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Humans↗
Biomedical subjects
R Coronel
Publications and source records attributed to R Coronel.
Submissions, editorial process and impact factor 1992-2000: focus on Europe.
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Bibliometrics↗
Reviewer's recommendations predict impact: why you have to send us your very best work.
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Cardiology↗
Laplacian electrograms and the interpretation of complex ventricular activation patterns during ventricular fibrillation.
INTRODUCTION: During ventricular fibrillation (VF), interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicability of Laplacian electrograms for detection of the moment of local activation during VF. METHODS AND RESULTS: From isolated perfused porcine intact hearts, 247 local unipolar electrograms were recorded simultaneously (13 x 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF. Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms and its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation indicated by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance. Following epicardial stimulation, Laplacian amplitude was significantly larger than during a breakthrough pattern. During VF, identical unipolar electrograms corresponded to Laplacian complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearance of activity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of sustained episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block). CONCLUSION: Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied to automatic sensing devices, such as the internal defibrillator, may optimize defibrillation success.
Action Potentials↗
Repolarisation and refractoriness during early ischaemia in humans.
OBJECTIVES: To determine whether effective refractory period (ERP) shortens or lengthens in the first minutes of ischaemia in humans, and the relation between ERP changes and action potential duration (APD). METHODS: ERP and monophasic action potential duration (MAPD) were measured from a single left ventricular epicardial site in 26 patients undergoing coronary artery surgery. Cardiopulmonary bypass was instituted and normothermia maintained. Refractory period was determined by the extrastimulus technique at a basic cycle length of 500 ms, at four times (group 1, 15 patients) or two times (group 2, 11 patients) the preischaemic diastolic threshold. A three minute period of ischaemia was instituted by aortic cross clamping between the input from the pump oxygenator and the heart. RESULTS: After three minutes of ischaemia, mean (SEM) ERP lengthened from 232 (5) ms (control) to 246 (7) ms (p < 0.005) in group 1, and from 256 (10) ms (control) to 348 (25) ms (p < 0.005) in group 2. In the same time MAPD shortened from 256 (5) ms (control) to 189 (9) ms (p < 0.001) with no difference between groups. Thus postrepolarisation refractoriness developed during ischaemia. Before ischaemia, ERP showed a good correlation with APD (R(2) = 0.64) but by one minute of ischaemia the correlation was poor (R(2) = 0.29). CONCLUSIONS: These results show that during the first three minutes of global ischaemia in patients with coronary artery disease: (1) ERP lengthened in response to both a low and a high stimulus strength; and (2) there was a good correlation between ERP and APD before ischaemia, which was lost by one minute as APD decreased and ERP increased. These findings may have important implications in arrhythmogenesis.
Action Potentials↗
Intracellular Ca2+ and delay of ischemia-induced electrical uncoupling in preconditioned rabbit ventricular myocardium.
OBJECTIVE: Short periods of ischemia and reperfusion alter myocardial Ca2+ handling and temporarily induce a mild increase of [Ca2+]i. We hypothesized that these alterations are involved in the cardioprotective mechanism of ischemic preconditioning, possibly via a Ca(2+)-dependent activation of protein kinase C (PKC). METHODS AND RESULTS: In arterially perfused rabbit papillary muscles, we determined Ca2+ transients (indo 1) and indicators of the onset of irreversible ischemic damage, including [Ca2+]i rise, electrical uncoupling and contracture. We tested three protocols of ischemic preconditioning (1-3). In addition, the effects of infusion of staurosporine, a blocker of PKC (4), or glibenclamide, a blocker of K+ATP channels (5) were analyzed. Furthermore, pretreatment with phorbol 12-myrisate 13-acetate (PMA), an activator of PKC (6), or cyclopiazonic acid (CPA), an inhibitor of the SR Ca2+ pump (7) was tested. During periods of reperfusion in the preconditioning protocols, the duration of the Ca2+ transient and the diastolic Ca2+ level temporarily increased. Only if sustained ischemia was induced during these changes of the transients, cardioprotection was present. Similar alterations of the Ca2+ transient concurring with cardioprotection were induced by pretreatment with PMA as well as CPA. Staurosporine and glibenclamide antagonized the reperfusion-induced changes of the Ca2+ transients as well as cardioprotection. If reperfusion was extended until the Ca2+ transient had normalized, cardioprotection was also absent. Under all conditions tested, the diastolic Ca2+ elevation or the Ca2+ transient prolongation prior to sustained ischemia correlated with the postponement of ischemic injury. CONCLUSIONS: A pre-ischemic mild increase of [Ca2-]i presents a common effector of preconditioning. Our data suggest that activation of PKC or opening of K+ATP channels may initiate the pathway leading to an alteration of Ca2+ metabolism and a protected status of the myocardium.
