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Jes Olesen - One of the best experts on this subject based on the ideXlab platform.
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ehmti 0165 acetazolamide infusion induces immediate and delayed headache and intracranial Artery Dilatation in healthy volunteers
Journal of Headache and Pain, 2014Co-Authors: Nanna Arngrim, Jes Olesen, Henrik Winther Schytz, Faisal Mohammad Amin, Anders Hougaard, Vibeke Andree Larsen, Pjh De Koning, H B W Larsson, Messoud AshinaAbstract:Methods Twelve healthy women received injection of 1 g acetazolamide or placebo on two separate days in a randomized double-blind crossover study design. We recorded headache on a verbal rating scale from 0-10 during an immediate phase (0-90 min) and a delayed phase (2-12 h). The circumferences of cranial arteries were measured in a blinded fashion using 3T high-resolution magnetic resonance angiography 30 and 60 min after acetazolamide injection.
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bibn4096bs antagonizes human α calcitonin gene related peptide induced headache and extracerebral Artery Dilatation
Clinical Pharmacology & Therapeutics, 2005Co-Authors: Jes Olesen, Kenneth A Petersen, Lisbeth H Lassen, Steffen Birk, Lynna LeskoAbstract:Background and Objective Calcitonin gene-related peptide (CGRP) plays a pivotal role in migraine pathogenesis. BIBN4096BS is the first CGRP receptor antagonist available for human studies, and its efficacy in the acute treatment of migraine has been demonstrated. We investigated the ability of BIBN4096BS to inhibit human αCGRP (h-αCGRP)–induced headache and cerebral hemodynamic changes in healthy volunteers. Methods Ten healthy volunteers completed this double-blind, placebo-controlled crossover study with 2.5 mg BIBN4096BS and placebo as pretreatments before a 20-minute intravenous infusion of h-αCGRP (1.5 Μg/min). Transcranial Doppler ultrasonography was used to measure blood flow velocity in the middle cerebral Artery (MCA); regional and global cerebral blood flow (CBF) was measured by xenon 133 inhalation single-photon emission computed tomography. The temporal and radial Artery diameter was measured by high-frequency ultrasound. Systemic hemodynamics, end-tidal partial pressure of carbon dioxide (PETCO2), and headache were monitored. Results Of the 10 volunteers, 6 had a CGRP-induced headache during the in-hospital phase after placebo pretreatment but none after BIBN4096BS (P = .031). BIBN4096BS did not affect changes in the diameter of the MCA or changes in CBF induced by h-αCGRP. VasoDilatation of the extracranial arteries was, however, significantly inhibited (P < .001 for temporal Artery and P = .001 for radial Artery). Conclusions These results show that BIBN4096BS effectively prevents CGRP-induced headache and extracerebral vasoDilatation but does not significantly affect the induced cerebral hemodynamic changes. Clinical Pharmacology & Therapeutics (2005) 77, 202–213; doi: 10.1016/j.clpt.2004.10.001
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the role of cgmp hydrolysing phosphodiesterases 1 and 5 in cerebral Artery Dilatation
European Journal of Pharmacology, 2001Co-Authors: Christina Kruuse, Jes Olesen, Sergei D Rybalkin, Tejvir S Khurana, Inger Jansenolesen, Lars EdvinssonAbstract:Abstract The aim was to investigate the presence and activity of cGMP hydrolysing phosphodiesterases in guinea pig basilar arteries and the effect of selective and non-selective phosphodiesterase inhibitors on cerebral Artery Dilatation involving the nitric oxide (NO)–guanosine cyclic 3′5-monophosphate (cGMP) pathway. Immunoreactivity to phosphodiesterases 1A, 1B and 5, but not phosphodiesterase 1C was found in fractions of homogenised cerebral arteries eluted by high-pressure liquid chromatography (HPLC). Both the phosphodiesterase 1 inhibitor 8-methoxymethyl-1-methyl-3-(2methylpropyl)-xanthine (8-MM-IBMX) and the phosphodiesterase 5 inhibitors zaprinast and dipyridamole induced Dilatation of cerebral arteries. The dilatory response to 8-MM-IBMX was reduced by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (10 μM) and endothelial removal and restored by sodium nitroprusside (0.1 μM) pretreatment, indicating a close relation to the nitric oxide–cGMP pathway. The responses to zaprinast and dipyridamole, however, were not only moderately affected, but also restored by sodium nitroprusside (0.1 μM) pretreatment. At high concentrations, the dilatory effects of zaprinast and dipyridamole were partly caused by cGMP-independent mechanisms. Targeting the phosphodiesterases present in cerebral arteries, with selective inhibitors or activators of phosphodiesterase, may be a possible new way of treating cerebrovascular disease.
