The latest consensus on perforator atherosclerosis in China is released, and one article summarizes the consensus on guidelines

Perforating branch atheromatous disease (BAD) is a common type of acute ischemic stroke.

Common perforating arteries include lenticulostriate arteries (LSA), paramedian pontine arteries (PPA), thalamic geniculate artery, anterior choroidal artery, Heubner's artery and thalamic perforating artery.

BAD accounts for 10% to 15% of all causes of ischemic stroke, and is clinically manifested as early neurological deterioration (END) dominated by progressive motor deficiency (PDM).
The clinical prognosis is poor at 48-72h after onset.

Traditional imaging is difficult to find the vascular lesions of BAD, which makes early diagnosis difficult in clinical practice.

Based on this, considering the lack of uniform standards for the diagnosis and treatment of BAD, the Cerebral Small Vascular Disease Branch of the Chinese Stroke Society established an expert group, combined with the current research status at home and abroad, to write this expert consensus to guide the clinical diagnosis and treatment of BAD.

 1 Pathogenesis of vascular risk factors.
Studies have shown that the incidence of traditional vascular risk factors such as hypertension, diabetes, and hyperlipidemia in patients with BAD and cerebrovascular disease is similar; but there are also studies that suggest that large-vessel atherosclerotic plaques Block position is closely related to BAD.

The risk factors of BAD are basically the same as those of large atherosclerosis, including hypertension, diabetes, hyperlipidemia, smoking, and hyperhomocysteinemia.

The current understanding of BAD tends to be more closely related to large vessel atherosclerosis.

 Pathology currently believes that there are four main pathogenesis of BAD: ①The atherosclerotic plaque of the carrier artery blocks the opening of the perforating artery, and the mechanism of causing BAD is large atherosclerosis; ②The atherosclerotic plaque of the carrier artery extends to the penetrating artery.
The opening of the branch artery causes vascular occlusion, and the plaque that causes BAD is located at the junction of the responsible aorta and the perforating artery; ③Atherosclerotic plaque at the opening of the perforating artery causes vascular occlusion; ④Unstable plaque at the opening of the perforating artery The mass falls off and causes vascular occlusion (Figure 1).

The application of high-resolution MRI angiography can clearly show the responsible aorta plaque, the plaque at the junction of the responsible aorta and the perforating artery, and the plaque at the opening of the perforating artery to identify the cause of BAD.

2 Clinical manifestations The common age of onset of BAD is between 54 and 75 years old, most of which are men.

The clinical manifestations of BAD are diverse, ranging from minor strokes with mild symptoms and recurrent TIAs to severe dysphagia with severe clinical symptoms, complete paralysis of one side of the limbs, and even death.

According to the blood supply area, BAD is divided into LSA and PPA lesions.

The clinical manifestations of ischemic cerebrovascular disease in the blood supply area of ​​LSA (diameter 300～840μm) often include: lateral movement disorder (high incidence, severe symptoms), eccentric sensory disorder, cognitive decline, and dominant hemispheric disease may appear Aphasia and mental and psychological disorders, non-dominant hemisphere lesions can cause hemispheric neglect, etc.

The clinical manifestations of ischemic cerebrovascular disease in the blood supply area of ​​PPA (200～300μm in diameter) often include: lateral movement disorder (hemiparesis-complete paralysis, multiple upper limbs than lower limbs), dysarthria, hemisensory disorder, ataxia , Central facial paralysis and other symptoms.

 3 Diagnosis is limited by the fact that traditional MRI technology cannot clearly display the perforating artery.
The current diagnostic criteria used in BAD are based on the area of ​​the perforating artery blood supply and imaging examinations that show the characteristics of the lesion.

 LSA regional ischemic stroke: ①Meet the diagnostic criteria of acute ischemic stroke; ②DWI shows that the infarcts in the corresponding blood supply area involve 3 levels and above in the horizontal position; ③The blood supply area of ​​LSA is: most of the putamen and the outer part of the globus pallidus , The head and body of the caudate nucleus, the forelimbs of the internal capsule, the upper part of the internal capsule and the radial crown around the ventricle (Figure 2).

 PPA regional ischemic stroke: DWI showed that the infarct was connected to the brain surface on the ventral side of the pons, and the lesion was close to the midline, on one side, and no more than the midline (Figure 3).

 Exclusion criteria: ①imaging showed that the responsible large vessel stenosis ≥50%; ②imaging showed that the intracranial aorta, external carotid artery and vertebral artery had unstable plaques that could cause arterial-arterial embolism; ③DWI showed the presence of cortical infarction and watershed infarction And multiple cerebral infarctions; ④ Cerebral infarctions caused by other clear causes, such as immune or infectious vasculitis, cardiogenic cerebral embolism, fat embolism, abnormal platelet and coagulation function, etc.