Adenosine Triphosphate↗
Cellular uncoupling during ischemia in hypertrophied and failing rabbit ventricular myocardium: effects of preconditioning.
BACKGROUND: Patients with heart failure show a very high incidence of arrhythmias and sudden death that is often preceded by ischemia; however, data on electrophysiological changes during ischemia in failing myocardium are sparse. We studied electrical uncoupling during ischemia in normal and failing myocardium. METHODS AND RESULTS: Tissue resistance, intracellular Ca2+ concentration (Indo-1 fluorescence ratio), and mechanical activity were simultaneously determined in arterially perfused right ventricular papillary muscles from 11 normal and 15 failing rabbits. Heart failure was induced by combined volume and pressure overload. Before sustained ischemia, muscles were subjected to control perfusion (non-PC) or ischemic preconditioning (PC). The onset of uncoupling during ischemia was equal in non-PC normal (13.6+/-0.9 minutes of ischemia) and non-PC failing hearts (13.3+/-0.7 minutes of ischemia). PC postponed uncoupling in normal hearts by 10 minutes. In failing hearts, however, PC caused a large variability in the onset of uncoupling during ischemia (mean, 12.2+/-2.1; range, 5 to 22 minutes of ischemia). The duration of uncoupling process was prolonged in failing hearts (12.9+/-0.9 minutes) compared with normal hearts (7.8+/-0.4 minutes). The degree of heart failure and relative heart weight of the failing hearts significantly correlated with the earlier uncoupling after PC and the duration of uncoupling. In every experiment, the start of Ca2+ rise and contracture preceded uncoupling during ischemia. CONCLUSIONS: The duration of the process of ischemia-induced electrical uncoupling in failing hearts is prolonged compared with that in normal hearts. Ischemic PC has detrimental effects in severely failing papillary muscles because it advances the moment of irreversible ischemic damage.
Animals↗
Energy-dependent transport of calcium to the extracellular space during acute ischemia of the rat heart.
OBJECTIVE: Acute ischemia is associated with rapidly decreasing contractility and Ca2+-transients. Diastolic intracellular Ca2+, however, only mildly increases until development of contracture. The purpose of this study was to investigate whether changes of cellular calcium handling during the early phase of ischemia are associated with active sarcolemmal calcium transport. METHODS: Changes of extracellular concentration of calcium ([Ca2+]o) and tetramethylammonium ([TMA+]o), to estimate extracellular space, were simultaneously measured with ion-specific electrodes in the globally ischemic rat heart. The magnitude and direction of sarcolemmal calcium transport were calculated from [Ca2]o corrected for changed extracellular water content. Energy dependence of sarcolemmal calcium transport was investigated by application of iodoaceticacid (IAA) to inhibit anaerobic glycolysis, and the involvement of the sarcoplasmic reticulum (SR) was studied by application of thapsigargin. The effect of anoxia and thapsigargin on cytosolic and SR calcium was studied in isolated myocytes with the fluorescent indicator indo-1. RESULTS: [Ca2+]o increased and extracellular space gradually decreased in the ischemic intact heart. During the first 7 min, the increase of [Ca2+]o was associated with net outward transport of calcium. Subsequently, net re-uptake occurred. IAA completely abolished outward transport and influx was accelerated and enhanced. Application of thapsigargin attenuated outward transport. In electrically-stimulated myocytes, anoxia caused little change of diastolic calcium and depletion of SR. Thapsigargin reduced both calcium transient amplitude and SR calcium without affecting diastolic calcium. During three successive short episodes of ischemia/reperfusion (preconditioning), outward transport of calcium progressively decreased. CONCLUSION: During the early phase of global ischemia, energy dependent transport of calcium to the extracellular space occurs. At least part of this calcium originates from SR. During the later stage of ischemia, re-uptake of calcium occurs, which is associated with development of contracture.
