M A Allessie

Maastricht University, Maestricht, Limburg, Netherlands

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Publications (199)1370.4 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is characterized by sustained high atrial activation rates and arrhythmogenic cellular Ca2+ signaling instability; however, it is not clear how a high atrial rate and Ca2+ instability may be related. Here, we characterized subcellular Ca2+ signaling after 5 days of high atrial rates in a rabbit model. While some changes were similar to those in persistent AF, we identified a distinct pattern of stabilized subcellular Ca2+ signaling. Ca2+ sparks, arrhythmogenic Ca2+ waves, sarcoplasmic reticulum (SR) Ca2+ leak, and SR Ca2+ content were largely unaltered. Based on computational analysis, these findings were consistent with a higher Ca2+ leak due to PKA-dependent phosphorylation of SR Ca2+ channels (RyR2s), fewer RyR2s, and smaller RyR2 clusters in the SR. We determined that less Ca2+ release per [Ca2+]i transient, increased Ca2+ buffering strength, shortened action potentials, and reduced L-type Ca2+ current contribute to a stunning reduction of intracellular Na+ concentration following rapid atrial pacing. In both patients with AF and in our rabbit model, this silencing led to failed propagation of the [Ca2+]i signal to the myocyte center. We conclude that sustained high atrial rates alone silence Ca2+ signaling and do not produce Ca2+ signaling instability, consistent with an adaptive molecular and cellular response to atrial tachycardia.
    The Journal of clinical investigation. 10/2014;
  • Maurits Allessie, Natasja Groot
    The Journal of Physiology 08/2014; 592(15). · 4.38 Impact Factor
  • Maurits Allessie, Natasja Groot
    The Journal of Physiology 08/2014; 592(15). · 4.38 Impact Factor
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    Maurits Allessie, Natasja de Groot
    Circulation Arrhythmia and Electrophysiology 12/2013; 6(6):1056-1058. · 5.95 Impact Factor
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    ABSTRACT: Isolation of the pulmonary veins may be an effective treatment modality for eliminating atrial fibrillation (AF) episodes but unfortunately not for all patients. When ablative therapy fails, it is assumed that AF has progressed from a trigger-driven to a substrate-mediated arrhythmia. The effect of radiofrequency ablation on persistent AF can be attributed to various mechanisms, including elimination of the trigger, modification of the arrhythmogenic substrate, interruption of crucial pathways of conduction, atrial debulking, or atrial denervation. This review discusses the possible effects of pulmonary vein isolation on the fibrillatory process and the necessity of cardiac mapping in order to comprehend the mechanisms of AF in the individual patient and to select the optimal treatment modality.
    Netherlands heart journal: monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation 10/2013; · 1.41 Impact Factor
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    Maurits Allessie, Natasja de Groot
    European Heart Journal 10/2013; · 14.72 Impact Factor
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    Circulation Arrhythmia and Electrophysiology 10/2013; 6(5):1041-1046. · 5.95 Impact Factor
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    ABSTRACT: BACKGROUND: -Endo- epicardial dissociation of electrical activations (EED) resulting in transmural conduction of fibrillation waves (breakthroughs) has been postulated to contribute to the complexity of the substrate of atrial fibrillation (AF). The aim of this study was to elucidate the correlation between EED and incidence of breakthrough, and to test the plausibility of transmural conduction versus ectopic focal discharges as sources of breakthrough. METHODS AND RESULTS: -We analyzed high-resolution simultaneous endo-epicardial in vivo mapping data recorded in left atrial free walls of goats with acute AF, 3 weeks and 6 months of AF (all n=7). Waves were analyzed for number, size and width, and categorized according to their origin outside (peripheral wave) or within the mapping area (breakthrough). Breakthrough-incidence was lowest (2.1±1.0%) in acute AF, higher (11.4±6.1%) after 3 weeks (p<0.01 vs acute AF) and highest (14.2±3.8%) after 6 months AF (p<0.001 vs acute AF) and similar in the epicardium and endocardium. The majority of breakthroughs (86%, n=564) could be explained by transmural conduction while only 13% (n=85) could be explained by ectopic focal discharges. Transmural micro-reentry did not play a role as source of breakthrough. CONCLUSIONS: -This is the first study to present simultaneous endo-epicardial in vivo mapping data at sites of breakthrough events. Breakthrough incidence and degree of EED increased with increasing AF substrate complexity. In goat left atrial free walls, the majority of breakthroughs can be explained by transmural conduction while ectopic focal discharges play a limited role as source of breakthrough.