 4 The treatment manifests itself as the treatment of repeated TIA ➤ Intravenous thrombolysis: Intravenous thrombolysis is currently the most important measure to restore cerebral blood flow.
Thrombolytic drugs include rt-PA, urokinase and tenecteplase, etc.
, rt-PA and urokinase It is the main thrombolytic drug currently used in my country.

It is currently believed that the thrombolytic time window that can effectively save the ischemic penumbra tissue is within 4.
5h or within 6h.

 ➤Antiplatelet therapy: Although the current research shows that for BAD, the efficacy of antiplatelet drugs is uncertain and controversial, there are still case reports with a small sample size suggesting that antiplatelet drug therapy is effective.

 ➤Anticoagulant therapy: Anticoagulant drugs include unfractionated heparin, low molecular weight heparin, heparin, oral anticoagulant and thrombin inhibitor.

The use of anticoagulants for stroke types other than cardiogenic stroke is still controversial, and there are no reports of long-term anticoagulants for the treatment of internal capsule warning syndrome.

 ➤Statins: Observational studies suggest that high-intensity statins can improve the prognosis of patients with acute ischemic stroke, but the efficacy of BAD needs to be confirmed by further high-quality randomized controlled studies.

 ➤Neuroprotective drugs: In theory, neuroprotective drugs can improve the prognosis of patients with ischemic stroke.

Animal studies have shown that neuroprotective drugs can improve neurological deficits, but clinical research conclusions are still inconsistent, and the efficacy needs to be further confirmed.

 The treatment of acute lacunar infarction is recommended for patients with acute lacunar infarction who meet the criteria for intravenous thrombolysis.
rt-PA intravenous thrombolysis is recommended.

For patients who exceed the intravenous thrombolytic time window, it is recommended to follow the treatment plan for small strokes in the efficacy study of clopidogrel in the treatment of acute non-disabling cerebrovascular events.
The specific treatment is: the first dose of clopidogrel 300 mg, followed by each 75mg per day, combined with aspirin 100mg per day for 21 days.

 Treatment of early neurological deterioration.
Specific treatments include improving cerebral perfusion and circulation (intravenous thrombolysis, antiplatelet, anticoagulation, fibrillation, volume expansion, etc.
), statins and neuroprotective treatments.

 5 Experts suggest that no matter which form of BAD is onset, there is a lack of strong evidence-based medical evidence in the current treatment, which needs to be confirmed by further clinical studies.

It is recommended that no matter what kind of clinical manifestations, on the basis of early rt-PA intravenous thrombolysis, head MRA+DWI examinations should be completed as soon as possible, and HR-MRI and enhanced sequence examinations should be carried out if possible.

For patients with END, experts unanimously recommend the use of tirofiban within 12-24 hours (intravenous infusion of tirofiban 0.
4μg·kg-1·min-1 for 30 minutes, followed by intravenous infusion of 0.
1μg·kg-1 ·Min-1 for at least 24 to 48 hours); for patients with clinical manifestations of TIA, most experts believe that the application of tirofiban is effective, and experts recommend that tirofiban be used immediately when symptoms appear (intravenous infusion of tirofiban 0.
4 μg·kg-1·min-1 for 30 min, followed by intravenous infusion of 0.
1 μg·kg-1·min-1 for at least 24 to 48 hours).

Subsequent to cilostazol-based dual antiplatelet therapy, or cilostazol combined with anticoagulant therapy.

Cilostazol 200 mg daily combined with aspirin 100 mg daily (load 300 mg) or clopidogrel daily 75 mg (load 225 mg) combined for at least 1 week after changing to any antiplatelet drug alone can significantly slow the progression of the disease, if it fails , You can switch to cilostazol combined with argatroban or low-molecular-weight heparin anticoagulation therapy.

 Yimaitong is compiled from: Men Xuejiao, Chen Weiqi, Xu Yuyuan, Zhu Yicheng, Hu Wenli, Cheng Xin, Bai Feng, Wang Lihua, Mao Ling, Qu Hui, Lu Peiyuan, Liu Jun, Sun Zhongwu, Sun Li, Li Yusheng, Wu Zhongliang, Wu Danhong, Wu Bo,Gu Wenping,Fan Yuhua,Zhou Guoyu,Ni Jun,Gao Feng,Huang Shixiong,Cao Yongjun,Peng Dantao,Xie Chunming,Cai Zhiyou,Xu Yun,Wang Yilong,Lu Zhengqi.
Consensus of Chinese Experts on Perforating Atherosclerosis[J].
Chinese Journal of Stroke ,2021,16(05):508-514.