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Biomedical subjects

J B Martins

Publications and source records attributed to J B Martins.

At least 19 recordsLinked to original sources
PubMed2001

Atrial fibrillation: a risk factor for increased mortality--an AVID registry analysis.

Emerging evidence suggests that atrial fibrillation is not a benign arrhythmia. It is associated with increased risk of death. The magnitude of association is controversial and potential causes remain unknown. Patients in the registry of the Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial form the basis for this report. Baseline variables, in particular the presence or absence of a history of atrial fibrillation/flutter, were examined in relation to survival. Multivariate Cox regression was used to adjust for differences in important baseline co-variables using 27 pre-selected variables. There were 3762 subjects who were followed for an average of 773+/-420 days; 1459 (39 %) qualified with ventricular fibrillation and 2303 (61 %) with ventricular tachycardia. A history of atrial fibrillation/flutter was present in 24.4 percent. There were many differences in baseline variables between those with and those without a history of atrial fibrillation/flutter. After adjustment for baseline differences, a history of atrial fibrillation/flutter remained a significant independent predictor of mortality, (relative risk=1.20; 95 % confidence intervals=1.03-1.40; p=0.020). Antiarrhythmic drug use, other than amiodarone or sotalol, was also a significant independent predictor of mortality (relative risk 1.34; 95 % confidence intervals 1.07-1.69, p=0.011. Atrial fibrillation/flutter is a significant independent risk factor for increased mortality in patients presenting with ventricular tachyarrhythmias. This risk may have been overestimated in previous studies that could not adjust for the proarrhythmic effects of antiarrhythmic drugs other than amiodarone or sotalol.

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PubMed2001

Myocardial ischemia-reperfusion damage impacts occurrence of ventricular fibrillation in dogs.

To define the relationship between ischemia-reperfusion-induced myocardial damage (IRD) and the occurrence of ventricular tachycardia (VT) and fibrillation (VF), we studied 23 dogs with a three-dimensional activation mapping system. Left anterior descending (LAD) coronary artery occlusion and reperfusion were performed while recording electrograms during VF and atrial pacing. Prior nonischemic sites showing IRD, defined as at least 10% loss of electrogram voltage after reperfusion, had the longest ventricular effective refractory periods (ERPs). IRD sites also occurred more frequently in dogs with reperfusion VF (44 +/- 2 sites, P < 0.01) compared with dogs with VT (18 +/- 5 sites) and no VT (16 +/- 3 sites). In dogs (n = 3) with 3 h of reperfusion, 95% of IRD sites still had lower voltage than those recorded during occlusion. Activation mapping of the first eight complexes of VF had Purkinje or endocardial focal origin in 57%, and complexes originated from IRD sites in 28%. In contrast, dogs with only reperfusion VT also had Purkinje or endocardial focal origin in 79%, but only 5% (P < 0.01 vs. VF dogs) of the sites of origin had IRD. Therefore, dogs with reperfusion VF had more IRD sites where the ERP was longest, and more focal ventricular complexes originated from IRD sites, indicating that IRD may be one important factor in the occurrence of VF during reperfusion.

Animals↗
PubMed2001

Prevention of ischemic ventricular tachycardia of Purkinje origin: role for alpha(2)-adrenoceptors in Purkinje?

Recent studies have shown the presence of postjunctional alpha(2)-adrenergic receptors on canine Purkinje fibers but not muscle cells. Stimulation of these receptors results in prolongation of the action potential duration and the Purkinje relative refractory period. We studied the effect of alpha(2)-adrenergic agonists on inducible ischemic ventricular tachycardia (VT) of both Purkinje fiber and myocardial origin. Open-chest dogs in whom VT was induced with extrastimuli after occlusion of the anterior descending coronary artery were studied. A mapping system, incorporating Purkinje signals, characterized the mechanisms of VT. The alpha(2)-adrenergic agonists clonidine (0.5-4.0 microg/kg) or UK 14,304 (4-5 microg/kg) versus saline were given intravenously after reproducibility of inducible sustained monomorphic VT had been demonstrated. Eighteen dogs were given clonidine, eleven of which had focal Purkinje VT. Of these 11 dogs, clonidine blocked VT induction in 9 (81.9%) and rendered VT nonsustained in 1 (9.1%), and VT remained inducible in 1 dog (9.1%), although this was focal midmyocardial VT only. In the seven dogs with VT of myocardial origin, six (85.6%) remained inducible with clonidine, whereas one dog (14.4%) had only nonsustained VT after clonidine. Of the six dogs, UK 14,304 blocked VT induction in four (66.6%) and rendered VT nonsustained in one (16.7%), and VT remained inducible in one dog (16.7%). In four dogs with VT of myocardial origin, VT remained inducible. In the eight control dogs that were given saline, focal Purkinje VT was repeatedly inducible. Pharmacological stimulation of postjunctional alpha(2)-adrenoceptors on Purkinje fibers may selectively prevent induction of VT of Purkinje fiber origin in the ischemic canine ventricle.

