Impact of Supratentorial Cerebral Hemorrhage on the Complexity of Heart Rate Variability in Acute Stroke.

Acute stroke commonly affects cardiac autonomic responses resulting in reduced heart rate variability (HRV). Multiscale entropy (MSE) is a novel non-linear method to quantify the complexity of HRV. This study investigated the influence of intracerebral hemorrhage (ICH) locations and intraventricular hemorrhage (IVH) on the complexity of HRV. We recruited 93 supratentorial ICH patients (male 59%, mean age 61 years), and the locations of ICH included basal ganglia (n = 40), thalamus (n = 35), and lobar (n = 18) group. Continuous one-hour electrocardiography signals were obtained from patients after admission, and the complexity index was defined as the area under the MSE curve. The complexity index was lower in lobar ICH (21.6 ± 7.9) than basal ganglia (27.9 ± 6.4) and thalamus (28.5 ± 7.2) groups. The complexity index was inversely correlated with initial stroke severity (r = -0.26), size of hematoma (r = -0.35) and ICH score (r = -0.26), especially among patients with intraventricular hemorrhage (r = -0.60, -0.60, and -0.41 respectively). A higher complexity can predict a good functional outcome (adjusted odds ratio 1.09, 95% confidence intervals 1.00-1.19) at post-stroke 3 months. In summary, more severe stroke and larger hematoma volume resulted in lower complexity of HRV. Lobar hemorrhage and IVH had great impacts on the cardiac autonomic function.

2017 Taiwan lipid guidelines for high risk patients.

In Taiwan, the prevalence of hyperlipidemia increased due to lifestyle and dietary habit changes. Low density lipoprotein cholesterol (LDL-C) and non-high density lipoprotein cholesterol (non-HDL-C) are all significant predicting factors of coronary artery disease in Taiwan. We recognized that lipid control is especially important in patients with existed atherosclerotic cardiovascular diseases (ASCVD), including coronary artery disease (CAD), ischemic stroke and peripheral arterial disease (PAD). Because the risk of ASCVD is high in patients with diabetes mellitus (DM), chronic kidney disease (CKD) and familial hypercholesterolemia (FH), lipid control is also necessary in these patients. Lifestyle modification is the first step to control lipid. Weight reduction, regular physical exercise and limitation of alcohol intake all reduce triglyceride (TG) levels. Lipid-lowering drugs include HMG-CoA reductase inhibitors (statins), cholesterol absorption inhibitors (ezetimibe), proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, nicotinic acids (niacin), fibric acids derivatives (fibrates), and long-chain omega-3 fatty acids. Statin is usually the first line therapy. Combination therapy with statin and other lipid-lowering agents may be considered in some clinical settings. For patients with acute coronary syndrome (ACS) and stable CAD, LDL-C < 70 mg/dL is the major target. A lower target of LDL-C <55 mg/dL can be considered in ACS patients with DM. After treating LDL-C to target, non-HDL-C can be considered as a secondary target for patients with TG ≥ 200 mg/dL. The suggested non-HDL-C target is < 100 mg/dL in ACS and CAD patients. For patients with ischemic stroke or transient ischemic attack presumed to be of atherosclerotic origin, statin therapy is beneficial and LDL-C < 100 mg/dL is the suggested target. For patients with symptomatic carotid stenosis or intracranial arterial stenosis, in addition to antiplatelets and blood pressure control, LDL-C should be lowered to < 100 mg/dL. Statin is necessary for DM patients with CV disease and the LDL-C target is < 70 mg/dL. For diabetic patients who are ≥ 40 years of age, or who are < 40 years of age but have additional CV risk factors, the LDL-C target should be < 100 mg/dL. After achieving LDL-C target, combination of other lipid-lowering agents with statin is reasonable to attain TG < 150 mg/dL and HDL-C >40 in men and >50 mg/dL in women in DM. LDL-C increased CV risk in patients with CKD. In adults with glomerular filtration rate (GFR) < 60 mL/min/1.73m2 without chronic dialysis (CKD stage 3-5), statin therapy should be initiated if LDL-C ≥ 100 mg/dL. Ezetimibe can be added to statin to consolidate the CV protection in CKD patients. Mutations in LDL receptor, apolipoprotein B and PCSK9 genes are the common causes of FH. Diagnosis of FH usually depends on family history, clinical history of premature CAD, physical findings of xanthoma or corneal arcus and high levels of LDL-C. In addition to conventional lipid lowering therapies, adjunctive treatment with mipomersen, lomitapide, or PCSK9 inhibitors become necessary to further reduce LDL-C in patients with FH. Overall, these recommendations are to help the health care professionals in Taiwan to treat hyperlipidemia with current scientific evidences. We hope the prescription rate of lipid lowering drugs and control rate of hyperlipidemia in high risk patients could be increased by implementation of the clinical guidelines. The major purpose is to improve clinical outcomes of these high risk patients through the control of hyperlipidemia.

Cerebral Lipiodol Embolism in Hepatocellular Carcinoma Patients Treated with Transarterial Embolization/Chemoembolization.

