Vasospasm In Patients Research Articles

Prolonged Cerebral Circulation Time Is the Best Parameter for Predicting Vasospasm during Initial CT Perfusion in Subarachnoid Hemorrhagic Patients.

PurposeWe sought to imitate angiographic cerebral circulation time (CCT) and create a similar index from baseline CT perfusion (CTP) to better predict vasospasm in patients with subarachnoid hemorrhage (SAH).MethodsForty-one SAH patients with available DSA and CTP were retrospectively included. The vasospasm group was comprised of patients with deterioration in conscious functioning and newly developed luminal narrowing; remaining cases were classified as the control group. The angiography CCT (XA-CCT) was defined as the difference in TTP (time to peak) between the selected arterial ROIs and the superior sagittal sinus (SSS). Four arterial ROIs were selected to generate four corresponding XA-CCTs: the right and left anterior cerebral arteries (XA-CCTRA2 and XA-CCTLA2) and right- and left-middle cerebral arteries (XA-CCTRM2 and XA-CCTLM2). The CCTs from CTP (CT-CCT) were defined as the differences in TTP from the corresponding arterial ROIs and the SSS. Correlations of the different CCTs were calculated and diagnostic accuracy in predicting vasospasm was evaluated.ResultsIntra-class correlations ranged from 0.96 to 0.98. The correlations of XA-CCTRA2, XA-CCTRM2, XA-CCTLA2, and XA-CCTLM2 with the corresponding CT-CCTs were 0.64, 0.65, 0.53, and 0.68, respectively. All CCTs were significantly prolonged in the vasospasm group (5.8–6.4 s) except for XA-CCTLA2. CT-CCTA2 of 5.62 was the optimal cut-off value for detecting vasospasm with a sensitivity of 84.2% and specificity 82.4%ConclusionCT-CCTs can be used to interpret cerebral flow without deconvolution algorithms, and outperform both MTT and TTP in predicting vasospasm risk. This finding may help facilitate management of patients with SAH.

Acute effects of intraventricular nicardipine on cerebral hemodynamics: A preliminary finding

ObjectiveIntraventricular nicardipine (IVTN) is a treatment option for severe vasospasm in patients with subarachnoid hemorrhage (SAH). However, its acute effects on cerebral hemodynamics have not been studied in detail. MethodsBetween June 2008 and December 2010, IVTN was administered (mainly 4mg every 8h) to 11 SAH patients (54 doses) with multimodality monitoring for refractory vasospasm. Retrospective analyses on physiological parameters were made from baseline and up to 6h after IVTN injection. Statistical analysis was performed with a mixed-effects model. ResultsMean intracranial pressure (ICP) increased slightly, reaching its peak at 20min after IVTN injection (2.5±0.9mmHg (mean±standard error), P<0.01), and decreased gradually thereafter over the next hour. Mean cerebral perfusion pressure transiently decreased 20–30min after injection (3.7±1.8mmHg, P<0.05). Mean arterial pressure, partial pressure of brain oxygen tension (PbtO2), cerebral blood flow (CBF), autoregulation indices did not change significantly. Lactate/pyruvate ratio and glucose remained stable. One patient underwent transcranial Doppler ultrasonography monitoring while on IVTN, which showed a transient increase in mean flow velocity with concomitant decrease in Pulsatility index, suggesting vasodilation in the distal resistance vessels. ConclusionsThe vasodilatory effect of IVTN transiently increased ICP, but did not significantly affect PbtO2, CBF or oxidative glucose metabolism in the immediate phase after injection.

