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Trauma Case Reports Jun 2019Coronary vasospasm is characterized by focal or diffuse spasm of an epicardial coronary artery. Definitive diagnosis is usually made with coronary angiography, when...
Coronary vasospasm is characterized by focal or diffuse spasm of an epicardial coronary artery. Definitive diagnosis is usually made with coronary angiography, when resolution of stenosis is observed after administration of intracoronary vasodilators. Coronary vasospasm is rarely a consequence of a blunt force injury to the chest. Among trauma induced cardiac complications, coronary vasospasm has been the least common with only one other reported case of coronary vasospasm induced by trauma. We report a rare case of severe spontaneous coronary vasospasm in a patient with polytrauma successfully treated with intracoronary, intravenous and oral vasodilator therapy. The mechanism is thought to be due to compensatory catecholamine response to trauma, and coronary vasospasm should be strongly suspected in trauma patients with unexplained hypotension, new conduction abnormalities or evidence of ischemia on the ECG.
PubMed: 31049387
DOI: 10.1016/j.tcr.2019.100194 -
Neurology India 2022Stellate ganglion block (SGB) causes blockage of sympathetic nerve activity, which may lead to intracerebral vessel dilatation and relieve cerebral vasospasm in patients...
BACKGROUND
Stellate ganglion block (SGB) causes blockage of sympathetic nerve activity, which may lead to intracerebral vessel dilatation and relieve cerebral vasospasm in patients of aneurysmal subarachnoid hemorrhage (aSAH).
OBJECTIVE
The aim of this study was to evaluate the efficacy and safety of SGB to relieve cerebral vasospasm on clinicoradiological parameters.
MATERIALS AND METHODS
We prospectively included 20 patients with clinical and angiographic evidence of vasospasm post aneurysmal clipping. Cerebral blood flow velocity and Lindegaard ratio were assessed using transcranial Doppler (TCD). Location of vasospasm, vessel diameter, vasospasm severity, parenchymal filling time, and venous sinus filling time were assessed on digital subtraction angiography (DSA). Patients received ultrasound-guided SGB with 10 mL of 0.5% bupivacaine on the ipsilateral side of the vasospasm. After 30 minutes, the neurological status, TCD, and DSA parameters were reevaluated.
RESULTS
After SGB, there was statistically significant reduction in the middle cerebral artery (MCA) peak systolic velocity (P = 0.005), mean flow velocity (P = 0.025), and Lindegaard ratio (P = 0.022) on TCD. We observed significant dilatation in the mean vessel diameter measured at the mid-M1 segment of MCA (P = 0.003) and mid-A1 segment of ACA (P = 0.002) on DSA. The mean parenchymal filling time and mean venous sinus filling time decreased nonsignificantly after SGB (P = 0.163/0.104). Neurological improvement was observed in five (25%) patients.
CONCLUSION
SGB has positive clinicoradiological influence in the management of cerebral vasospasm of large vessels. However, its effect on cerebral microvasculature is limited and needs a larger database for further analysis.
Topics: Cerebrovascular Circulation; Humans; Prospective Studies; Stellate Ganglion; Subarachnoid Hemorrhage; Ultrasonography, Doppler, Transcranial; Vasospasm, Intracranial
PubMed: 35263898
DOI: 10.4103/0028-3886.338735 -
Scientific Reports Nov 2020Cerebral vasospasm is a dreaded sequelae of aneurysmal subarachnoid hemorrhage (aSAH), requiring timely intervention with therapeutic goals of improving brain perfusion....
Cerebral vasospasm is a dreaded sequelae of aneurysmal subarachnoid hemorrhage (aSAH), requiring timely intervention with therapeutic goals of improving brain perfusion. There are currently no standardized real-time, objective assessments of the interventional procedures performed to treat vasospasm. Here we describe real-time techniques to quantify cerebral perfusion during interventional cerebral angiography. We retrospectively analyzed 39 consecutive cases performed to treat clinical vasospasm and quantified the changes in perfusion metrics between pre- and post- verapamil administrations. With Digital Subtraction Angiography (DSA) perfusion analysis, we are able to identify hypoperfused territories and quantify the exact changes in cerebral perfusion for each individual case and vascular territory. We demonstrate that perfusion analysis for DSA can be performed in real time. This provides clinicians with a colorized map which directly visualizes hypoperfused tissue, combined with associated perfusion statistics. Quantitative thresholds and analysis based on DSA perfusion may assist with real-time dosage estimation and help predict response to treatment, however future prospective analysis is required for validation.
