Results of Cryoenergy and Radiofrequency-Based Catheter Ablation for Treating Ventricular Arrhythmias Arising From the Papillary Muscles of the Left Ventricle, Guided by Intracardiac Echocardiography and Image Integration.

BACKGROUND: Catheter radiofrequency ablation of ventricular arrhythmias (VAs) arising from the left ventricle's papillary muscles has been associated with inconsistent results. The use of cryoenergy versus radiofrequency has not been compared yet. This study compares outcomes and complications of catheter ablation of VA from the papillary muscles of the left ventricle with either cryoenergy or radiofrequency. METHODS AND RESULTS: Twenty-one patients (40±12 years old; 47% males; median ejection fraction 59±7.3%) with drug refractory premature ventricular contractions or ventricular tachycardia underwent catheter cryoablation or radiofrequency ablation. VAs were localized using 3-dimensional mapping, multidetector computed tomography, and intracardiac echocardiography, with arrhythmia foci being mapped at either the anterolateral papillary muscle or posteromedial papillary muscles of the left ventricle. Focal ablation was performed using an 8-mm cryoablation catheter or a 4-mm open-irrigated radiofrequency catheter, via transmitral approach. Acute success rate was 100% for cryoenergy (n=12) and 78% for radiofrequency (n=9; P=0.08). Catheter stability was achieved in all patients (100%) treated with cryoenergy, and only in 2 (25%) patients treated with radiofrequency (P=0.001). Incidence of multiple VA morphologies was observed in 7 patients treated with radiofrequency (77.7%), whereas none was observed in those treated with cryoenergy (P=0.001). VA recurrence at 6 months follow-up was 0% for cryoablation and 44% for radiofrequency (P=0.03). CONCLUSIONS: Cryoablation was associated with higher success rates and lower recurrence rates than radiofrequency catheter ablation, better catheter stability, and lesser incidence of polymorphic arrhythmias.

Angiotensin (1-7) re-establishes impulse conduction in cardiac muscle during ischaemia-reperfusion. The role of the sodium pump.

INTRODUCTION: The effect of angiotensin (1-7) (Ang 1-7) on membrane potential and excitability of rat heart muscle under ischaemia/reperfusion was investigated. MATERIALS AND METHODS: The hearts of adult rats were removed under deep anaesthesia and perfused using the Langendorff method. After 40 minutes of global no-flow ischaemia, the heart was reperfused for five minutes and the right ventricle was dissected out and transferred to a transparent chamber, through which normal oxygenated Krebs solution flowed continuously (37 degrees C). Measurements of membrane potential were performed using an intracellular microelectrode connected to a high impedance preamplifier. The muscle was stimulated with rectangular current pulses (3 ms duration; 0.6 Hz) generated by an electronic stimulator and isolation unit. To study the influence of Ang (1-7) on sodium pump current, isolated myocytes were voltage-clamped at -40 mV and the current generated by the pump was recorded before and after the administration of Ang (1-7) (10-8 M) to the bath. RESULTS: Ang (1-7) (10-8 M) hyperpolarised the ischaemic heart fibre and re-established impulse propagation. The increment of resting potential was related to the activation of the sodium pump. Indeed, Ang (1-7) (10-8 M) enhanced the transient outward current generated by an electrogenic sodium pump. Both effects of Ang (1-7) on membrane potential and pump current were abolished by ouabain (10-7 M). The cardiac refractoriness was also increased by Ang (1-7) (10-8 M). CONCLUSIONS: Ang (1-7) activates the sodium pump, hyperpolarises the heart cell and re-establishes the impulse conduction during ischaemia/reperfusion. These effects of Ang (1-7), and the increment of cardiac refractoriness, provide an explanation for the reduced incidence of arrhythmias during ischaemia/reperfusion in the presence of Ang (1-7).

Effects of the new imidazopyridine CL 86-02-01 on isolated papillary muscle of guinea-pig hearts.

Inotropic activity and the effect of CL 86-02-01 (2-(3-methoxy-5-methylsulfinyl-2-thienyl)-1H-imidazo[4,5-c]pyridine hydrochloride, CAS 109 792-24-7) on membrane resting and action potentials were studied in isolated guinea-pig papillary muscles. Membrane resting potential and action potential parameters were not significantly changed, while CL 86-02-01 exerted a concentration-dependent inotropic effect by increasing the maximum rate of force development and maximum rate of force relaxation. Time to peak force, relaxation time and total contraction time were reduced. These effects are similar to those of beta-adrenergic drugs and phosphodiesterase inhibitors, but markedly differ from those described for other positive inotropic agents like cardiac glycosides, calcium agonists, alpha-adrenergic drugs or increased extracellular calcium concentration.