    Circulation Arrhythmia and Electrophysiology 03/2013; · 5.95 Impact Factor
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    ABSTRACT: OBJECTIVE: We studied the electrophysiologic effects of acute atrial dedilatation and subsequent dilatation, in patients with long-lasting persistent atrial fibrillation (AF) with structural heart disease undergoing elective cardiac surgery. METHODS: Nine patients were studied. Mean age was 71±10 years, and left ventricular ejection was 46±6%. Patients had at least moderate mitral valve regurgitation and dilated atria. After sternotomy and during extracorporal circulation, mapping was performed on the beating heart with 2 multi-electrode arrays (60 electrodes each, interelectrode distance 1.5 mm) positioned on the lateral wall of the right atrium (RA) and left atrium (LA). Atrial pressure and size were altered by modifying extracorporal circulation. Atrial fibrillation electrograms were recorded at baseline, after dedilation and after dilatation of the atria afterwards. RESULTS: At baseline median, AF cycle length (mAFCL) was 184±27ms in RA and 180±17ms in LA. After dedilatation, mAFCL shortened significantly to 168±13 in RA and to 168±20ms in LA. Dilatation lengthened mAFCL significantly in RA to 189±17ms and in LA to 185±23ms. Conduction block (CB) at baseline was 14.3±3.6% in RA and 17.3±5.5% in LA. CB decreased significantly with dedilatation to 7.4±2.9 in RA and to 7.9±6.3% in LA. CB increased significantly with dilatation afterwards to 15.0±8.3% in RA and to 18.5±16.0% in LA. CONCLUSIONS: Acute dedilatation of the atria in patients with longstanding persistent atrial fibrillation causes a decrease in mAFCL in both atria. Subsequent dilatation increased mAFCL. The amount of CB decreased with dedilatation and increased with dilatation afterwards, in both atria.
    Heart rhythm: the official journal of the Heart Rhythm Society 11/2012; · 4.56 Impact Factor
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    ABSTRACT: Post-operative atrial fibrillation (POAF) is one of the most frequent complications of cardiac surgery and an important predictor of patient morbidity as well as of prolonged hospitalization. It significantly increases costs for hospitalization. Insights into the pathophysiological factors causing POAF have been provided by both experimental and clinical investigations and show that POAF is 'multi-factorial'. Facilitating factors in the mechanism of the arrhythmia can be classified as acute factors caused by the surgical intervention and chronic factors related to structural heart disease and ageing of the heart. Furthermore, some proarrhythmic mechanisms specifically occur in the setting of POAF. For example, inflammation and beta-adrenergic activation have been shown to play a prominent role in POAF, while these mechanisms are less important in non-surgical AF. More recently, it has been shown that atrial fibrosis and the presence of an electrophysiological substrate capable of maintaining AF also promote the arrhythmia, indicating that POAF has some proarrhythmic mechanisms in common with other forms of AF. The clinical setting of POAF offers numerous opportunities to study its mechanisms. During cardiac surgery, biopsies can be taken and detailed electrophysiological measurements can be performed. Furthermore, the specific time course of POAF, with the delayed onset and the transient character of the arrhythmia, also provides important insight into its mechanisms. This review discusses the mechanistic interaction between predisposing factors and the electrophysiological mechanisms resulting in POAF and their therapeutic implications.