Adrenergic alpha-Agonists↗
PubMed1998

Electrophysiologic effects of civamide (zucapsaicin) on canine cardiac tissue in vivo and in vitro.

The cardiac electrophysiologic effects of civamide (zucapsaicin), the cis-isomer of the alkyl vanillylamide, capsaicin, were evaluated in intact dogs and isolated Purkinje fibers. In anesthetized dogs, the mechanism of ventricular tachycardia inducible from 1 to 3 h after coronary artery occlusion was determined by activation mapping. Of 16 dogs studied, nine had ventricular tachycardia of focal endocardial origin; four, a reentrant mechanism; and three had no inducible arrhythmia. Civamide (50 microg/kg) was administered to 10 of 13 dogs that were inducible, but three dogs were used as time controls. Transmural activation times were unaltered by civamide, but mean arterial pressure decreased from 76 +/- 10 to 66 +/- 10 mm Hg (p < 0.05), and muscle refractory periods shortened from 138 +/- 3 to 132 +/- 4 ms (p < 0.05). Civamide altered inducibility in five of six dogs with ventricular tachycardia of focal endocardial origin, but those with epicardial reentrant mechanisms were not affected in three of four dogs. With microelectrode techniques in vitro, civamide (10(-5) M) shortened the action-potential duration at 50% repolarization (APD50) from 193 +/- 13 to 177 +/- 12 ms (p < 0.01) and APD90 from 260 +/- 15 to 248 +/- 13 ms (p < 0.01) in isolated Purkinje fibers (n = 10). Nifedipine prevented the effects of civamide in vitro. These results show that civamide may alter inducibility of ventricular tachycardia with focal endocardial origin and shorten APD of Purkinje fibers in vitro. The effects of civamide in vitro are prevented by preexposure of the Purkinje fibers to nifedipine, suggesting that the electrophysiologic effects of civamide may be mediated through blockade of calcium channels.

Action Potentials↗
PubMed1997

Role of the Purkinje system in spontaneous ventricular tachycardia during acute ischemia in a canine model.

BACKGROUND: A role for the Purkinje system in the development of spontaneous ventricular tachycardia (VT) during acute ischemia has been suspected but not proved. We used a three-dimensional activation mapping system incorporating Purkinje signals to characterize the mechanism and site of origin of spontaneous VT occurring in the first 30 minutes after coronary artery occlusion in a dog model. METHODS AND RESULTS: The left anterior descending coronary artery was occluded in 48 dogs after instrumentation of the risk zone with 21 multipolar plunge needles, each recording 6 bipolar electrograms through the myocardial wall. VT of Purkinje origin was defined as a focal endocardial VT with a Purkinje potential identified before muscle potential on the electrode recording the earliest activity. Purkinje potentials were identified on an average of 10 of the 21 plunge needles. During atrial pacing at cycle lengths of 300 to 700 ms, a total of 25 VTs were observed from 18 of the 48 dogs (37.5%). Of the VTs, 15 (60.0%) were of focal Purkinje origin, 1 (4.0%) of focal endocardial origin, 2 (8.0%) of focal midmyocardial origin, and 2 (8.0%) of focal epicardial origin; 3 (12.0%) had a reentrant mechanism, whereas in 2 (8.0%), the mechanism could not be defined. The mean cycle length of all VTs was 265+/-17 ms (mean+/-SEM, n=25). Of the 25 VTs, 19 originated from an ischemic area as defined by significant decreases in voltages of muscle electrograms at the time of occurrence of the VT, 4 originated from an ischemic border zone, and the origin of 2 could not be determined. CONCLUSIONS: In this model, VT with a focal mechanism is commonly seen in the early ischemic period. Sixty percent of the VTs were of focal Purkinje origin as characterized by three-dimensional activation mapping. The results of this study indicate that Purkinje tissue may play an important role in the development of early ischemic VT.