Prevention of action potentials during extracellular electrical stimulation of long duration.

INTRODUCTION: This study investigated if action potentials can be prevented by electrical field stimuli of long duration. METHODS AND RESULTS: The transmembrane potential was recorded by a double-barrel micro-electrode during field stimulation given across a papillary muscle from 10 guinea pigs. After 10 stimuli (S) with a 200-msec S-S interval, a 400-msec square wave shock was given just before or after the end of the effective refractory period following the 10th stimulus through electrodes 1 cm on either side of the papillary muscles. Another two stimuli (S' and S") having the same 200-msec S-S interval were given during the shock pulse to test if the action potentials induced by these two stimuli could be prevented by the shock. The shock strength was increased until the shock field prevented the action potentials induced by the S' and S" stimuli. The resting membrane potential was -85.5 +/- 2.9 mV. For shocks causing depolarization at the recording site, the field strength required to prevent S'- and S"-induced action potentials was 1.5 +/- 0.4 V/cm, which depolarized the transmembrane potential to -55.3 +/- 8.9 mV and -58.1 +/- 7.2 mV from the resting membrane potential at the time of the S' and S" stimuli, respectively. The strength of shocks causing hyperpolarization required to prevent S'- and S" -induced action potentials was 5.0 +/- 0.8 V/cm, which hyperpolarized the transmembrane potential to -105 +/- 6.5 mV and -115.6 +/- 6.9 mV from the resting membrane potential at the time of the S' and S" stimuli, respectively. CONCLUSION: Both depolarization and hyperpolarization caused by an electrical field can prevent action potentials.

Electrical heterogeneity and conduction block in reoxygenated guinea pig papillary muscles.

To investigate the changes in electrical activity after reoxygenation, guinea pig papillary muscles were reoxygenated with 5 mM glucose solution after various durations (30-120 min) of substrate-free hypoxia. Action potential duration recovered to the control level on reoxygenation following 30-120 min hypoxia. The recovery of developed tension or resting tension was incomplete after reoxygenation following longer periods of hypoxia. There was a high incidence of arrhythmias on reoxygenation after 60 min hypoxia, which have been shown to be triggered activities due to delayed afterdepolarizations. In some muscles reoxygenated after prolonged hypoxia (90-120 min), there was electrical heterogeneity which was shown by variable action potential durations and configurations. There was also conduction block around the microelectrode site in muscle. It was suggested that the electrical heterogeneity and conduction block could predispose to reentry, and that triggered activities and reentry could be involved in the genesis of arrhythmias on reperfusion.

High voltage shock induced cellular electrophysiological effects: transient refractoriness and bimodal changes in action potential duration.

The cellular electrophysiological effects of defibrillation shocks on the myocardium during ventricular fibrillation are not clear. The present study investigated the effects of high voltage shocks on membrane potentials of isolated guinea pig and pig papillary muscles during rapid activations simulating ventricular fibrillation. High voltage shocks induced an action potential with a prolonged duration, followed by a transient refractory state. Subsequent action potentials following this refractory state had shortened durations. The duration of the transient refractory state varied in proportion to shock intensity and stimulation rate, whether the shock was biphasic or monophasic. Shock induced prolonged depolarization was not a consistent finding and mainly observed with slow stimulation rates. In conclusion, high voltage shocks induce bimodal changes of the action potential duration associated with a transient refractory state during rapid activation. The rate dependency of this refractory state suggests that the duration of the shock induced refractory state may be longer in the fibrillating than the normal beating heart, and may contribute to successful defibrillation.

Prolongation and shortening of action potentials by electrical shocks in frog ventricular muscle.

