From the *Division of Cardiovascular Medicine, University of Louisville, and §Jewish Hospital Rudd Heart and Lung Institute, Louisville, Kentucky. The authors report no conflicts of interest regarding the content herein. Manuscript submitted February 3, 2009, provisional acceptance given February 17, 2009, and final version accepted February 20, 2009. Address for correspondence: Michael P. Flaherty, MD, Division of Cardiology, 550 S. Jackson Street, ACB 3rd Floor, University of Louisville, Louisville, KY 40292. E-mail: firstname.lastname@example.org
_______________________________________________ ABSTRACT: We report an unusual case of unstable angina resulting from a rare subacute submedial intramural hematoma within the mid-proximal segment of the left anterior descending coronary artery 3 days after successful coronary angioplasty and stenting. An additional stent was deployed to contain the hemorrhage with good angiographic and clinical results.
J INVASIVE CARDIOL 2009;21:e128–e131 Symptoms of myocardial ischemia that present subacutely following elective percutaneous transluminal coronary interventions (PCI) typically raise the suspicion for either stenotic interplay within a new plaque or subacute closure of the treated vessel. Since the advent of coronary stents, subacute vessel closure (in-stent thrombosis) occurs in less than 1% of patients.1 Alternatively, acute coronary syndromes due to vessel closure or near vessel closure, owing to dissection and intramural hematoma formation (with or without an intact intima), are less rare, yet, almost invariably present acutely, manifesting often within 6 hours after the procedure.2–6 In contrast, subacute manifestations of coronary intramural hematomas in the post-PCI period are either extremely uncommon or underreported.7,8 We present a rare cause of unstable angina presenting subacutely following coronary artery stenting. Case Presentation. A 36-year-old diabetic male with chronic stable angina and evidence of inducible myocardial ischemia in two large segments in the anteroseptal and apicolateral regions by myocardial perfusion imaging underwent diagnostic cardiac catheterization. Coronary angiography revealed two severe, diffuse, irregular calcified lesions in the mid-proximal left anterior descending (LAD) and mid-distal left circumflex (LCx) arteries (Figure 1A). The plan was to perform a staged angioplasty of both lesions beginning with the LAD. A 0.014 inch Balanced Middleweight Universal® guidewire (Abbott Vascular, Abbot Park, Illinois) was placed across the LAD lesion into the distal LAD. Using a Galaxy 2 intravascular ultrasound (IVUS) imaging system and a 40 MHz, Atlantis Plus catheter (Boston Scientific, Natick, Massachusetts), the reference vessel diameter was estimated at approximately 3.7 mm. Angioplasty was performed initially with a 3.5 mm x 6 mm Flextome® Cutting Balloon® (Boston Scientific) inflated at 6 and then 9 atm. Additional angioplasty and stenting was performed on the LAD lesion using a 3.5 mm x 20 mm Taxus® Express2™ paclitaxel-eluting stent (Boston Scientific) deployed at nominal pressure, followed by postdilatation of the stent with a 3.5 mm x 12 mm Quantum Maverick® balloon (Boston Scientific) at 16 atm. Figure 1B demonstrates a very good angiographic result, save for minor overdilitation of the distal edge of the stent and resultant slight reference vessel mismatch. Notably, no acute dissection or evidence of intramural hematoma was noted angiographically (Figure 1B) or by IVUS (Figures 1C–D). Prior to the procedure, the patient was loaded with 600 mg of clopidogrel and following the procedure, continued on clopidogrel (75 mg) and aspirin (325 mg) daily. The patient was brought back 3 days later for elective PCI of the LCx lesion, at which time the patient was complaining of worsening, and now unstable, angina that began 2 days after the index procedure. The electrocardiogram revealed new, deep symmetric T-wave inversions in leads V1–V6. Coronary angiography demonstrated a new severe and eccentric tapering luminal narrowing immediately proximal to the edge of the stent and extending proximally toward the LAD ostium (Figure 2A). There was no angiographic evidence of in-stent narrowing or coronary artery dissection. The stenosis did not respond to intracoronary nitroglycerin (300 µg). Angiographic suspicion for coronary artery intramural hematoma was corroborated using IVUS. IVUS images in Figure 2 demonstrate a crescent-shaped extraluminal area with patchy echogenic/echolucent zones indicative of a large intramural hematoma causing significant luminal narrowing that extended from the proximal edge of the stent just prior to the LAD ostium. Interestingly, while confirming the diagnosis of intramural hematoma, the complete IVUS examination revealed no evidence of intimal or medial dissection or disruption (Figure 2C). In an attempt to contain the occlusive hemorrhage, direct (1:1) stenting across the intramural hematoma using a Taxus Express2 stent (3.5 mm x 24 mm) deployed nominal pressure, and postdilatation with a 3.75 mm x 15 mm Quantum Maverick balloon was performed. The distal edge of the stent overlapped 3 mm into the proximal edge of the first stent and landed approximately 4 mm from the ostium of the LAD with an excellent angiographic result (Figure 3) that was confirmed with IVUS. Angiography performed during follow-up stenting of the LCX 1 week later demonstrated no luminal narrowing within either of the LAD stents. Discussion. The estimated overall incidence of iatrogenic coronary artery intramural hematomas complicating PCI is approximately 7%, occurring most often in diabetics at any site along the normal and/or within the treated (diseased) segment.5 Importantly, this number also includes those hematomas resulting from accumulation of blood within the media, owing to intimal dissection without re-entry (exit), accounting for approximately 50% of all cases.5 A slightly less common (incidence
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