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a nitric oxide donor nitroglycerin triggers genuine migraine attacks
European Journal of Neurology, 1994Co-Authors: L L Thomsen, Christina Kruuse, Helle K Iversen, Jes OlesenAbstract:Supersensitivity to induction of headache and arterial Dilatation by a donor of nitric oxide (nitroglycerin) has recently been demonstrated in migraine sufferers. The aims of the present study were to examine whether the nitric oxide donor nitroglycerin may induce a typical migraine attack, to exclude placebo-related effects and to describe the relation between middle cerebral Artery Dilatation and provoked migraine. Nitroglycerin (0.5 μg/kg/min for 20 min) or placebo was infused into 12 migraine patients in a double-blind cross-over trial. Blood velocity in the middle cerebral Artery was measured with transcranial Doppler and characteristics of headache and accompanying symptoms were recorded frequently. Headache occurred during the nitroglycerin infusion as previously described but peak headache intensity did first occur 5.5 h after infusion. At this time the induced headaches in 8 of 10 completing patients fulfilled the diagnostic criteria for migraine without aura of the International Headache Society. Furthermore, all patients who normally had unilateral spontaneous migraine attacks also had unilateral headaches after nitroglycerin. Only one subject developed migraine after placebo (p < 0.03). The time pattern of headache and estimated middle cerebral Artery Dilatation corresponded well. The study therefore demonstrates that activation of the nitric oxide cGMP pathway may cause typical migraine attacks.
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migraine pain associated with middle cerebral Artery Dilatation reversal by sumatriptan
The Lancet, 1991Co-Authors: Lars Friberg, Jes Olesen, B Sperling, Helle K IversenAbstract:Abstract The combination of measurements of regional cerebral blood flow (rCBF) and blood velocity in the middle cerebral arteries (MCA) by transcranial doppler sonography was used to investigate cerebrovascular involvement in migraine. Ten migraine patients with unilateral headache were studied during an attack and when they had been free of attacks for 5 days (non-attack). On both occasions they were given an intravenous infusion of sumatriptan (2 mg), a 5-HT 1 -like receptor agonist, which relieved the symptoms within 30 min without affecting rCBF. The MCA velocity was normal on both sides on the non-attack day and on the unaffected side during the attack. However, during the attack the MCA velocity on the headache side was significantly lower than that on the non-headache side (45 vs 61 cm/s:mean difference 16·3 [95% confidence interval 10·3-22·3]; p=0·02). The MCA velocity on the headache side returned to normal after treatment with sumatriptan and recovery. Since rCBF in the MCA supply territory was unaffected, the lower velocity can be explained only by Dilatation of the MCA. The mean MCA diameter increase was estimated to be 20%. Thus, headache was associated with intracranial large arterial Dilatation on the headache side. Sumatriptan predominantly had effects on the distended Artery, which suggests that the 5-HT receptor system has a role in the pathogenesis of migraine.
Nagib Dahdah - One of the best experts on this subject based on the ideXlab platform.