Effects of electrical shocks on myocardium are important for defibrillation. We measured effects of shocks (5 ms, 1-40 V/cm) in isolated frog ventricular strips. We recorded contraction strength and intracellular action potential (AP) with a shock-voltage cancellation technique to allow recordings immediately after shocks. Shocks of > or = 5 V/cm produced a dose- and latency-dependent prolongation of the AP ongoing during the shock. Stronger shocks of 28-40 V/cm decreased the duration, maximum diastolic potential, amplitude, and maximum rate of rise of the phase zero depolarization of paced APs that began after the shock. The contraction strength increased 43 and 59% during the 10 s after the stronger shocks. The transmembrane potential was shifted toward 0 mV immediately after the stronger shocks. We concluded that weak or strong shocks prolong the AP ongoing during the shock, whereas sufficiently strong shocks also shorten APs that begin after the shock. AP prolongation and shortening may be important for defibrillation and acceleration of tachycardia after failed cardioversion shocks.

Dynamics of circus movement re-entry across canine Purkinje fibre-muscle junctions.

1. To determine the cellular electrophysiological mechanisms for unidirectional conduction block and re-entrant excitation, single cycles of circus movement re-entry were induced in canine Purkinje fibre-papillary muscle preparations containing two Purkinje fibre-muscle junctions (PMJs). The preparations were mounted in a partitioned tissue bath that permitted independent superfusion of each PMJ. The pre-existing dispersion of refractoriness between PMJs was accentuated by superfusing PMJ1 with normal Tyrode solution or Tyrode solution containing 6-8 mM KCl and superfusing PMJ2 with Tyrode solution containing 0.5 mM heptanol and 4-10 mM KCl. 2. Premature stimuli delivered to the Purkinje fibre induced unidirectional anterograde conduction block at PMJ2. Conduction proceeded from Purkinje cells to papillary muscle at PMJ1 and from papillary muscle retrogradely across the previously blocked PMJ2. 3. The difference in refractory periods between the two PMJs defined a range of premature coupling intervals within which re-entry was inducible. Conduction block at the PMJ occurred in papillary muscle at short coupling intervals and in the Purkinje fibre at longer intervals. 4. Once initiated, re-entry could be reset or annihilated by properly timed subthreshold current pulses delivered to cells at the PMJ. 5. To define better the mechanisms for conduction block and re-entry, an analytical model was developed using non-linear regression analysis to derive equations from the experimental results. Varying parameters within the constraints of the model reproduced the key features of the rate-dependent conduction block observed experimentally. Critical elements of the model included the induction of significant activation delays at short diastolic intervals and a reduction in the rate of action potential duration restitution after exposure to heptanol. 6. These results help to establish the conditions necessary for induction of one-dimensional circus movement re-entry and to define the roles of non-linearities of activation delay and excitability in the dynamics of conduction block at the PMJ.

Presynaptic beta-adrenoceptors in guinea pig papillary muscle: evidence for adrenaline-mediated positive feedback on noradrenergic transmission.

Guinea pig papillary muscles were preincubated in the presence of 5 x 10(-9) mol/L unlabeled noradrenaline or adrenaline then incubated with (3H)-noradrenaline and superfused. Electrical field stimulation with 180 pulses delivered at 1 or 3 Hz was used to induce overflow of radioactivity. Comparison of the effects of preexposure of the tissue to adrenaline or noradrenaline revealed that adrenaline incubation caused an enhancement of stimulation-evoked overflow of (3H)noradrenaline and a reduction of the effect of exogenously added isoprenaline. Furthermore, the selective beta 2-adrenoceptor antagonist ICI 118,551 (10(-7) mol/L), but not the selective beta 1-adrenoceptor antagonist ICI 89,406 (10(-7) mol/L), reduced electrically evoked overflow of (3H)noradrenaline in tissue preincubated with adrenaline but not in tissue preincubated with noradrenaline. The overflow-reducing effect of ICI 118.551 occurred at stimulation with 3 Hz but not at stimulation with 1 Hz. The present results support the hypothesis that noradrenergic transmission in guinea pig papillary muscle is facilitated via beta 2-adrenoceptors, and that adrenaline may serve as transmitter in this positive feedback mechanism after its incorporation into sympathetic nerves.

On the physiologic role of beta-2 adrenoceptors in the human heart: in vitro and in vivo studies.

