Treatment of Saphenous Vein Graft Thrombosis with Distal
Protection, Thrombectomy, and Adenosine Prior to Reperfusion:
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ABSTRACT: We report the treatment of an acute myocardial infarction presenting late with thrombotic total occlusion of a saphenous vein graft. A novel approach was used to prevent microvascular obstruction and reperfusion injury, with a distal protection system, a thrombectomy device, and administration of intracoronary adenosine prior to restoration of flow, so that initial reperfusion was done with maximal microvascular vasodilatation. J INVAS CARDIOL 2004;16:336–338 Key words: acute myocardial infarction; myocardial reperfusion injury; percutaneous transluminal coronary angioplastys While the timely restoration of infarct-artery patency is central to the optimal treatment of the patient with an acute myocardial infarction (AMI), the ultimate goal of early reperfusion therapy is to re-establish normal myocardial metabolism. While epicardial coronary atherosclerosis and thrombosis initiate most acute ischemic events, complete treatment of these conditions requires both rapid and effective epicardial coronary reperfusion as well as attention to preserving microvascular integrity. The closely related phenomena of microvascular obstruction and reperfusion injury underlie the often-observed paradox of a patent epicardial infarct artery yet poor distal runoff, whether manifest as slow or no reflow, reduced myocardial perfusion, or continuing or worsening ischemic injury after reperfusion. The present case describes a novel technique combining distal protection and thrombectomy devices with specific drug therapy given at the time of reperfusion to prevent microvascular obstruction. Case Report. A 74-year-old woman was free of angina since undergoing 2-vessel coronary bypass surgery in 1998. She had sudden onset of severe chest pain, nausea and diaphoresis at 10:30 pm, persisting through the night. The following day she presented to an emergency department and had 3.0 mm ST elevation in leads II, III, and aVF. She was treated with metoprolol, heparin, and eptifibatide and transferred for emergency angiography, 16 hours after the onset of pain. Angiography showed a patent LIMA graft to the LAD. The native LAD was totally occluded after the first septal and diagonal branches. The LAD diagonal had a proximal 70% stenosis and was a medium-to- large caliber vessel. The native left circumflex was patent. The large first circumflex marginal had several 50% stenoses. The native RCA was totally occluded. The saphenous vein graft to the distal right coronary was totally occluded in its midportion with a large thrombus meniscus (Figure 1). The RCA vein graft was treated using an 8 French MPA guide catheter (Cordis, Warren New Jersey). A temporary pacing lead was inserted. The total occlusion was crossed directly using the Guardwire distal protection system (Medtronic Inc., Minneapolis Minn.), which was then inflated to 4 mm. Unfractionated heparin and an additional bolus of eptifibatide (Integrilin, Millenium Pharmaceuticals, Cambridge, Mass.) were given. Rheolytic thrombectomy was done using the Angiojet XMI catheter (Possis Medical, Minneapolis Minn.) while the Guardwire was inflated (Figure 2). After completing 3 runs, the Angiojet catheter was positioned in the distal part of the graft, and adenosine (4 mg) was instilled through the Angiojet catheter while the Guardwire was being deflated, so that initial reperfusion occurred with maximal microvascular vasodilatation. There was transient demand pacing. Angiography was done to evaluate a severe mid-graft stenosis (Figure 3). The Guardwire was reinflated, and the graft lesion was treated with a 4.0 x 28 mm Ultra stent (Guidant Corporation, Santa Clara Calif.). A refractory stenosis in the stented segment yielded to high-pressure inflation with a 4.0 x 13 mm Powersail balloon (Guidant Corporation). The Angiojet was passed twice again, and reperfusion was done with instillation of another 4 mg Adenosine. Final angiography showed 0% stenosis (Figure 4) and TIMI 3 flow with a myocardial blush and somewhat delayed washout (TIMI Myocardial Perfusion Grade 2; Figure 5). Chest pain and injury pattern improved immediately. Creatine Kinase (IU/L) and CK-MB (mg/L) were 2,021 and 399 immediately after intervention, and fell thereafter. Discussion. Intervention upon thrombus-containing saphenous vein grafts is particularly likely to produce complications from microvascular obstruction. In the present case an additional insult to microvascular integrity was the late presentation with total occlusion. Angiographically-apparent