Animals↗
PubMed1996

Mechanism of alpha-2 adrenergic modulation of canine cardiac Purkinje action potential.

We reported recently that stimulation of postjunctional alpha-2 adrenergic receptors prolongs the action potential durations (APD) of isolated canine Purkinje fibers. With standard microelectrode techniques, we examined the ionic mechanism through which alpha-2 adrenergic stimulation prolonged Purkinje APD, by measuring the effects of inhibitors of the various plateau currents on the alpha-2-mediated prolongation of APD. The alpha-2-specific agonist UK 14,304 (0.1 microM) prolonged the Purkinje APD at 50% repolarization and the APD at 90% repolarization, and these effects were inhibited by yohimbine (0.1 microM). The Purkinje APD at 50% repolarization and the APD at 90% repolarization were prolonged significantly with the transient outward potassium current inhibitor 4-aminopyridine (1 mM), the rapid component of delayed rectifier potassium current inhibitor d-sotalol (10 microM), the slow component of delayed rectifier potassium current inhibitor indapamide (0.1 microM) and the chloride current inhibitor mefenamic acid (10 nM) and were shortened significantly with the calcium current inhibitor nifedipine (0.3 microM). Prolongation of Purkinje APD at 50% repolarization and APD at 90% repolarization by UK 14,304 remained intact in the presence of d-sotalol, indapamide, mefenamic acid and nifedipine. All of these UK 14,304 effects were significantly reversed by yohimbine. Only in the presence of 4-aminopyridine did UK 14,304 fail to prolong Purkinje APD. The phase 1 magnitudes of Purkinje action potentials were also significantly inhibited by UK 14,304. This effect was completely abolished only in the presence of 4-aminopyridine. These results suggest that inhibition of the 4-aminopyridine-sensitive transient outward potassium current is the major ionic mechanism by which alpha-2 adrenergic stimulation prolongs Purkinje APD.

Action Potentials↗
PubMed1995

Electrophysiological effects of alpha 2-adrenergic stimulation in canine cardiac Purkinje fibers.

The effects of alpha 2-adrenergic stimulation on action potentials were measured in isolated canine Purkinje fibers. Action potential durations at 50 and 90% of repolarization (APD50 and APD90) were significantly prolonged by 0.25 microM l-norepinephrine + 0.5 microM dl-propranolol (NE+P) from baseline values of 166 +/- 7 and 249 +/- 9 (SE) ms (n = 7) to 174 +/- 7 and 265 +/- 9 ms, respectively (P < 0.05 for both). Selective alpha 2-blockade with 0.01 microM yohimbine (YO) reduced this prolongation by NE+P in APD50 and APD90 to 169 +/- 7 and 256 +/- 8 ms, respectively (P < 0.05 compared with NE+P). Additional selective alpha 1-blockade with 0.01 microM prazosin (PZ) completely blocked the effects of NE+P, returning APD50 and APD90 to 163 +/- 7 and 250 +/- 9 ms (not different from baseline). After incubation of isolated Purkinje fibers with pertussis toxin (1 microgram/ml), which reduced the availability of a 41-kDa membrane protein for ADP ribosylation by 70 +/- 7% (n = 4, P < 0.05), YO failed to reverse the prolongation in action potential durations brought on by NE+P, but the effects of PZ were intact. The effects of alpha 2-stimulation on beta-adrenergic-induced delayed afterdepolarizations (DADs) were studied by burst pacing of Purkinje fibers in Tyrode solution containing 7.5 mM Ca2+. The DADs induced in the presence of NE+PZ (beta- + alpha 2-stimulation) were significantly smaller in amplitude and required a shorter pacing cycle length to reach threshold than those induced in the presence of NE+PZ+YO (unopposed beta-adrenergic stimulation). Furthermore sustained triggered activity, seen in five of eight preparations under beta-stimulation, could no longer be elicited in the presence of beta- + alpha 2-stimulation. These results suggest that the postjunctional alpha 2-adrenergic receptors in canine Purkinje fibers are coupled to a pertussis toxin-sensitive G protein and that stimulation of these receptors leads to action potential prolongation and suppression of DADs induced by beta-adrenergic stimulation.

