R Nadeau

Hôpital du Sacré-Coeur de Montréal, Montréal, Quebec, Canada

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Publications (124)450.83 Total impact

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    ABSTRACT: Measurement of QT intervals during atrial flutter (AFL) is relevant to monitor the safety of drug delivery. Our aim is to compare QT and QTc intervals in AFL patients before and after catheter ablation in order to validate QT measurement during AFL. 25 patients suffering from AFL underwent catheter ablation; 9 were in sinus rhythm and 16 were in AFL at the time of the procedure. Holter ECGs were continuously recorded before, during and after the procedure. In AFL signals, flutter waves were subtracted using a previously-validated deconvolution-based method. Fridericia's QTc was computed before and after ablation after hysteresis reduction. Comparing QTc values obtained before and after ablation showed that (1) the intervention did not significantly affect QTc, and (2) the QTc during AFL was concordant with the QTc value in sinus rhythm. QTc can be reliably measured in patients with AFL using flutter wave subtraction and hysteresis reduction.
    Journal of electrocardiology 11/2013; DOI:10.1016/j.jelectrocard.2013.11.002 · 1.36 Impact Factor
  • Journal of electrocardiology 11/2013; 46(6):624. DOI:10.1016/j.jelectrocard.2013.09.029 · 1.36 Impact Factor
  • The Canadian journal of cardiology 10/2013; 29(10):S186-S187. DOI:10.1016/j.cjca.2013.07.297 · 3.94 Impact Factor
  • Journal of Electrocardiology 07/2013; 46(4):e34. DOI:10.1016/j.jelectrocard.2013.05.125 · 1.36 Impact Factor
  • The Canadian journal of cardiology 09/2012; 28(5):S325. DOI:10.1016/j.cjca.2012.07.546 · 3.94 Impact Factor
  • Journal of Electrocardiology 11/2011; 44(6):752. DOI:10.1016/j.jelectrocard.2011.09.036 · 1.36 Impact Factor
  • The Canadian journal of cardiology 09/2011; 27(5):S267. DOI:10.1016/j.cjca.2011.07.471 · 3.94 Impact Factor
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    ABSTRACT: This paper reports two attempts at estimating the magni-tude of atrial flutter amplitude modulation caused by atrial motion during heart contraction. The first approach con-sists in analyzing the ECG of a patient in flutter with atrio-ventricular block and an implanted pacemaker. These con-ditions facilitate QRST cancellation, even in the presence of time-varying flutter wave amplitude. The second ap-proach is based on a computer model of atrial flutter em-bedded in a torso model featuring predetermined motion of the atria. The results suggests that this lead-dependent effect is usually not large enough to preclude reasonably accurate QRST cancellation or T-wave extraction.
  • Journal of Hypertension 01/2004; 22(Suppl. 1):S63. DOI:10.1097/00004872-200402001-00263 · 4.22 Impact Factor
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    ABSTRACT: Severe disorders of the heart rhythm can be treated by radiofrequency (RF) catheter ablation. However, the precise localization of the arrhythmogenic sites and the positioning of the RF catheter are currently problematic. To shorten the duration of the RF ablation procedure and increase its efficacy, we have developed a catheter navigation system. Our prototype consists of a Pentium III computer, a frame grabber and an analog to digital converter. It can: 1) localize the catheter tips from fluoroscopic images of the heart; 2) automatically measure the local activation times on the electrograms recorded with the catheter at multiple sites, and 3) superimpose over the fluoroscopic images, animated and translucent color lines depicting the electrical activation sequence from which the cardiologist can precisely localize the arrhythmogenic site with respect to the RF catheter. In this paper we describe our first achievements and failures with the development of a fluoroscopic navigation system to guide RF catheter ablation of cardiac arrhythmias.
