Emergent Primary PCI of Anomalous LAD

Approximately 0.3–2% of patients may have anomalous origins of the coronary arteries.^1,2 Anomalous origin of the left coronary artery (LCA) or left anterior descending (LAD) artery from the right sinus has been well described. In persons in whom the course involves an interarterial track between the aorta (Ao) and pulmonary artery (PA), an increased incidence of sudden death has been reported,³ particularly during or shortly after exercise. This has been felt to be due to transient occlusion of the anomalous LAD from increased blood flow through the Ao and PA as the anomalous LAD courses between them, possibly causing myocardial ischemia.^4–6 In an elective setting, further anatomic delineation with other methodologies such as cardiac magnetic resonance (MR) imaging is recommended. In this case report we present an emergent percutaneous coronary intervention (PCI) of an anomalous LAD arising from the right sinus of Valsalva and coursing between the Ao and PA in a nonsurgical candidate. Case Report. An elderly 75-year-old Caucasian male presented to the emergency department with increasing shortness of breath and decreased mental status. The patient had a history of hypothyroidism, hypertension, hyperlipidemia, peripheral vascular disease and mild aortic stenosis with mild aortic insufficiency. The patient had a new left bundle branch block (LBBB) and wide complex tachycardia requiring electrical cardioversion in the emergency department, where he was also electively intubated. The patient’s initial BNP was elevated at 2,470, initial troponin was elevated at 43, creatine kinase (CK) was elevated at 680, CK-MB was elevated at 71, and CK-MB percentage was elevated at 10.5%. The patient’s chest X-ray was consistent with pulmonary edema. He was admitted to the CCU department. An echocardiogram was performed and revealed an ejection fraction of 10–15% with global hypokinesis and mild aortic valve disease. The patient continued to demonstrate wide complex tachycardias, LBBB and increasing cardiac enzymes. Creatinine clearance at this time was calculated at 34 cc/minute. At that juncture, the patient was brought emergently to the cardiac catheterization laboratory. Cardiac catheterization was performed. The right coronary artery (RCA) was occluded, with filling of the distal RCA and posterior descending artery (PDA) from left-to-right collaterals. The LCA supplied the lateral and anterior lateral wall. The LAD arose from the right sinus and had an interarterial course as deduced from the RAO view and the location of the “dot” sign.8 A 70% hazy lesion with angiographic evidence of thrombus was noted in the proximal portion. Further angiography was limited in light of the patient’s renal status. Given the critical nature of his clinical condition, it was decided to proceed with PCI. The patient was given bivalirudin (Angiomax™, The Medicines Company, Cambridge, Massachusetts) at the standard dose of 0.75 mg/kg intravenous bolus followed by standard intravenous infusion. A 6 Fr JR4 guiding catheter (Medtronic, Inc., Minneapolis, Minnesota) was advanced to the ostium of the anomalous LAD. With difficulty, a 0.014 in. x 180 cm Prowater guidewire (Abbott Laboratories, Redwood City, California) was advanced into the distal LAD. A 2.5 x 12 mm Taxus® II drug-eluting stent (Boston Scientific Corporation, Natick, Massachusetts) was advanced and deployed at 12 atmospheres. This was followed by overlapping proximally, with a 2.5 x 8 mm Taxus II drug-eluting stent. The angiographic result was excellent, with 0% residual stenosis. There was no dissection, tear or perforation. TIMI 3 flow was observed upon completion of the procedure. The patient’s postprocedure course was uneventful. He was quickly weaned from ventilatory support. His cardiac enzymes and ECG returned to baseline. The patient was discharged home 4 days postprocedure. His predischarge echocardiogram revealed an increase in left ventricular function, with an ejection fraction estimated at approximately 30%. Discussion. Sudden cardiac death and/or myocardial ischemia have been described in patients with an anomalous LAD or LCA. Several mechanisms have been brought into play, including anatomic configurations at the ostium and the anatomic course of the anomalous vessel. The ostial abnormalities have been thought to include a slit-like orifice, ostial tissue flaps or ridges or acute angle of origin. The arterial course of the anomalous vessel includes a posterior, interarterial, anterior or septal course. In the absence of symptoms or demonstrable ischemia, the posterior, anterior and septal courses have been felt to generally have a benign course.^9,10 However, there have been reported cases of these routes requiring revascularization.¹¹ In these case reports, as in most cases of an interarterial route, a surgical approach was utilized. The increased incidence of sudden death has been attributed to physiologic phenomena. It has been hypothesized that during or after exercise, enlargement of the PA and Ao may cause compression or kinking of the anomalous vessel resulting in flow impairment.¹² Further confirmation of the interarterial route with imaging such as cardiac MR is recommended. In most previous cases, surgery appears to have been the revascularization method of choice.¹³ In our review of the literature, we could find only two previous cases of stenting (primary or otherwise) of anomalous LCA/LAD.^14,15 To our knowledge, this is the first case report demonstrating stenting of the anomalous LAD coursing between the Ao and PA, as well as the first involving the use of a drug-eluting stent. This case report adds to the small, but growing body of evidence suggesting that with adequate guide support and guidewire manipulation in selected patients with anomalous origins of coronary vessels, primary PCI can be performed safely with acceptable short-term clinical outcomes.

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