Action Potentials↗
PubMed1994

Refractory period response of cardiac Purkinje tissue to alpha 1- and alpha 2-adrenergic influences.

Our purpose was to characterize Purkinje responses in vivo to alpha 1- and alpha 2-adrenergic stimulation in sinoaortically denervated and vagotomized dogs pretreated with metoprolol (1 mg/kg). We measured Purkinje relative refractory period (PRRP) responses to norepinephrine (NE) and phenylephrine (PE) with prazosin and/or yohimbine, WB-4101, and chloralethylclonidine (CEC) in varying doses. Results were as follows: PE infusion (25 micrograms.kg-1.min-1) prolonged PRRP (9.6 +/- 1.4 ms; a 4.1 +/- 0.4% change). Prazosin blocked PRRP prolongation with PE at 7 x 10(-8) M/kg (P < 0.05). Yohimbine did not attenuate PRRP prolongation with PE either alone or in combination with prazosin. NE infusion (0.8 micrograms.kg-1.min-1) also prolonged PRRP (9.2 +/- 2.3 ms; a 4.8 +/- 1.0% change). In contrast neither prazosin nor yohimbine at any dose (up to 10(-6) M/kg) totally blocked the prolongation with NE infusion. However, with prazosin (2 x 10(-7) M/kg) pretreatment, yohimbine blocked PRRP prolongation, significant at 7 x 10(-8) M/kg (P < 0.05). In separate experiments with yohimbine pretreatment at 7 x 10(-8) M/kg, PRRP prolongation with either PE or NE infusion was blocked equipotently with WB-4101 and CEC at 7 x 10(-8) M/kg. However, CEC did not block mean arterial pressure (MAP) responses to PE or NE infusion unlike WB-4101. We concluded that both subclasses of alpha 1-adrenergic antagonists equipotently block PRRP prolongation by alpha-agonists despite different effects on MAP. Purkinje refractoriness is also prolonged by alpha 2-adrenergic stimulation acting at the cell membrane.

Adrenergic alpha-Antagonists↗
PubMed1993

Transient depression of responses to sympathetic nerve stimulation overlying a subendocardial infarct.

In previous work, the normal epicardial rim overlying a subendocardial infarct was demonstrated to be parasympathetically denervated. In the present study, we determined responses of effective refractory period (ERP) in this rim during sympathetic nerve stimulation (SNS). Eighteen dogs were studied 1-3 days after a 1-h or permanent coronary artery occlusion (group I). SNS shortened ERP in sites basal, septal, and lateral in the rim by 8 +/- 2, 7 +/- 2, and 7 +/- 2% (SE), respectively, which were similar to sites remote from the infarct (10 +/- 1%). These results were not altered by site of infarction or by atropine administration. To eliminate dissection of the coronary vessel and spontaneous ventricular tachycardia, 19 dogs were studied 6 h after a permanent bead embolization of a coronary artery (group II). In contrast to group I, ERP shortening in the rim sites of group II was depressed (3 +/- 3, 0 +/- 2, and 1 +/- 2%, respectively) compared with remote sites (10 +/- 1%, P < 0.05). In this group, collateral blood flow in the rim was no different than remote epicardium before and during SNS, and norepinephrine shortened ERP in the rim equivalent to remote sites. In an additional 31 animals (group III), the alteration in ATP-dependent K+ channel function was evaluated. Pretreatment with glyburide (an ATP-dependent K+ channel blocker) preserved ERP response to SNS (9 +/- 1% shortening of ERP vs. 12 +/- 2% at baseline) compared with only 3 +/- 0% shortening of ERP with vehicle (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Impulse propagation in the Purkinje system and myocardium of intact dogs.

