Sinoatrial Nodal Artery Fistula to Bronchial Arteries Originating From the Right Coronary Artery in the Setting of Chronic Bronchiectasis and Coronary Artery Disease

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We present a 67-year-old man with a medical history of hyperlipidemia, hypertension, and emphysema, and who was a former smoker, with dyspnea on exertion and chest pain. Electrocardiogram showed right bundle-branch block without ischemic changes. Transthoracic echocardiogram (TTE) showed a normal ejection fraction over 55% and without any valvular heart disease. Given his symptoms and risk factors, the patient was referred for coronary computed-tomography angiography (CCTA), which showed obstructive disease in the distal left main coronary artery (LMCA) measuring at 60% stenosis with calcified and non-calcified plaque, another significant lesion in the mid-left anterior descending artery (LAD) with 70% stenosis, and normal left circumflex (LCx) artery and right coronary artery (RCA). The total calcium score was 426, which is in the 89th percentile for the patient's age and ethnicity. The patient was referred for cardiac catheterization.

The patient underwent cardiac catheterization from the right radial artery. Selective coronary angiography (CAG) was completed with a 5-French Tiger catheter (Terumo). CAG revealed an 80% stenosis of the LAD. The LMCA and LCx were unremarkable.  The patient subsequently received percutaneous coronary intervention (PCI) of the LAD. A 3.5 x 24-mm Synergy stent (Boston Scientific) was placed in the LAD without issue. The RCA was normal, however, an aberrant vessel was noted traversing into the left lung field beyond the pulmonary artery into the left lower lobe of the lung (Figure 1).  Opacification of a discrete mass of pulmonary parenchyma was observed as well (Video).

Bronchiectasis is defined as irreversible bronchial dilatation. It is usually associated with structural abnormalities of the bronchial wall, and a chronic or recurrent infection is usually present. Bronchiectasis may occur because of numerous pathologic processes and thus may be a feature of a number of various lung and airway diseases. Patients with bronchiectasis may have symptoms related to both airway infection and underlying or associated conditions, such as chronic bronchitis, emphysema, asthma, or bronchiolitis obliterans. Nearly all patients with bronchiectasis have chronic cough with purulent sputum production and recurrent pulmonary infections.¹ In addition, bronchial arteries in the setting of bronchiectasis can be hypertrophied and recruit systemic arteries to increase perfusion.

The sinoatrial nodal artery (SAN) branch most commonly originates from the right coronary artery (68.0%), with the left circumflex being the second most common point of origin (22.1%). The most common course of SAN was found to be retrocaval (47.1%), followed by precaval (38.9%) and pericaval (14.0%).² Precaval SANs course across the crest of the right auricle, while the retrocaval track through the interatrial groove. The pericaval course is toward the SAN and runs more frequently anterior to the superior vena cava. Very little data is available on anomalous SAN and on arterial collateralization of patients with chronic bronchiectasis from coronary arteries. Our patient undergoing cardiac catheterization demonstrated a SAN in direct communication with bronchial arteries and lung parenchyma.

Anomalous vessels and collaterals arising from the RCA are not an uncommon finding in the cardiac catheterization laboratory; collaterals from the RCA to other coronary arteries is almost commonplace in contemporary coronary angiography. Fistulas to the pulmonary artery are also observed during coronary angiography and have been reported to be present in approximately 0.1% to 0.2% of cases during invasive coronary angiography, and 0.9% by CCTA.^3,4 However, direct communication with lung parenchyma is extremely rare. Initially, it was thought that this was a pseudo sequestration to the lung; however, further evaluation of the CCTA proved otherwise. CCTA confirmed that the SAN traversed superior and posterior into the mediastinum, and volume rendered imaging demonstrated a fistula between the SAN and bronchial arteries (Figure 2). Saccular ballooned bronchiectasis was noted in addition to hypertrophied bronchial arteries, which recruited perfusion from the SAN (Figure 3); this was also apparent on coronary angiography with opacified saccular structures. Bronchial circulatory dilatation and collateral vessels are a response to chronic pulmonary ischemia and decreased pulmonary blood flow through hypertrophy and enlargement in an effort to maintain blood flow to the affected lung and maintain gas exchange through systemic-pulmonary arterial anastomoses.⁵ Bronchial artery collateral flow is a more common finding with systemic arteries usually stemming from the aorta; however, in this case, the collateral flow was recruited directly from the SAN.

Bronchiectasis on CTA may have air-fluid levels and appear as large, cystic areas with a honeycomb appearance. Several mechanisms are involved in the development of bronchiectasis. These include bronchial infection, inflammation, peribronchial fibrosis, and bronchial obstruction. Underlying structural abnormalities of the bronchial wall, either congenital or acquired, may also be present in some patients.⁵ In many patients with bronchiectasis, several mechanisms mutually contribute to the development of airway deformities, and infection is almost always present. Bronchial artery hypertrophy can accompany this as well, as evidenced by this case.

Upon follow-up, our patient had marked improvement with angina and dyspnea following PCI, therefore treatment of the fistula was conservative. Possible treatment can be percutaneous intervention with coils; a surgical approach with ligation of the vessel can be considered as well if it is determined that the fistula was the cause of dyspnea.

Affiliations and Disclosures

From the Department of Cardiology, Maimonides Medical Center, Brooklyn, New York, USA.

Consent statement: Our patient has given explicit written and fully informed consent that images pertaining to his procedure and the nature of his pathology will be used for publication and educational purposes. Full document can be furnished upon request.

Disclosures: The authors report no financial relationships or conflicts of interest regarding the content herein.

Address for correspondence: Richard Casazza, MAS, Department of Cardiology, Maimonides Medical Center, 4802 10th Avenue, Brooklyn, NY, 11219, USA. Email: rcasazza@maimonidesmed.org; X: @tesslagra

References

1. Chang AB, Redding GJ. Bronchiectasis and chronic suppurative lung disease. In: Wilmott R, Bush A, Deterding R, Ratjen F, Sly P, Zar H, Li AP, eds. Kendig's Disorders of the Respiratory Tract in Children. Elsevier; 2019:439-459.e6. doi: 10.1016/B978-0-323-44887-1.00026-2
2. Vikse J, Henry BM, Roy J, et al. Anatomical variations in the sinoatrial nodal artery: a meta-analysis and clinical considerations. PLoS One. 2016;11(2):e0148331. doi: 10.1371/journal.pone.0148331
3. Andreou AY, Georgiou GM, Avraamides PC. Right posterior sinoatrial node artery showing a pericaval course: a previously undescribed mode of termination. Surg Radiol Anat. 2010;32(6):609-612. doi: 10.1007/s00276-009-0593-9
4. Yildiz A, Okcun B, Peker T, Arslan C, Olcay A, Bulent Vatan M. Prevalence of coronary artery anomalies in 12,457 adult patients who underwent coronary angiography. Clin Cardiol. 2010;33(12):E60-64. doi: 10.1002/clc.20588
5. Walker CM, Rosado-de-Christenson ML, Martínez-Jiménez S, Kunin JR, Wible BC. Bronchial arteries: anatomy, function, hypertrophy, and anomalies. Radiographics. 2015;35(1):32-49. doi: 10.1148/rg.351140089

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