M A Allessie

Maastricht University, Maestricht, Limburg, Netherlands

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Publications (226)1482.83 Total impact

  • Eva A.H. Lanters · Maurits A Allessie · Natasja M.S. de Groot
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    ABSTRACT: The incidence and appearance of focal fibrillation waves on the right and left atrial epicardial surface were visualized during 10 seconds of persistent atrial fibrillation in a 71-year-old woman with valvular heart disease. The frequent, non-repetitive, widespread and capricious distribution of focal waves suggest that transmural conduction of fibrillation waves is most likely the mechanism underlying focal fibrillation waves. This article is protected by copyright. All rights reserved.
    No preview · Article · Dec 2015 · Pacing and Clinical Electrophysiology
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    ABSTRACT: Focal waves appear frequently at the epicardium during persistent atrial fibrillation (AF), however, the origin of these waves is under debate. We performed simultaneous endo-epicardial mapping of the right atrial wall during longstanding persistent AF in a patient undergoing cardiac surgery. During 10 seconds 53 and 59 focal waves appeared at random at respectively the endocardium and epicardium. Repetitive focal activity did not last longer than 3 cycles. Transmural asynchrony and conduction may be the origin of focal waves. Asynchronous propagating fibrillation waves in three dimensions would stabilize the arrhythmia and could explain the limited success of persistent AF ablation.
    No preview · Article · Dec 2015 · The Canadian journal of cardiology
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    ABSTRACT: Atrial fibrillation is a progressive arrhythmia, the exact mechanism underlying the progressive nature of recurrent AF episodes is still unknown. Recently, it was found that key players of the protein quality control system of the cardiomyocyte, i.e. Heat Shock Proteins, protect against atrial fibrillation progression by attenuating atrial electrical and structural remodeling (electropathology). HALT & REVERSE aims to investigate the correlation between electropathology, as defined by endo- or epicardial mapping, Heat Shock Protein levels and development or recurrence of atrial fibrillation following pulmonary vein isolation, or electrical cardioversion or cardiothoracic surgery. Study design This study is a prospective observational study. Three separate study groups are defined: (1) cardiothoracic surgery, (2) pulmonary vein isolation and (3) electrical cardioversion. An intra-operative high-resolution epicardial (group 1) or endocardial (group 2) mapping procedure of the atria is performed to study atrial electropathology. Blood samples for Heat Shock Protein determination are obtained at baseline and during the follow-up period at 3 months (group 2), 6 months (groups 1 and 2) and 1 year (group 1 and 2). Tissue samples of the right and left atrial appendages in patients in group 1 are analysed for Heat Shock Protein levels and for tissue characteristics. Early post procedural atrial fibrillation is detected by continuous rhythm monitoring, whereas late post procedural atrial fibrillation is documented by either electrocardiogram or 24-h Holter registration. HALT & REVERSE aims to identify the correlation between Heat Shock Protein levels and degree of electropathology. The study outcome will contribute to novel diagnostic tools for the early recognition of clinical atrial fibrillation. Trial Registrations: Rotterdam Medical Ethical Committee MEC-2014-393, Dutch Trial Registration NTR4658
    Full-text · Article · Nov 2015 · Journal of Translational Medicine