    Engineering in Medicine and Biology Society, 2003. Proceedings of the 25th Annual International Conference of the IEEE; 10/2003
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    ABSTRACT: Background: The prolongation of the QRS complex of the electrocardiogram (ECG) can predict arrhythmic events after myocardial infarction; we investigated the hypothesis that QRS prolongation can be caused by ventricular dilatation in a canine model of pacing-induced heart failure. Method: Pacemakers were implanted in 23 dogs. The right ventricle was paced at 240 bpm for periods ranging between 4 and 8 weeks. At the end of each week, the left ventricular diastolic volume (LVDV) was measured with apical echocardiograms and the ECG was measured with 3 orthogonal leads while the animals were briefly anesthetized with isoflurane. During the terminal experiments, propagation velocities were measured with a plaque electrode array (192 leads) placed over the left ventricle. Results: For the 16 animals who survived more than 6 weeks, the QRS duration significantly increased (P [lt ] .001) from 36[plusmn]5 ms to 53[plusmn]10 ms while the LVDV also showed a significant increase (P [lt ] .001) from 63[plusmn]12 mL to 110[plusmn]19 mL. A very significant correlation between QRS duration and LVDV was found (r =.54, P [lt ] .0001). The longitudinal and transversal propagation velocities (0.62[plusmn]0.12 m/s and 0.27[plusmn]0.12 m/s, respectively) measured during the last experiment showed no difference with propagation velocities previously measured in normal dogs (0.67[plusmn]0.15 m/s and 0.34[plusmn]0.06 m/s). Conclusion: Because no slowing of the conduction velocity was found, QRS prolongation can be explained by a lengthening of the conduction pathway due to ventricular dilatation.
    Journal of Electrocardiology 10/2001; 34(4):326-326. DOI:10.1054/jelc.2001.0340326 · 1.36 Impact Factor
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    ABSTRACT: ST segment deviation conveys crucial information concerning diagnosis, therapy and prognosis during acute coronary syndromes, but the understanding of the genesis of different ST shift polarities and the rationale for optimal lead placement during ischemic monitoring are incomplete. Ninety-nine continuous recordings were made with orthogonal X, Y and Z leads in 35 patients during ST elevation myocardial infarction (MI), in 30 patients during single vessel, elective coronary angioplasty (PTCA), and in 34 patients with unstable angina or acute non-Q wave MI. Each lead was sampled at 500 Hz, and dominant QRS-T complexes were averaged every 47 s. In PTCA, 10 s averages were analyzed. Trend plots of ST + 60 ms for each lead and ST vector angles phi and theta were constructed and edited. ST shift polarity (depression or elevation) and vector orientation (phi and theta) were noted for the greatest ST shift 50 microV or greater on any lead for each patient. Coronary angiographical data were consulted when available. By constructing polar plots of phi and theta, it was evident that ST depression vectors were confined to a small, lateral cardiac region despite a variety of coronary lesions, while ST elevation vectors were oriented according to the territory of the occluded artery (difference of direction means, P<0.002). ST depression in acute coronary syndromes is maximal over the left thorax regardless of coronary lesion location, indicating that the mechanism of ST depression is not fully understood. In ambulatory monitoring where ST depression is expected, a lateral lead may suffice.
    The Canadian journal of cardiology 01/2001; 17(1):57-62. · 3.94 Impact Factor
  • J Feng, R Chahine, R Nadeau
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    ABSTRACT: The objective of this study was to investigate if a variation in extracellular-K+ concentrations alters the effects of global pre-conditioning on ischemia-induced arrhythmias. Rat hearts were Langendorff-perfused with Krebs-Henseleit solution and randomised in 8 groups (n = 12/group): four control groups (K+: 2, 4, 6, or 8 mmol/L) which underwent 30-min coronary artery occlusion and four preconditioned groups (K+: 2, 4, 6, or 8 mmol/L) in which the 30-min regional ischemia was preceded by 2 cycles of 3 min global ischemia. In the presence of low K+ (2 mmol/L), there were no differences between control and preconditioning groups in the number of ventricular premature beats (VPBs): 194 +/- 64 vs. 217 +/- 81, the incidence of ventricular tachycardia (VT): 100% vs. 100% and of ventricular fibrillation (VF): 100% vs. 100%. In the presence of normal K+ concentration (4 mmol/L), ischemic preconditioning reduced the number of VPBs from 88 +/- 26 to 25 +/- 10, (p < 0.05), the incidence of VT from 100 to 50% (p < 0.05), and of VF from 67 to 16% (p < 0.05). In the condition of higher K+ concentration (6 mmol/ L), VPBs (34 +/- 8 vs. 11 +/- 4), the incidence of VT (100% vs. 25%; p < 0.05 ) and VF (25% vs. 8%) were further reduced in preconditioned hearts. In the condition of K+ concentration (8 mmol/L), there were no differences in VPBs (11 +/- 3 vs. 7 +/- 2), the incidence of VT (8% vs. 0%) and VF (8% vs. 0%) between control and preconditioned hearts. Our data show that ischemic preconditioning affords protection against arrhythmias during coronary artery occlusion in the isolated rat heart and that hypokalemia abolishes the antiarrhythmic effects of global preconditioning.
