Dissection of the Right Coronary Ostium and Sinus of Valsalva during Right Coronary Artery Angioplasty

Author Affiliations: From the Department of Cardiology and Hypertension, Institute of Cardiology, Jagiellonian University Medical College, Cracow, Poland, and the *Department of Interventional Cardiology, Institute of Cardiology, Jagiellonian University, Medical College, Cracow, Poland. The authors report no conflicts of interest regarding the content herein. Manuscript submitted February 27, 2008, provisional acceptance given May 23, 2008, and accepted June 19, 2008. Address for correspondence: Leszek Bryniarski MD, PhD, FESC, Department of Cardiology and Hypertension, Institute of Cardiology, Jagiellonian University Medical College, Cracow, Poland. E-mail: l_bryniarski@poczta.fm

_______________________________________________ ABSTRACT: We describe a case of dissection of the coronary ostium and sinus of Valsalva during a recanalization procedure to address chronic total occlusion of the right coronary artery (RCA). The patient was treated conservatively, and 1 month later, underwent angioplasty of the RCA and marginal branch. Based on a review of the incidence of, management strategies for, and causes of dissection of the RCA and ascending aorta, we conclude that the frequency of this condition may be underestimated and, in view of the increasing number of elderly patients, will rise over time.

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J INVASIVE CARDIOL 2008;20:E277–E280 Successful angioplasty, especially recanalization of a chronic total occlusion (CTO) of the coronary artery, depends on support provided by a catheter.1 Catheters that provide good support are relatively “aggressive” for the right coronary ostium, the proximal segment of the right coronary artery (RCA) and the left main artery (LM), and place the patient at risk of arterial dissection. Dissection of the coronary ostium may be accompanied by dissection of the sinus of Valsalva. This complication is unusual, but may lead to dissection of the ascending aorta, a life-threatening condition.2–9,13–17 Diagnosis and management of this complication is crucial for patient survival. Case Report. In May of 2003 we admitted a 67 year-old male with CCS Class III angina pectoris to the Department of Cardiology and Hypertension, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland for coronary angiography. His medical history included coronary heart disease for 10 years, anteroseptal infarction 7 years previously and inferolateral infarction 6 weeks previously. The patient had hypercholesterolemia, and his electrocardiogram (ECG) at rest showed a sinus rhythm of 70 beats per minute, a QS complex in leads V1–V4, pathological Q-wave, negative T-wave in leads II and III, aVF and a flat T- wave in leads V5–V6. Chest X-rays showed normal pulmonary vascular markings, a normal heart and an elongated aorta. Echocardiography indicated left ventricular enlargement (d-63 mm, s-40 mm), an ejection fraction (EF) of 40%, akinesis of the basal segments of the posterior and lateral walls, akinesis of the apical segments of the ventricular septum and lateral wall; the left atrium, 48 mm; the left ventricular posterior wall, 9 x 9 mm, the ventricular septum, 9 x 14 mm; thin and mobile mitral leaflets, a 32 mm aortic ring, aortic cusps that were slightly thickened, separation of 19 mm, right ventricle of 21 mm, mitral regurgitation grade 2/3 and aortic regurgitation grade 1. All laboratory tests were within normal limits. Physical examination revealed blood pressure (BP) of 100/70 mmHg and mitral regurgitation murmur on auscultation. The patient was taking bisoprolol (10 mg/day), perindopril (2 mg/day), isosorbide mononitrate (100 mg/day), molsidomine (8 mg/day), simvastatin (20 mg/day), acetylsalicylic acid (100 mg/day), ticlopidine (500 mg/day) and nitroglycerine (as needed). Coronary angiography showed disseminated lesions in the left coronary artery (LCA), 20% stenosis of the LM at the bifurcation, 20–30% stenosis of the left anterior descending artery (LAD), 60–65% stenosis of the proximal diagonal branch, 80% stenosis of the proximal marginal artery bifurcating into two branches, with 90% ostial stenosis. The predominant RCA was occluded in the proximal segment, with relatively good peripheral filling from the LCA collaterals (Figure 1). On ventriculography, we observed akinesis of the posterobasal segment, hypokinesis of the apical and anterolateral segment, and a left ventricular EF of ~40%. Following coronary angiography, we selected the patient for double-vessel angioplasty (RCA and marginal-branch angioplasty). For this procedure we used a 6 Fr Judkins Zooma right guiding catheter (Medtronic, Inc., Minneapolis, Minnesota) and a standard guidewire (Boston Scientific Corp., Natick, Massachusetts). After placement of the guiding catheter and contrast injection, we observed stasis of the contrast dye beyond the proximal RCA and retrograde stasis within the sinus of Valsalva (Figure 2). The patient reported strong retrosternal pain. The ECG was unchanged and his BP and heart rate (HR) were similar to baseline readings. We administered intravenous morphine (5 mg) and protamine sulphate (30 mg) and terminated the procedure. After 30 minutes the patient’s hemodynamics were stable and there was unchanged stasis of the dye in the sinus of Valsalva, so the patient was transferred to the coronary care unit. Emergent transthoracic echocardiography (TTE) and computed tomography (CT) showed no evidence of aortic dissection, pericardial fluid or any progression of aortic regurgitation. Echocardiography (performed each day) showed no progression of the dissection. After 5 days transesophageal echocardiography was used to assess both sinuses of Valsalva and both proximal parts of the coronary arteries. Normal blood flow was seen in the LM, LAD and circumflex (Cx) arteries, but there was no flow in the proximal RCA and no dissection of the right sinus of Valsalva or the proximal RCA. Markers of myocardial necrosis were negative. We discharged the patient on the seventh day with a prescription for all drugs noted previously except for ticlopidine. A month later, the patient was readmitted for follow-up coronary angiography and angioplasty. The RCA was unchanged and there was no dissection (Figure 3). We used a 7 Fr Judkins Zooma right guiding catheter for angioplasty and a standard guidewire to force the occlusion. One inflation with a balloon (1.5 x 20 mm, 12 atm pressure) indicated significant stenosis in the proximal and mid-RCA. Several subsequent inflations with a balloon (3.5 x 20 mm, 12 atm pressure) in the entire vessel provided good results with residual stenosis

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