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STEMI Induced by Coronary Artery Dilatation
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A53-year-old male presented with chest pain at a pre-hospital care provider, and an ECG showed an anterior MI. The patient received 60-mg oral prasugrel (Effient, Eli Lilly/Daiichi Sankyo; Efient, Lilly France), 250-mg IV aspirin and 0.35-mL IV enoxaparin, and was transferred to the cath lab. He had no significant medical history except for dyslipidemia.
Coronary angiography (Figure 1) was performed using left radial access, which revealed left anterior descending (LAD) artery total occlusion of the middle segment with diffuse proximal disease involving all coronary arteries with dilatation/ectasia and irregularities. PCI was performed via a right common femoral artery approach to ensure maximal guide catheter support. Before PCI, we delivered glycoprotein IIb/IIIa inhibitors (bolus plus infusion) and catheterized the left main artery with a 6F JL 3.5 guiding catheter. A guidewire (BMW, Abbott Vascular) was positioned in the distal segment of the LAD and manual thrombus aspiration was performed. After aspiration, TIMI 3 flow was obtained with severe stenosis of the mid LAD. A bare-metal stent (Multi-Link, Abbott Vascular; 12 mm x 3.5 mm) was deployed (Figure 2, panel A) because the result after aspiration of the thrombus was not optimal. Although the result after stent deployment was not ideal, we chose not to further intervene because of the risk of occluding the side branch, given the trifurcation of the LAD distal to the location of the stent.
Romain Didier
The final result is shown in Figure 2, panel B. No complications occurred during the 5-day hospital stay. Dual antiplatelet therapy (aspirin 75 mg plus clopidogrel 75 mg) and warfarin were prescribed for 1 month with follow-up aspirin plus warfarin thereafter.
Definition and Classification
Figure 1. Coronary angiography showed diffuse proximal dilatation. Panel A: Left anterior descending artery with middle occlusion. Panel B: The right coronary artery.
Figures 1 and 2 provided by Didier, et al; printed with permission
Figure 2. Panel A: Angioplasty with a bare-metal stent. Panel B: The final angiographic result.
Figure 3. Classification of coronary artery dilatation. In fusiform aneurysms, the length (L) of the dilated portion of the coronary artery is more than its transverse diameter (T), whereas in saccular aneurysms, as shown in the diagram, the length (L) of the dilated portion is less than its transverse diameter (T).
Figure provided by Didier, et al. Reproduced and modified with permission from Díaz-Zamudio M, et al. Radiographics. 2009;29:1921-1938.
Figure 4. Potential causes of coronary artery dilatation.
Abbreviations: CA, coronary artery; CAA, coronary artery aneurysm; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.
Figure provided by Didier, et al. Reproduced and modified with permission from Díaz-Zamudio M, et al. Radiographics. 2009;29:1921-1938.
Figure 5. Three episodes of acute MI in heavily dilated right coronary arteries. The second and third MI occurred just after warfarin administration was discontinued.
Abbreviations: AMI, acute MI; tPA, tissue plasminogen activator.
Reproduced from Sakakura K, et al. 2005 with permission of Japanese College of Cardiology.
Coronary artery aneurysms are defined as coronary artery segments that have a diameter exceeding the diameter of normal adjacent coronary segments or the diameter of the patient’s largest coronary vessel by 1.5 times, and involve less than 50% of the total length of the vessel. Coronary artery aneurysms have been classified in three different ways on the basis of the vessel wall composition and the morphologic structure (Figure 3).
In the first method of classification, coronary artery aneurysms can be either “true” aneurysms or “false” aneurysms (pseudoaneurysms), a distinction that is based on the number of layers in the vessel wall. The vessel wall in true aneurysms is composed of three layers: the tunica intima, tunica media and tunica adventitia. However, in pseudoaneurysms there is a loss of wall integrity, as well as transition from the three-layered wall to an outwardly single/double layer as a result of disruption of the media and external elastic membrane. Pseudoaneurysms are frequently a result of blunt chest trauma or catheter-based coronary interventions.
Second, coronary artery aneurysms can be classified by their morphologic appearance. In saccular aneurysms, the transverse diameter is greater than the longitudinal measurement of the aneurysm, whereas in fusiform aneurysms, the longitudinal measurement is greater than the transverse diameter. Saccular aneurysms are frequently seen distal to an area of proximal-related stenosis, are often multisegmental and are more prone to thrombosis and rupture. In contrast, fusiform aneurysms are not known to be related to a proximal stenosis.
Third, in most reports, a giant aneurysm is defined as a maximal diameter exceeding 20 mm in adults or 8 mm in children.
Ectasia, on the other hand, is dilatation of the coronary vessel 1.5 times the diameter of normal adjacent coronary segments and involves more than 50% of the total length of the vessel. This classification may have prognostic implications, with the worst outcomes observed in types I and II (Figure 3).
The most common etiology of coronary artery aneurysm is atherosclerosis. However, there are numerous causes of coronary ectasia or aneurysms (Figure 4), such as Kawasaki disease in children with focal dilatation or inflammatory disorders with diffuse arterial disease. More rarely, fistulous communication with the pulmonary artery also can induce this phenomenon.
Prognosis
The natural history of atherosclerotic aneurysms is usually favorable, but there are conflicting reports. The prognosis is directly related to the severity of the concomitant obstructive CAD. According to the Coronary Artery Surgery Study (CASS) Registry, there was no difference in 5-year survival between patients with and without aneurysms who had occlusive CAD.
Treatment
There are no controlled clinical studies to evaluate optimal therapy for coronary artery aneurysms because of the rarity of this condition. Medical management depends on the presence or absence of coexisting obstructive CAD rather than the sole presence of coronary ectasia or aneurysm. In the absence of obstructive CAD, treatment is not well established because it is based mainly on case reports and, as a result, continues to be a therapeutic dilemma.
Nicolas Amabile
After acute MI, some cases (Figure 5) were described using conservative measures. This treatment consists of attempts to prevent thromboembolic complications with anticoagulant therapy and administration of antiplatelet drugs. Sakakura and colleagues presented three acute MIs in the same patient with diffuse coronary dilatation induced by atherosclerosis. They found that for each new recurrence, interruption of warfarin was detrimental, resulting in repeat thrombosis. We believe that a stent should be considered only if the result after manual aspiration is not satisfactory, as stents act like a foreign body and are more likely to induce repeat thrombosis after discontinuation of anticoagulants.
Renu Virmani
Surgery may be considered as a means to avoid complications, but only for patients who present with obstructive CAD or evidence of embolization leading to myocardial ischemia, as well as for patients with evidence of enlargement of saccular coronary artery aneurysms with an increased risk for rupture.
Conclusion
Atherosclerosis is the most common etiology of coronary artery dilatation. The majority of the time, aneurysms are asymptomatic, but the management of acute thrombotic events is coronary angiography followed by aspiration, and stenting should be avoided. The conservative measures appear to provide the best results; in other words, use of manual aspiration only, when possible, and anticoagulant and antiplatelet therapies to prevent recurrence of acute events.