    Europace 08/2011; 14(2):159-74. · 2.77 Impact Factor
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    ABSTRACT: Hyperaldosteronism is associated with an increased prevalence of atrial fibrillation (AF). However, it is unclear whether this is the consequence of altered haemodynamics or a direct aldosterone effect. It was the aim of the study to demonstrate load-independent effects of aldosterone on atrial structure and electrophysiology. Osmotic mini-pumps delivering 1.5 µg/h aldosterone were implanted subcutaneously in rats (Aldo). Rats without aldosterone treatment served as controls. After 8 weeks, surface electrocardiogram, the inducibility of AF, and atrial pressures were recorded in vivo. In isolated working hearts, left ventricular function was measured, and conduction in the right atrium (RA) and the left atrium (LA) was mapped epicardially. The atrial effective refractory period (AERP) was determined. Atrial tissue was analysed histologically. Neither systolic nor diastolic ventricular function nor atrial pressures were altered in Aldo rats. All Aldo (11/11) showed inducible atrial arrhythmias vs. two of nine controls (P = 0.03). In Aldo, the P-wave duration and the total RA activation time were longer. Prolongation of local conduction times occurred more often in Aldo, whereas the AERP did not differ between both groups. In Aldo, atrial fibroblasts and interstitial collagen were increased, active matrix metalloproteinase 13 was reduced, and atrial myocytes were hypertrophied. The connexin 43 content was unaltered. Aldosterone causes a substrate for atrial arrhythmias characterized by atrial fibrosis, myocyte hypertrophy, and conduction disturbances. The described model imputes atrial proarrhythmia directly to aldosterone, since ventricular haemodynamics appeared unaltered in this model. This mechanism may have therapeutical impact for primary and secondary prevention of AF.
    European Heart Journal 08/2011; 33(16):2098-108. · 14.72 Impact Factor
  • Maurits Allessie
    Journal of Cardiovascular Electrophysiology 12/2010; 22(4):402-4. · 3.48 Impact Factor
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    ABSTRACT: The electropathological substrate of persistent atrial fibrillation (AF) in humans is largely unknown. The aim of this study was to compare the spatiotemporal characteristics of the fibrillatory process in patients with normal sinus rhythm and long-standing persistent AF. During cardiac surgery, epicardial mapping (244 electrodes) of the right atrium (RA), the left lateral wall (LA), and the posterior left atrium (PV) was performed in 24 patients with long-standing persistent AF. Twenty-five patients with normal sinus rhythm, in whom AF was induced by rapid pacing, served as a reference group. A mapping algorithm was developed that separated the complex fibrillation process into its individual elements (wave mapping). Parameters used to characterize the substrate of AF were (1) the total length of interwave conduction block, (2) the number of fibrillation waves, and (3) the ratio of block to collision of fibrillation waves (dissociation index). In 4403 maps of persistent AF, no evidence for the presence of stable foci or rotors was found. Instead, many narrow wavelets propagated simultaneously through the atrial wall. The lateral boundaries of these waves were formed by lines of interwave conduction block, predominantly oriented parallel to the atrial musculature. Lines of block were not fixed but continuously changed on a beat-to-beat basis. In patients with persistent AF, the total length of block in the RA was more than 6-fold higher than during acute AF (median, 21.1 versus 3.4 mm/cm(2); P<0.0001). The highest degree of interwave conduction block was found in the PV area (33.0 mm/cm(2)). The number of fibrillation waves during persistent AF was 4.5/cm(2) compared with 2.3 during acute AF, and the dissociation index was 7.3 versus 1.5 (P<0.0001). The interindividual variation of these parameters among patients was high. Electric dissociation of neighboring atrial muscle bundles is a key element in the development of the substrate of human AF. The degree of the pathological changes can be measured on an individual basis by electrophysiological parameters in the spatial domain.
    Circulation Arrhythmia and Electrophysiology 12/2010; 3(6):606-15. · 5.95 Impact Factor
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    ABSTRACT: This study aims to determine the degree and mechanisms of endo-epicardial dissociation of electrical activity during atrial fibrillation (AF) and endo-epicardial differences in atrial electrophysiology at different stages of atrial remodelling. Simultaneous high-density endo-epicardial mapping of AF was performed on left atrial free walls of goats with acute AF, after 3 weeks, and after 6 months of AF (all n = 7). Endo-epicardial activation time differences and differences in the direction of conduction vectors were calculated, endocardial and epicardial effective refractory periods (ERP) were determined, and fractionation of electrograms was quantified. Histograms of endo-epicardial activation time differences and differences in the direction of conduction vectors revealed two distinct populations, i.e. dissociated and non-dissociated activity. Dyssynchronous activity (dissociated in time) increased from 17 ± 7% during acute AF to 39 ± 17% after 3 weeks, and 68 ± 13% after 6 months of AF. Dissociation was more pronounced in thicker parts of the atrial wall (thick: 49.3 ± 21.4%, thin: 42.2 ± 19.0%, P < 0.05). At baseline, endocardial ERPs were longer when compared with epicardial ERPs (ΔERP, 21.8 ± 18 ms; P < 0.001). This difference was absent after 6 months of AF. The percentage of fractionated electrograms during rapid pacing increased from 9.4 ± 1.9% (baseline) to 18.6 ± 0.6% (6 months). During AF, pronounced dissociation of electrical activity occurs between the epicardial layer and the endocardial bundle network. The increase in dissociation is due to owing to progressive uncoupling between the epicardial layer and the endocardial bundles and correlates with increasing stability and complexity of the AF substrate.