Eosinophilia-Associated Coronary Artery Vasospasm in Patients with Aspirin-Exacerbated Respiratory Disease

Eosinophilia is known to be associated with coronary artery vasoconstriction that does not respond to conventional vasodilator treatment but does respond to eosinophil-suppressing treatment. The prevalence of eosinophilia-associated coronary vasospasm in patients with aspirin-exacerbated respiratory disease (AERD), an inflammatory disease characterized by blood and respiratory tissue eosinophilia, is unknown. We observed that some patients with AERD report angina-type chest pain that responds to corticosteroid therapy. We sought to understand the cause of and determine the most appropriate treatment for such chest pain. A retrospective chart review of patients with AERD followed at Brigham and Women’s Hospital was performed. Patients who reported chest pain were assessed for presence of cardiac risk factors, eosinophilia, and chest pain response to conventional and unconventional treatments. One hundred fifty three patients were reviewed; 10 had a history of angina-like chest pain. Eight of the 10 patients had undergone aspirin desensitization and initiated high-dose aspirin; of those, 6 reported an increase in the frequency or severity of chest pain while on high-dose aspirin with improvement after aspirin discontinuation or dose reduction. Most patients had no traditional cardiac risk factors but did have significant eosinophilia. Their chest pain did not improve with typical anti-anginal treatments but did respond to corticosteroid therapy. Though uncommon, patients with AERD can develop eosinophilia-associated coronary artery vasospasm, which is occasionally worsened by high-dose aspirin. AERD patients who present with chest pain, particularly if they are on high-dose aspirin, should be screened for eosinophilia as early treatment with corticosteroids could be life saving.

Is There an Influence of Routine Daily Transcranial Doppler Examination on Clinical Outcome in Patients After Aneurysmal Subarachnoid Hemorrhage?

Transcranial Doppler (TCD) is widely used as a daily routine method to detect vasospasm in patients after aneurysmal subarachnoid hemorrhage (aSAH); however, there are only limited data about the real benefit of this examination. Therefore, the clinical outcome of 2 cohorts with and without daily TCD after aSAH was assessed. All patients included in this study received a standardized diagnostic and treatment protocol. Fifty patients admitted with aSAH from January 2013 to December 2013 received daily TCD measurements; 39 patients admitted from January 2014 to September 2014 received no TCD measurements. Data on clinical grade (Hunt and Hess grade), severity of bleeding (Barrow Neurological Institute grade), localization of aneurysm, and angiographic or clinically relevant vasospasm were collected prospectively. The Glasgow Outcome Scale, modified Rankin Scale, and the National Institute of Health Stroke Scale were used as clinical outcome parameters. Patient baseline characteristics and clinical data were comparable; treatment modality of the aneurysm was not different between the groups (P= 0.7756). No significant difference between the Hunt and Hess grade (P= 0.818) and the Barrow Neurological Institute grade (P= 0.1551) was observed. There was also no significance concerning the incidence of angiographic or clinically relevant vasospasm between both groups (P= 0.5842 and P= 0.7933). Glasgow Outcome Scale, mRS, and National Institute of Health Stroke Scale as the primary outcome parameters showed no significant difference in morbidity and mortality between both groups (mortality P= 0.8544). With the limitation of an explorative cohort study, the results indicate that routine TCD studies do not improve the overall outcome of patients after aSAH.

Antihypertensive drugs

Antihypertensive drugs

Modified Glasgow Coma Scale Score as an Early Indicator of Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage

Introduction Cerebral vasospasm (CV) is a delayed narrowing of cerebral arteries, occurring 4 to 14 days after subarachnoid hemorrhage (SAH). CV is a possible cause of delayed deterioration of patients after aneurysmal SAH (aSAH). Timely diagnostics and therapy of CV could reduce the morbidity and mortality after ruptured intracranial aneurysm (IA). Important diagnostic tool for the early detection of CV in conscious patients is neurological examination. The modified Glasgow Coma Scale score (mGCS) is derived from the Glasgow Coma Scale score (GCS) assessment of eye opening, verbal, and motor response. The mGCS score is calculated as the sum of the eye-opening response, the verbal response, and the worst motor response.

Cerebral Vasospasm in Patients With Severe Traumatic Brain Injury

Cerebral vasospasm (CV) occurs in 18-70% of patients with severe traumatic brain injury (sTBI) and is one of the main reasons for the development of secondary ischemic brain damage and a risk factor for adverse neurodevelopmental outcome.