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coronary Artery Dilatation in viral myocarditis mimics coronary Artery findings in kawasaki disease
Pediatric Cardiology, 2016Co-Authors: Anne Fournier, Ibtissama Boukas, Marie-josée Raboisson, Soha Racheddastous, Nagib DahdahAbstract:Coronary Artery (CA) Dilatations are typical to Kawasaki disease (KD) in the pediatric population. CA involvement is a useful feature to help establish the diagnosis of KD. Since myocarditis is omnipresent in the acute phase of KD, we sought to investigate whether viral myocarditis may cause CA Dilatation. This retrospective study reviewed 14 consecutive patients diagnosed with acute myocarditis at CHU Sainte-Justine, Montreal. KD diagnosis was excluded for all patients. All echocardiography studies were reviewed by an independent experienced echocardiographer for CA size and myocardial function parameters. CA involvement was classified under three categories: definite Dilatation (Z-score ≥2.5 in one or more CA), occult Dilatation (Z-score variation ≥2 points for the same CA on two different echocardiograms, but maximum Z-score always <2.5), and no Dilatation otherwise. Demographics, laboratory values, microbial etiology testing, and diagnostic studies were collected from medical records. Mean age at presentation was 1.67 ± 3.22 years, where 11/14 (78 %) presented with acute and three with subacute myocarditis. Five (36 %) patients had normal CA measurements, six (43 %) had occult Dilatation, and three (21 %) had definite Dilatation. Maximal CA Z-score was within the first 8 days of presentation. Patients with viral myocarditis can present CA Dilatation during the acute phase of the illness. This finding should be taken into account when KD diagnosis is being based on the CA involvement as the two illnesses may present with similar features.
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n terminal pro brain natriuretic peptide in acute kawasaki disease correlates with coronary Artery involvement
Cardiology in The Young, 2015Co-Authors: Philippe Mahouna Adjagba, Anne Fournier, Laurent Desjardins, Linda Spigelblatt, Martine Montigny, Nagib DahdahAbstract:Background We have lately documented the importance of N-terminal pro-brain natriuretic peptide in aiding the diagnosis of Kawasaki disease. Objectives We sought to investigate the potential value of N-terminal pro-brain natriuretic peptide pertaining to the prediction of coronary Artery Dilatation (Z-score>2.5) and/or of resistance to intravenous immunoglobulin therapy. We hypothesised that increased serum N-terminal pro-brain natriuretic peptide level correlates with increased coronary Artery Dilatation and/or resistance to intravenous immunoglobulin. Methods We carried out a prospective study involving newly diagnosed patients treated with 2 g/kg intravenous immunoglobulin within 5–10 days of onset of fever. Echocardiography was performed in all patients at onset, then weekly for 3 weeks, then at month 2, and month 3. Coronary arteries were measured at each visit, and coronary Artery Z-score was calculated. All the patients had N-terminal pro-brain natriuretic peptide serum level measured at onset, and the Z-score calculated. Results There were 109 patients enrolled at 6.58±2.82 days of fever, age 3.79±2.92 years. High N-terminal pro-brain natriuretic peptide level was associated with coronary Artery Dilatation at onset in 22.2 versus 5.6% for normal N-terminal pro-brain natriuretic peptide levels (odds ratio 4.8 [95% confidence interval 1.05–22.4]; p=0.031). This was predictive of cumulative coronary Artery Dilatation for the first 3 months (p=0.04–0.02), but not during convalescence at 2–3 months (odds ratio 1.28 [95% confidence interval 0.23–7.3]; p=non-significant). Elevated N-terminal pro-brain natriuretic peptide levels did not predict intravenous immunoglobulin resistance, 15.3 versus 13.5% (p=1). Conclusion Elevated N-terminal pro-brain natriuretic peptide level correlates with acute coronary Artery Dilatation in treated Kawasaki disease, but not with intravenous immunoglobulin resistance.