Animals↗
Effects of intracavitary blood flow and electrode-target distance on radiofrequency power required for transient conduction block in a Langendorff-perfused canine model.
OBJECTIVES: We sought to quantify the effects of electrode-target distance and intracavitary blood flow on radiofrequency (RF) power required to induce transient conduction block, using a Langendorff-perfused canine ablation model. BACKGROUND: Given the thermally mediated nature of RF catheter ablation, cooling effects of intracavitary blood flow and electrode-target distance will influence lesion extension and geometry and electrophysiologic effects. METHODS: In eight Langendorff-perfused canine hearts, the right ventricular free wall was opened, and the right bundle branch (RBB) carefully localized by multielectrode activation mapping. The right atrium was paced at cycle length of 500 ms. Proximal and distal electrodes were attached at the endocardial aspect of the RBB, and the perfused heart was submerged in heparinized blood at 37 degrees C. A standard 4-mm tip ablation electrode was positioned at a constant contact pressure of 5 g between the two electrodes at the site of maximal RBB potential (0 mm) and 2 and 4 mm distant from this site along a line perpendicular to the RBB. RF pulses (500 kHz) were delivered for 30 s at 0.5-W increments until transient bundle branch block. In four hearts, intracavitary flow was simulated by directing a 30-cm/s jet of blood parallel to the septum at the ablation site, and the protocol was repeated to assess the effects on power required for block. In one heart, the effect of variable flow was assessed (0, 15 and 30 cm/s). RESULTS: An exponential distance-related increase was seen in power required for block, from 1.8 +/- 0.9 W (mean +/- SD) at 0 mm to 5.4 +/- 1.1 W at 4 mm. In the presence of 30-cm/s flow, an increase to 3.9 +/- 0.8 W at 0 mm and 13.1 +/- 2.4 W at 2 mm was seen. At 4 mm, coagulum formation invariably occurred before block could be induced. For 15-cm/s flow, less power was required: 3 and 7 W at 0 and 2 mm, respectively. CONCLUSIONS: Increasing the ablation electrode-target distance causes an exponential increase in power required for conduction block; this relation is profoundly influenced by intracavitary flow. Given the geometry of endomyocardial RF lesions, these findings are particularly relevant for directly subendocardial ablation targets.
Animals↗
Profibrillatory effects of intracoronary thrombus in acute regional ischemia of the in situ porcine heart.
BACKGROUND: An intracoronary thrombus during regional ischemia is related to life-threatening arrhythmias. The electrophysiological consequences of a thrombus are unknown. METHODS AND RESULTS: In open chest pigs, regional ischemia was induced by intracoronary injection of a thrombus (protocol 1). In protocol 2, coronary ligation was followed by injection of heparinized blood. Three consecutive episodes of ischemia (10 minutes) and reperfusion (20 minutes) were studied in protocols 3 and 4 (ligation). During the former, an intracoronary thrombus started the third period of ischemia. Multiple (78) local electrograms were recorded simultaneously, and activation patterns were determined. In a first period of ischemia, ventricular fibrillation (during the first 10 minutes) occurred more often after intracoronary thrombosis than during the other protocols (4/7 versus 2/19, P<.05) despite similar size of the ischemic tissue. The incidence of delayed arrhythmias (between 15 and 30 minutes) was not different. Epicardial activation delay was larger 2 to 4 minutes after intracoronary thrombosis compared with ligation. ST elevation was larger with than without a thrombus (2 minutes of ischemia, 12.9+/-4.1 versus 8.2+/-3.0 mV; +/-SD, P<.05). In protocols 3 and 4 the second period and third period of ischemia were similar irrespective of the presence of an intracoronary thrombus. CONCLUSIONS: More conduction slowing underlies the profibrillatory effect of an intracoronary thrombus relative to coronary ligation. After preconditioning with ischemia, the profibrillatory effects are no longer detectable.