To study the physiologic role of human myocardial beta-2 adrenoceptors, the beta adrenoceptor subtype(s) involved in the effects of catecholamines in vitro on the force of contraction and in vivo on heart rate were characterized. In vitro on both isolated electrically driven right and left atrial and left papillary muscle preparations, isoprenaline and adrenaline caused positive inotropic effects via beta-1 and beta-2 adrenoceptor stimulation. In the atria both beta-1 and beta-2 adrenoceptor stimulation increased contractile force to a maximum; in left papillary muscle, however, only beta-1 adrenoceptor stimulation maximally increased contractile force, whereas beta-2 adrenoceptor stimulation caused only submaximal increases. Noradrenaline, on the other hand, caused a positive inotropic effect nearly exclusively via atrial and ventricular beta-1 adrenoceptor stimulation. In vivo in 10 healthy volunteers isoprenaline-induced tachycardia was antagonized with equal potency by the beta-2 adrenoceptor-selective antagonist ICI 118,551 and the beta-1 adrenoceptor-selective antagonist bisoprolol indicating that it is mediated by cardiac beta-1 and beta-2 adrenoceptor stimulation to about the same degree. In contrast, exercise-induced tachycardia (that is mediated mainly by noradrenaline released from the neurons) was antagonized only by bisoprolol but not by ICI 118,551. It is concluded that in humans under normal physiologic conditions contractility and/or heart rate is regulated only by cardiac beta-1 adrenoceptors. In situations of stress, however, when large amounts of adrenaline are released from the adrenal medulla, stimulation of cardiac beta-2 adrenoceptors could contribute to additional increases in contractility, heart rate, or both.

Myocardial beta-adrenoceptor changes in heart failure: concomitant reduction in beta 1- and beta 2-adrenoceptor function related to the degree of heart failure in patients with mitral valve disease.

In patients suffering from end-stage congestive cardiomyopathy, cardiac beta 1-adrenoceptor function is markedly reduced, whereas cardiac beta 2-adrenoceptor function is nearly normal. To determine whether beta 1-adrenoceptor function is impaired in heart failure selectively, beta 1- and beta 2-adrenoceptor density and functional responsiveness in the right and left atria and the left papillary muscles from patients with mitral valve disease (functional class III to IV) were studied. In all three tissues concomitantly beta 1- and beta 2-adrenoceptor density gradually declined when the degree of heart failure increased from functional class III to IV. This decrease in beta 1- and beta 2-adrenoceptor density was accompanied by similar decreases in the contractile response of isolated electrically driven right atrial and left ventricular papillary muscles to beta-adrenergic agonists. It is concluded that a decrease in cardiac beta-adrenoceptor function is a general phenomenon in heart failure, and its extent is related to the degree of heart failure. However, in contrast to congestive cardiomyopathy, in mitral valve disease the decrease in cardiac beta-adrenoceptor function is due to a concomitant decrease in beta 1- and beta 2-adrenoceptors.

Contractile performance of papillary muscles of renovascular hypertensive and isoproterenol-pretreated rats.

Previous studies suggested that left ventricle papillary muscles from neurogenic hypertensive rats with 15 days of sino-aortic denervation (SAD) develop intense depression of their inotropic state. Considering that these animals have an increased cardiac sympathetic tonus that could produce the observed depression of the contractile response we did the present study simulating a cardiac sympathetic hyperactivity pretreating rats, during 15 days, with isoproterenol (IPA, 0.1 mg/kg, i.p., divided in 3 daily doses). Because SAD rats also develop hypertension, the effect of blood pressure overload was studied in rats with 15 days of renovascular hypertension (RHR), Goldblatt 1K1C, to compare, separated, the effects of sympathetic hyperactivity and hemodynamic overload. Results showed that RHR had muscles that developed larger force than their controls (C: 7.31 +/- 0.34 g/mm2, RHR: 12.8 +/- 0.40 g/mm2), meanwhile IPA pretreated rats had muscles developing less force than their respective controls (C: 13.8 +/- 0.37 g/mm2, IPA: 8.61 +/- 0.24 g/mm2). These results are according to the proposition that the contractile state depression is related to the sympathetic hyperactivity, as suggested by the IPA pre-treated group and because the animals with isolated pressure overload showed a better contractile performance when compared to their uninephrectomized controls.

Low Ba-induced pacemaker current in well-polarized cat papillary muscle.