To characterize Purkinje activation (PA) patterns, we studied 15 alpha-chloralose-anesthetized dogs. During left ventricular basal or apical pacing, PA was mapped with a row of four to eight multipolar electrodes placed in the left ventricular wall to record Purkinje and muscle potentials. PA times increased linearly with distance from the pacing site (r = 0.8, slope 1.8 +/- 0.15 mm/ms, P < 0.05). With a single premature stimulus (S2) delivered from the apical or basal site, delay of PA times was first evident at remote sites (> or = 50 mm) with S1-S2 = 185 +/- 5 (SD) ms, while at peripacing sites (< or = 10 mm), delay was first evident when S1-S2 = 176 +/- 6 ms (Purkinje relative refractory period; P < 0.05). With S2,...S5 such that S1-S2 = S2-S3, and so on, an alternating mode of conduction, both temporally and spatially, occurred. The alternation was due to refractoriness and conduction interactions. With short premature intervals, remote coupling intervals were 30 ms less than the premature intervals. Conduction delay in Purkinje fibers with premature stimuli allowed remote epicardium to be activated by alternate routes. Conduction of constant-rate stimuli in the Purkinje system is relatively uniform. With single premature stimuli, conduction is delayed first remotely from the pacing site, whether apical or basal stimulation was employed. When S1-S2 is less than Purkinje relative refractory period, the usual endocardial-to-epicardial activation sequence is altered. Multiple premature stimuli cause remote coupling intervals to alternate.

Animals↗
PubMed1993

Reversal of lidocaine effects on sodium currents by isoproterenol in rabbit hearts and heart cells.

We demonstrated recently that isoproterenol enhanced the cardiac voltage-dependent sodium currents (INa) in rabbit ventricular myocytes through dual G-protein regulatory pathways. In this study, we tested the hypothesis that isoproterenol reverses the sodium channel blocking effects of class I antiarrhythmic drugs through modulation of INa. The experiments were performed in rabbit ventricular myocytes using whole-cell patch-clamp techniques. Reversal of lidocaine suppression of INa by isoproterenol (1 microM) was significant at various concentrations of lidocaine (20, 65, and 100 microM, P < 0.05). The effects of isoproterenol were voltage dependent, showing reversal of INa suppression by lidocaine at normal and hyperpolarized potentials (negative to -80 mV) but not at depolarized potentials. Isoproterenol enhanced sodium channel availability but did not alter the steady state activation or inactivation of INa nor did it improve sodium channel recovery in the presence of lidocaine. The physiological significance of the single cell INa findings were corroborated by measurements of conduction velocities using an epicardial mapping system in isolated rabbit hearts. Lidocaine (10 microM) significantly suppressed epicardial impulse conduction in both longitudinal (theta L, 0.430 +/- 0.024 vs. 0.585 +/- 0.001 m/s at baseline, n = 7, P < 0.001) and transverse (theta T, 0.206 +/- 0.012 vs. 0.257 +/- 0.014 m/s at baseline, n = 8, P < 0.001) directions. Isoproterenol (0.05 microM) significantly reversed the lidocaine effects with theta L of 0.503 +/- 0.027 m/s and theta T of 0.234 +/- 0.015 m/s (P = 0.014 and 0.004 compared with the respective lidocaine measurements). These results suggest that enhancement of INa is an important mechanism by which isoproterenol reverses the effects of class I antiarrhythmic drugs.

Animals↗
PubMed1992

Effect of direct, reflex and exercise-provoked increases in sympathetic tone on idiopathic ventricular tachycardia.

Exercise treadmill testing and direct enhancement of sympathetic influence with agents such as isoproterenol are often used to reproduce ventricular tachycardia (VT). The cardiac effects of, and arrhythmia responses to, graded exercise, isoproterenol infusion and lower body negative pressure (the latter 2 with and without atrial and ventricular stimulation) were studied in 11 patients with idiopathic VT. During maximal exercise, substantial increases in heart rate and blood pressure occurred, but only 2 of 9 exercised patients had VT (during recovery in both). During programmed stimulation alone, VT was initiated in 6 patients. During maximum levels of lower body negative pressure (-60 cm of water in most), mean systolic blood pressure decreased by 10 mm Hg, heart rate increased by 15 beats/min, and ventricular refractory period decreased by 10 ms. In 4 patients VT occurred spontaneously during lower body negative pressure; in 2, lower body negative pressure was the only intervention producing VT. During isoproterenol infusion VT occurred spontaneously in 2 patients; both had VT initiated during other interventions. Lower body negative pressure and isoproterenol increased VT rate, but did not prolong it. It is concluded that there is significant variability in arrhythmia responses to sympathetic augmentation, suggesting that additional covariables such as parasympathetic input and ventricular volume may also have a role in arrhythmia occurrence.

Adult↗
PubMed1992

NMR relaxation times in acute myocardial infarction: relative influence of changes in tissue water and fat content.