Effect of Red Blood Cell Transfusion on Unfavorable Neurologic Outcome and Symptomatic Vasospasm in Patients with Cerebral Aneurysmal Rupture: Old versus Fresh Blood

Red blood cell (RBC) transfusion, especially with "old" blood, is associated with adverse clinical outcomes. We compared the effects of fresh blood versus old blood transfusion on poor neurologic outcomes and symptomatic vasospasm in patients with ruptured cerebral aneurysms. In this retrospective study, 211 patients with aneurysmal rupture were divided into 3 groups: nontransfusion (n = 136), fresh blood (RBC storage ≤ 14 days) transfusion (n = 39), and old blood (RBC storage >14 days) transfusion (n = 36). Unfavorable neurologic outcomes (modified Rankin Scale score ≥ 3) and symptomatic cerebral vasospasm were assessed. The incidence of unfavorable neurologic outcomes was significantly higher in the fresh blood and old blood transfusion groups compared with the nontransfused group (71.8% and 58.3% vs. 21.3%; P < 0.01); the incidence of symptomatic vasospasm was significantly higher in the old blood group compared with the fresh blood and nontransfusion groups (57.1% vs. 26.7% and 22.2%; P < 0.05). On binary logistic regression, old age, Hunt and Hess grade 3-4, high postoperative C-reactive protein level, RBC transfusion, delayed infarction, and hydrocephalus were independent predictors of unfavorable neurologic outcomes. Young age, Fisher grade 3-4, old RBC transfusion, and surgical clipping were independent predictors of postoperative symptomatic vasospasm. RBC transfusion itself, regardless of the duration of RBC storage, was associated with unfavorable neurologic outcomes in patients with ruptured cerebral aneurysms. Also, old blood transfusion, but not fresh blood transfusion, was associated with increased symptomatic cerebral vasospasm.

Effects of Clot Removal by Meticulous Irrigation and Continuous Low-Dose Intravenous Nicardipine on Symptomatic Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage Treated by Clipping

Symptomatic cerebral vasospasm (SCV) is the second most common of morbidity and mortality in aneurysmal subarachnoid hemorrhage (aSAH) after rebleeding. Blood breakdown products are one of the leading causes of vasospasm. We hypothesized that meticulous subarachnoid clot removal in addition to continuous low-dose intravenous nicardipine (CLIN) could reduce the incidence of SCV. SCV was defined as new focal neurologic signs, consciousness deterioration, or both when the cause was believed to be ischemia attributable to vasospasm after other possible causes of worsening were excluded. Initial brain damage was defined as continued consciousness disturbance after clipping without acute hydrocephalus, ischemic lesions, or focal sign before clipping. Poor outcome was defined as a Glasgow Outcome Scale score of 3-5 at 30 days. We compared the variables for 460 aSAH patients with and without SCV, and with and without poor outcome by multivariate analysis. All patients underwent clipping with meticulous irrigation for clot removal, and SCV was observed in 56 patients (12%). SCV was observed in 2 patients (2.9%) among 70 patients treated with CLIN. There was a higher proportion of patients who were older than 65 years (P = 0.032) and female (P = 0.038), and a lower proportion of patients with CLIN (P = 0.026) among patients with SCV. The outcomes for 109 patients (27%) were poor; age greater than 65 years (P < 0.0001) and initial brain damage (P = 0.008) were related to the poor outcomes. The present study showed that meticulous irrigation for clot removal and CLIN might reduce the incidence of SCV in patients with aSAH.

Vasospasm Is a Consistent Finding in Pernio (Chilblains) and a Possible Clue to Pathogenesis

Background/Aims: Pernio (chilblains) is an inflammatory condition classically characterized by localized erythema and swelling of acral sites upon exposure to cool and damp conditions. We sought to determine whether cold-induced vasospasm has a role in the development of pernio. Methods: We retrospectively reviewed 5 patients with pernio who were seen at our institution between January 1, 2000 and December 31, 2011, and had undergone a noninvasive arterial vascular study of the upper extremities that corresponded to a site of clinical involvement of pernio and who had also undergone vasospastic testing and ice water immersion as part of the noninvasive arterial vascular study protocol. Results: Vascular testing in all patients (mean age 37.8 years; 4 women) demonstrated vasospasm with ice water immersion. Conclusion: Our findings suggest that vasospasm likely has a role in the pathophysiology of pernio and may also provide a rationale for the pharmacological treatment of vasospasm in patients with pernio.