    Cardiovascular Research 10/2010; 89(4):816-24. · 5.81 Impact Factor
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    ABSTRACT: Over a time course of months, the stability of atrial fibrillation (AF) gradually increases and the efficacy of pharmacological cardioversion declines both in humans and in animal models. Changes in fibrillatory conduction over this period largely are unexplored. Goats were instrumented with an atrial endocardial pacemaker lead and a burst pacemaker. AF was maintained for 3 weeks (short-term AF [ST], n = 10) or 6 months (long-term AF [LT], n = 7). AF could be cardioverted pharmacologically at the early time point (persistent AF), but not at the later time point (permanent AF). At follow-up, a high-resolution mapping electrode was used to record epicardial conduction patterns in the free walls of the right atrium (RA) and left atrium (LA). A new method for mapping of fibrillation waves was used to describe AF conduction patterns. Wavefronts propagated uniformly during slow pacing in both groups, although conduction velocity was significantly lower in the LT group (LA, 93 ± 14 versus 72 ± 10 cm/s; RA, 94 ± 8 versus 78 ± 8 cm/s). Median AF cycle length (AFCL) was not significantly different between the groups. However, the LT group showed highly complex activation patterns during AF, with an increased number of simultaneously propagating waves (LT group RA, 8.4 ± 3.0 waves/AFCL; LA, 12.8 ± 2.4 waves/AFCL; versus ST group RA, 4.3 ± 2.2 waves/AFCL; LA, 4.5 ± 2.5 waves/AFCL). Fibrillation waves in the LT group showed pronounced dissociation with large activation time differences. The incidence of waves newly appearing within the recording area also was increased in both atria. These alterations in conduction were accompanied by myocyte hypertrophy and increased endomysial fibrosis. Long-term AF in goats leads to dissociated conduction in the atrial free walls that may contribute to increased AF stability.
    Circulation Arrhythmia and Electrophysiology 10/2010; 3(6):590-9. · 5.95 Impact Factor
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    ABSTRACT: During persistent atrial fibrillation (AF), waves with a focal spread of activation are frequently observed. The origin of these waves and their relevance for the persistence of AF are unknown. In 24 patients with longstanding persistent AF and structural heart disease, high-density mapping of the right and left atria was performed during cardiac surgery. In a reference group of 25 patients, AF was induced by rapid pacing. For data analysis, a mapping algorithm was developed that separated the fibrillatory process into its individual wavelets and identified waves with a focal origin. During persistent AF, the incidence of focal fibrillation waves in the right atrium was almost 4-fold higher than during acute AF (median, 0.46 versus 0.12 per cycle per 1 cm² (25th to 75th percentile, 0.40 to 0.77 and 0.01 to 0.27; P<0.0001). They were widely distributed over both atria and were recorded at 46 ± 18 of all electrodes. A large majority (90.5) occurred as single events. Repetitive focal activity (>3) happened in only 0.8. The coupling interval was not more than 11 ms shorter than the average AF cycle length (P=0.04), and they were not preceded by a long interval. Unipolar electrograms at the site of origin showed small but clear R waves. These data favor epicardial breakthrough rather than a cellular focal mechanism as the underlying mechanism. Often, conduction from a site of epicardial breakthrough was blocked in 1 or more directions. This generated separate multiple wave fronts propagating in different directions over the epicardium. Focal fibrillation waves are due to epicardial breakthrough of waves propagating in deeper layers of the atrial wall. In patients with longstanding AF, the frequency of epicardial breakthroughs was 4 times higher than during acute AF. Because they provide a constant source of independent fibrillation waves originating over the entire epicardial surface, they offer an adequate explanation for the high persistence of AF in patients with structural heart disease.