    Molecular and Cellular Biochemistry 11/2000; 214(1-2):75-80. DOI:10.1023/A:1007183311209 · 2.39 Impact Factor
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    ABSTRACT: To investigate a noninvasive technique to localize the atrial insertion site of concealed accessory pathways based on the analysis of body surface potential maps (BSPMs) of retrograde P waves in dogs with simulated retrograde pathways. Orthodromic tachycardias were simulated by atrial stimulations at eight different sites around the atrioventricular ring with long (250 ms and 300 ms) and short (100 ms and 130 ms) coupling times in 14 anesthetized dogs to have P waves well separated from the T wave or occurring during the T wave, respectively. The distance between pacing sites was 15 to 40 mm in group 1 (eight dogs) and 2 mm (in the right atrial free wall region) in group 2 (six dogs). Beats were signal-averaged during 30 s and BSPMs were constructed from 63 unipolar leads. The P wave BSPM pattern for any specific stimulation site was stable and reproducible (correlation coefficient greater than 0.98), and similar in different dogs at long coupling interval stimulations. The thoracic distribution of negative potentials and position of the potential minimum clearly identified the stimulation site when long coupling time stimulations were used. The spatial resolution of the technique as determined by comparison of correlation coefficients in group 2 was 6 mm (P<0.05). When short coupling time stimulations were used (fast tachycardia simulation), the T wave masked the P wave potential distribution in four of eight dogs, but the retrograde P wave map could still be accurately extracted by subtracting a straight line joining the onset and offset of the P wave in 24 of 28 (86%) of the tachycardia simulation sites in these four dogs. The BSPM patterns of simulated retrograde P waves are specifically related to the site of atrial stimulation. Although the T wave altered these BSPM patterns, a subtraction technique recovered the pattern of the retrograde P wave in 93% of all simulated orthodromic tachycardias. The spatial resolution of the retrograde P wave BSPM method was 6 mm.
    The Canadian journal of cardiology 02/2000; 16(2):175-82. · 3.94 Impact Factor
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    ABSTRACT: The purpose of this study was to examine the spontaneous changes in cycle length during episodes of sustained monomorphic (MVT) and polymorphic (PVT) ventricular tachycardias and to relate these changes with the earliest epicardial activation site of the beat. Isochronal activation maps were obtained from 127 unipolar electrograms recorded from the surface of both ventricles with a sock electrode array in 24 open chest anesthetized dogs. After atrioventricular block, the left anterior descending coronary artery was occluded for 60 min under ventricular pacing (140/min), followed by reperfusion. In 7 dogs the left stellate ganglion was stimulated 5 min after reperfusion. In 7 MVTs (reperfusion) and 4 PVTs (sympathetic stimulation), cycle length changes showed an initial acceleration, reaching a minimum cycle length and then decelerating before termination. Isochronal maps showed radial spread from earliest activation, without conduction block. Cycle length (481 +/- 80 msec) in MVT had beat to beat variations of 15 +/- 17 msec corresponding to small shifts in sites of the earliest activation, clustered along the border of the ischemic myocardium. In PVTs the cycle length (352 +/- 90 msec, p < 0.01) had a variability of 62 +/- 23 msec, corresponding to wide changes in the sites of earliest activation in right and left ventricles. Linear regression analysis showed a strong and significant correlation between cycle length variability and the number of electrodes with the earliest activation (r = 0.77, p < 0.0001). In these models of monomorphic and polymorphic ventricular tachycardias, cycle length variability showed a significant correlation with the number of electrodes with the earliest activation. MVTs showed concentrated origins with regular cycle length, whereas PVTs showed dispersed origins with irregular cycle length. These results suggest that the earliest epicardial activation site of the beat could be a factor in determining the dynamics in the cycle length.
    Archivos del Instituto de Cardiología de México 01/2000; 70(1):9-18.