BACKGROUND AND PURPOSE: Liver cancer is the third leading cause of cancer mortality worldwide. The aim of this study was to investigate the frequency and characteristics of cerebral lipiodol embolism (CLE) in patients with hepatocellular carcinoma (HCC) receiving transarterial embolization/chemoembolization (TAE/TACE). METHODS: We reviewed all HCC patients who received TAE/TACE during the period of 2007 and 2013 at a university medical center. The frequency of CLE per procedure and the clinical manifestations of CLE, including the review of previous reported cases (n = 24), were analyzed. RESULTS: During the study period, a total of 7855 TAE/TACE procedures were conducted on 3277 patients. There were 8 patients (mean age 59±11 years; 5 males and 3 females) who developed CLE. The frequency of TAE/TACE-related CLE was 1.02 (95% CI, 0.44-2.01) per 1000 procedures. Acute disturbance of consciousness and respiratory distress after TAE/TACE were the most common presentations of CLE. All patients had disseminated infarcts involving both the anterior and posterior cerebral circulations. For 3 patients with shunting between the tumor feeding artery and the pulmonary vein, a specific imaging pattern of coexisting scattered hyperdense spots was found. Furthermore, combined with our 8 cases, the total of 32 cases indicated that old age and female sex were the two risk factors for poor outcome after CLE. CONCLUSIONS: CLE is a rare but potentially serious complication in HCC patients receiving TAE/TACE. The clinical characteristics of CLE summarized in our study would help facilitate the ability of clinicians to provide timely diagnosis and management.

Targeting P(2)X(7) receptor for the treatment of central post-stroke pain in a rodent model.

Stroke is a leading cause of death and disability in industrialized countries. Approximately 8-14% of stroke survivors suffer from central post-stroke pain (CPSP) when hemorrhagic stroke occurs in lateral thalamic regions, which severely affects their quality of life. Because the mechanisms of CPSP are not well understood, effective treatments have not been developed. In the present study, we tested the hypothesis that persistent CPSP is caused by P(2)X(7)receptor activation after brain tissue damage and subsequent elevations in inflammatory cytokines. A thalamic hemorrhagic rat model was used, characterized by thermal and mechanical allodynia that develops in the subacute to chronic phases upon CPSP onset. We found a significant increase in P(2)X(7) expression in reactive microglia/macrophages in thalamic peri-lesion tissues at 5 weeks post-hemorrhage. Thalamic P(2)X(7) receptors were directly involved in pain transmission and hypersensitivity. The systemic targeting of P(2)X(7) receptors during the acute stage of hemorrhage rescued abnormal pain behaviors and neuronal activity in the thalamocingulate pathway by reducing reactive microglia/macrophage aggregation and associated inflammatory cytokines. After CPSP onset, the targeting of interleukin-1ß reversed abnormal pain sensitivity. The aberrant spontaneous thalamocortical oscillations in rats with CPSP were modulated by blocking P(2)X(7) receptors. Taken together, our results suggest that targeting P(2)X(7) may be bi-effective in the treatment of CPSP, as both a pain blocker and immunosuppressant that inhibits inflammatory damage to brain tissue. P(2)X(7)receptors may serve as a potential target to prevent the occurrence of CPSP and may be beneficial for the recovery of patients from stroke.

Dissection of the posterior inferior cerebellar artery in a young adult with cerebellar infarct.

The posterior inferior cerebellar artery (PICA) is frequently involved in dissection of the vertebral artery (VA); however, isolated PICA dissection has rarely been reported. A 37-year-old man experienced acute and progressive drowsiness, vertigo, occipital headache, vomiting, and ataxia. There was no precedent trauma or chiropractic manipulation. Neurologically, he had dysmetria of the left extremities. His NIHSS score was 3. Brain magnetic resonance imaging showed an acute cerebellar infarct in the left PICA territory. Magnetic resonance angiography showed a faint signal adjacent to the junction of the left VA and PICA, suggesting a vascular shadow. Catheter angiography showed focal stenosis with a post-stenotic fusiform aneurysmal dilatation of the left proximal PICA that was highly suggestive of dissection with pseudoaneurysm formation. He was treated with clopidogrel and was free of neurological symptoms 3 months after the stroke event. Isolated PICA dissection may be considered in patients with PICA territory infarct or subarachnoid hemorrhage. Treatment depends on the manifestations; ruptured dissecting aneurysms are often treated with surgery or embolization, and infarcts are usually treated with antithrombotic agents.

Migrainous infarction involving two different arterial territories: report of two cases.

It is reasonable to speculate that migrainous infarction may develop in different territories of cerebral arteries. However, this condition was rarely reported before. Here we described two patients (one woman, 29 year-old; one man, 47 year-old) with a history of migraine with aura, had ischemic strokes during the migraine attack. The ischemic stroke of the female patient involved the territories of the posterior cerebral and anterior choroidal arteries; whereas the male patient had two episodes of ischemic strokes, involving the territories of the middle and posterior cerebral arteries sequentially. Both patients recovered well during the follow-up periods. We suggest that migrainous infarction can involve different arterial territories.