It has previously been reported that superfusion of normally quiescent mammalian ventricular muscle with low concentrations of Ba (less than 0.3 mM) can induce spontaneous activity with maximum diastolic potentials (MDP) that are similar to the normal resting potential (-80 mV or larger). The mechanism for this activity was studied in cat papillary muscle sucrose-gap preparations under current clamp and voltage-clamp conditions. Hyperpolarizing current pulses decreased or abolished the amplitude of the pacemaker potential in a voltage-dependent manner. When Ba concentration was increased to 2 mM the MDP depolarized by approximately 20 mV. Hyperpolarizing steps under these conditions abolished the diastolic depolarization, also in a voltage-dependent manner. Voltage clamping the preparation at the MDP during superfusion of 0.2 mM Ba revealed a time-dependent, inwardly directed current. Hyperpolarizing voltage-clamp steps from a holding potential of -50 mV showed that this current was maximal at approximately -70 mV and frequently reversed at membrane potentials of approximately -95 to -115 mV. The time course of this current was biexponential, and the time constant of the faster component decreased with larger hyperpolarization. When the same voltage-clamp protocol was repeated in the presence of 2 mM Ba, no time-dependent current change was detected. In four out of five experiments, Cs (2.5 mM) reduced (but never abolished) the amplitude of the low Ba-induced current. Our results do not support the hypothesis that a hyperpolarization-induced current (iF-like current) is responsible for the automaticity in well-polarized ventricular muscle at low Ba concentrations. Instead, our data suggest that this pacemaker activity is the result of a Ba-induced, time-dependent blockade of the inward rectifier potassium current (iK1).

Steric aspects of agonism and antagonism at beta-adrenoceptors: experiments with the enantiomers of terbutaline and pindolol.

The enantiomers of terbutaline, a beta 2-selective adrenoceptor agonist, and pindolol, an unselective antagonist with partial agonist activity, were examined with respect to their ability to react in vitro on adrenoceptors in the trachea (mostly beta 2), the soleus muscle (beta 2) and in the papillary muscle of the left ventricle (beta 1) from the guinea-pig (+)-terbutaline was more than 3,000 times less potent than (-)-terbutaline in relaxing the trachea and in depressing subtetanic contractions of the soleus muscle. (+)-terbutaline did not inhibit the effects of (-)-terbutaline in these tissues. The effect of (-)-terbutaline on the papillary muscle was about 200 times weaker than on the soleus. (+)-terbutaline had a negligible inotropic effect on the papillary muscle and it did not inhibit the effect of isoprenaline. The enantiomers of pindolol did not show any consistent agonistic activity under the present experimental conditions. (-)-pindolol inhibited competitively the effect of isoprenaline to the same extent in all three tissues. (+)-pindolol was about 200 times less potent in this respect. Our data do not reveal any qualitative differences in the pharmacological properties between the optical isomers of terbutaline and pindolol, respectively.

Effects of in vivo treatment with isoprenaline or prenalterol on beta-adrenoceptor mechanisms in the heart and soleus muscle of the cat.

The full agonist isoprenaline (5.3-6.6 nmol/kg . min) and the partial beta-adrenoceptor agonist prenalterol (10.6-13.3 nmol/kg . min) were administered to cats continuously via osmotic minipumps (i.p.). After seven days the functional and adenylate cyclase responsiveness to the agonists, as well as the beta-adrenoceptor-binding characteristics, were studied in cardiac and soleus muscle preparations in vitro. After isoprenaline pretreatment, the papillary muscles and soleus muscle strips wer 15-18 times less sensitive to isoprenaline compared with muscles from control cats. The stimulatory potency (pD2) of prenalterol in the papillary muscle was not changed significantly. The affinity of the agonists to the beta-adrenoceptors was unaffected in both tissues by the pretreatment, but the densities of beta-adrenoceptors were significantly reduced, by 36% (myocardium) and 47% (soleus) respectively. In the cat papillary muscle the intrinsic sympathomimetic activity (ISA) of prenalterol on contractile parameters was reduced from 84 (Tmax), 69 (dT/dtmax) and 71% (dT/ dtmin ) in control animals, to 33, 22 and 28%, respectively in the animals pretreated with isoprenaline. Prenalterol pretreatment did not induce any marked changes, either in the stimulatory potency or affinity of the agonists in the two tissues or in the maximal response (ISA) of prenalterol in the papillary muscle. The marked reduction in the stimulatory potency of isoprenaline and the reduced ISA of prenalterol in the myocardium after isoprenaline pretreatment can not be explained by the reduction in beta- adrenoceptor density alone. Since the affinity to the beta- adrenoceptors is unaffected, a reduced efficiency in the signal transmission must be the main cause.(ABSTRACT TRUNCATED AT 250 WORDS)

What role do alpha- and beta-adrenoceptors play in the regulation of the heart?

