Large Coronary Aneurysm Complicated by Acute Myocardial Infarction: Combined Intravascular Ultrasound Imaging and Doppler Flow A

Antonio L. Bartorelli, MD, Luca Grancini, MD, Piero Montorsi, MD, Daniela Trabattoni, MD, Franco Fabbiocchi, MD
Antonio L. Bartorelli, MD, Luca Grancini, MD, Piero Montorsi, MD, Daniela Trabattoni, MD, Franco Fabbiocchi, MD
Coronary artery aneurysms (CAA) are characterized by abnormal dilatation of a localized or diffuse segment of the coronary arterial tree, up to 1.5 times the diameter of an adjacent normal segment.1 In Western populations, the incidence ranges between 1.5–4.9% and the most common association is with atherosclerotic coronary artery disease (CAD), which is considered the major cause of their formation.2 A congenital or inflammatory origin is found in 20–30% and 10–20% of cases, respectively.3 A high incidence (15–35%) of CAA has been reported in Japanese patients with Kawasaki’s disease.4 The role that CAA play in causing myocardial ischemia in an otherwise normal coronary arterial tree has been debated. Angina pectoris, silent myocardial ischemia and, occasionally, acute myocardial infarction have been reported in patients with CAA, even in the absence of underlying CAD.5 CAA repair has been recommended for those patients who are symptomatic or develop complications.6,7 We report a patient with a large CAA and no coexistent CAD, who developed myocardial infarction. This article describes the CAA clinical features, morphologic appearance as assessed by angiography and intravascular ultrasound (IVUS), and coronary flow dynamics studied with pulsed wave Doppler before and after successful obliteration with stent graft implantation. Case Report.A 64-year-old white woman with a history of moderate hypertension and hypercholesterolemia was admitted to a different hospital 3 hours after sudden onset of severe prolonged chest pain. She had no personal or family history of CAD or other remarkable diseases. Electrocardiogram (ECG) revealed T-wave inversion in the precordial leads. Serum levels of creatine kinase (CK) and CK-MB rose to 407 U/L (normal, Discussion. In this case, the etiology of the CAA could not be determined with certainty. Apart from moderate hypertension and hypercholesterolemia, both medically treated, there were no other risk factors for CAD. In addition, angiography and IVUS excluded coronary atherosclerosis in the aneurysmal and adjacent LAD wall. Furthermore, there was neither history suggesting Kawasaki’s disease nor laboratory evidence of collagen, infectious or inflammatory diseases. Finally, although a congenital origin could be inferred, this patient did not have arteriovenous fistula or other congenital abnormalities, which are often associated with this rare etiology.3 The CAA characteristics were studied with IVUS. This diagnostic technique was particularly useful to exclude underlying atherosclerosis and to determine CAA wall architecture, diameter and length (allowing the appropriate size of the stent graft to be selected) and to evaluate the adequacy of stent graft implantation. Interestingly, the CAA was not associated with atherosclerotic coronary lesions (a much less common condition compared to the coexistence of CAA and coronary obstruction)8 and was complicated by acute myocardial infarction. From a pathogenetic standpoint, CAA can cause stasis of blood, which in turn may promote in situ thrombosis with total lumen occlusion or distal embolization from mural thrombus.9–12 These flow alterations associated with thrombotic complications may have played a role in our patient, promoting myocardial ischemia and resulting in acute myocardial infarction. However, it is noteworthy that despite absence of coronary atherosclerosis, the Doppler flow study showed a marked reduction of CFR. The mechanism of this finding is not completely clear. Possible explanations could be a concomitant microcirculatory impairment13 or a CFR “pseudoreduction” due to the relatively high APV. The lack of a reference vessel CFR measurement makes it difficult to rule out the first hypothesis. However, diseases impairing microcirculation, such as diabetes, left ventricular hypertrophy or dilated cardiomyopathy, were excluded in our patient. Moreover, the significant reduction of APV and the normalization of CFR after CAA obliteration suggest that high baseline flow velocity could be the more likely explanation. High baseline flow velocity could be the result of compensatory arteriolar vasodilation induced by flow reduction inside the aneurysm. Alternatively, the anatomical condition of this CAA (spherical, with the inlet and outlet asymmetrically located) may have induced a whirling flow inside the aneurysmal lumen with a persistent acceleration of the blood beyond it. From the available data, however, it is not possible to attribute a causative role to the altered CAA flow dynamics in the pathogenesis of the acute ischemic event. Surgical treatment of CAA has been recommended for patients who develop symptoms or complications, but is still controversial.5–7 This is due to the lack of randomized data showing superiority of this strategy in comparison with medical therapy. The purpose of surgery, usually consisting of coronary artery bypass grafting and, if possible, aneurysm resection, is to prevent myocardial infarction, rupture or infection of the CAA. Endovascular techniques with newer interventional devices have been recently proposed in large and symptomatic CAA14 as an alternative to surgery. Spring coil embolization, although successfully used,15 may be complicated by parent vessel thrombosis or distal coil embolization. A novel and more appealing transcatheter technique uses composite endoluminal stent grafts to provide precise and effective aneurysm obliteration with preservation of lumen patency. Initially, autologous-vein coated stents were employed.16,17 This approach is limited by the large lumen (10 Fr) guiding catheter needed for delivery and the cumbersome and time-consuming stent-graft preparation, which includes surgical harvesting of a patient’s vein and accurate vein sewing to the stent ends. New stent grafts consisting of a thin elastic PTFE membrane integrated between two metal stents have been recently developed to overcome these limitations.18 These devices are currently under investigation for the percutaneous management of coronary artery rupture, aneurysm and fistula, and for the treatment of degenerated saphenous graft lesions or thrombus-containing lesions. In this patient, the previous myocardial infarction and the proximal LAD location of the CAA were the main reasons for our attempt to exclude the aneurysm with a PTFE-covered stent. Our acute result is consistent with the few cases in which the same device was successfully used to percutaneously obliterate CAA. However, in 2 out of the 3 previous reports, CAAs developed following PTCA or stenting and were smaller in size.19–21 Some concern has been created by other reports of late thrombo-occlusive events of PTFE-covered stents implanted for the treatment of occlusive coronary artery disease.18 Thrombus formation is likely due to delayed graft reendothelialization.22 Studies in a small number of patients have shown that prolonged antiplatelet therapy and high-pressure expansion of the stent graft monitored with IVUS may prevent thrombotic complications.23 However, further clinical experience is required to substantiate these observations. Severe in-stent graft restenosis was found at angiographic and IVUS follow-up in our patient, suggesting that exuberant tissue in-growth induced by the biomaterial may be another limitation. Experimental studies demonstrated that transmural endothelialization of PTFE grafts is minimal and that neointimal hyperplasia occurs mainly from the graft ends.24 These observations seem confirmed by the proximal location of the severe hyperplastic response observed in this case. Previous reports suggested that this could be due to the length of metallic struts not covered by the PTFE layer on each side of the Jomed stent graft.20 Since we used the newer generation of this device, which features nearly complete coverage of the stent, a direct interaction between the PTFE material and the vascular wall response could be inferred. Neointimal hyperplasia of coronary PTFE stent grafts may pose new problems for interventional treatment. Balloon angioplasty of in-stent graft restenosis could be limited by the inability to extrude the hyperplastic tissue through the PTFE membrane, while debulking techniques may carry the risk of graft material damage. These observations suggest that PTFE stent grafts can undoubtedly benefit from adjunctive technologies such as thrombo-resistant coatings25 and antiproliferative drugs delivered by the covering.26
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