Acute Disease↗
Differential electrophysiology of repolarisation from clone to clinic.
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Animals↗
Gene therapy in the cardiovascular system.
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Cardiovascular Diseases↗
Electrophysiologic and extracellular ionic changes during acute ischemia in failing and normal rabbit myocardium.
The incidence of ventricular arrhythmias is higher in failing hearts than in control hearts, especially during acute ischemia. Electrophysiological and extracellular ionic changes during acute ischemia in normal and failing rabbit myocardium were assessed. Heart failure was induced in rabbits by combined volume and pressure overload. In perfused papillary muscles, the onset of electrical uncoupling and changes in action potential duration and conduction velocity during acute ischemia were determined. In Langendorff-perfused rabbit hearts the changes in extracellular potassium concentration ([K+]o) and pH during acute global ischemia were studied. In perfused papillary muscles, during the first 10 min of ischemia, action potential duration at 80% of repolarization decreased more in preparations from failing than from control hearts (from 174 to 104 ms and from 156 to 119 ms respectively (P < 0.001)). Conduction velocity was significantly lower in failing hearts during ischemia (P < 0.005). The onset of electrical uncoupling was similar in failing and control hearts (mean +/- S.E.M., 17 +/- 1 and 15 +/- 1 min respectively, n.s.). Langendorff-perfused hearts [K+]o, after 10 min of ischemia, was 11.0 +/- 0.4 mM in failing and 9.5 +/- 0.3 mM in control hearts (P < 0.01), while the change in pH was the same. After pretreatment with glibenclamide, an ATP sensitive K+ channel blocker, [K+]o reached lower values after 10 min of ischemia in both failing (8.8 +/- 0.5 mM) and control hearts (7.2 +/- 0.4 mM). During ischemia, action potential duration shortening is more pronounced and conduction velocity is lower in failing myocardium than in control myocardium. [K+]o reaches higher values during acute ischemia in failing compared with normal myocardium. These changes are not caused by an earlier activation of IK.ATP. Increased spatial dispersion in electrophysiological parameters and [K+]o over the ischemic border in failing hearts may explain the higher propensity for reentrant arrhythmias during acute regional ischemia in failing hearts.
Action Potentials↗
Intracellular Ca2+, intercellular electrical coupling, and mechanical activity in ischemic rabbit papillary muscle. Effects of preconditioning and metabolic blockade.
During myocardial ischemia, electrical uncoupling and contracture herald irreversible damage. In the present study, we tested the hypothesis that an increase of intracellular Ca2+ is an important factor initiating these events. Therefore, we simultaneously determined tissue resistance, mechanical activity, pH(0), and intracellular Ca2+ (with the fluorescent indicator indo 1, Molecular Probes, Inc) in arterially perfused rabbit papillary muscles. Sustained ischemia was induced in three experimental groups: (1) control, (2) preparations preconditioned with two 5-minute periods of ischemia followed by reperfusion, and (3) preparations pretreated with 1 mmol/L iodoacetate to block anaerobic metabolism and minimize acidification during ischemia. In a fourth experimental group, intracellular Ca2+ was increased under nonischemic conditions by perfusing with 0.1 mmol/L ionomycin and 0.1 mumol/L gramicidin. Ca2+ transients and contractions rapidly disappeared after the induction of ischemia. In the control group, diastolic Ca2+ began to rise after 12.6 +/- 1.3 minutes of ischemia; uncoupling, after 14.5 +/- 1.2 minutes of ischemia; and contracture, after 12.6 +/- 1.5 minutes of ischemia (mean +/- SEM). Preconditioning significantly postponed Ca2+ rise, uncoupling, and contracture (21.5 +/- 4.0, 24.0 +/- 4.1, and 23.0 +/- 5.3 minutes of ischemia, respectively). Pretreatment with iodoacetate significantly advanced these events (1.9 +/- 0.7, 3.6 +/- 0.9, and 1.9 +/- 0.2 minutes of ischemia, respectively). In all groups, the onset of uncoupling always followed the start of Ca2+ rise, whereas the start of contracture was not different from the rise in Ca2+. Perfusion with ionomycin and gramicidin permitted estimation of a threshold [Ca2+] for electrical uncoupling of 685 +/- 85 nmol/L. In conclusion, the rise in intracellular Ca2+ is the main trigger for cellular uncoupling during ischemia. Contracture is closely associated with the increase of intracellular Ca2+ during ischemia.
