Flow-Dependent Changes Resulting in Restoration of Patency of the Left Internal Mammary Artery Graft After Documented Atresia
- Volume 23 - Issue 5 - May 2011
- Posted on: 4/29/11
- 0 Comments
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ABSTRACT: The left internal mammary artery (LIMA) has been the conduit of choice in coronary artery bypass grafting (CABG). Atresia of the LIMA is a common finding after CABG in patients with less than critical disease of the native vessel. However, it is extremely rare for an atretic LIMA to restore its normal caliber after progression of native coronary artery disease. We report a patient in whom the LIMA was occluded 2 years after CABG, but was found to be completely patent 5 years later, after worsening of the left anterior descending artery disease.
J INVASIVE CARDIOL 2011;23:207–209
The left internal mammary artery (LIMA) has been the conduit of choice in coronary artery bypass grafting (CABG).1 Atresia of the LIMA is a common finding after CABG in patients with less than critical disease of the native vessel.2 However, it is extremely rare for an atretic LIMA to restore its normal caliber after progression of native coronary artery disease. We report a patient in whom the LIMA was occluded 2 years after CABG, but was found to be completely patent 5 years later, after worsening of the left anterior descending artery (LAD) disease.
A 67-year-old female was admitted with diarrhea. She underwent CABG in 2005 for severe triple-vessel coronary artery disease. She was found to have an atretic LIMA graft on a subsequent angiogram 2 years later (Figure 1).
At that time, percutaneous coronary intervention (PCI) of the native LAD was successfully performed using drug-eluting stents (DES). She remained asymptomatic since then. The patient denied any cardiac complaints on this admission. Her initial work-up was unremarkable. On the second hospital day, she complained of chest pain and was found to be diaphoretic and hypotensive. Electrocardiography (ECG) showed atrial fibrillation with rapid ventricular response and ST elevation in leads V1–V2. Hemodynamic stabilization was achieved with amiodarone and digoxin. Emergency left-heart catheterization was performed and thrombus was noted at the site of the prior stent without flow in the distal vessel (Figure 2). The right coronary artery and LIMA graft, respectively, were not visualized, as they were known to be totally occluded and atretic.
Primary percutaneous coronary intervention (PCI) of the LAD was performed. Thrombus was aspirated and balloon-facilitated PCI using DES was accomplished uneventfully. ECG changes normalized after intervention and restoration of thrombolysis in myocardial infarction (TIMI) 3 flow, accompanied by relief of the chest pain. Post-PCI angiography showed competitive flow in the distal LAD (Figure 3).
The LIMA graft was engaged for further evaluation and selective angiography showed a widely patent LIMA graft with prompt opacification of the LAD antegradely and retrogradely to the anastomosis site (Figure 4). The patient remained hemodynamically stable and had an uneventful hospital course.
After the initial development by Dr. Green,1 LIMA grafting to the LAD gained widespread acceptance as the arterial conduit of choice. Initial enthusiasm was limited by early post-operative spasm resulting in catastrophic consequences.3 Later comparison of arterial and venous conduits showed clear benefit of the LIMA graft with long-term patency rates of 90–95%, as compared to 50–60% for venous grafts at 10 years.4-6 Development of atherosclerosis in the LIMA is extremely rare and usually is not flow-restrictive. The most common cause of initial failure of a LIMA graft is generally due to technical issues at the anastomosis site.7 Despite overall excellent patency, it is not uncommon to find diffuse narrowing ultimately leading to graft failure. Various causes have been suggested including damage during harvesting, lack of innervations and vascular supply of the dissected graft, spasm and inflammation as a result of post-pericardiotomy syndrome7 and steal physiology from a large, undivided proximal branch of the LIMA.8 Competitive flow9 from a less than severely diseased native vessel leading to the longitudinal narrowing of LIMA was first described by Barner10 in 1974 and was thought to be a result of disuse atrophy. Same phenomenon was later described by Geha and Baue11 and named “distal thread phenomenon."12 Case series and observational studies were highly sugestive of the competitive flow from the native vessel as the underlying mechanism of this entity.13–15
Flow dynamics in arterial grafts are different from venous grafts.16 The diameter and flow reserve in a venous graft does not change with time. However, early after surgery, the LIMA has higher flow velocities compensating for the smaller diameter and low flow reserve. With progression of the native coronary artery disease, there is a fall of pressure in the distal arterial bed that increases the diameter of the LIMA with improved flow reserve and a decrease in the flow velocity. This physiologic change in the caliber of the LIMA is therefore a result of autoregulation that occurs in response to changes in the competitive flow in the native recipient vessel and its distal bed.17 In this case report, we described a patient in whom the LIMA had the distal thread phenomenon 2 years after implantation as a result of less than critical disease in the native LAD. With the progression of the disease in the native vessel, the flow dynamics reversed and there was a fall in the distal pressure that led to augmentation of flow in the LIMA. Resultant shear stress enhanced the release of endothelial nitrous oxide leading to smooth muscle relaxation and restoration of patency of the LIMA graft. Thus, although the LIMA may have appeared to become non-functional during high flow in the native LAD, flow through the LIMA can markedly increase when needed if the recipient artery becomes occluded proximally. Surgical guidelines have consequently been expanded to include arterial grafting of coronary arteries with less than critical stenosis.18,19 Another mechanism was described by Shammas et al,20 who reported a case of string sign reversal after interruption of rich collateral flow to the distal vessel supplied by the graft. They went on to suggest that the adaptability of the IMA graft may be explained, at least in part, by the preservation of the vasavasorum and nervorum, as it is mobilized as a lymphovascular pedicle. This would also be consistent with observations that an IMA graft can increase its size and augment its flow to match the physiologic demand of the territory supplied.21
Our case raises the question: Why was the LIMA closed in 2007, when presumably severe disease in the LAD was present, and its caliber restored in 2010 when the patient presented with stent thrombosis? If we believe that the LIMA restores its caliber when there is decline of the flow in the native vessel, then it should have reopened at the previous event when LAD intervention had to be performed for significant disease in the LAD. We reviewed the angiogram from 2007 and it was noted that there was a moderate-to-severe lesion in the LAD. Unfortunately there was no functional assessment of the lesion done at that time and the operator opted to perform PCI of the LAD in light of the patient’s symptoms and the fact that the LIMA was atretic. Certainly, it would have been useful to have more functional information at that time in terms of stress test or fractional flow reserve to answer this question.
Conclusion. Although very rarely22–24 described in the literature, this case highlights the importance of understanding the flow dynamics in arterial grafts, especially the LIMA. If LIMA appears to be atretic after CABG, there is a possibility of reopening of the LIMA with progression of coronary artery disease in the native vessel. Moreover, the question arises of whether we should use the LIMA for a moderate lesion in a patient who is undergoing open heart surgery for valvular lesions or significant multivessel disease with less severe stenosis of the native LAD. Further investigation into the underlying mechanisms and the determinants of this ability to maintain a recruitable patency are clearly indicated and will provide important clinical insight into the care of such patients.