    Circulation 10/2010; 122(17):1674-82. · 15.20 Impact Factor
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    ABSTRACT: The small GTPase Rac1 seems to play a role in the pathogenesis of atrial fibrillation (AF). The aim of the present study was to characterize the effects of Rac1 overexpression on atrial electrophysiology. In mice with cardiac overexpression of constitutively active Rac1 (RacET), statin-treated RacET, and wild-type controls (age 6 months), conduction in the right and left atrium (RA and LA) was mapped epicardially. The atrial effective refractory period (AERP) was determined and inducibility of atrial arrhythmias was tested. Action potentials were recorded in isolated cells. Left ventricular function was measured by pressure-volume analysis. Five of 11 RacET hearts showed spontaneous or inducible atrial tachyarrhythmias vs. 0 of 9 controls (P < 0.05). In RacET, the P-wave duration was significantly longer (26.8 +/- 2.1 vs. 16.7 +/- 1.1 ms, P = 0.001) as was total atrial activation time (RA: 13.6 +/- 4.4 vs. 3.2 +/- 0.5 ms; LA: 7.1 +/- 1.2 vs. 2.2 +/- 0.3 ms, P < 0.01). Prolonged local conduction times occurred more often in RacET (RA: 24.4 +/- 3.8 vs. 2.7 +/- 2.1%; LA: 19.1 +/- 6.3 vs. 1.2 +/- 0.7%, P < 0.01). The AERP and action potential duration did not differ significantly between both groups. RacET demonstrated significant atrial fibrosis but only moderate systolic heart failure. RacET and statin-treated RacET were not significantly different regarding atrial electrophysiology. The substrate for atrial arrhythmias in mice with Rac1 overexpression is characterized by conduction disturbances and atrial fibrosis. Electrical remodelling (i.e. a shortening of AERP) does not play a role. Statin treatment cannot prevent the structural and electrophysiological effects of pronounced Rac1 overexpression in this model.
    Cardiovascular Research 03/2010; 87(3):485-93. · 5.81 Impact Factor
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    ABSTRACT: This study introduces the use of wavelet decomposition of unipolar fibrillation electrograms for the automatic detection of local activation times during complex atrial fibrillation (AF). The purpose of this study was to evaluate this technique in patients with structural heart disease and longstanding persistent AF. In 46 patients undergoing cardiac surgery, unipolar fibrillation electrograms were recorded from the right atrium, using a mapping array of 244 electrodes. In 25 patients with normal sinus rhythm, AF was induced by rapid pacing, whereas 21 patients were in persistent AF. In patients with longstanding AF, the atrial electrograms showed a high degree of fractionation. In each patient, 12 s of AF were analyzed by wavelet transformation (15 scales). The finest scales (1-7) were used to reconstruct a "local" fibrillation electrogram, whereas with the coarse scales (9-15), a far-field signal was generated. With these local and far-field electrograms, the "primary" fibrillation potentials, due to wave propagation underneath the electrode, could be distinguished from double potentials and multiple components generated by remote wavefronts. Wavelet transformation resulted in AF histograms with a closely gaussian distribution and the automatically generated activation maps showed a good resemblance with fibrillation maps obtained by laborious manual editing. A special chaining algorithm was developed to detect multiple components in fractionated electrograms. The degree of fractionation showed a positive correlation with the complexity of fibrillation, thus providing an objective quantification of the degree of electrical dissociation of the atria. Wavelet transformation can be a useful technique to detect the primary potentials and quantify the degree of fractionation of fibrillation electrograms. This could enable real-time mapping of complex cases of human AF and classification of the underlying electropathological substrate.
    IEEE transactions on bio-medical engineering 02/2010; 57(6):1388-98. · 2.15 Impact Factor
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    ABSTRACT: We investigated clinical correlates of atrial fibrillation (AF) progression and evaluated the prognosis of patients demonstrating AF progression in a large population. Progression of paroxysmal AF to more sustained forms is frequently seen. However, not all patients will progress to persistent AF. We included 1,219 patients with paroxysmal AF who participated in the Euro Heart Survey on AF and had a known rhythm status at follow-up. Patients who experienced AF progression after 1 year of follow-up were identified. Progression of AF occurred in 178 (15%) patients. Multivariate analysis showed that heart failure, age, previous transient ischemic attack or stroke, chronic obstructive pulmonary disease, and hypertension were the only independent predictors of AF progression. Using the regression coefficient as a benchmark, we calculated the HATCH score. Nearly 50% of the patients with a HATCH score >5 progressed to persistent AF compared with only 6% of the patients with a HATCH score of 0. During follow-up, patients with AF progression were more often admitted to the hospital and had more major adverse cardiovascular events. A substantial number of patients progress to sustained AF within 1 year. The clinical outcome of these patients regarding hospital admissions and major adverse cardiovascular events was worse compared with patients demonstrating no AF progression. Factors known to cause atrial structural remodeling (age and underlying heart disease) were independent predictors of AF progression. The HATCH score may help to identify patients who are likely to progress to sustained forms of AF in the near future.
