Acute anterior myocardial infarction due to aortosaphenous vein graft occlusion with very large thrombus burden

Abstract

A 75-year-old man, with a previous history of myocardial infarction and three-vessel coronary artery bypass grafting, presented with an acute anterior ST-elevation myocardial infarction. The vein graft to the left anterior descending artery was occluded with heavy thrombus burden, and the other grafts were patent. After administering a bolus dose of tirofiban and then undergoing percutaneous coronary intervention without stenting to the left anterior descending artery saphenous vein graft, intracoronary thrombolytic infusion was performed to maintain the patency of the vein graft. The patient was asymptomatic after medical follow-up. This may be an effective treatment option in patients with large thrombus burden and requires further investigation through large-scale trials.

Saphenous vein graft occlusion with thrombus formation is a substantial cause of acute myocardial infarction (MI) in patients who have recently or previously undergone coronary artery bypass graft (CABG) surgery. The therapeutic approach to thrombotic occlusions of sapheneous grafts in acute MI is still controversial. We present a case of acute anterior MI due to aortosaphenous vein graft occlusion with very large thrombus burden.

CASE PRESENTATION

A 75-year-old man was admitted to an emergency unit within 2 h of the onset of typical severe chest pain. He was a smoker, with a previous history of MI and hypertension, and had undergone CABG surgery (aortosaphenous vein grafts to the left anterior descending artery, obtuse marginalis branch of the circumflex artery and distal region of the circumflex artery) 10 years previously. Electrocardiography showed 3 mm ST-segment elevations in the precordial leads. A physical examination revealed a blood pressure of 130/80 mmHg and a pulse rate of 92 beats/min. He had no signs or symptoms of pulmonary congestion. The patient was admitted to the intensive care unit with a diagnosis of acute anterior MI. After admission, he was given 8000 U intravenous heparin, 5 mg intravenous metoprolol, 300 mg oral acetylsalicylic acid and 600 mg oral clopidogrel, and an emergency coronary catheterization was performed.

Coronary angiography revealed diffuse noncritical plaques within the right coronary artery, a patent aortocircumflex obtuse marginalis vein graft, an occluded aortocircumflex vein graft and an acutely occluded aorto-left anterior descending saphenous vein graft with very large thrombus burden (Figure 1).

Figure 1.

Coronary angiography revealing an acutely occluded aorto-left anterior descending saphenous vein graft with very large thrombus burden

Intravenous tirofiban (25 μg/kg bolus) was administered because of the diffuse thrombus image. Baloon angioplasty was performed using 3.0×30 mm Sprinter Semi-Compliant Over-the-Wire Balloon Dilatation Catheter (Medtronic Inc, USA), and Thrombolysis in Myocardial Infarction grade 2 flow was achieved (Figure 2). A distal protection device could not be used, because the device was not readily available at the centre. Subsequently, low-dose intracoronary tissue plasminogen activator (5 mg/h) was infused over 8 h because of the diffuse thrombus image after coronary angioplasty and the age of the patient. However, stenting was not considered in the acute phase, because data from previous studies have suggested that stenting can increase the risk of procedural complications in the acute phase with large thrombus burden (1,2). Postprocedural electrocardiography revealed complete resolution of ST-segment elevations and diminished chest pain. Treatment with acetylsalicylic acid, clopidogrel, heparin and metoprolol was reinitiated. Control coronary angiography was planned for one week later, but the consent of the patient could not be obtained. The patient was discharged on 300 mg of acetylsalicylic acid, 75 mg of clopidogrel, 50 mg of metoprolol, 40 mg of atorvastatin, 2.5 mg of ramipril and 5 mg of warfarin (target international normalized ratio of 2.0 to 3.0).

Figure 2.

Coronary angiography revealing thrombolysis in myocardial infarction grade 2 flow after balloon angioplasty

DISCUSSION

Acute MI involving vein grafts is an interesting clinical challenge for cardiologists. In patients with a saphenous vein graft as the culprit vessel in acute MI, mortality within one year is 20% (3,4). However, recent studies (3–5) indicate that vein graft infarcts carry a greater mortality risk than those involving native vessels, and that previous CABG surgery is an independent predictor of mortality.

