Vasospasm of the basilar artery following spontaneous SAH-clinical observations and implications for vascular research.

The basilar artery (BA), as a reference vessel for laboratory investigations of cerebral vasospasm (CVS) in many experimental models, warrants a sufficient blood supply despite hemodynamic changes during CVS. In a prospective evaluation study, we analyzed  patients who were admitted to our department with subarachnoid hemorrhage (SAH) for the occurrence and sequelae of CVS. Specifically, we sought to identify patients with CVS of the BA. As per institutional protocol, all patients with CVS detected in the posterior circulation had magnetic resonance imaging (MRI) examinations instead of CTA. Between January and December 2016, 74 patients were treated for spontaneous SAH. CVS occurred in 45 (61%) patients, and 31 (42%) patients developed associated cerebral infarctions (CI). CVS was significantly associated with CI (p < 0.0001; OR 44). In 18 (24.3%) patients, CVS significantly affected the basilar artery. Poor admission clinical state, younger age, and treatment modalities were significantly associated with BACVS. BACVS was more often detected in patients with severe CVS (p < 0.046; OR 4.4). Patients with BACVS developed cerebral infarction in a frequency comparable to other patients with CVS (61% vs. 70%, p = 0.7), but none of these infarctions occurred in the brain stem or pons even though vessel diameter was dramatically reduced according to CT- and/or MR-angiography. BACVS does not appear to be followed by cerebral infarction in the BA territory, presumably due to a vascular privilege of this vessel and its perforating branches. In contrast, brain ischemia can frequently be observed in the territories of other major arteries affected by CVS.

Decision-making in a patient with cardiac arrest due to venous thromboembolism within 24 h after glioblastoma resection.

In the fulminant VTE form with cardiac arrest, systemic thrombolysis remains the most effective therapy. However, several contraindications restrict the use such as intracranial neoplasm or a recent history of intracranial surgery. Here, we report the case of a 59-year-old man who underwent glioblastoma resection and suffered from a fulminant pulmonary embolism with cardiac arrest. After CPR, continuous tPA infusion via an endovascularly placed pulmonary catheter was maintained over a period of 8 h. In this case, we report on our decision-making process and the use of local thrombolysis as a successful therapy in a patient with multiple contraindications.

Biglycan is required for adaptive remodeling after myocardial infarction.

BACKGROUND: After myocardial infarction (MI), extensive remodeling of extracellular matrix contributes to scar formation and preservation of hemodynamic function. On the other hand, adverse and excessive extracellular matrix remodeling leads to fibrosis and impaired function. The present study investigates the role of the small leucine-rich proteoglycan biglycan during cardiac extracellular matrix remodeling and cardiac hemodynamics after MI. METHODS AND RESULTS: Experimental MI was induced in wild-type (WT) and bgn(-/0) mice by permanent ligation of the left anterior descending coronary artery. Biglycan expression was strongly increased at 3, 7, and 14 days after MI in WT mice. bgn(-/0) mice showed increased mortality rates after MI as a result of frequent left ventricular (LV) ruptures. Furthermore, tensile strength of the LV derived from bgn(-/0) mice 21 days after MI was reduced as measured ex vivo. Collagen matrix organization was severely impaired in bgn(-/0) mice, as shown by birefringence analysis of Sirius red staining and electron microscopy of collagen fibrils. At 21 days after MI, LV hemodynamic parameters were assessed by pressure-volume measurements in vivo to obtain LV end-diastolic pressure, end-diastolic volume, and end-systolic volume. bgn(-/0) mice were characterized by aggravated LV dilation evidenced by increased LV end-diastolic volume (bgn(-/0), 111+/-4.2 microL versus WT, 96+/-4.4 microL; P<0.05) and LV end-diastolic pressure (bgn(-/0), 24+/-2.7 versus WT, 18+/-1.8 mm Hg; P<0.05) and severely impaired LV function (EF, bgn(-/0), 12+/-2% versus WT, 21+/-4%; P<0.05) 21 days after MI. CONCLUSIONS: Biglycan is required for stable collagen matrix formation of infarct scars and for preservation of cardiac hemodynamic function.