Increased Arterial Stiffness is a Predictor of Delayed Ischaemic Stroke After Subarachnoid Haemorrhage.

BACKGROUND: Subarachnoid haemorrhage (SAH) accounts for 5-10% of strokes and its prognosis may be influenced by different complications, including delayed cerebral ischaemia (DCI). The pathophysiology of DCI is complex and still unknown. Many different mechanisms may contribute to the occurrence of DCI. Arterial stiffness (AS), a well-known risk factor for cardiovascular events, also associated with the development and rupture of cerebral aneurysms, may represent a novel contributing risk factor. The aim of our study was to investigate a possible link between AS and DCI after SAH. METHOD: Fifty-nine (59) patients with SAH (age [mean±standard deviation], 62±12 years) underwent neuroimaging examination, and 24-hour heart rate and blood pressure monitoring, including AS index (ASI) measurement. RESULTS: Of 59 patients, DCI occurred in 12. ASI was significantly higher in patients with DCI than in patients without it (0.70±0.1 vs 0.62±0.1; p=0.03). ASI was a significant predictor for DCI (odds ratio [for an increase of 0.20 points in ASI], 5.99; 95% confidence interval, 1.23-29.22; p=0.03). CONCLUSIONS: Arterial stiffness index is a simple and inexpensive tool that is able to predict the risk of DCI in patients with SAH. This marker can impact on intensive care unit monitoring, early recognition, and treatment, contributing to optimal acute management of patients with SAH.

Methamphetamine spasm in the large caliber arteries-the severity is likely underestimated.

This report describes two cases of rarely reported, severe large arterial vascular spasms seen on computed tomography images after methamphetamine abuse. Although the effects of methamphetamine on the central nervous system and smaller arteries are relatively well known, its effects on large caliber arteries are rarely discussed. We present two cases of severe large arterial multisegmented vasospasm, captured on contrast-enhanced computed tomography, several hours after methamphetamine abuse. One of the patients was discharged without apparent tissue loss or organ failure. The other developed severe heart failure, liver failure, and toe gangrene. The publication of the de-identified images has been approved by the VA Central California Health Care System's Research and Development Committee and Privacy Officer. Vascular surgeons and, perhaps, acute care physicians, who are usually aware of small arterial vasospastic conditions, should also be aware of this methamphetamine-induced large arterial finding, which can be quite dramatic in appearance on imaging.

Severe Cerebral Vasospasm Caused by Acute on Top of Chronic Spontaneous Subdural Hematoma: A Case Report and Review of the Literature.

Cerebral vasospasm is a well-known phenomenon that has been associated with subarachnoid hemorrhage due to aneurysmal bleeding. It can lead to serious outcomes if not recognized and treated promptly. It happens most frequently following cases of aneurysmal subarachnoid hemorrhage. Other causes include traumatic brain injury, reversible cerebral vasoconstriction syndrome, post-tumor resection, and non-aneurysmal subarachnoid hemorrhage. We describe a case of severe clinical vasospasm following acute on top of chronic spontaneous subdural hematoma in a patient with corpus callosum agenesis. Also, a small literature review of the possible risk factors of such occurrence is discussed.

Analysis of risk factors correlated with angiographic vasospasm in patients with aneurysmal subarachnoid hemorrhage using explainable predictive modeling.

Cerebral vasospasm (CAV) is a major complication of aneurysmal subarachnoid hemorrhage (aSAH) in patients with ruptured intracranial aneurysm. Explainable artificial intelligence (XAI) was used to analyze the contribution of risk factors on the development of CAV. We obtained data about patients (n = 343) treated for aSAH in our hospital. Predictive factors including age, aneurysm size, Hunt and Hess grade, and modified Fisher grade were used as input to analyze the contribution and correlation of factors correlated with CAV using a random forest regressor. An analysis conducted using an XAI model showed that aneurysm size (27.6%) was most significantly associated with the development of CAV, followed by age (20.7%) and Glasgow coma scale score (7.1%). In some patients with an estimated artificial intelligence-selected CAV value of 51%, the important risk factors were aneurysm size (9.1 mm) and location, and hypertension is also considered a major influencing factor. We could predict that Fisher grade 3 contributed to 20.3%, and the group using Antiplatelet contributed to 12.2% which is expected to lower cerebral CAV compared to the Control group (16.9%). The accuracy rate of the XAI system was 85.5% (area under the curve = 0.88). Using the modeling, aneurysm size and age were quantitatively analyzed and were found to be significantly associated with CAV in patients with aSAH. Hence, XAI modeling techniques can be used to analyze factors correlated with CAV by schematizing prediction results in some patients. Moreover, poor Fisher grade and use of postoperative antiplatelet agent are important factors for prediction of CAV.

Regulation of RhoA/ROCK and sustained arterial contraction by low cytosolic Ca2+ levels during prolonged depolarization of arterial smooth muscle.