Saphenous vein grafts exhibit different pathologies at different intervals after operation. Between 3% and 12% of saphenous vein grafts occlude within the first month after bypass surgery (6). At this early stage, the principal underlying mechanism is graft thrombosis, which is caused by a combination of diffuse endothelial disruptions, changes in blood rheology and alterations in flow dynamics. Most saphenous vein grafts examined more than two to three months after operation have developed a proliferative intimal fibroplasia. This is not friable, and is rarely a cause of stenosis or occlusion. However, vein graft atherosclerosis is a distinct pathological process that is often recognized as early as three to four years after operation and is characterized by lipid infiltration in areas of intimal fibroplasia. It is very friable and it is often associated with overlying mural thrombus. Vein graft atherosclerosis is seen in the majority of late saphenous vein graft stenoses. Some clinical trials (7,8) have shown that by 10 years after operation, approximately 30% of vein grafts are totally occluded and 30% of patent grafts exhibit some degree of stenosis or intimal irregularities characteristic of vein graft atherosclerosis.

The optimal strategy for treating these lesions remains unclear. Percutaneous coronary intervention (PCI) is the best treatment option in ST-segment elevation acute MI. However, contrary to the native vessels, PCI of saphenous vein grafts is mostly associated with serious complications such as distal embolization, no reflow and slow flow. To overcome these problems, there are embolic protection devices available for eligible patients. In some trials (Saphenous vein graft Angioplasty Free of Emboli Randomized [SAFER] [9], etc), use of distal protection devices during PCI of stenotic venous grafts was associated with a highly significant reduction in major adverse events. However, this study was performed with nonacute, stenotic and degenerated saphenous grafts. There is no evidence supporting the use of embolic protection devices in emergency situations, such as in patients with acute MI. In our patient, distal protection devices could not be used, because the device was not readily available at our centre.

With intracoronary stents, the outcomes of vein graft interventions have improved; however, there are no data suggesting that stents reduce the frequency of distal embolization. Observational data from another study (1,2) suggested that stenting should not be used in patients with large thrombus burden in the acute phase. Therefore, balloon dilation without stenting in acute phase, followed by stents if the patient is eligible, such as in our case, may be a therapeutic option.

Thrombolysis is also another treatment option for these patients and is an important therapeutic approach in the early phase of acute MI (10). Protocols, including dose, rate of infusion and type of thrombolytic agent, are not standardized and vary widely among institutions. In one study (11), intracoronary fibrin-specific thrombolytic infusion was suggested for fascilitating percutaneous recanalization of chronic total occlusion. In our patient, intracoronary thrombolytic infusion after PCI was administered according to this suggestion. However, there are no reliable data about intracoronary thrombolysis in patients with acute occluded saphenous vein grafts. In a recent report (10), it was shown that the administration of low-dose intracoronary streptokinase immediately after primary PCI improved myocardial perfusion. Also, in a comparative study (12), recanalization occurred in 71.4% of patients receiving intracoronary streptokinase compared with 25% of patients receiving intravenous streptokinase for acute MI (P<0.05). Because of the relationship between late saphenous graft occlusion and progression of the atherosclerotic process, antiplatelet therapy can potentially benefit the treatment for these patients. Thus, available data indicate that acetylsalicylic acid is effective in improving vein graft patency if commenced the day after surgery (6).

The platelet glycoprotein (GP) IIb/IIIa receptor antagonists have been shown to reduce the complications of PCI, which include slow-flow or noreflow phenomena, when given prophylactically to patients presenting with acute coronary syndrome with large thrombus (13). However, there are no adequate data about the possible role of GPIIb/IIIa antagonists alone before PCI in thrombus-associated vein graft lesions. Oral anticoagulants (warfarin), at any dose, are not routinely recommended because of an increased bleeding risk and no observable improvement in graft patency (6). Nevertheless, observational data from another study (14) suggest that warfarin in patients with acute coronary syndrome associated with large thrombus should be used to prevent persistant occlusion. In our patient, a GPIIb/IIIa antagonist was given prophylactically before PCI to maintain patency, and warfarin was commenced before discharge (target international normalized ratio of 2.0 to 3.0) to prevent any possible thrombus formation. Thus, in ST-segment elevation MI associated with thrombus in aortosaphenous graft, this treatment option (PCI plus low-dose thrombolysis) may be a good alternative strategy.