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    ABSTRACT: To discriminate between monomorphic (MVT) and polymorphic (PVT) ventricular tachycardias in humans using cycle length variability (CLV), and to characterize the onset of MVT and PVT using power spectral analysis of the CLV during sinus rhythm and the number of ventricular extrasystoles before onset of arrhythmia. Medtronic, Inc's Spontaneous Ventricular Tachy- arrhythmia Database was analyzed. This data base contains sets of 1000 RR intervals (n=135) that preceded spontaneous onset of ventricular tachycardia or fibrillation and sets of controls (n=135) without spontaneous ventricular tachycardia or fibrillation from 78 patients with the Medtronic Model 7218 implantable cardioverter defibrillator. CLV was measured as the standard deviation of RR intervals normalized by the mean RR value. Power spectral analysis based on the fast Fourier transform analysis was performed on 128 RR samples, and the normalized power spectrum of the low frequency band (0.04 to 0.15 Hz) and of the high (NHF) frequency band (0.15 to 0.4 Hz) were estimated. During PVT the CLV was much greater (0. 133+/-0.095) than during MVT (0.04+/-0.035) (P<0.0001). Also, 64% of patients who developed PVT had more than 27 extrasystoles compared with 40% of patients during control conditions (P=0.03). This parameter was not significantly different in patients with MVT. Due to the high incidence of extrasystoles in this population, only 36% of PVT and 43% of MVT recordings could be analyzed for CLV during sinus rhythm. NHF characterizing parasympathetic activity decreased from 50.6% (PVT control) to 34.4% (PVT onset) (P=0.06) and from 47. 4% (MVT control) to 43.7% (MVT onset) (P=0.18). Discrimination between MVT and PVT episodes was possible based on CLV analysis. The onset of PVT was characterized by a greater number of preceding extrasystoles compared with the control. During sinus rhythm, the NHF spectral power activity decreased at the onset of both types of arrhythmic episodes compared with control, although statistical significance was marginal.
    The Canadian journal of cardiology 11/1999; 15(11):1223-8. · 3.94 Impact Factor
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    ABSTRACT: The sympathetic nervous system is a major modulator of cardiovascular function. Over the past three decades, numerous studies, using various methodologies, have reported the existence of a variety of pre- and postsynaptic sympathetic dysfunctions in essential hypertension. Most of these abnormalities facilitate sympathetic neurotransmission, resulting in a chronic increase in the sympathetic tone and reactivity in a significant proportion of hypertensive patients. Chronic sympathetic activation is also associated with major alterations in the balance among postsynaptic adrenergic receptors in cardiovascular tissues. Indeed, an attenuation of beta-adrenergic function and a potentiation of alpha1-adrenergic function has been demonstrated in cardiovascular tissues in hypertensive patients, suggesting the development of a sympathetic postsynaptic alpha1 dominance during the development and evolution of hypertension. Chronic activation of the sympathetic system is deleterious and could contribute to the development of most cardiovascular complications associated with hypertension. One of the major aims of antihypertensive therapy should thus be to attenuate pre- or postsynaptic sympathetic tone. Most antihypertensive drugs have been found to improve either pre- or postsynaptic sympathetic function in hypertensive patients. At the presynaptic level, diuretics were found to increase the liberation of noradrenalin, presumably through baroreflex sympathetic activation. In contrast, beta-blockers were shown to attenuate noradrenalin release from sympathetic nerves by blocking presynaptic facilitatory beta-receptors, thus reducing the sympathetic tone on postsynaptic receptors. Similarly, angiotensin-converting enzyme inhibitors or angiotensin II type 1 (AT1) receptor antagonists have been found to reduce sympathetic reactivity by acting on the central nervous system, but also by blocking AT1-mediated facilitatory mechanisms located on sympathetic fibres and in the adrenal medulla. Short acting dihydropyridine calcium channel blockers (CCBs) were found to enhance noradrenalin release from sympathetic nerves, but longer acting CCBs seems to have variable effects. Indeed, while the chronic slow release formulation of nifedipine gastrointestinal therapeutic system (GITS) did not raise circulating noradrenalin levels, treatment with amlodipine increased circulating noradrenalin levels, suggesting that nifedipine GITS is neutral on the sympathetic tone but that amlodipine chronically activates the sympathetic system. At the postsynaptic level, however, dihydropyridine CCBs were shown to attenuate the sympathetic tone on alpha1-adrenoceptors. In conclusion, it appears that most antihypertensive drugs interfere with pre- or postsynaptic sympathetic mechanisms and that these mechanisms could contribute to their hypotensive effects.