Animals↗
Heterogeneities in [K+]o and TQ potential and the inducibility of ventricular fibrillation during acute regional ischemia in the isolated perfused porcine heart.
BACKGROUND: The relation between the inducibility of ventricular fibrillation (VF) and heterogeneity of the extracellular potassium concentration ([K+]o) and of TQ potential is unknown. METHODS AND RESULTS: Data from 78 epicardial DC electrodes or from up to 32 intramural K+ electrodes were acquired simultaneously. Induction of VF was attempted with one or two ventricular premature beats induced in normal myocardium in isolated porcine hearts during (1) regional perfusion of the left anterior descending artery (LAD) with a normoxic, hyperkalemic solution ([K+] 6 to 19.6 mmol/L), (2) simulated ischemia, ie, LAD perfusion with a glucose-free, hypoxic solution ([K+] 4 to 16 mmol/L, PO2 < 5 mm Hg, pH 6.98), and (3) regional ischemia produced by stopping LAD flow. During normoxic, hyperkalemic LAD perfusion, no VF could be induced (12 interventions, 7 hearts). During simulated ischemia (27 interventions), VF could be induced only when [K+]o was between 8 and 13.5 mmol/L. After 5 minutes of true regional ischemia, more sites with [K+]o between 8 and 13.5 mmol/L were present than after 10 minutes. VF could be induced with 1 ventricular premature beat in 11 of 17 interventions after 5 minutes and in 0 of 14 interventions after 10 minutes of ischemia (P < .001). Regional simulated ischemia presents a relatively homogeneous condition compared with 5 minutes of regional ischemia (SD +/- SEM of TQ potential in LAD tissue, 0.9 +/- 0.05 versus 2.1 +/- 0.13 mV, respectively). True ischemia superimposed on regional simulated ischemia caused the rapid development of heterogeneities in [K+]o and TQ potential and caused VF after 45 +/- 7 seconds in all interventions. Activation maps of induction of VF suggest a different mechanism of unidirectional block during simulated ischemia from that in true ischemia. CONCLUSIONS: (1) In the presence of hypoxia and acidosis, [K+]o between 8 and 13.5 mmol/L provides the conditions necessary for the induction of VF; (2) after 5 minutes of ischemia, these conditions are present in a larger area and inducibility of VF is higher than after 10 minutes of ischemia; and (3) small heterogeneities within the intermediate K(+)-concentration domain (8 to 13.5 mmol/L) are associated with high inducibility of VF.
Animals↗
Thrombolysis and reocclusion in experimental jugular vein and coronary artery thrombosis. Effects of a plasminogen activator inhibitor type 1-neutralizing monoclonal antibody.