Tissue changes known to occur with acute myocardial infarction include increases in tissue water and lipid content. We sought to evaluate the relative contribution of alterations in tissue water and fat content to the changes of T1 and T2 relaxation times with infarction. Nine mongrel dogs underwent coronary artery occlusion for 6-12 h. T1 and T2 at 20 MHz and tissue water and fat content of normal and infarcted tissue were measured. Tissue water content, T1, and T2 were significantly greater in infarcted myocardium compared to normal (P less than 0.05). Tissue fat content, while not significantly different, increased linearly in infarcted samples as a function of duration of ischemia (r = 0.77). Despite this increase in fat content, only tissue water content was significantly linearly related to T1 (r = 0.97) and T2 (r = 0.91). Increases in T1 and T2 of infarcted tissue appeared to be most significantly influenced by changes in tissue water content. While total tissue fat content increased with duration of ischemia, it did not appear to significantly alter T1 or T2.

Animals↗
PubMed1992

Hemodynamic and reflex sympathetic control of transmural activation and rate of ventricular tachycardia in ischemic and hypertrophic ventricular myocardium of the dog.

BACKGROUND: A previous study found that the electrophysiological response to ischemia is altered in hypertrophic myocardium, resulting in prolonged transmural activation time (TAT) associated with induction of sustained monomorphic ventricular tachycardia. This study investigated the role of hemodynamics in modulating TAT and the cycle length of induced ventricular tachycardia (VT) in dogs with left ventricular hypertrophy (LVH). METHODS AND RESULTS: Anesthetized open-chest dogs underwent 3 hours of uninterrupted circumflex coronary occlusion. During atrial drive, TAT was recorded between endocardial and epicardial bipolar pairs on the same multipolar plunge needle placed in nonischemic and ischemic zones, documented by triphenyltetrazolium chloride staining. TAT and VT induced by up to three extrastimuli were studied during hypertension (control), during normotension produced most frequently by nitroprusside infusion (3-6 micrograms/kg/min), and during further hypertension most frequently produced by phenylephrine infusion (1-5 micrograms/kg/min). Twenty-five dogs with chronic hypertension and LVH (group 1) produced by a single-kidney renal clamp mechanism and 15 control dogs were studied. In the latter, neither intervention altered TAT, and no VT was inducible. In group 1, however, nitroprusside reversibly prolonged TAT within the ischemic zone (mean +/- SEM, 31 +/- 3 to 34 +/- 3 msec, p less than 0.005) and cycle length of induced VT (204 +/- 19 to 240 +/- 17 msec, p less than 0.01). Phenylephrine reversibly shortened both TAT in the ischemic zone (33 +/- 2 to 28 +/- 2 msec, p less than 0.05) and cycle length of VT (219 +/- 17 to 165 +/- 11 msec, p less than 0.025). Cycle length of VT and TAT were dissociated from blood pressure elevation in two dogs with LVH; when blood pressure was elevated by sympathetic nerve stimulation, cycle length of VT and TAT were prolonged. In 11 dogs with LVH (group 2), prolongation of TAT with nitroprusside infusion was prevented by intravenous metoprolol (1.0 mg/kg). Of 12 dogs with LVH and inducible VT (group 3), seven still had VT inducible after metoprolol, but the cycle length of VT was still prolonged with nitroprusside infusion. CONCLUSIONS: These results suggest that 1) TAT in acutely ischemic LVH was uniquely responsive to hemodynamic influences, an effect prevented by beta-blockade with metoprolol, and 2) the cycle length of VT was also uniquely regulated by hemodynamic influences but not blocked by metoprolol.

Adrenergic beta-Antagonists↗
PubMed1992

Post-mortem observations of a recent radiofrequency catheter ablation site.

The acute and chronic gross and microscopic morphologic changes present in myocardium after radiofrequency catheter ablation have been previously described in animal experiments. Acute changes have also been described in four cadaveric human specimens. We describe post-mortem observations of a recent radiofrequency catheter ablation site in a patient who underwent successful ablation for refractory ventricular tachycardia. Our gross and microscopic observations are similar to those previously described in animal experiments and confirm that the animal experimental results can be extrapolated to human hearts. As the use of radiofrequency becomes more prevalent as an alternative treatment for refractory cardiac tachycardias, pathologists will be called upon to identify post-mortem the lesions described. These lesions can be specifically identified, which can serve as a useful verification for this procedure.

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