microvascular obstruction and reperfusion injury portend worsened clinical outcomes in AMI. A meta-analysis of five thrombolytic trials confirmed the tight association between death and the failure to achieve brisk epicardial coronary flow, with diminished 30–day survival in patients having TIMI 0 and 1 vs. TIMI 2 versus TIMI 3 flow at 90 minutes. Even among patients with TIMI 3 epicardial flow, the TIMI myocardial perfusion (TMP) grade can further predict clinical outcomes. With this angiographic assessment of tissue-level flow, TMP grade 0 has no ground-glass myocardial blush, TMP grade 1 has myocardial blush that does not clear (“no reflow”), TMP grade 2 blush clears slowly, and TMP grade 3 blush largely clears within 3 cardiac cycles of the washout phase. In the TIMI 10b angiographic study, among patients with TIMI grade 3 epicardial flow after thrombolysis, TMP grade 0 or 1 was associated with a 5.0% mortality at 30 days, TMP grade 2 with 2.9% mortality, and TMP grade 3 with 0.7% mortality. Adenosine is an endogenously-produced molecule; its release in the myocardium is increased during ischemia as a result of the breakdown of ATP. Adenosine has a variety of effects at crucial signaling points. It is a potent short-acting vasodilator, giving it an autoregulatory effect in the case of ischemia. Multiple lines of evidence suggest an important role of endogenous adenosine in the myocardial protection associated with ischemic preconditioning. In animal models, intracoronary adenosine infusion mimics the benefits of ischemic preconditioning at maintaining coronary perfusion despite stenosis and thrombosis. Similar findings have been reported for patients undergoing PCI after pretreatment with intracoronary adenosine. A direct protective effect against reperfusion injury on cardiac myocytes has also been proposed, including in cardiac surgery. Adenosine also prolongs conduction through the atrioventricular node. Administration of adenosine, whether intravenous or intracoronary, can produce heart block and profound bradycardia. Rheolytic thrombectomy also commonly produces heart block requiring the use of a temporary pacemaker during intervention. Marzilli et al. demonstrated dramatic benefits from intracoronary adenosine in mitigating reperfusion injury during primary angioplasty for AMI. Upon the initial inflation of an over-the-wire balloon across the obstruction in the infarct artery, the guidewire was withdrawn and a high dose of intracoronary adenosine (4 mg) was slowly infused through the central lumen of the balloon catheter. On balloon deflation, reperfusion was released into the now-dilated distal bed. Interestingly, there were no episodes of bradyarrhythmias or AV block. Compared with controls, the adenosine-treated group achieved more TIMI 3 flow, with trends toward decreased CK release. There was a significant decrease in the cumulative clinical endpoint of recurrent ischemia, nonfatal MI, heart failure, and cardiac death in the adenosine-treated group, and improvement in LV function one week post-infarct was significantly greater in the adenosine-treated group. In trials evaluating the Percusurge system, totally occluded grafts were excluded. The technique described allows treatment of a totally occluded graft. In three cases we have noted that crossing an acute infarct occlusion of a vein graft with the Guardwire allows contrast penetration to the graft beyond the occlusion site; thus we have taken care to be prepared to inflate the distal protection balloon quickly once a “landing” position is identified. The approach used in this case has applicability limited to vein graft lesions or similarly easy-to-cross lesions, requiring that the total occlusion can be crossed directly with the Guardwire. In all subsequent cases attempted, this could be done. Exchange of the Angiojet catheter over-the-wire requires care not to bend the relatively fragile Guardwire. A rapid-exchange thrombectomy device (including the Percusurge Export device) might be used in some cases, though it is our impression that the Angiojet is a more efficient tool for removal of a large amount of thrombus. Either device allows delivery of drugs directly to the distal circulation. The Angiojet catheter has not been designed for drug injection; it is possible that the outflow lumen might contain particles that would be embolized when used this way, particularly if care is not taken to aspirate this lumen completely first. The seal around the guidewire can inspire air unless care is taken to tighten it completely. In cases at high risk for reperfusion injury, this technique may be useful for preserving microvascular integrity.