    Journal of the American College of Cardiology 02/2010; 55(8):725-31. · 14.09 Impact Factor
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    ABSTRACT: Previous studies suggest that a short temporal excitable gap exists between the fibrillation waves during atrial fibrillation (AF). The aim of this study was to investigate the role of that gap in the development of sustained AF in goats. Eight female goats were instrumented with left atrium (LA) electrodes, and sustained AF (>24 h) was induced by intermittent rapid atrial pacing for 9.3+/-4.6 days. In the process of sustained AF development, the atrial effective refractory period (AERP), refractory period during AF (RP(AF)), mean AF cycle length (AFCL), temporal excitable gap during AF (EG(AF) = AFCL - RP(AF)) and degree of fractionation of fibrillation electrograms at LA were studied. When the induced AF lasted for 3-10 min, AFCL, RP(AF) and EG(AF) were 98.3+/-11.0 ms, 90.5+/-13.2 ms and 7.8+/-2.4 ms, respectively. During sustained AF, the values were 84.9+/-5.2 ms, 63.0+/-4.8 ms and 21.9+/-3.5 ms, respectively (P<0.05). Percentage of single potentials was 94.2+/-3.9% and 75.6+/-5.5%, respectively (P<0.05). In this model progressive shortening of atrial refractoriness and widening of the temporal excitable gap induced by electrical remodeling created an electrophysiologic substrate for the perpetuation of AF.
    Circulation Journal 02/2010; 74(4):655-63. · 3.58 Impact Factor

Publication Stats

9k Citations
1,370.40 Total Impact Points


  • 1986–2014
    • Maastricht University
      • • Department of Physiology
      • • Cardiothoracale Chirurgie
      • • Cardiologie
      Maestricht, Limburg, Netherlands
  • 2012
    • Isala Klinieken
      • Department of Cardiology
      Zwolle, Overijssel, Netherlands
  • 2008
    • Federal University of Rio de Janeiro
      Rio de Janeiro, Rio de Janeiro, Brazil
    • Radboud University Medical Centre (Radboudumc)
      Nymegen, Gelderland, Netherlands
  • 2007
    • St. George's School
      Middletown, Rhode Island, United States
  • 2005
    • Maastricht Universitair Medisch Centrum
      Maestricht, Limburg, Netherlands
  • 2004
    • East Carolina University
      North Carolina, United States
  • 2000–2001
    • Leiden University Medical Centre
      • Department of Radiology
      Leiden, South Holland, Netherlands
  • 1998
    • University of Groningen
      • Department of Cardiology
      Groningen, Province of Groningen, Netherlands
  • 1995
    • Leiden University
      Leyden, South Holland, Netherlands
  • 1994–1995
    • Dallas Zoo
      Dallas, Texas, United States
    • Università degli Studi di Trento
      • Department of Physics
      Trento, Trentino-Alto Adige, Italy
  • 1993
    • University of Barcelona
      Barcino, Catalonia, Spain
    • United Arab Emirates University
      Al Ain, Abu Dhabi, United Arab Emirates
  • 1991–1993
    • Aristotle University of Thessaloniki
      • Division of Electrical Energy
      Saloníki, Central Macedonia, Greece
  • 1992
    • Université de Nîmes
      Nismes, Languedoc-Roussillon, France
  • 1988
    • Columbia University
      • College of Physicians and Surgeons
      New York City, NY, United States
  • 1987
    • Transnationale Universiteit Limburg
      Box Elder, South Dakota, United States
  • 1974–1976
    • University of Amsterdam
      • Department of Plant Physiology
      Amsterdamo, North Holland, Netherlands