Risk Factors for Postoperative Cerebral Vasospasm After Surgical Resection of Acoustic Neuroma

Cerebral vasospasm is an important cause of morbidity after subarachnoid hemorrhage, but can also occur after resection of acoustic neuroma. This study aimed to identify factors associated with postoperative cerebral vasospasm in patients with acoustic neuroma. This was a retrospective analysis of patients with acoustic neuroma (diagnosed by preoperative magnetic resonance imaging and postoperative pathology) treated between April 2013 and February 2014 in a hospital in China. Patients with other intracranial abnormalities, postoperative vasoactive drug use, or postoperative abnormalities in consciousness, vital signs, blood electrolytes, or arterial blood gases were excluded. The neurilemmoma was removed using the suboccipital retrosigmoid sinus approach, with care taken to minimize bleeding and protect the facial, trigeminal, and lower cranial nerves and brainstem. Flow velocities in the bilateral internal carotid, middle cerebral, and anterior cerebral arteries, assessed with transcranial Doppler ultrasonography before surgery and on postoperative days 1, 3, 5, 7, and 9, were used to detect cerebral vasospasm (mild, 120-140 cm/s; moderate, 141-200 cm/s; severe, >200 cm/s). Factors associated with vasospasm were identified by univariate and multivariate analyses. Forty-three (53.8%) of the 80 patients (36 men) included were diagnosed with cerebral vasospasm: 5 (11.6%) were categorized as mild, 36 (83.7%) as moderate, and 2 (4.7%) as severe. Multivariate analysis showed that younger patient age, larger tumor size, and firm tumor consistency were independently associated with postoperative cerebral vasospasm (P <0.05). Younger patient age, larger tumor size, and firmer tumor consistency were independently associated with postoperative cerebral vasospasm in patients with acoustic neuroma.

A hypothesis on possible neurochemical mechanisms of action of cervical spinal cord stimulation in prevention and treatment of cerebral arterial vasospasm after aneurysmal subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) is associated with the high incidence of development of cerebral vasospasm that results in morbidity and mortality due to delayed cerebral ischemia. So far there are no consistently effective therapies for treatment of vasospasm in patients suffering from SAH. It is well known that cervical spinal cord stimulation (SCS) can induce vasodilatation and increase cerebral blood flow (CBF). Based on the experiments in animals and the studies in humans, we have proposed the possibility to use SCS as a therapeutic strategy for prevention and treatment of cerebral vasospasm after SAH. However, the physiological mechanisms of action of SCS in this regard are poorly understood. Better understanding of the pathophysiology of vasospasm after SAH may provide insight into the role of SCS in such conditions. We hypothesize that effect of SCS on vasodilatation may be related to modulation of activity of phosphodiesterases 5 (PDE-5) and nitric oxide synthase (eNOS), resulting in enhancement of nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway, which may help prevent and/or treat vasospasm after SAH. Further investigations on the physiological mechanisms of action of SCS would be necessary to support this hypothesis.

Efficacy and safety of intravenous nimodipine administration for treatment of hypertension in&amp;nbsp;patients with intracerebral hemorrhage

BackgroundNicardipine (NC) is the most commonly used antihypertensive drug in neurological patients with hypertension. Although nimodipine (NM) is widely used to treat cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage, trials exploring its antihypertensive effect after intravenous administration in subjects with intracerebral hemorrhage (ICH) are scarce.MethodsA retrospective study was carried out to compare the safety and efficacy of NC and NM administered intravenously in patients with ICH. Therapeutic responses were assessed by achievement of goal blood pressure (BP); use of additional medications for BP control; proportion of time spent within goal; variability in BP; time to goal BP; number of dose adjustments; variability in ICH volume, Glasgow Coma Scale score, and intracranial pressure; and drug-related complications.ResultsA total of 87 patients were eligible for analysis (n=46 [NC]; n=41 [NM]), and baseline characteristics between groups were similar. Both agents were effective in achieving goal BP during infusion, with 93.5% and 87.8% patients in the NC and NM groups achieving goal, respectively. Fewer additional medications were needed to control BP in the NC group. BP variability was similar and no differences were observed in the mean time to goal BP and mean numbers of dose adjustments between both groups. Interestingly, intracranial pressure declined (P=0.048) during NC administration but increased (P=0.066) after NM treatment. Finally, the incidences of hematoma expansion, neurological deterioration, and adverse drug events were similar in both groups.ConclusionNM is effective and safe for BP control in patients with ICH.