Topics: Adolescent; Adult; Angiography, Digital Subtraction; Female; Humans; Male; Middle Aged; Perfusion Imaging; Retrospective Studies; Subarachnoid Hemorrhage; Treatment Outcome; Vasospasm, Intracranial; Verapamil; Young Adult
PubMed: 33139791
DOI: 10.1038/s41598-020-75365-2 -
Acta Neurochirurgica. Supplement 2008Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide... (Review)
Review
Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation, and chemoregulation. Subarachnoid haemorrhage (SAH) interrupts this regulation of cerebral blood flow. Hemoglobin, gradually released from erythrocytes in the subarachnoid space destroys nNOS-containing neurons in the conductive arteries. This deprives the arteries of NO, leading to the initiation of delayed vasospasm. But such vessel narrowing increases shear stress, which stimulates eNOS. This mechanism normally would lead to increased production of NO and dilation of arteries. However, a transient eNOS dysfunction evoked by an increase of the endogenous competitive nitric oxide synthase (NOS) inhibitor, asymmetric dimethyl-arginine (ADMA), prevents this vasodilation. eNOS dysfunction has been recently shown to be evoked by increased levels of ADMA in CSF in response to the presence of bilirubin-oxidized fragments (BOXes). A direct cause of the increased ADMA CSF level is most likely decreased ADMA elimination due to the disappearance of ADMA-hydrolyzing enzyme (DDAH II) immunoreactivity in the arteries in spasm. This eNOS dysfunction sustains vasospasm. CSF ADMA levels are closely associated with the degree and time-course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, the exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme (IPRMT3) or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of preclinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.
Topics: Humans; Intracranial Aneurysm; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase; Nitric Oxide Synthase Type I; Nitroglycerin; Subarachnoid Hemorrhage; United States; Vasospasm, Intracranial
PubMed: 18456999
DOI: 10.1007/978-3-211-75718-5_28 -
Annals of Biomedical Engineering Sep 2007The etiology, and hence most effective treatment, of cerebral vasospasm remains unknown, thus this devastating sequela to subarachnoid hemorrhage continues to be...
The etiology, and hence most effective treatment, of cerebral vasospasm remains unknown, thus this devastating sequela to subarachnoid hemorrhage continues to be responsible for significant morbidity and mortality. Based on abundant and diverse clinical and laboratory observations, we hypothesize that vasospasm and its subsequent resolution result from a short-term chemo-dominated turnover of cells and matrix in evolving vasoconstricted states that produces a narrowed lumen and thicker wall, which is stiffer and largely unresponsive to exogenous vasodilators, and a subsequent mechano-dominated turnover of cells and matrix in evolving vasodilated states that restores the vessel toward normal. There is, however, a pressing need for a mathematical model of arterial growth and remodeling that can guide the design and interpretation of experiments to test this and competing hypotheses. Toward this end, we present a new biochemomechanical framework that couples a 2-D model of the evolving geometry, structure, and properties of the affected arterial wall, a 1-D model of the blood flow within the affected segment, and a 0-D model of the biochemical insult to the segment. We submit that such a framework can capture salient features of the time-course of vasospasm and its potential resolution, as illustrated numerically in part II of this paper.
Topics: Biomechanical Phenomena; Cerebral Arteries; Cerebrovascular Circulation; Humans; Models, Cardiovascular; Subarachnoid Hemorrhage; Vasoconstriction; Vasospasm, Intracranial
PubMed: 17487586
DOI: 10.1007/s10439-007-9321-y -
Cerebrovascular Diseases (Basel,... 2017Early diagnosis of vasospasm following subarachnoid hemorrhage can prevent cerebral ischemia and improve neurological outcomes. This study numerically evaluates the...
BACKGROUND
Early diagnosis of vasospasm following subarachnoid hemorrhage can prevent cerebral ischemia and improve neurological outcomes. This study numerically evaluates the relevance of extracranial blood velocity indices to detect vasospasm.
METHODS
A numerical model of cerebral blood flow was used to evaluate the hemodynamics associated with anterior and posterior vasospasm under normal and impaired cerebral autoregulation conditions. Extracranial blood velocities at the carotid and vertebral arteries and their ratios between ipsilateral and contralateral, anterior and posterior, and downstream and upstream arteries were monitored during vasospasm progression.
