Case report
Left main coronary artery stenting in a patient with acute coronary syndrome complicated by embolisation of the diagonal branch of the left descending artery. Intra-vessel ultrasound/virtual histology findings

Introduction

Pathological studies have shown that necrotic rich core plaques at high risk of rupture – so-called thin cap fibroatheroma (TCFA) – are infrequently present in the left main coronary artery (LMCA), while they are common in the proximal segments of three main coronary arteries [1]. Similarly, angiographic studies as well as intra-vessel ultrasound analyses have observed that plaque rupture rarely occurs in the LMCA or distal part of coronary arteries, whereas it is far more common in the proximal part of coronary vessels, especially in the left anterior descending artery [2, 3]. The reasons why vulnerable plaques tend to spare the LMCA are still poorly under­stood [4].

We present the case of a female patient with acute coronary syndrome caused by vulnerable plaque in LMCA con­firmed by the novel method of coronary artery imaging/ virtual histology (IVUS/VH).

Case report

The 44-year-old woman, a regular smoker, presented with diffuse chest pain. The first anginal symptoms on exertion started 2 weeks earlier. Six h before admission she felt prominent chest discomfort at rest with severe apprehension. She had elevated cholesterol levels, and positive family history. On admission, she was haemo­dynamically stable; her blood pressure was 160/80 mmHg, and the heart rate 75/min. No symptoms of heart failure were observed. The electrocardiogram demonstrated normal sinus rhythm 75/min, ST-depressions in lead I, aVL, and negative T wave in lead V2-V5. The cardiac troponin I level was markedly elevated (10.2 ng/ml). Loading doses of clopidogrel (600 mg), and aspirin (300 mg) were given, and urgent coronary angiography was performed. It revealed LMCA stenosis and occluded small postero-lateral branch of the left circumflex artery (fig. 1). The dominant right coronary artery was without any significant lesions. The intravascular ultrasound examination (IVUS) was performed, to estimate the true LMCA diameter. The minimal lumen area was 4.2 mm² (fig. 2 A), and no symptoms of fresh thrombus were found. The virtual histology (VH) analysis revealed a thin cap fibroatheroma, with a large necrotic core (32%) and 12% of dense calcium (fig. 2 B). We decided to perform percutaneous coronary intervention of LMCA. A 0.014’’ guidewire was passed down the left anterior descending artery (LAD), and 4.0 × 16 mm TAXUS Liberte (Boston Scientific, USA), paclitaxel-eluting stent was implanted, using the direct-stenting method. The stent was then post-dilated, with a 4.0 × 12 mm non-compliant balloon, at the pressure of 22 atm. On angiography no residual stenosis was revealed, and in IVUS, the MLA increased to 10.1 mm².

After completion of the procedure the patient reported the recurrence of anginal pain. The electrocardiogram showed ST-segment elevations in leads I, aVL, V4-V6. Coronary angiography revealed no signs of thrombosis within the implanted stent, but it showed occluded middle part of the large first diagonal branch (fig. 3). An intracoronary bolus of abciximab was administered, and then intravenous infusion was started. The lesion was crossed with a guidewire with difficulty, and balloon angioplasty was performed, with perfect angiographic results (no residual stenosis, TIMI 3 flow). After the procedure, the infusion of abciximab was continued for 12 h. The patient also received unfractionated heparin, aspirin, clopidogrel, atorvastatin, metoprolol and ramipril. She responded well to the therapy. The peak troponin I level was 37.6 ng/ml, and peak CK-MB 42 IU/l. Echocardiography showed left ventricular ejection fraction of 48% with akinesia of the lateral wall and hypokinesia of the anterior wall. She made an uneventful recovery. The patient was discharged 10 days later in good general condition, on aspirin, clopidogrel, atorvastatin, ramipril and metoprolol. After 9 months she was still asymptomatic and had no complaints.

Discussion

Left main coronary artery stenosis is the most challenging lesion in patients with acute coronary syndromes. Since the mass of myocardium at risk is very high, the patient is often in cardiogenic shock, and the risk of death is high. In the present case we decided to perform angioplasty of the left main coronary artery despite having on-site cardiac surgery. Coronary artery bypass grafting is currently the routine treatment for unprotected LMCA disease, but with the substantial progress in interventional techniques and equipment there is a growing body of evidence that LMCA lesions may be treated effectively and safely by interventionalists [4, 5]. Our decision also resulted from the fact that the patient had non-ST-elevation acute myocardial infarction, with a prominent unstable plaque in LMCA requiring urgent revascularization. The presence of a dominant right coronary artery, without any significant changes, further reduced the risk of the procedure.

The novel method of coronary artery imaging – spectral analysis of IVUS radiofrequency, virtual histology (IVUS/VH) – was used in the presented case to measure the size of the vessel, as well as to confirm the presence of unstable plaque. The IVUS/VH data gave us the opportunity to obtain detailed quantitative information both on the overall plaque composition and the anatomical relation of specific plaque components to the lumen of the vessel [6]. We found a large extent of necrotic core and other elements of atherosclerotic plaque, as well as the presence of TCFA. The presence of TCFA, with large avascular, hypocellular lipid cores, makes the plaque very prone to rupture, which may result in epicardial artery occlusion, myocardial infarction and sudden cardiac death [1, 7].

In our case, although the stent was implanted without predilatation, the procedure was

complicated by distal embolisation and occlusion of a large diagonal artery [8]. Since the occlusion was very difficult to cross, and no thrombus was found on baseline IVUS examination, it is highly probable that the embolic material was composed of the squized plaque. This rare but possible complication should always be taken into consideration while treating unstable patients, especially when the lesion is situated in a proximal part of a large vessel. We also advise evaluating the final angiogram after the procedure very carefully, to avoid overlooking the presence of distal embolisation. The administration of GP IIb/IIIa receptor blockers may not be helpful in such cases, and the role of distal protection devices is yet to be established.

References

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