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    ABSTRACT: Purpose: A new technique is demonstrated for extensive high-resolution intra-operative atrial mapping that will facilitate the localization of atrial fibrillation (AF) sources and identification of the substrate perpetuating AF. Methods: Prior to the start of extra-corporal circulation, a 8 × 24-electrode array (2-mm inter-electrode distance) is placed subsequently on all the right and left epicardial atrial sites, including Bachmann's bundle, for recording of unipolar electrograms during sinus rhythm and (induced) AF. AF is induced by high-frequency pacing at the right atrial free wall. A pacemaker wire stitched to the right atrium serves as a reference signal. The indifferent pole is connected to a steal wire fixed to subcutaneous tissue. Electrograms are recorded by a computerized mapping system and, after amplification (gain 1000), filtering (bandwidth 0.5-400 Hz), sampling (1 kHz) and analogue to digital conversion (16 bits), automatically stored on hard disk. During the mapping procedure, real-time visualization secures electrogram quality. Analysis will be performed offline. Results: This technique was performed in 168 patients of 18 years and older, with coronary and/or structural heart disease, with or without AF, electively scheduled for cardiac surgery and a ventricular ejection fraction above 40 %. The mean duration of the entire mapping procedure including preparation time was 9 ± 2 min. Complications related to the mapping procedure during or after cardiac surgery were not observed. Conclusions: We introduce the first epicardial atrial mapping approach with a high resolution of ≥1728 recording sites which can be performed in a procedure time of only 9±2 mins. This mapping technique can potentially identify areas responsible for initiation and persistence of AF and hopefully can individualize both diagnosis and therapy of AF.
    Full-text · Article · Oct 2015 · Journal of Interventional Cardiac Electrophysiology
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    ABSTRACT: Atrial fibrillation (AF) is the most common age-related cardiac arrhythmia. It is a progressive disease, which hampers successful treatment. The progression of AF is caused by the accumulation of damage in cardiomyocytes which makes the atria more vulnerable for AF. Especially structural remodeling and electrical remodeling, together called electropathology, are sustainable in the atria and impair functional recovery to sinus rhythm after cardioversion. The exact electropathological mechanisms underlying persistence of AF are at present unknown. High resolution wavemapping studies in patients with different types of AF showed that longitudinal dissociation in conduction and epicardial breakthrough were the key elements of the substrate of longstanding persistent AF. A double layer of electrically dissociated waves propagating transmurally can explain persistence of AF (Double Layer Hypothesis) but the molecular mechanism is unknown. Derailment of proteasis –defined as the homeostasis in protein synthesis, folding, assembly, trafficking, guided by chaperones, and clearance by protein degradation systems – may play an important role in remodeling of the cardiomyocyte. As current therapies are not effective in attenuating AF progression, step-by-step analysis of this process, in order to identify potential targets for drug therapy, is essential. In addition, novel mapping approaches enabling assessment of the degree of electropathology in the individual patient are mandatory to develop patient-tailored therapies. The aims of this review are to 1) summarize current knowledge of the electrical and molecular mechanisms underlying AF, 2) discuss the shortcomings of present diagnostic instruments and therapeutic options and 3) to present potential novel diagnostic tools and therapeutic targets.
    Full-text · Article · Sep 2015 · Journal of Atrial Fibrillation
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    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.
    Full-text · Article · Oct 2014 · Journal of Clinical Investigation
  • Maurits Allessie · Natasja de Groot