    The Canadian journal of cardiology 04/1999; 15 Suppl A:8A-14A. · 3.94 Impact Factor
  • Journal of Electrocardiology 01/1999; 32:48-48. DOI:10.1016/S0022-0736(99)90037-7 · 1.36 Impact Factor
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    ABSTRACT: To compare the acute and chronic effects of nifedipine retard (NPA), nifedipine gastrointestinal therapeutic system (NGITS) and amlodipine at trough and peak plasma concentrations of drug on blood pressure and heart rate, and on plasma norepinephrine and epinephrine levels in patients with mild-to-moderate hypertension (diastolic blood pressure 95-115 mmHg). After 3-4 weeks' placebo treatment, patients of both sexes were randomly allocated to be administered 10 or 20 mg NPA twice a day, 30 or 60 mg NGITS once a day, and 5 or 10 mg amlodipine once a day for 6 weeks. Initially, for the first 2 weeks, the lowest dose of each drug was used, but higher doses were administered after 2 weeks if sitting diastolic blood pressure was > 90 mmHg. Patients were evaluated after administration of the first dose and after 6 weeks' therapy in a hospital setting. Blood samples were taken for high-performance liquid chromatography measurement of catecholamine and drug levels at various intervals for a period covering trough to peak drug level ranges. Administration of all three drugs reduced clinic blood pressure to the same level after 6 weeks' therapy, but heart rate was increased slightly only with amlodipine (P < 0.05). Administration of NPA reduced blood pressure more abruptly whereas administrations of NGITS and amlodipine induced smoother falls after acute and chronic treatments: a significant increase in heart rate was observed with amlodipine after chronic treatment. Both acute and chronic treatments with NPA (n = 19) increased norepinephrine levels (P < 0.01) transiently (2-4 h). In contrast, administration of NGITS (n = 22) did not increase norepinephrine levels and even induced a slight but significant decrease in norepinephrine levels 5-6 h after chronic treatments. Although administration of amlodipine (n = 22) did not increase norepinephrine levels transiently either after acute or after chronic administration, it did induce a sustained rise in basal norepinephrine levels by more than 50% after chronic therapy (P < 0.01). Plasma epinephrine levels were not increased by any of the treatments and even a slight decrease was observed 4 h after administration of a dose following chronic treatments with NGITS and amlodipine (P < 0.05). The transient increase in norepinephrine levels observed with NPA and the sustained increases in norepinephrine levels observed after chronic treatment with amlodipine suggest that sympathetic activation occurs with those two drugs. The lack of increase in norepinephrine levels after administration of NGITS suggests that this formulation does not activate the sympathetic system. The lowering of epinephrine levels after administrations of NGITS and amlodipine suggests that inhibition of release of epinephrine by the adrenal medulla occurs with longer-acting dihydropyridine formulations.
    Journal of Hypertension 12/1998; 16(11):1357-69. DOI:10.1097/00004872-199816090-00017 · 4.22 Impact Factor
  • A Mokrane, R Nadeau
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    ABSTRACT: Electrical stimulation of the right cardiac sympathetic nerve was used to achieve a step increase of norepinephrine concentration at the sinus node. The heart rate (HR) response to sympathetic stimulation was characterized by a first-order process with a time delay. For moderate to high intensities of stimulation the mean delay and time constant were 0.7 and 2.1 s, respectively, and for low intensities of stimulation they were 0.4 and 1.1 s, respectively. From the analysis of the HR response to different patterns of nerve stimulation, in vivo neurotransmitter kinetics were estimated. The time constant of norepinephrine dissipation averaged approximately 9 s. These results combined with computer simulations revealed two facets of sympathetic neural control of HR: 1) negligible role of the sympathetic system in beat-to-beat regulation of HR under stationary conditions and 2) ability of HR to react relatively quickly (within a few seconds) to sharp increases in sympathetic nerve traffic.
    The American journal of physiology 10/1998; 275(3 Pt 2):H995-1001. · 3.28 Impact Factor

Publication Stats

1k Citations
450.83 Total Impact Points


  • 1975–2013
    • Hôpital du Sacré-Coeur de Montréal
      Montréal, Quebec, Canada
  • 1973–1999
    • Université de Montréal
      • • Department of Radiology, Radiation Oncology and Nuclear Medicine
      • • Department of Physiology
      • • Faculty of Medicine
      Montréal, Quebec, Canada
  • 1997
    • Keio University
      Edo, Tōkyō, Japan
  • 1995
    • Jewish General Hospital
      Montréal, Quebec, Canada
    • Dalhousie University
      Halifax, Nova Scotia, Canada
  • 1987–1995
    • Université du Québec à Montréal
      • • Department of Chemistry
      • • Department of Sociology
      Montréal, Quebec, Canada
  • 1994
    • Polytechnique Montréal
      • Institute of Biomedical Engineering
      Montréal, Quebec, Canada