The role of L-type Ca2+ channels (LTCCs) and RhoA/Rho kinase (ROCK) on depolarization-induced sustained arterial contraction lasting several minutes is already known. However, in vivo, vascular smooth muscle cells can be depolarized for longer periods, inducing substantial inactivation of LTCCs and markedly reducing Ca2+ influx into the myocytes. We have examined, in femoral arterial rings, the role of LTCCs and RhoA/ROCK during long-lasting depolarization. Our results reveal a new vasoreactive response after 20-30min of depolarization in 2.5mM external Ca2+ that has not been identified previously with shorter stimuli. Prolonged depolarization-induced arterial contraction was permanently abolished when arterial rings were treated with 100nM external Ca2+ or 20nM nifedipine. However, when Ca2+ influx was restricted, applying ~7µM external Ca2+ solution or 3nM nifedipine, vasorelaxation was transient, and isometric force slowly increased after 30min and maintained its level until the end of the stimulus. Under these conditions, arterial contraction showed the same temporal course of RhoA activity and was sensitive to fasudil, nifedipine and cyclopiazonic acid. Ca2+-response curve in ß-escin permeabilized arteries was also sensitive to ROCK inhibitors. Thus, although long-lasting depolarization inactivates LTCCs, the reduced Ca2+ entry can induce a detectable arterial contraction via RhoA/ROCK activation.

Low-dose combination of Rho kinase and L-type Ca(2+) channel antagonists for selective inhibition of depolarization-induced sustained arterial contraction.

L-type Ca(2+) channels (LTCCs) are involved in the maintenance of tonic arterial contractions and regulate the RhoA/Rho-associated kinase (ROCK) sensitization cascade. We have tested effects of individual and combined low concentrations of LTCCs and ROCK inhibitors to produce arterial relaxation without the adverse side effects of LTCCs antagonists. We have also studied whether this pharmacological strategy alters Ca(2+)-dependent electrical properties of isolated arterial and cardiac myocytes as well as cardiac contractility. Rat basilar, human carotid and coronary arterial rings were mounted on a small-vessel myograph to measure isometric tension and cardiac contractility was measured in Langendorff-perfused rat heart. Simultaneous cytosolic Ca(2+) concentration and arterial diameter were measured in intact pressurized arteries loaded with Fura-2. Patch-clamp techniques were used to measure electrical properties in isolated cardiac and arterial myocytes. Low concentrations of LTCCs and ROCK inhibitors reduced the tonic component of moderate depolarization-evoked contraction, leaving the phasic component practically unaltered. This selective vasorelaxant effect was more marked when the LTCCs and ROCK inhibitors were applied together. In the concentration range used (nM), Ca(2+) currents in arterial myocytes, cardiac action potentials and heart contractility were unaffected by this pharmacological approach. In conclusion, low doses of LTCCs and ROCK inhibitors could be used to selectively relax precontracted arteries in pathologic conditions such as hypertension, and cerebral or coronary spasms with minor side effects on physiological contractile properties of vascular and cardiac myocytes.

THE EFFECTS OF VASCULAR FREEZING TIME ON ARTERIAL VASOSPASM IN RATS

The outcomes of microvascular surgery may be jeopardized by factors that reduce the blood flow across the freshly the performed anastomosis Arterial vasospasm is one of such factors causing the failure of an anastomosis. Vascular spasm has treated by systemic or topical administration of pharmacologic agents. However, despite the works done to prevent and elucidate the cause of vasospasm, a apasmolytic agent Capable of consistently protecting against it or reversing it has not been found. Vascular freezing as an powerful spasmolytic maneuver has recently been reported. The purpose of the present study was to determine optimal vascular freezing time. The effect of vascular freezing time was examined on the relief of arterial vasospasm. The vascular was freezing was performed on the artery of rats whit hand-held liquid nitrogen oxide spray. the artery was frozen for 5, 15,or 30 seconds. Vascular spasm and patency were evaluated immediately after and 1, 3, 7, 14, and 56 days after the freezing. Femaral arteries were havested at 1, 3, 7, 14, and 56 days after freezing for histologc examination The results obtained were as follows : 1. immediately after the freezing-thawing, the vasospasm was relieved and not induced by spasmogenic induction manipulation in all groups. 2. Immediately after the freezing-thawing, the artery become dialated, the diameter of which was slightly more than the intial, ranging between 0-17% and the diameter of 5-second group was smaller than those of 15-and 30-second group(P<0.05). 3. One to 56 days after freezing, arteral diameter was still 1-22% larger than the initial and there was no significant difference among groups. 4. One to 56 days after the freezing, vasospasm was not induced by spasmogenic induction manipulation in all groups. 5. One day after the freezing, almost all the vessel wall died and the normal architeture of the layer was deranged in all group. The shorter was the duration of freezing, the more early was the healing of artery occurred, 6. Fifty-six days after the freezing, cellularity was increased and the architecture was regenerated, There was no significant differance among groups. It was suggested that vascular freezing for 5 seconds is useful to relieve the vasospasm and to lessen the injury of artery.