Do transfusion requirements increase after the diagnosis of vasospasm in patients with aneurysmal subarachnoid haemorrhage?

Abstract Background: Many patients experience impaired cerebral oxygen delivery secondary to vasospasm and delayed cerebral ischemia following aneurysmal subarachnoid haemorrhage (SAH). Anaemia is common after SAH affecting up to 50% patients, which may decrease cerebral oxygen delivery and is associated with worse clinical outcomes. Transfusion of allogeneic red cells increases the oxygen content of the blood but it not consistently associated with improved physiologic markers of clinical outcomes. The threshold for transfusion is not clear in patients with SAH. A recent survey found that most physicians would alter their transfusion threshold in SAH patients who develop delayed ischemia. The objective of our study is to identify the predictors of transfusion and to determine if the diagnosis of delayed ischemia increases the transfusion rates in patients with aneurysmal subarachnoid haemorrhage. Materials and Methods: We retrospectively reviewed the charts of 100 consecutive patients with SAH who were admitted to ICU for mechanical ventilation, and collected demographic and clinical data. Data were analyzed for the association between clinical factors and transfusion the differences in transfusion between the patients with and without vasospasm. Statistical methods included the t-test, univariate analysis and multivariate analysis. Results: Data from 96 patients were included in the analysis. Incidence of anaemia haemoglobin (Hb) &lt; 100 gm/l and vasospasm were 67% (64/96) and 39% (38/96) respectively. Of 64 patients with anaemia, 27 patients received transfusion, while 38 patients did not receive a transfusion. The transfusion rates were similar between those who had vasospasm and who did not. However, out of the 14 patients with vasospasm who received a transfusion, 11 patients had been transfused after experiencing vasospasm, while only 3 were transfused before. On multivariate analysis only female sex, starting Hb levels and lowest Hb levels were found to be predictors of transfusion. Presence or absence of vasospasm was not found to be a predictor. Conclusions: From our retrospective review, we conclude that the incidence of anaemia is higher in patients with vasospasm. Sex and starting and lowest Hb levels were the only predictors of transfusion likelihood in aneurysmal subarachnoid haemorrhage while presence of vasospasm was not.

Cranial Accelerometry Can Detect Cerebral Vasospasm Caused by Subarachnoid Hemorrhage.

We previously reported the presence of a cranial "bruit" in patients with cerebral vasospasm by signal processing cranial accelerometry signals time locked to the cardiac cycle. This shift to higher frequencies is likely related to the turbulence of blood flow produced by vascular narrowing. We sought to build a more quantitative model to predict cerebral vasospasm then test the accuracy of this technique to detect cerebral vasospasm in a prospective blinded study. Skull accelerometry was performed using an array of 6 highly sensitive accelerometers placed in contact with the scalp. Paired transcranial Doppler (TCD) recordings and accelerometry epochs were obtained in consecutive patients with subarachnoid hemorrhage undergoing TCD recordings for surveillance of cerebral vasospasm. The energy of rectified acceleration measurements within systolic and diastolic bands of the cardiac cycle were measured and correlated with TCD-defined spasm. This model was then tested prospectively in a blinded consecutive sample of subarachnoid hemorrhage patients to determine accuracy of the technique. We developed a model predicting cerebral vasospasm from analysis of 14 unblinded subjects with varying degrees of cerebral vasospasm as detected by TCD. We then recorded from 58 subjects obtaining 125-paired recordings of accelerometry and TCD to test this model in a blinded analysis. Accelerometry detection of any spasm versus non-spasm correlated with TCD-defined vasospasm (P<0.001). The model was 81% sensitive for detecting any cerebral vasospasm in patients, while the negative predictive value was 61%. Highly sensitive skull accelerometry can detect cerebral vasospasm with clinically meaningful accuracy. This tool holds promise in the ICU environment to detect as well as reject cerebral vasospasm as the cause of neurological deficits in subarachnoid hemorrhage.