BACKGROUND: Thrombolytic therapy for acute myocardial infarction is often complicated by reocclusion of the initially reperfused artery. Platelets have been shown to play an important role in this process. We determined the contribution of plasminogen activator inhibitor type 1 (PAI-1), stored in the alpha-granules of platelets, to thrombolysis resistance and to reocclusion. METHODS AND RESULTS: In a rabbit jugular vein thrombosis model, the effect of a PAI-1-neutralizing monoclonal antibody (CLB-2C8) on thrombolysis and thrombus growth was assessed. The effect on reperfusion, reocclusion, and duration of vessel patency was studied in a canine model of coronary artery thrombosis superimposed on a high-grade stenosis and endothelial damage. In the rabbit jugular vein model, the intravenous administration of 1 mg/kg anti-PAI-1 antibody significantly enhanced the endogenous thrombolysis from 5.5 +/- 1.3% in the animals treated with a nonspecific monoclonal antibody (control) to 13.7 +/- 2.6% in the animals treated with the anti-PAI-1 antibody. Thrombus growth was reduced significantly, from 41.3 +/- 2.6% in the control animals to 22.8 +/- 2.8% in the animals treated with the anti-PAI-1 antibody. In combination with a single bolus injection of recombinant tissue-type plasminogen activator (rTPA; 0.25 mg/kg), the anti-PAI-1 antibody reduced thrombus growth significantly, from 21.5 +/- 2.7% in the animals treated with rTPA alone to 12.2 +/- 2.6% in the animals treated with rTPA and the antibody. No additional effect of the anti-PAI-1 antibody was observed on rTPA-induced thrombolysis. In the canine coronary artery thrombosis model, the administration of a suboptimal dose of rTPA (0.45 mg/kg) induced reperfusion in 7 of the 8 dogs after 19.5 +/- 8.2 minutes. Reperfusion was followed by reocclusion in all animals after 3.3 +/- 2.6 minutes. Administration of the anti-PAI-1 antibody in combination with rTPA significantly reduced time to reperfusion (8.1 +/- 5.2 minutes) and delayed the occurrence of reocclusion to 11.6 +/- 12.5 minutes. CONCLUSIONS: Administration of the anti-PAI-1 antibody (CLB-2C8) results in increased endogenous thrombolysis and inhibition of thrombus growth in a venous thrombosis model in rabbits and facilitated reperfusion and reduction of reocclusion in a canine model of coronary artery thrombosis.
Animals↗
The relation between extracellular potassium concentration and pH in the border zone during regional ischemia in isolated porcine hearts.
During regional ischemia gradients of extracellular potassium concentration ([K+]o) and extracellular pH (pHo) exist. In globally ischemic papillary muscles increased PCO2 causes a rise in [K+]o. We studied whether pHo and [K+]o are causally related during acute regional ischemia in the isolated blood-perfused pig heart. Multiple pH- or K(+)-sensitive electrodes were inserted in the left ventricular midmyocardium. Local electrograms and ionic data were simultaneously acquired. Regional ischemia was produced by interrupting left anterior descending (LAD) artery flow (10 min). Up to 5 mm from the electrophysiological border the pH-K relation deviated from that in the central ischemic zone. Respiratory acidosis (pH about 7.10) of the perfusate in the presence of LAD-ischemia caused acidification of the ischemic border zone without a local change in [K+]o. We conclude that pHo changes are not related to changes of intramural [K+]o in the lateral border zone during regional ischemia.
Animals↗
Ventricular fibrillation is not always due to multiple wavelet reentry.
INTRODUCTION: It is not known whether ventricular fibrillation (VF) is always caused by multiple wavelet reentry, or if it could also be caused by a single wandering reentrant wavefront. Activation mapping of the entire ventricles during VF is practically impossible. METHODS AND RESULTS: We studied VF in a two-dimensional sheet of left ventricular subepicardial tissue of isolated, Langendorff-perfused pig hearts. Left and right endocardial cryoablation via probes filled with liquid nitrogen caused coagulation necrosis of the right ventricle, interventricular septum, and most of the left ventricular wall, leaving a thin subepicardial layer intact. Left ventricular epicardial activation patterns were constructed based on simultaneous recording of 128 unipolar extracellular electrograms. Regular pacing through a central electrode before and after freezing revealed that, following cryoablation, the activation pattern no longer showed evidence of involvement of the Purkinje system, and that it was compatible with propagation through a two-dimensional anisotropic tissue sheet. VF was induced by burst pacing. When the mass of surviving subepicardium was < 10 g, no VF could be induced; when it was between 10 and 20 g, VF was nonsustained; when it was > 20 g, VF was sustained. Unipolar extracellular electrograms during VF before and after cryablation could not be distinguished from each other; however, epicardial activation patterns were markedly different. In the intact left ventricle, up to six different wavefronts were simultaneously present during a 100-msec time window. In the "frozen heart," during a period of about 0.5 seconds, at most two wandering reentrant waves were simultaneously present; sometimes only one reentrant wave was seen in a 100-msec time window. CONCLUSION: The extracellular waveform during VF can be caused by different forms of reentry: multiple wavelet reentry (on the order of six different wavefronts), two independent wandering reentrant waves, and a single wandering reentrant wave.
Animals↗