Ahlquist described the existence of beta-adrenoceptors as structures mediating the positive effects of sympathetic nerve stimulation in the heart. Recently, the role of alpha-adrenoceptors has also been investigated by both biological and radioligand binding studies. The presence of alpha-adrenoceptors has now been demonstrated in the hearts of various mammalian species including man. Stimulation of beta-adrenoceptors causes positive ino-, chrono-, dromo- and bathmotropic effects while that of alpha-adrenoceptors is restricted to positive inotropic effects. Analysis of the effects mediated by alpha-stimulation as carried out in our department showed a clear-cut difference between the mechanisms underlying stimulation of beta- and of alpha-adrenoceptors: that evoked by beta-adrenoceptors is connected to an increase in cAMP, whereas that by alpha-adrenoceptors is not. Moreover, the effect of alpha-stimulation is evidently more dependent on heart rate and on the presence of Ca2+ than that of beta-stimulation. The nature of cardiac alpha-adrenoceptors is apparently distinct from that of other organs as they are stimulated by dopamine and adrenaline but not by the transmitter noradrenaline. Since the alpha-receptor-mediated increase in force of contraction is obviously less energy consuming than that via beta-receptors the heart gains a greater adaptability in adrenergic regulation especially in emergency situations such as myocardial infarction.

Active modulation of electrical coupling between cardiac cells of the dog. A mechanism for transient and steady state variations in conduction velocity.

Propagation velocities of action potentials were measured simultaneously along the longitudinal and transverse axes of cardiac fibers in ventricular muscle. The anisotropic distribution of propagation velocities was found to be altered transiently and in the steady state by the rate and pattern of stimulation and by ouabain. The relative amount of velocity change varied with the direction of propagation and was greatest in the direction perpendicular to the long fiber axis. None of the variables usually associated with the membrane ionic mechanism of depolarization--resting potential, Vmax, and taufoot--showed enough variation to account for the observed changes in velocity. A simplified anisotropic propagation model representing the internal current pathway as an alternating sequence of cytoplasmic and junctional resistance is presented, taking into account the larger contribution to the internal resistance made by the cell couplings in the transverse direction than in the longitudinal direction. On the basis of this model, it was concluded that the observed changes in velocity were due to changes in cell coupling. Both transient and steady state velocity changes were found to correspond to changes in the action potential duration, suggesting that there is a common factor, such as the internal calcium and/or sodium concentrations, linking the control of the action potential duration and the coupling resistance between cardiac cells.

Experimental production of papillary muscle and mitral valve lesions by vagal manipulations in rabbits.

The present paper describes peculiar lesions in papillary muscles and mitral valves produced by vagal manipulations. In the 109 rabbits killed one week after clipping or crushing of their cervical vagi, papillary muscle and mitral valve lesions were found in 53 (48.6%) and 52 (47.7%) hearts respectively. The lesions were identified by visible deposits of colloidal carbon which had been injected intravenously during the first 3 postoperative days. The left ventricular free wall, interventricular septum and right ventricle were free of carbon deposits. The papillary muscles involved were characterized by swelling and increased stiffness which corresponded to degeneration of the myocardial cells and interstitial fibrosis on microscopic observation. Hydroxyproline content of the papillary muscles involved was 1.4 times more than that of normal hearts, while there was no significant difference in hydroxyproline content of either interventricular septum or left ventricular free wall between the manipulated and the normal preparations. Heart murmurs were heard in 23 animals studied. Phonocardiograms revealed mid to late systolic murmurs with or without midsystolic click. These results indicate that the vagus nerve plays an important role in the pathogenesis of some forms of papillary muscle and mitral valve lesions.

[Morphology of 2 cardiomyocyte populations in the papillary muscles of the rat heart]. / K voprosu o morfologii dvukh populiatsii kardiomiotsitov v sosochkovykh myshtsakh serdtsa u krysy.

A light optic and quantitative electron microscope investigation has been performed in order to study papillary muscles in the rat heart. Certain quantitative differences have been revealed in the structure of the conducting and working myocardium. Innervation of the papillary muscles has been characterized. A new type of the conducting cardiomyocytes (IV) has been revealed which had not occurred in the composition of the sinuatrial and atrioventricular ganglia of the atrioventricular (His') bundle and its peduncles, their differences from other three types of the conducting cells revealed before are described. The data obtained are compared to morphological characteristics of the papillary cardiac muscles in other mammalian species.