SAPVF is a vascular anomaly characterized by the penetration of systemic chest wall arteries into the lung parenchyma and was first reported by Burchell and Clagett in 1947 [3]. SAPVF can be divided into congenital and non-congenital types. Approximately 15% of SAPVF are congenital [1], and non-congenital types develop in patients with postoperative, with trauma, or with various inflammatory or infectious diseases of the lung and pleura such as pneumonia, pneumothorax, or lung abscess [1, 2]. Specifically, most non-congenital types have been reported to be postoperative cases such as coronary artery bypass graft (CABG) or VATS surgery, and non-postoperative cases in adult are rare.

We compiled a list of cases with non-congenital, non-postoperative SAPVF described in the relevant literature [4,5,6,7]. The causes of these cases were listed as a complications of Takayasu's disease, trauma, and or various inflammatory or infectious diseases. In the present case, there was no obvious history of surgery, trauma, or various inflammatory or infectious disease. Furthermore, there were no serological or pathological findings suggesting the presence of fungal infection. The history of heavy smoking, and the presence of giant bullae and diffuse emphysematous changes suggested the presence of chronic inflammation in the thoracic cavity, which was considered to be the cause of SAPVFs.

The SAPVF has few symptoms and is often discovered by chance during routine physical examination. Patients with symptoms present with hemoptysis, dyspnea, pulmonary hypertension, and chronic chest pain. [2, 8]. The natural outcome of SAPVF is not yet well known. Described complications include hemoptysis or congestive heart failure [9]. Therefore, several authors said that intervention is recommended because of the future risk of endocarditis, angina pectoris, and congestive heart failure [9]. Contrast-enhanced CT should always be performed for SAPVF, as it plays an important role in detecting the causes of SAPVF and related complications. Angiography is considered essential in the diagnosis of SAPVF. It makes the full anatomic structure of the lesion more obvious and can clarify the extent and location of the lesion.

SAPVF can be treated by embolization or surgical resection. Recently, embolization has become the preferred method because it causes minor trauma, minimal loss of lung parenchyma, and does not require general anesthesia [9]. Embolization is thought to be more effective in patients with a single or few vessels than in those with many abnormal vessels. In patients, as in our case, who have many abnormal vessels, surgery is the treatment of choice to cure and prevent recurrence of SAPVF. Multiple non-congenital SAPVFs which had no obvious history of surgery, trauma, or various inflammatory or infection disease are very rare, and this case is the first report to describe the surgical treatment of multiple SAPVFs.

Surgical treatment includes local excision, segmental resection, lobectomy, ligation, and even pneumonectomy [10]; in recent years, VATS has been actively performed [11]. In the current case, adhesions between the SAPVF and chest wall, which contained many aberrant blood vessels, could be safely separated using a vessel sealing system during VATS. In fact, no complications, such as bleeding, were observed intra- or post-operatively, and the surgery was performed safely. Therefore, surgery should be considered as the first choice for SAPVF that is difficult to treat with embolization.