Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENDOCARDIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMed1986

Effects of halothane on the intramyocardial pressure of the canine left ventricle.

In the intact canine heart a gradient of systolic intramyocardial pressure from a minimum at the epicardial region to a maximum at the endocardial region is well established. No information is, however, available regarding the effects of various anaesthetic agents on this gradient. In the present study the effects of halothane on intramyocardial pressure recorded from subendocardial and subepicardial layers of the canine left ventricular free wall were assessed. Experiments were performed on seven anaesthetised mongrel dogs ventilated with 100% oxygen. Intramyocardial pressure was recorded simultaneously from the inner and outer regions of the myocardium using two Mikro-tip pressure transducers. Halothane concentration in the inspired gas varied from 0% to 2%. In the pentobarbital anaesthetised dog halothane does not significantly change the heart rate. With increasing concentrations of halothane in inspired gas systolic intramyocardial pressure at both endocardium and epicardium decreased significantly from control values. As the halothane concentration increased, the normal differential between systolic left ventricular pressure and endocardial intramyocardial pressure was abolished. The intramyocardial pressure gradient from endocardium to epicardium, however, persisted during systole. During diastole the pressure gradient was reversed, becoming maximum in the epicardial region and minimum in the endocardial region in both control and halothane treated animals. Over the range of 0-2% halothane concentration there was no significant effect on the diastolic intramyocardial pressure gradient. These results suggest that halothane affects the myocardial tissue pressure non-uniformly across the left ventricular free wall and therefore influence sth e transmural distribution of coronary blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Measurement of transmural distribution of phosphorus metabolites in the pig heart by 31P magnetic resonance spectroscopy.

We used the phase modulated rotating frame imaging technique to measure transmural distribution of phosphorus metabolites in 10 anaesthetised ventilated pigs using a double surface coil placed on the surface of the left ventricle. Anaesthesia was maintained in five animals with halothane, barbiturate and nitrous oxide and in five others with intravenous chloralose. 31Phosphorus spectra were acquired, gated to expiration and systole. From phantom experiments the resolution of the experiment was shown to be approximately 2 mm. The anatomical limits of the myocardium were identified by the appearance of 2,3-diphosphoglycerate peaks from red blood cells. The limits of the epicardium were confirmed by obtaining images after placing a phantom containing fluorophosphate on the surface of the heart. The endocardium was identified by inserting a small balloon catheter through the centre of the coil into the left ventricular cavity, filling it with 0.5 ml of fluorophosphate and pulling it gently against the endocardium. No transmural differences in phosphocreatine to ATP ratio were identified in the normal heart. The animals anaesthetised with chloralose showed a significantly higher phosphocreatine to ATP ratio compared to those anaesthetised with halothane and barbiturate. The chloralose animals tended to have a higher blood pressure and a lower heart rate when compared to the other animals. No transmural differences, however, were identified in either group. When regional ischaemia was produced using a snare to occlude the left coronary artery, phosphocreatine fell and the signal from the inorganic phosphate + 2,3-diphosphoglycerate region increased. The inner wall tended to become more acid compared to the outer wall during ischaemia. These experiments show that the phase modulated rotating frame imaging technique can be used to study the effects of changes in workload, ischaemia, or pharmacological intervention on transmural distribution of metabolites in the heart and thus help elucidate factors responsible for subendocardial vulnerability to stress.

2,3-Diphosphoglycerate↗
PubMed1991

Chemical ablation by subendocardial injection of ethanol via catheter--preliminary results in the pig heart.

This study was set up to discover how a subendocardial application of ethanol administered via a catheter would affect an animal model. A 7 F bipolar catheter with a lumen, through which a 2 mm needle was inserted, was placed in the left ventricle of 11 pigs. Altogether, 33 subendocardial injections into the left ventricular myocardium were performed under fluoroscopic control using a mixture of 0.5-1.5 ml ethanol and 0.5-1 ml iopamidol as contrast medium. The mixtures were injected into the apical, lateral and septal walls of the left ventricle. After 25 days, the hearts were removed and the lesions examined pathologically. The calculated volume of the lesions was about 60 mm3, the area in projection to the endocardium about 35 mm2, the depth relative to the endocardium about 1.5 mm and the maximum diameter about 8 mm. Perforation of the myocardial wall by pericardial injection occurred twice without further complications. Subendocardial application of concentrated ethanol by catheter caused a controlled local necrosis. This technique may become a new approach with which to treat ventricular tachycardia by chemical ablation.