Absorption, elimination and cerebrospinal fluid concentrations of nimodipine in healthy beagle dogs receiving human intravenous and oral formulation.

Nimodipine is an L-type calcium channel blocker and is used to treat vasospasm in patients with subarachnoid hemorrhage. Its putative mechanism of action is relaxation of smooth muscle cells in cerebral arteries. In addition, nimodipine may have pleiotropic effects against vasospasm. Systemic hypotension is an adverse effect when patients are treated with oral or intravenous nimodipine. Intracranial administration of nimodipine formulations may produce higher concentration of nimodipine in the cerebrospinal fluid (CSF) than is possible to achieve orally or intravenously, while resulting in lower incidence of systemic hypotension. The aim of this study was to provide information on plasma and CSF levels of nimodipine in beagle dogs as a comparative data for development of experimental intracranial treatment modalities. Plasma levels of nimodipine were measured after current 30 and 60mg single oral dose of nimodipine (Nimotop(®) 30mg tablets), a single intravenous bolus 0.72mg/dog of nimodipine (Nimotop(®) 0.2mg/ml infusion solution) and CSF levels after 60mg single oral dose of nimodipine. CSF/Plasma concentration ratio of nimodipine after oral administration of 60mg at 1h was 0.013±0.0005. The mean terminal elimination half-life of nimodipine after i.v. bolus dose 0.72mg was 1.8h and mean plasma clearance was 40.3 and 3.4l/h/kg. Absolute bioavailability was 22%. Maximum plasma concentration and area under the plasma concentration-time curve from time of administration until the last measurable plasma concentration increased in a dose-proportional manner comparing the exposure parameters at oral doses of 30 and 60mg. Individual variation in the kinetic profile of nimodipine was measured.

Cerebrospinal fluid from patients with subarachnoid haemorrhage and vasospasm enhances endothelin contraction in rat cerebral arteries.

IntroductionPrevious studies have suggested that cerebrospinal fluid from patients with subarachnoid hemorrhage (SAH) leads to pronounced vasoconstriction in isolated arteries. We hypothesized that only cerebrospinal fluid from SAH patients with vasospasm would produce an enhanced contractile response to endothelin-1 in rat cerebral arteries, involving both endothelin ETA and ETB receptors.MethodsIntact rat basilar arteries were incubated for 24 hours with cerebrospinal fluid from 1) SAH patients with vasospasm, 2) SAH patients without vasospasm, and 3) control patients. Arterial segments with and without endothelium were mounted in myographs and concentration-response curves for endothelin-1 were constructed in the absence and presence of selective and combined ETA and ETB receptor antagonists. Endothelin concentrations in culture medium and receptor expression were measured.ResultsCompared to the other groups, the following was observed in arteries exposed to cerebrospinal fluid from patients with vasospasm: 1) larger contractions at lower endothelin concentrations (p<0.05); 2) the increased endothelin contraction was absent in arteries without endothelium; 3) higher levels of endothelin secretion in the culture medium (p<0.05); 4) there was expression of ETA receptors and new expression of ETB receptors was apparent; 5) reduction in the enhanced response to endothelin after ETB blockade in the low range and after ETA blockade in the high range of endothelin concentrations; 6) after combined ETA and ETB blockade a complete inhibition of endothelin contraction was observed.ConclusionsOur experimental findings showed that in intact rat basilar arteries exposed to cerebrospinal fluid from patients with vasospasm endothelin contraction was enhanced in an endothelium-dependent manner and was blocked by combined ETA and ETB receptor antagonism. Therefore we suggest that combined blockade of both receptors may play a role in counteracting vasospasm in patients with SAH.

Comparative efficacy of meloxicam and placebo in vasospasm of patients with subarachnoid hemorrhage.