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abstract 165 coronary Artery Dilatation in kawasaki disease is associated with anatomical coronary dominance an angiography based study
Circulation, 2015Co-Authors: Baher Hanna, Anne Fournier, Chantale Lapierre, Frederick Trinh Tan, Larent Desjardins, Nagib DahdahAbstract:Introduction: Coronary Artery (CA) Dilatation in Kawasaki disease (KD) is best determined by elevated Z-scores. Z-score equations, do not take into account anatomical CA dominance. We hypothesize that, except for CA aneurysms, CA dominance influences Dilatation status in KD (Z-score > 2.5). Material and Methods: We retrospectively analyzed CA status in KD patients followed at our institution for persistent CA Dilatation. All patients who had a diagnostic catheterization between 2002 and 2012 were considered. Serial echocardiographic dimensions of LCA, RCA, and LAD upon diagnosis, 1 week, 2 weeks, 4 weeks, 2 months, 3-6 months, and 9-12 months later were normalized to BSA using published CA Z-score equations. Data were contrasted with CA angiography description of CA dominance: right or left dominance was adopted when the respective CA supplies both diaphragmatic LV free wall and posterior inter ventricular septum (IVS); Co-dominance was when posterior IVS was supplied by RCA and diaphragmatic LV free wall by LCA. Results: Of 69 potential patients, 16 were excluded (9 never presented a CA Dilatation and 7 had CA aneurysms). The interval between acute onset and selective CA angiography of the remaining 53 patients was 69.5±52.8months at 9.2±5.2years old. Of the latter, 20(37.7%) had LCA-dominance, 31(58.5%) RCA-dominance, and 2(3.8%) Co-dominance. Upon KD onset, the LCA-dominant subset had 14/20(70%) ipsilateral Dilatation vs. 6/20(30%) contralateral Dilatation. Similarly, RCA-dominant Dilatation was ipsilateral in 21/31(68%) vs. 10/31(32%) contralateral Dilatation (p=0.89). On late follow-up, persistent CA Dilatation was similar between LCA-dominance 6/14(43%) and RCA-dominance 10/21(47%) (p=0.94). The interval between onset and normalizing CA Z-score was 1.16±1.65 vs. 2.45±3.6years in ispilateral vs. contralateral subsets (p=0.19). From the inflammatory perspective, serum albumin was significantly lower in patients with contralateral CA Dilatation (p=0.02). Nevertheless, other inflammatory markers did not show a significant difference. Conclusion: Transitory CA Dilatation following KD is closely related to anatomical dominance. This may be a reflection of vasodilation during immune carditis rather than coronary vasculitis.
Anne Fournier - One of the best experts on this subject based on the ideXlab platform.
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coronary Artery Dilatation in viral myocarditis mimics coronary Artery findings in kawasaki disease
Pediatric Cardiology, 2016Co-Authors: Anne Fournier, Ibtissama Boukas, Marie-josée Raboisson, Soha Racheddastous, Nagib DahdahAbstract:Coronary Artery (CA) Dilatations are typical to Kawasaki disease (KD) in the pediatric population. CA involvement is a useful feature to help establish the diagnosis of KD. Since myocarditis is omnipresent in the acute phase of KD, we sought to investigate whether viral myocarditis may cause CA Dilatation. This retrospective study reviewed 14 consecutive patients diagnosed with acute myocarditis at CHU Sainte-Justine, Montreal. KD diagnosis was excluded for all patients. All echocardiography studies were reviewed by an independent experienced echocardiographer for CA size and myocardial function parameters. CA involvement was classified under three categories: definite Dilatation (Z-score ≥2.5 in one or more CA), occult Dilatation (Z-score variation ≥2 points for the same CA on two different echocardiograms, but maximum Z-score always <2.5), and no Dilatation otherwise. Demographics, laboratory values, microbial etiology testing, and diagnostic studies were collected from medical records. Mean age at presentation was 1.67 ± 3.22 years, where 11/14 (78 %) presented with acute and three with subacute myocarditis. Five (36 %) patients had normal CA measurements, six (43 %) had occult Dilatation, and three (21 %) had definite Dilatation. Maximal CA Z-score was within the first 8 days of presentation. Patients with viral myocarditis can present CA Dilatation during the acute phase of the illness. This finding should be taken into account when KD diagnosis is being based on the CA involvement as the two illnesses may present with similar features.
