Vertebral artery and posterior inferior cerebellar artery aneurysms: Results of microsurgical treatment of eighty patients.

BACKGROUND: The choice of surgical approaches and options for the microsurgical vertebral artery (VA) and posterior inferior cerebellar artery (PICA) aneurysms repair remains controversial. METHODS: A retrospective analysis of the clinical, surgical, and angiographic data of 80 patients with VA and PICA aneurysms treated from 2012 to 2018 was performed. RESULTS: The aneurysms were saccular in 50 cases (62.5%) and fusiform in 30 cases (37.5%). The median suboccipital craniotomy was the most common approach (73.8%). Retrosigmoid craniotomy was performed in 25% of patients. There were the following types of microsurgical operations: neck clipping (61.25%), clipping with the artery lumen formation (13.75%), trapping (10%), proximal clipping (5%), and deconstruction with anastomosis (10%). Fifty-seven (71.3%) patients were discharged without worsening of the clinical signs after surgery. The most common postoperative neurological disorder was palsy of IX and X cranial nerve revealed in 14 (17.5%) patients. No fatal outcomes or patients in vegetative state were identified. The complete occlusion of PICA and VA aneurysms according angiography was in 77 (96.3%) cases. CONCLUSION: Microsurgical treatment is an effective method for VA and PICA aneurysms. The majority of VA and PICA aneurysms do not require complex basal approaches. A thorough preoperative planning, reconstructive clipping techniques, and anastomoses creation, as well as patient selection based on the established algorithms and consultations with endovascular surgeons, may reduce the number of complications and increase the rate of complete microsurgical occlusion in VA and PICA aneurysms.

Formation During Lifetime of Arteriovenous Shunt in Developmental Venous Anomaly That Caused Intracerebral Hemorrhage.

BACKGROUND: Developmental venous anomaly (DVA) or venous angioma is a common anomaly of cerebral veins that is found incidentally in the majority of cases. There are few cases of arteriovenous shunting in DVA associated with a more malignant course of the disease. Whether these DVAs with shunts are of congenital pathology or lifetime formations is unclear. CASE DESCRIPTION: We report a case of lifetime arteriovenous shunt formation in DVA that caused intracerebral hemorrhage in a child. The patient underwent 2 sequential direct surgeries: an emergency evacuation of the intracerebral hematoma and a scheduled excision of the DVA with arteriovenous shunting. CONCLUSIONS: Arteriovenous shunting in DVA may develop during a lifetime and cause intracerebral hemorrhages. This case showed that localization of DVA with arteriovenous shunting in a noneloquent area enables its complete microsurgical excision with favorable functional outcomes.

Non-invasive risk stratification for sudden cardiac death by heart rate turbulence and microvolt T-wave alternans in patients after myocardial infarction.

AIMS: To evaluate the predictive value of heart rate turbulence (HRT) and microvolt T-wave alternans (mTWA) for sudden cardiac death (SCD) in patients after myocardial infarction (MI). METHODS AND RESULTS: We studied 111 patients with MI in the previous 60 days (median, 27 [9;84] months) before inclusion (84 men, mean age 64.1 ± 10.5 years, mean left ventricular ejection fraction 46.6 ± 12.2%). Heart rate turbulence and mTWA were evaluated using 24 h ambulatory electrocardiogram monitoring. The primary endpoint was SCD, and the secondary endpoint was all-cause mortality and non-sudden death from cardiovascular causes. During follow-up of 12 months, 15 SCD and 8 non-sudden cardiovascular deaths (including five fatal MI and three fatal strokes) occurred. Non-survivors had significantly higher mTWA values (83 [74;165] vs. 79 [78;94] mcV, P= 0.002), absolute turbulence onset (TO) values (0 [-0.005;0.01] vs. -0.01 [-0.013;-0.004], P= 0.004), and significantly lower absolute turbulence slope (TS) values (3.34 [2.10;4.83], vs. 3.82 [4.48;7.27], P< 0.001) compared with survivors. In patients with SCD, mTWA, and TO were significantly higher (92 [72;213] vs. 74 [65;86] mcV, P= 0.004 and 0 [-0.001;0.01] vs. -0.01 [-0.03;0.01], P= 0.007, respectively) and TS values were significantly lower (2.14 [1.10;4.56] vs. 4.41 [2.1;7.18], P= 0.005) than in patients with non-sudden death. All parameters were significantly worse in non-survivors than in survivors. We defined cut-off values for increased risk of SCD: for TO = -0.005, relative risk (RR) was 12.4 [95% confidence interval (CI) 2.6-38.2, P< 0.001; positive predictive value (PPV) 28.3%, negative predictive value (NPV) 96.9%], and for mTWA > 53.5 mcV at 100 b.p.m., RR was 5.01 (95% CI 1.5-17.0, P= 0.005; PPV 24.4%, NPV 93.9%). Notably, mTWA > 18.5 mcV at 05.00 AM significantly increased all-cause mortality [RR 7.5 (95% CI 1.4-38.7), P= 0.01; PPV 19.6%, NPV 90.8%]. CONCLUSION: In patients who died from cardiovascular causes, mTWA, and TO values were significantly higher and TS values were significantly lower than in survivors, and the subgroup with SCD was characterized by significantly increased mTWA and TO values and decreased TS values. mTWA > 53.5 mcV at 100 b.p.m. was an independent significant predictor of SCD and increased risk of SCD by five-fold.