Cerebral vasospasm considered to be a serious cause of morbidity and mortality following subarachnoid haemorrhage (SAH).Despite several available therapeutic options, current protocols do not prevent major consequences of vasospasm. Inflammation is believed to play an important role in post-haemorrhagic vasospasm. Meloxicam is a non-steroidal anti-inflammatory drug. The aim of this study was to compare the efficacy of meloxicam versus placebo on vasospasm in patients with SAH. In this randomized, double-blind, placebo-controlled trial, SAH patients randomly received 7.5 mg meloxicam or placebo twice daily for 7 days. End points were, middle cerebral artery velocity obtained with transcranial doppler, in-hospital mortality, hospital stay and discharge Glasgow Outcome Scale. Eighty-one patients enrolled in the study. (40 received meloxicam, 41 received placebo). Baseline characteristics were similar between the groups. There were no differences in length of hospitalization (17.4 ± 3.1 vs 18.6 ± 4.2 days; p = 0.145), in-hospital mortality rate (15 vs 22%; p-value=0.569), or GOS (p = 0.972) between the two groups. MCA velocity were slightly less in patients who had received meloxicam, but not to a significant degree (p-value=0. 564(. No side effect has been detected for meloxicam. This study did not prove meloxicam efficacy in vasospasm of SAH patients. But it demonstrated that clinical trial of meloxicam in these patients is feasible and probably safe. The effectiveness of meloxicam on cerebral vasospasm has to be studied in larger trials.

The Impact of Subclinical Hypothyroidism or Thyroid Autoimmunity on Coronary Vasospasm in Patients without Associated Cardiovascular Risk Factors.

Background and ObjectivesSubclinical hypothyroidism is associated with endothelial dysfunction and impaired coronary flow reserve. However, the effect of subclinical hypothyroidism or thyroid autoimmunity on variant angina has yet to be determined.Subjects and MethodsAmong 385 consecutive patients without associated cardiovascular risk factors who underwent coronary angiography with the ergonovine provocation test (EPT), 165 had a positive EPT {EPT(+)} and 220 had a negative EPT {EPT(-)}. The relationship between coronary artery spasm and the presence of subclinical thyroid dysfunction as well as serum thyroid peroxidase autoantibody (TPO Ab) was evaluated.ResultsThe proportion of patients with subclinical hypothyroidism among those who were EPT(+) was significantly higher than that in those who were EPT(-) (18% vs. 11%, p=0.001). However, there was no significant difference in the proportion of patients with subclinical hyperthyroidism between the groups. Moreover, EPT(+) patients showed significantly more positive TPO Ab (33% vs. 14%, p<0.001) than those with EPT(-). There was a positive correlation between EPT(+) and TPO positivity (r=0.226, p<0.001), subclinical hypothyroidism (r=0.112, p=0.033), and body mass index (r=0.123, p=0.018). Binary logistic regression analysis revealed that the significant predictors of EPT(+) were body mass index {adjusted odds ratio (OR)=1.042, 95% confidence interval (CI)=1.005-1.080}, presence of subclinical hypothyroidism (OR=3.047, 95% CI=1.083-8.572), TPO Ab titer (OR=1.028, 95% CI=1.015-1.041), and the presence of TPO Ab (OR=4.904, 95% CI=1.544-15.567).ConclusionSubclinical hypothyroidism and the presence of TPO Ab are significantly associated with coronary vasospasm in patients without cardiovascular risk factors.

Predictors of Symptomatic Vasospasm After Subarachnoid Hemorrhage: A Single Center Study of 457 Consecutive Cases.

We set forth to identify predictors of symptomatic vasospasm in patients with subarachnoid hemorrhage (SAH). We used multivariate logistic regression analysis of the prospective, hospital based, single center register of the Department of Neurosurgery, University of Debrecen, Hungary. Evaluated patients' characteristics were: sex, age, Hunt-Hess grade on admission, location of aneurysm, thickness of blood clot on initial CT scan (Fisher grade), hypertension. Between 1987 and 2004, 567 SAH cases were registered, 457 were included in this study. Symptomatic vasospasm developed in 22.5% of the cases. In univariate analysis, Hunt-Hess grades 2 and 3 and female sex were predictive for symptomatic vasospasm. In multivariate analysis, female sex remained a significant predictor: OR: 1.8 (1.005-3.2). Women are at more danger of developing symptomatic vasospasm after subarachnoid hemorrhage.