suggests benefit in patients in whom a distal filter device is employed.

The risk of restenosis with BMS is high (10–20%) and early data with DES show promising results in restenosis reduction.

There is no benefit in using of PTFE coated stents over BMS.

There is no evidence for the use of thrombectomy devices in vein graft PCI.

For vein graft PCI both the radial and femoral access routes can be employed.

INTRODUCTION

Since first implantation of coronary grafts in 1967 the success of venous conduits in relieving myocardial ischaemia has been limited by their temporal attrition. Although internal mammary grafts have unsurpassed long term patency, utilisation is limited by scarcity. The use of gastroepiploic and radial arteries has been shown to be less than optimal.¹ Consequently, in spite of declining surgical revascularization rates worldwide, the use of venous grafts seems unlikely to diminish and treatment of symptomatic patients with degenerated venous grafts will remain a problem for interventional cardiologists.

Atherosclerotic disease in vein grafts can be either discrete (focal) or diffuse and degenerative. Most clinical trials forming the evidence base for percutaneous intervention in vein grafts report outcomes in patients with discrete disease. Initial trials demonstrated a high percentage of adverse events. The recognition that these were largely secondary to distal embolisation led to development of protection devices that have revolutionized percutaneous intervention in vein grafts with a significant reduction in periprocedural adverse events.

Vein graft disease progression and its timing

Three interlinked pathological processes – thrombosis, neointimal hyperplasia and atherosclerosis, which are temporally distinct, contribute to vein graft disease.^2,³ Awareness of the processes and their timing may help in optimising outcome from intervention.

Vein graft attrition occurring within a month of surgery is almost always due to graft thrombosis and the occlusion rate is 3 to 12% per month. Early thrombosis of vein grafts is caused by the combination of a prothrombotic state and technical factors present at the time of surgery.

Neointimal hyperplasia is defined as the accumulation of smooth muscle cells and extra cellular matrix in the intima and is the main pathological process that occurs one month to one year after graft implantation. It is similar to pathological changes that occur in native coronary arteries after balloon angioplasty.

Atherosclerosis is the main pathological process that contributes to vein graft occlusion one year and beyond after surgery.² The predisposing factors and the basic process of atheroma development are similar to those documented in native coronary arteries. However, there are a few distinct topographic, temporal, and histological differences in the pathology of vein graft disease.

The distinct morphological difference seen in vein grafts compared to native coronary arteries is that vein graft atheroma is diffuse, concentric, and friable with poorly developed or absent fibrous cap with little calcification. Intravascular ultrasound studies reveal the absence of focal compensatory enlargement (‘Glagov’s law’) of diseased vein graft segments.^3,⁴ Late graft thrombosis triggers recurrent ischaemia and is frequently seen in old degenerating grafts with advanced atherosclerotic disease.⁵

REVASCULARISATION FOR VEIN GRAFT DISEASE

Redo surgery

Recurrence of anginal symptoms is seen in up to 20% of patients within one year following surgical revascularisation followed by 4% of patients annually during the next 5 years, 19% at 10 years and 31% at 12 years.⁶

There are limited data comparing percutaneous revascularisation to repeat surgery in patients with angina recurrence. Repeat surgery achieves complete revascularisation in 92% of patients compared to 38% in the percutaneous intervention group. However, in-hospital complications are more common in surgical patients: death (7.3 % vs. 0.3%), Q-wave MI (6.1% vs. 0.9%), and low output syndromes (24% vs. 9%). Both procedures result in equal survival rates at one and six years with equal relief of angina but repeat intervention and/or revascularisation is more frequent in the percutaneous group (64% vs. 8%) at six years.^7,⁸

Given the high morbidity and mortality of re-operation reduced symptomatic benefit as compared to first bypass surgery,^8,⁹ percutaneous revascularisation should be the preferred first route for post surgery angina recurrence.

Percutaneous coronary intervention

Lesion pathology explains the different outcomes in vein grafts when compared to native coronary arteries.

Balloon angioplasty for vein graft disease has moderate procedural success limited by high periprocedural complication rate, high incidence of restenosis (35%) and high repeat revascularisation rate.^10,¹¹ Clinical trials show BMS to be superior to balloon angioplasty in vein graft lesions. The use of stents is associated with a high procedural success, superior clinical outcome, and reduced TLR. However, as compared to native vessels the restenosis rate remains high^12,¹³ coupled with higher periprocedural complications.

The high incidence of periprocedural complications is in the guise of myocardial necrosis resulting from distal embolisation. The major advance in vein graft intervention has been the advent of embolic protection devices for which extensive trial evidence exists for reducing complications from embolisation (vide infra).

The significant problems associated with vein graft intervention are:

1. distal embolisation;

2. no reflow; and

3. aggressive restenosis.

The use of DES in native coronary arteries has shown promising results with significant reduction in restenosis rates.^14,¹⁵ Limited data is available on the long term efficacy of DES in patients with vein graft disease. Most studies confirm a high procedural success rate but there is conflicting data on how DES would affect the clinical outcome. Two nonrandomized trials have shown a trend towards a reduction in MACE at six to nine months follow up.^16,¹⁷ The use of DES was associated with a lower restenosis rate (10% vs. 26.7%, P=0.03) and TVR (4.9% vs. 23.1%, P <0.01) at six to nine months. However, one study showed similar clinical outcome at 30 days, 60 days and 1 year.¹⁸