Giant right sinus of Valsalva aneurysm led to proximal right coronary artery occlusion.

Introduction

Coronary artery stenosis or occlusion due to sinus of Valsalva aneurysm (SVA) is rare, while SVA leading to right coronary artery occlusion is extremely rare (1-3). We present a case of a giant right SVA combined with proximal right coronary obstruction, wherein good results were achieved in the patient with early surgical intervention.

Case Report

A 56-year-old male was admitted to our hospital with a 6-month history of shortness of breath and palpitation following physical exertion. Transthoracic echocardiography revealed a giant right SVA. The aortic valve was tricuspid with trivial aortic regurgitation and the ascending and descending aorta were within normal limits. The bi-dimensional images confirmed the presence of a right coronary sinus aneurysm with maximum dimensions of 56.82 mm×49.67 mm (Fig. 1). A computed tomography (CT) scan showed the giant right SVA. The proximal right coronary artery (RCA) was not visible, whereas the middle and distal RCA were clearly visible (Fig. 2a-2c). Electrocardiogram was normal.

Figure 1

Transthoracic echocardiography showing (a) a giant right SVA, parasternal short axis view at great vessels level, (b) aneurysm measuring: 56.82 mm×49.67 mm

SVA - sinus of Valsalva aneurysm

Figure 2

Preoperative and postoperative CT scan showing (a) Giant right SVA with proximal RCA occlusion, (b) Right sinus reconstruction and coronary artery bypass grafting to RCA, (c) Giant right SVA, (d) Right sinus reconstruction

SVA - sinus of Valsalva aneurysm; RCA - right coronary artery

Surgery was performed through a median sternotomy. Cardiopulmonary bypass was established by ascending aorta, superior vena cava, and inferior vena cava cannulation with left heart venting through the atrial septum. A giant SVA was observed at the right sinus (Fig. 3a). After cross-clamping the ascending aorta, cardioplegia solution was infused through the ascending aorta. The ascending aorta was opened at the border of the SVA and normal ascending aorta. The SVA involved the total right sinus, protruded forward and downward, and the orifice of the RCA could not be found inside (Fig. 3b). The proximal RCA on the SVA was occluded and the proximal RCA on the atrioventricular groove had a small lumen and a very thin wall. The middle RCA on the atrioventricular groove was normal. Coronary artery bypass to the middle RCA was performed immediately with greater saphenous vein (GSV) grafting, and cardioplegia solution was infused through the GSV graft (Fig. 3c). The right sinus was reconstructed with a vascular prosthesis patch ranging from the aortic annulus to the normal ascending aorta and from commissure to commissure (Fig. 3c). The proximal GSV graft was anastomosed to the normal ascending aorta. The cardiopulmonary bypass time was 148 min and cross-clamp time was 108 min.

Figure 3

Intraoperative images. (a) Giant SVA, (b) SVA involving the total right sinus, (c) Right sinus reconstruction with a vascular prosthesis patch and coronary artery bypass grafting with GSV graft to RCA

SVA - sinus of Valsalva aneurysm; GSV - greater saphenous vein;

RCA - right coronary artery

The duration of mechanical ventilation support was 27.25 h. The patient’s duration of stay in the intensive care unit was 89.83 h. The patient’s recovery was uneventful. He was discharged from the hospital 6 days after surgery. A postoperative CT scan showed good aortic root morphology (Fig. 2b, 2d).

Discussion

An unruptured SVA is usually asymptomatic in early years with symptoms typically manifesting between 30 and 45 years of age (4). During its expansion, it could cause obstruction of the right ventricular outflow tract, aortic regurgitation, conduction disorders, and more rarely, myocardial ischemia due to compression of the coronary arteries.

The reduction of coronary flow due to SVA compression is a rare condition and may lead to myocardial ischemia or infarction. Approximately 70% of SVAs occur in the right coronary sinus, 29% in the non-coronary sinus, and only 1% in the left coronary sinus (5). However, according to the literature, there is more risk of myocardial ischemia with left SVA than with right SVA (6). This may be associated with the space structure of the proximal left coronary artery, surrounded by the SVA, left atrium, and pulmonary trunk, whereas proximal RCA has more space to compensate for SVA compression. According to a collective review of the literature, the mechanism of coronary obstruction due to SVA is considered to be initiated by hyperextension of the coronary artery due to the bulge in the sinus of Valsalva. The coronary artery obstruction is caused by a thrombus within the aneurysm (7, 8). Most patients of SVA-associated coronary obstruction undergo coronary artery bypass grafting to guarantee a distal myocardial perfusion, despite the fact that there are reports of the successful treatment with SVA repair alone (9). In our case, giant right SVA led to occlusion of proximal RCA. Our viewpoint regarding the mechanism of SVA-associated coronary obstruction is novel. We believe that the right SVA expanded gradually, which may have made proximal RCA form a sharp angle, resulting in coronary flow reduction and proximal RCA occlusion. The proximal RCA on the atrioventricular groove had a small lumen and very thin wall due to this reduction in flow. The middle and distal RCA had normal lumen due to collateral circulation compensatory (Fig. 2a).

Conclusion

Surgery was performed to reconstruct right sinus with a vascular prosthesis patch and coronary artery bypass grafting with GSV to the middle RCA. The patient, reported herein, successfully recovered after surgical treatment with good early results. However, continued follow-up is required for long-term results.