Stroke is a life-threatening condition in which accurate diagnoses and timely treatment are critical for successful neurological recovery. The current acute treatment strategies, particularly non-invasive interventions, are limited, thus urging the need for novel therapeutical targets. Arginine vasopressin (AVP) receptor antagonists are emerging as potential targets to treat edema formation and subsequent elevation in intracranial pressure, both significant causes of mortality in acute stroke. Here, we summarize the current knowledge on the mechanisms leading to AVP hyperexcretion in acute stroke and the subsequent secondary neuropathological responses. Furthermore, we discuss the work supporting the predictive value of measuring copeptin, a surrogate marker of AVP in stroke patients, followed by a review of the experimental evidence suggesting AVP receptor antagonists in stroke therapy. As we highlight throughout the narrative, critical gaps in the literature exist and indicate the need for further research to understand better AVP mechanisms in stroke. Likewise, there are advantages and limitations in using copeptin as a prognostic tool, and the translation of findings from experimental animal models to clinical settings has its challenges. Still, monitoring AVP levels and using AVP receptor antagonists as an add-on therapeutic intervention are potential promises in clinical applications to alleviate stroke neurological consequences.

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Objective: Intracranial carotid artery calcification (ICAC), as a strong contributor to the occurrence of ischemic stroke, might be present in the medial or intimal arterial layer. Traditional vascular risk factors are associated with ICAC; however, its association with new markers of vascular function are less understood. The paper aims to evaluate the relationship between carotid-femoral pulse wave velocity (CF-PWV) and ICAC subtypes. Design and method: We enrolled 65 patients with acute ischemic stroke. CF-PWV, systolic, diastolic and mean blood pressure, and pulse pressure (SBP, DBP, MBP, PP) were measured within 6±2 days of stroke onset. CT was performed within 24 hours of stroke onset and ICAC on the stroke site was classified by two methods: volume- and score-based. Tertiles of ICAC volume were determined, and low-grade ICAC (T1) was regarded as a reference. According to the score-based method, medial and intimal ICAC subtypes were determined. Data were analyzed with multivariate logistic regression. Results: Medial and intimal ICAC subtypes were found in 34 (52%) and 24 (37%) patients, respectively. In 11% of patients no ICAC calcifications were found. CF-PWV was higher in patients with high-grade ICAC (OR = 1.56, 95%CI = 1.03-2.35, p = 0.035). CF-PWV was higher in patients with the medial ICAC subtype than in patients with the intimal ICAC subtype (OR = 1.60, 95%CI = 1.00-2.55, p = 0.049) after adjustment for age, MBP, diabetes mellitus, arterial hypertension, hyperlipidemia, and smoking status. Conclusions: Our study demonstrates that among patients with ischemic stroke, aortic stiffness is independently associated with ICAC, and that medial ICAC, compared with intimal ICAC, is accompanied by more advanced aortic stiffness.