    No preview · Article · Aug 2014 · The Journal of Physiology
  • Maurits Allessie · Natasja de Groot

    No preview · Article · Aug 2014 · The Journal of Physiology
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    Maurits Allessie · Natasja de Groot

    Full-text · Article · Dec 2013 · Circulation Arrhythmia and Electrophysiology
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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.
    Full-text · Article · Oct 2013 · Netherlands heart journal: monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation
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    Maurits Allessie · Natasja de Groot

    Full-text · Article · Oct 2013 · European Heart Journal
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    Full-text · Article · Oct 2013 · Circulation Arrhythmia and Electrophysiology
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    ABSTRACT: Background: Endo-epicardial dissociation (EED) of electric activations 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 versus acute AF) and highest (14.2±3.8%) after 6 months AF (P<0.001 versus acute AF) and similar in the epicardium and endocardium. Most of the breakthroughs (86%; n=564) could be explained by transmural conduction, whereas only 13% (n=85) could be explained by ectopic focal discharges. Transmural microreentry 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, most of the breakthroughs can be explained by transmural conduction, whereas ectopic focal discharges play a limited role as source of breakthrough.
    Full-text · Article · Mar 2013 · Circulation Arrhythmia and Electrophysiology
  • Natasja de Groot · Maurits Allessie
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    ABSTRACT: The electropathological alterations of the atria responsible for development of a substrate of persistent atrial fibrillation (AF) in humans are still unknown. In this chapter we evaluate a new mapping algorithm (wave-mapping) by comparing the spatiotemporal characteristics of the fibrillatory process in patients with normal sinus rhythm and long-standing persistent AF. In patients with structural heart disease, the electropathological substrate was determined by electrical dissociation between atrial muscle bundles (longitudinal dissociation) and a high incidence of endo-epicardial breakthroughs. Longitudinal dissociation was quantified by measuring the total length of lines of block per cm2 per AF cycle. These lines of block were predominantly oriented parallel to the major atrial muscle bundles. Endo-epicardial breakthroughs occurred over the entire atrial surface, both in the left and the right atrium. They are considered as an important source of “new” fibrillation waves, because they represent transmural junction sites and bifurcation points between fibrillation waves propagating in the dissociated endo- and epicardial layers of the atrial wall. We hypothesize that the high persistence of AF in patients with valvular disease is due to the existence of a double layer of fibrillation waves, resulting from electrical dissociation of the endo- and epicardial layers. In patients with structural heart disease, AF is maintained by a constant “ping-pong” of multiple fibrillation waves between the endo-and epicardial layers of the atrial wall.
    No preview · Chapter · Dec 2012
  • Arif Elvan · Ahmet Adiyaman · Rypko J Beukema · Hauw T Sie · Maurits A Allessie
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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.
    No preview · Article · Nov 2012 · Heart rhythm: the official journal of the Heart Rhythm Society
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    Bart Maesen · Jan Nijs · Jos Maessen · Maurits Allessie · Ulrich Schotten
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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.
    Full-text · Article · Aug 2011 · Europace
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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.
    Preview · Article · Aug 2011 · European Heart Journal
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    ABSTRACT: Cardiac experimental electrophysiology is in need of a well-defined Minimum Information Standard for recording, annotating, and reporting experimental data. As a step towards establishing this, we present a draft standard, called Minimum Information about a Cardiac Electrophysiology Experiment (MICEE). The ultimate goal is to develop a useful tool for cardiac electrophysiologists which facilitates and improves dissemination of the minimum information necessary for reproduction of cardiac electrophysiology research, allowing for easier comparison and utilisation of findings by others. It is hoped that this will enhance the integration of individual results into experimental, computational, and conceptual models. In its present form, this draft is intended for assessment and development by the research community. We invite the reader to join this effort, and, if deemed productive, implement the Minimum Information about a Cardiac Electrophysiology Experiment standard in their own work.
    Full-text · Article · Jul 2011 · Progress in Biophysics and Molecular Biology
  • Maurits Allessie

    No preview · Article · Dec 2010 · Journal of Cardiovascular Electrophysiology
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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.
    Full-text · Article · Dec 2010 · Circulation Arrhythmia and Electrophysiology

Publication Stats

14k Citations
1,482.83 Total Impact Points


  • 1984-2015
    • Maastricht University
      • • Department of Physiology
      • • Department of Cardiology
      Maestricht, Limburg, Netherlands
  • 2011
    • Maastricht Universitair Medisch Centrum
      Maestricht, Limburg, Netherlands
  • 2004
    • East Carolina University
      • Department of Surgery
      North Carolina, United States
  • 2000
    • Leiden University Medical Centre
      • Department of Radiology
      Leyden, South Holland, Netherlands
  • 1997-1999
    • University of Groningen
      • Department of Cardiology
      Groningen, Groningen, Netherlands
  • 1994-1995
    • Dallas Zoo
      Dallas, Texas, United States
  • 1993
    • University of Barcelona
      Barcino, Catalonia, Spain
  • 1992
    • Emirates University
      Arab, Alabama, United States
    • Aristotle University of Thessaloniki
      Saloníki, Central Macedonia, Greece
  • 1987-1990
    • Transnationale Universiteit Limburg
      United States
  • 1982-1988
    • Columbia University
      • • Department of Pharmacology
      • • College of Physicians and Surgeons
      New York, New York, United States
  • 1973-1976
    • University of Amsterdam
      • Department of Plant Physiology
      Amsterdamo, North Holland, Netherlands