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n terminal pro brain natriuretic peptide in acute kawasaki disease correlates with coronary Artery involvement
Cardiology in The Young, 2015Co-Authors: Philippe Mahouna Adjagba, Anne Fournier, Laurent Desjardins, Linda Spigelblatt, Martine Montigny, Nagib DahdahAbstract:Background We have lately documented the importance of N-terminal pro-brain natriuretic peptide in aiding the diagnosis of Kawasaki disease. Objectives We sought to investigate the potential value of N-terminal pro-brain natriuretic peptide pertaining to the prediction of coronary Artery Dilatation (Z-score>2.5) and/or of resistance to intravenous immunoglobulin therapy. We hypothesised that increased serum N-terminal pro-brain natriuretic peptide level correlates with increased coronary Artery Dilatation and/or resistance to intravenous immunoglobulin. Methods We carried out a prospective study involving newly diagnosed patients treated with 2 g/kg intravenous immunoglobulin within 5–10 days of onset of fever. Echocardiography was performed in all patients at onset, then weekly for 3 weeks, then at month 2, and month 3. Coronary arteries were measured at each visit, and coronary Artery Z-score was calculated. All the patients had N-terminal pro-brain natriuretic peptide serum level measured at onset, and the Z-score calculated. Results There were 109 patients enrolled at 6.58±2.82 days of fever, age 3.79±2.92 years. High N-terminal pro-brain natriuretic peptide level was associated with coronary Artery Dilatation at onset in 22.2 versus 5.6% for normal N-terminal pro-brain natriuretic peptide levels (odds ratio 4.8 [95% confidence interval 1.05–22.4]; p=0.031). This was predictive of cumulative coronary Artery Dilatation for the first 3 months (p=0.04–0.02), but not during convalescence at 2–3 months (odds ratio 1.28 [95% confidence interval 0.23–7.3]; p=non-significant). Elevated N-terminal pro-brain natriuretic peptide levels did not predict intravenous immunoglobulin resistance, 15.3 versus 13.5% (p=1). Conclusion Elevated N-terminal pro-brain natriuretic peptide level correlates with acute coronary Artery Dilatation in treated Kawasaki disease, but not with intravenous immunoglobulin resistance.
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abstract 165 coronary Artery Dilatation in kawasaki disease is associated with anatomical coronary dominance an angiography based study
Circulation, 2015Co-Authors: Baher Hanna, Anne Fournier, Chantale Lapierre, Frederick Trinh Tan, Larent Desjardins, Nagib DahdahAbstract:Introduction: Coronary Artery (CA) Dilatation in Kawasaki disease (KD) is best determined by elevated Z-scores. Z-score equations, do not take into account anatomical CA dominance. We hypothesize that, except for CA aneurysms, CA dominance influences Dilatation status in KD (Z-score > 2.5). Material and Methods: We retrospectively analyzed CA status in KD patients followed at our institution for persistent CA Dilatation. All patients who had a diagnostic catheterization between 2002 and 2012 were considered. Serial echocardiographic dimensions of LCA, RCA, and LAD upon diagnosis, 1 week, 2 weeks, 4 weeks, 2 months, 3-6 months, and 9-12 months later were normalized to BSA using published CA Z-score equations. Data were contrasted with CA angiography description of CA dominance: right or left dominance was adopted when the respective CA supplies both diaphragmatic LV free wall and posterior inter ventricular septum (IVS); Co-dominance was when posterior IVS was supplied by RCA and diaphragmatic LV free wall by LCA. Results: Of 69 potential patients, 16 were excluded (9 never presented a CA Dilatation and 7 had CA aneurysms). The interval between acute onset and selective CA angiography of the remaining 53 patients was 69.5±52.8months at 9.2±5.2years old. Of the latter, 20(37.7%) had LCA-dominance, 31(58.5%) RCA-dominance, and 2(3.8%) Co-dominance. Upon KD onset, the LCA-dominant subset had 14/20(70%) ipsilateral Dilatation vs. 6/20(30%) contralateral Dilatation. Similarly, RCA-dominant Dilatation was ipsilateral in 21/31(68%) vs. 10/31(32%) contralateral Dilatation (p=0.89). On late follow-up, persistent CA Dilatation was similar between LCA-dominance 6/14(43%) and RCA-dominance 10/21(47%) (p=0.94). The interval between onset and normalizing CA Z-score was 1.16±1.65 vs. 2.45±3.6years in ispilateral vs. contralateral subsets (p=0.19). From the inflammatory perspective, serum albumin was significantly lower in patients with contralateral CA Dilatation (p=0.02). Nevertheless, other inflammatory markers did not show a significant difference. Conclusion: Transitory CA Dilatation following KD is closely related to anatomical dominance. This may be a reflection of vasodilation during immune carditis rather than coronary vasculitis.