RESULTS
For current clinical indices that track blood velocities at vasospastic arterial segments using transcranial Doppler (TCD), we observed that velocities increased initially and then decreased with vasospasm progression. This nonmonotonic behavior can lead to false-negative decisions in moderate to severe vasospasm. Alternatively, volumetric flow decreased monotonically at the affected arteries, leading to blood velocities upstream of the vasospastic artery also decreasing monotonically. Based on this principle, we demonstrate that velocity ratios between the carotid and vertebral arteries may better identify moderate to severe vasospasm and improve sensitivity and specificity of vasospasm detection.
CONCLUSION
The velocity indices proposed in this study may enable new or improved noninvasive diagnosis of vasospasm using extracranial Doppler ultrasound. Compared to current clinical indices, the new indices may improve the handling of (1) scenarios of severe vasospasm or impaired cerebral autoregulation, (2) systemic changes in blood pressure and cardiac output, (3) vasospasm occurring in arteries distal to the cerebral circle region, and (4) cases with insufficient acoustic bone window for TCD. The results provide a concrete basis for future clinical evaluation of extracranial indices for vasospasm detection.
Topics: Blood Flow Velocity; Carotid Arteries; Cerebrovascular Circulation; Computer Simulation; Hemodynamics; Homeostasis; Humans; Models, Cardiovascular; Numerical Analysis, Computer-Assisted; Subarachnoid Hemorrhage; Time Factors; Ultrasonography, Doppler, Transcranial; Vasospasm, Intracranial; Vertebral Artery
PubMed: 28241122
DOI: 10.1159/000454992 -
Journal of Cerebral Blood Flow and... Jul 2018Statins have pleiotropic effects that are considered beneficial in preventing cerebral vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage... (Randomized Controlled Trial)
Randomized Controlled Trial
Statins have pleiotropic effects that are considered beneficial in preventing cerebral vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (aSAH). Many studies using statins have been performed but failed to show remarkable effects. We hypothesized that a long-acting statin would be more effective, due to a longer half-life and stronger pleiotropic effects. Patients with aSAH were randomly assigned to a pitavastatin group (4 mg daily; n = 54) and a placebo group ( n = 54) after repair of a ruptured aneurysm. The primary efficacy end point was vasospasm-related delayed ischemic neurological deficits (DIND), and the secondary end points were cerebral vasospasm evaluated by digital subtraction angiography (DSA), vasospasm-related new cerebral infarctions, and outcome at three months. Severe cerebral vasospasms on DSA were statistically fewer in the pitavastatin group than in the placebo group (14.8% vs. 33.3%; odds ratio, 0.32; 95% confidence interval, 0.11-0.87, p = 0.042); however, the occurrence of DIND and new infarctions and outcome showed no statistically significant differences between the groups. The present study is the first to prove the definite, statin-induced amelioration of cerebral vasospasm on DSA. However, administration of any type of statin at the acute phase of aSAH is not recommended.
Topics: Adult; Aged; Aneurysm, Ruptured; Delayed-Action Preparations; Double-Blind Method; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Intracranial Aneurysm; Male; Middle Aged; Quinolines; Subarachnoid Hemorrhage; Vasospasm, Intracranial
PubMed: 28762878
DOI: 10.1177/0271678X17724682 -
Journal of Translational Medicine Apr 2012Subarachnoid hemorrhage (SAH) frequently results in several complications, including cerebral vasospasm, associated with high mortality. Although cerebral vasospasm is a...
BACKGROUND
Subarachnoid hemorrhage (SAH) frequently results in several complications, including cerebral vasospasm, associated with high mortality. Although cerebral vasospasm is a major cause of brain damages after SAH, other factors such as inflammatory responses and oxidative stress also contribute to high mortality after SAH. Trehalose is a non-reducing disaccharide in which two glucose units are linked by α,α-1,1-glycosidic bond, and has been shown to induce tolerance to a variety of stressors in numerous organisms. In the present study, we investigated the effect of trehalose on cerebral vasospasm, inflammatory responses, and oxidative stress induced by blood in vitro and in vivo.
