We reported a rare case of SSS without stenosis induced by multiple SAA that was diagnosed via comprehensive head and neck ultrasonography. The report was consented with the patient. The pathophysiological changes of SSS are stenosis or occlusion of the subclavian artery proximal to the origin of the VA. The most common cause is the atherosclerotic stenosis. The hemodynamic mechanism of SSS is the abnormal pressure gradient between the bilateral vertebral arteries due to the lesion of subclavian. 1 In general, a duplex ultrasound can be used to observe the characteristic spectrum of alternating directions in VA, due to SSS. Previous studies have shown that SSS is often associated with the degree of subclavian artery stenosis proximal to the VA to some extent.3
We found that the pathophysiological mechanisms of vertebral artery hemodynamics in SAA patients and subclavian artery stenosis patients were similar. Although uncommon, multiple SAA on the right is the cause of vertebral arterial blood reflux in our case. The origin of VA in our case was located on the aneurysm. SSS may be explained by Bernoulli's equation and Venturi-style management theory.9 According to the Bernoulli equation, the potential energy of Newton's liquid is inversely proportional to the kinetic energy. As the velocity (i.e., kinetic energy) increases, the pressure (i.e., potential energy) decreases. Vice versa,the pressure inside the aneurysm decreases, and the blood flow speed inside the aneurysm will inevitably accelerate. According to the Venturi tube principle, the acceleration of blood flow at the vertebral artery opening will cause the reduction of pressure at the same point, and then the aneurysm originating from the VA will "suck" the blood from the basilar artery or the contralateral VA༌which can cause vertebrobasilar insufficiency. Depending on the severity of SSS, there will be a variety of ischemic symptoms in the posterior circulation, which might be the source of occasional dizziness of our patient.
The symptoms of different SAAs are variable. 10 Nearly up to a third of patients with SAA were asymptomatic. 11 Saliou and his team explained that intrathoracic SAA is largely asymptomatic and difficult to detect on physical examination, and that symptoms may be directly related to the size of the aneurysm.12 However, upon reviewing previous studies, we found that the diagnosis of SAA was mostly achieved through advanced imaging examination, which gave the message of the location and size of SAA.10 However, most of these examinations could not provide hemodynamic parameters, such as CT, CTA, and MRA. Few studies analyzed the possible hemodynamic changes in the VA of patients with SAA. Ultrasonography is a reliable method for the evaluation of the VA hemodynamics. In general, it might be the only diagnostic tool sensitive enough to detect SSS I .3 In our case ,during the doppler detection of right VA, the spectrum changed from a mid-systolic inversion to a full cardiac cycle inversion while the patient kept fist-releasing with his right hand (Fig. 3).Through this clinical trials, the increased demand of blood in the right upper extremity resulted in the patient moving from SSS II to SSS III; the continuous variation in the form of vertebral artery spectrum was recorded vividly by VA ultrasonography. These advantages of ultrasonography lead us to recommend this method for the early and accurate diagnosis and follow-up of low-pressure lesions in the subclavian artery.
Compared with the aforementioned cases (Table 1), 5−8 the patient we reported were younger, with no obvious signs of arteriosclerosis, which suggests the right SAA was more likely to be congenital. In addition, our patient had multiple SAAs, and as the number increased, so did the severity of SSS. In the case of Otto, 5 the aneurysm was substantially large, and the patient's degree of SSS was also aggravated compare with other reports. Therefore, we speculated that the number and size of aneurysms might be responsible for the severity of SSS. In summary, our case provide increasing evidence that SAA is a possible underlying cause of SSS, suggesting that low-pressure lesions in the subclavian artery are a potential cause of vertebrobasilar insufficiency.