Alain Nitenberg - One of the best experts on this subject based on the ideXlab platform.
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loss of flow dependent coronary Artery Dilatation in patients with hypertension
Circulation, 1995Co-Authors: Isabelle Antony, Guy Lerebours, Alain NitenbergAbstract:Background Abnormal endothelium-dependent coronary response to acetylcholine has been shown in patients with essential hypertension. We tested the hypothesis that flow-dependent Dilatation, which has been shown in normal human coronary arteries, is impaired in hypertensive patients. Methods and Results The coronary vasomotor response to maximal increase of blood flow induced by papaverine was studied in 10 control subjects and in 14 hypertensive patients with no other risk factors and angiographically normal coronary arteries. After the injection of papaverine in the midportion of the left anterior descending coronary Artery (LAD), the diameter of the proximal LAD (LAD1) was measured by quantitative angiography, whereas that of the proximal circumflex Artery (LCx) served as control segment. Estimates of coronary blood flow in the distal LAD (LAD2) were calculated by intracoronary Doppler flow velocity measurements. An increase in LAD2 blood flow of 521±41% ( P <.001) in control subjects was associated with a 17.0±3.3% Dilatation of the LAD1 ( P <.001) and with no significant change in the diameter of the LCx. In hypertensive patients, despite a comparable increase in LAD2 blood flow of 406±32% ( P <.001), the LAD1 failed to dilate (−0.4±0.6%, NS). The dilative response to isosorbide dinitrate was similar in control subjects and hypertensive patients (30.0±4.1%, P <.001 and 21.9±1.9%, P <.001, respectively). Conclusions Thus, the flow-mediated coronary Dilatation is lost in hypertensive patients, and this may impair normal Dilatation observed in response to an increase in myocardial metabolic demand.
Kevi J Shoemake - One of the best experts on this subject based on the ideXlab platform.
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sodium nitroglycerin induces middle cerebral Artery vasoDilatation in young healthy adults
Experimental Physiology, 2018Co-Authors: J M Schulz, Araa K Alkhazraji, Kevi J ShoemakeAbstract:NEW FINDINGS: What is the central question of this study? Nitric oxide causes Dilatation in peripheral vessels; however, whether nitric oxide affects basal cerebral Artery Dilatation has not been explored. What is the main finding and its importance? This study demonstrated that vasoDilatation occurs in the right middle cerebral Artery in response to exogenous nitric oxide. However, blood velocity decreased and, therefore, overall cerebral blood flow remained unchanged. This study provides new insight into the role of nitric oxide in cerebral blood flow control. ABSTRACT: Recent evidence indicates that basal cerebral conduit vessels dilate with hypercapnia, with a nitric oxide (NO) mechanism explaining one way in which parenchymal cerebral arterioles dilate. However, whether NO affects basal cerebral Artery Dilatation remains unknown. This study quantified the effect of an exogenous NO donor [sodium nitroglycerin (NTG); 0.4 mg sublingual spray] on the right middle cerebral Artery (rMCA) cross-sectional area (CSA), blood velocity and overall blood flow. Measures of vessel CSA (7 T magnetic resonance imaging) and MCA blood velocity (transcranial Doppler ultrasound) were made at baseline (BL) and after exogenous NTG or placebo (PLO) administration in young, healthy individuals (n = 10, two males, age range 20-23 years). The CSA increased in the rMCA [BL, 5.2 ± 1.2 mm2 ; PLO, 5.4 ± 1.5 mm2 ; NTG, 6.6 ± 1.5 mm2 , P < 0.05; mean ± SD]. Concurrently, rMCA blood velocity decreased from BL during NTG compared with PLO (BL, 67 ± 10 cm s-1 ; PLO, 62 ± 10 cm s-1 ; NTG, 59 ± 9.3 cm s-1 , P < 0.05; mean ± SD]. However, total MCA blood flow did not change with NTG or PLO [BL, 221 ± 37.4 ml min-1 ; PLO, 218 ± 35.0 ml min-1 ; NTG, 213 ± 46.4 ml min-1 ). Therefore, exogenous NO mediates a dilatory response in the rMCA, but not in its downstream vascular bed.
