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Dive into the research topics where Floris Vanmolkot is active.

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Featured researches published by Floris Vanmolkot.


Ultrasound in Medicine and Biology | 2001

Does B-mode common carotid artery intima-media thickness differ from M-model?

Luc M. Van Bortel; Floris Vanmolkot; Janneke J. van der Heijden-Spek; Marsel Bregu; Jan A. Staessen; Arnold P.G. Hoeks

An increased intima-media thickness of the common carotid artery is thought to be an early sign of atherosclerosis. Both B- and M-mode ultrasonographic techniques are used to measure the intima-media thickness of the common carotid artery (B-IMT and M-IMT, respectively). The present study compares intima-media thickness of the common carotid artery measured with the two techniques. Intima-media thickness was measured in a random population sample of 250 subjects. Comparison was made by mean and 95% confidence intervals of differences between B-IMT and M-IMT, by linear regression analysis, and by intraclass and concordance correlation coefficients. M-IMT was + 0.011 +/- 0.091 mm (95% confidence intervals: -0.167 to + 0.188 mm) larger than B-IMT, which was 0.661 +/- 0.136 mm (range: 0.380 to 1.120 mm). Intraclass and concordance correlation coefficients were 0.802 and 0.801, respectively. In conclusion, acceptable agreement exists between the two methods and there was no important systematic difference between B-IMT and M-IMT.


BMC Neurology | 2010

Endothelial function in migraine: a cross-sectional study

Floris Vanmolkot; Jan de Hoon

BackgroundMigraine has been associated with cardiovascular disorders. Endothelial dysfunction may be a mechanism underlying this association. The present study tested the hypothesis that endothelium-dependent vasodilation, basal endothelial nitric oxide release and endothelial fibrinolytic capacity are impaired in migraine patients.MethodsGraded doses of sodium nitroprusside (SNP, 0.2 to 0.8 μg.min-1.dL-1 forearm), substance P (0.2 to 0.8 pmol.min-1.dL-1 forearm) and NG-monomethyl-L-arginine (L-NMMA, 0.1 to 0.4 μmol.min-1.dL-1 forearm) were infused into the brachial artery of 16 migraine patients with or without aura during a headache-free interval and 16 age- and sex-matched subjects without a history of migraine. Forearm blood flow (FBF) was measured by strain-gauge venous occlusion plethysmography. Local forearm release of tissue plasminogen activator (t-PA) in response to substance P infusion was assessed using the arteriovenous plasma concentration gradient. Responses to infused drugs were compared between patients and matched controls by analysis of variance.ResultsIn both migraine patients and control subjects, SNP and substance P caused a dose-dependent increase, and L-NMMA a dose-dependent decrease in FBF (P < 0.001 for all responses). In both groups, substance P caused an increase in t-PA release (P < 0.001). FBF responses and t-PA release were comparable between migraine patients and control subjects.ConclusionsThe absence of differences in endothelium-dependent vasodilation, basal endothelial nitric oxide production and stimulated t-PA release between migraine patients and healthy control subjects argues against the presence of endothelial dysfunction in forearm resistance vessels of migraine patients.


Cardiovascular Drugs and Therapy | 1997

Quality of life comparison between bisoprolol and nifedipine retard in hypertension

Jan de Hoon; Floris Vanmolkot; Louis L.M. van de Ven; Luc M. Van Bortel

Quality of life with the selective beta1-blocker bisoprolol and the calcium channel blocker nifedipine as a retard formulation was compared in patients with essential hypertension. A multicenter randomized, double-blind, two-way, crossover study design was used. After a placebo run-in period (4–6 weeks), during which all antihypertensive therapy was withdrawn, 82 patients were randomized. During the active treatment periods (8 weeks each), patients received either bisoprolol once daily or nifedipine retard twice daily, using the double-dummy technique. A washout period (4–6 weeks) separated the treatment periods. Data at baseline (at randomization) and at the end of each treatment period were compared. Seventy-five patients completed the study. Blood pressure (168 ± 2/103 ± 1 mmHg) decreased (p > 0.001) similarly with bisoprolol (153 ± 2/90 ± 1 mmHg) and nifedipine (154 ± 2/90 ± 1 mmHg). Compared with baseline values, none of the quality of life variables investigated changed during bisoprolol or nifedipine retard use. Neither in the intention-to-treat nor the efficacy analysis were differences between bisoprolol and nifedipine found in quality of life variables, such as the Health Status Index, somatic symptoms, anxiety, depression, total psychiatric morbidity, cognitive symptoms, and hostility score. Only in the efficacy analysis did Health Status Index tend to be better (p = 0.055) during nifedipine intake when compared with bisoprolol. This trend was not present in the intention-to-treat analysis. The number of dropouts during bisoprolol (n = 2) and nifedipine (n = 3) treatment, and the number of patients reporting side effects (21% and 16%, respectively) did not differ (p = 0.64) between both treatments. It can be concluded that at equipotent antihypertensive dosages, an 8-week treatment period with the selective beta1-blocker bisoprolol or the calcium antagonist nifedipine as a retard formulation does not result in any difference in quality of life variables. It is not clear whether the trend of Health Status Index to become better during nifedipine intake, which was only found in the efficacy analysis and not in the intention-to-treat analysis, is of clinical relevance.


Cephalalgia | 2003

A human in vivo model to investigate the potency of CGRP receptor antagonists

Floris Vanmolkot; Jan de Hoon


Basic & Clinical Pharmacology & Toxicology | 2007

Endothelial function in migraine

Floris Vanmolkot; Jan de Hoon


Journal of Headache and Pain | 2006

Cardiovascular risk factors in young migraineurs.

Floris Vanmolkot; Jan de Hoon


Archive | 2005

Increased augmentation index in young migraine patients

Floris Vanmolkot; Jan de Hoon


Cephalalgia | 2004

Further evaluation of a human in vivo pharmacodynamic model to assess the efficacy of CGRP-receptor antagonists.

Floris Vanmolkot; Jan de Hoon


Cephalalgia | 2003

CGRP8-37 inhibits CGRP-induced vasodilation in the human forearm.

Floris Vanmolkot; Jan de Hoon


Cephalalgia | 2001

Assessment of selective 5-HT1B/1D-receptor agonists-induced peripheral vascular effects in humans.

Jan de Hoon; Floris Vanmolkot; P. Barrington; R. Peck; N. Dallow; P. Williams; J. McColm

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Jan de Hoon

Katholieke Universiteit Leuven

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Jan A. Staessen

Katholieke Universiteit Leuven

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Jan de Hoon

Katholieke Universiteit Leuven

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