METHODS
Enzyme immunoassay for eicosanoids, pro-inflammatory cytokines, and endothelin-1, and western blotting analysis for cyclooxygenase-2, inducible nitric oxide synthase, and inhibitor of NF-κB were examined in macrophage-like cells treated with hemolysate. After treatment with hemolysate and hydrogen peroxide, the levels of lipid peroxide and amounts of arachidonic acid release were also analyzed. Three hours after the onset of experimental SAH, 18 Japanese White rabbits received an injection of saline, trehalose, or maltose into the cisterna magna. Angiographic and histological analyses of the basilar arteries were performed. In a separate study, the femoral arteries from 60 rats were exposed to fresh autologous blood. At 1, 3, 5, 7, 10, and 20 days after treatment, cryosections prepared from the femoral arteries were histologically analyzed.
RESULTS
When cells were treated with hemolysate, trehalose inhibited the production of several inflammatory mediators and degradation of the inhibitor of NF-κB and also suppressed the lipid peroxidation, the reactive oxygen species-induced arachidonic acid release in vitro. In the rabbit model, trehalose produced an inhibitory effect on vasospasm after the onset of experimental SAH, while maltose had only a moderate effect. When the rat femoral arteries exposed to blood were investigated for 20 days, histological analysis revealed that trehalose suppressed vasospasm, inflammatory response, and lipid peroxidation.
CONCLUSIONS
These data suggest that trehalose has suppressive effects on several pathological events after SAH, including vasospasm, inflammatory responses, and lipid peroxidation. Trehalose may be a new therapeutic approach for treatment of complications after SAH.
Topics: Animals; Cells, Cultured; Disease Models, Animal; Hemolysis; Humans; Inflammation; Lipid Peroxidation; Male; Mice; NF-kappa B; Oxidative Stress; Rabbits; Rats; Rats, Sprague-Dawley; Rats, Wistar; Reactive Oxygen Species; Signal Transduction; Subarachnoid Hemorrhage; Trehalose; Vasospasm, Intracranial
PubMed: 22546323
DOI: 10.1186/1479-5876-10-80 -
BMC Neurology Sep 2020Delayed symptomatic vasospasm is a rare complication following clipping of an unruptured intracranial saccular aneurysm. There have been ten reported cases of delayed...
BACKGROUND
Delayed symptomatic vasospasm is a rare complication following clipping of an unruptured intracranial saccular aneurysm. There have been ten reported cases of delayed symptomatic vasospasm and only two of these occurred after 2 weeks from initial intervention. Our case is the first to document the refractory nature of such vasospasm despite aggressive first line therapy.
CASE PRESENTATION
Here, we present a 67-year-old female who had surgical clipping of a 10x7mm right middle cerebral artery (MCA) bifurcation aneurysm. Her surgery and initial postoperative course were uncomplicated, but she presented with acute left hemiparesis, dysarthria, headache and vomiting on post-op day 29 secondary to vasospasm of M2. She was initially stabilized with intra-arterial verapamil then managed with volume expansion, permissive hypertension, and nimodipine. She developed recurrent vasospasm of M2 the following day and was again treated with intra-arterial verapamil. Magnetic resonance imaging (MRI) brain showed an infarction involving the right basal ganglia, frontal lobe, and parietal lobe and her hospital course was complicated by super-refractory status epilepticus. At her follow up appointment she displayed continued left lower extremity weakness, left visual field defect, and left-sided neglect.
CONCLUSIONS
Overall, cerebral vasospasms associated with unruptured aneurysms remain rare complications and are not often monitored for after initial recovery. Reviewing the documented cases highlights the unpredictability of when these events occur with our current knowledge. Current hypotheses for the mechanisms responsible for delayed and refractory vasospasms include: blood-derived breakdown products, mechanically induced vasospastic responses, and delayed reactions from the trigemino-cerebrovascular system (TCVS). The uncertainly of these events warrants further research and supports a strong argument for monitoring patients with initial surgical clipping up to a month out from their initial procedure.
Topics: Aged; Female; Headache; Humans; Hypertension; Intracranial Aneurysm; Neurosurgical Procedures; Vasospasm, Intracranial
PubMed: 32919459
DOI: 10.1186/s12883-020-01925-8 -
JACC. Cardiovascular Interventions Aug 2020
Topics: Acetylcholine; Angina, Stable; Coronary Vasospasm; Coronary Vessels; Follow-Up Studies; Humans; Treatment Outcome
PubMed: 32739306
DOI: 10.1016/j.jcin.2020.06.044