Animals↗
PubMed1991

Intracoronary isoflurane causes marked vasodilation in canine hearts.

Previous studies of coronary vasomotor effects of isoflurane were complicated by changes in systemic hemodynamic conditions and in global cardiac work demands. Accordingly, in the current study, the left anterior descending coronary artery (LAD) of 11 open-chest dogs anesthetized with fentanyl and pentobarbital was cannulated and perfused with isoflurane-free arterial blood or with arterial blood equilibrated in an extracorporeal oxygenator with isoflurane (0.5, 1.0, 2.0% in 95.5% oxygen-4.5% carbon dioxide). Steady-state changes in coronary blood flow (CBF) in LAD were measured electromagnetically, and their transmural distribution (endocardium: epicardium ratio) was evaluated with 15-microns radioactive microspheres. Venous blood was obtained from the anterior interventricular vein and analyzed for oxygen tension (PO2) and oxygen content. Myocardial oxygen consumption (MVO2) was calculated using the Fick equation. Cardiac responses during isoflurane were compared to those during maximal vasodilation with intracoronary adenosine. Perfusion pressure was maintained at 100 mmHg. CBF increased 271, 279, and 503% with 0.5, 1.0, and 2.0% isoflurane, respectively, with no change in the endocardium:epicardium ratio. With 2.0% isoflurane, the increase in CBF was 80% of the maximal, adenosine-induced response. The increases in CBF caused by isoflurane were accompanied by greater than proportional increases in venous PO2 and decreases in the arteriovenous oxygen difference, reflecting the reduction (approximately 40% in MVO2. In conclusion, isoflurane has a direct, concentration-dependent relaxing effect on coronary vascular smooth muscle in the canine heart in situ. The ability of isoflurane to increase CBF nearly maximally while also significantly reducing local myocardial oxygen requirements attests to the potency of isoflurane's direct vasodilator action.

Adenosine↗
PubMed1989

Effects of Ro 40-5967, a novel calcium antagonist, on myocardial function during ischemia induced by lowering coronary perfusion pressure in dogs: comparison with verapamil.

Ro 40-5967 is a structurally novel calcium antagonist that binds to the verapamil binding site but has very weak negative inotropic effects compared to verapamil. The goals of the present study were to assess the effects of Ro 40-5967 on myocardial function during ischemia, and to compare them to those of verapamil. For this purpose, in anesthetized dogs where the circumflex coronary artery was cannulated and perfused at controlled pressure, myocardial function was measured using piezo electric crystals implanted into the endocardium. Myocardial distribution of coronary blood flow was assessed using radioactive microspheres. Ischemia was produced by lowering perfusion pressure from 100 to 15 mm Hg in steps. During ischemia, Ro 40-5967 partially prevented the decrease of segmental shortening (p less than 0.01) and increased coronary flow, especially in the endocardium (p less than 0.01). In contrast, verapamil did not improve myocardial function during ischemia. The protective effect of Ro 40-5967 could be partially explained by the decrease of arterial pressure and heart rate induced by Ro 40-5967. However, Ro 40-5967 injected directly inside the coronary artery did not induce systemic effects, but still had protective effects (p less than 0.05). Verapamil injected intracoronary produced severe cardiac depression. We conclude that in the present model during ischemia Ro 40-5967 has no negative inotropic effects, and in contrast to verapamil can improve the myocardial function.

Animals↗
PubMed1992

Induction of vascular adhesion molecules during rejection of human cardiac allografts.

Adhesion of leukocytes to vascular endothelium is a necessary step leading to the migration of cells into underlying tissues. Vascular adhesion molecules regulate this process and may play an important role in graft rejection. Immunocytochemical studies have been used to investigate the expression of vascular adhesion molecules (ICAM-1, PECAM, VCAM-1, and ELAM-1) in normal donor heart (n = 15) and myocardial biopsies from heart transplant patients with acute rejection (n = 15). Sections were also stained with antibodies against endothelium, leukocytes, MHC antigens, and markers of cell activation. In donor heart EN4, vWF, ICAM-1, PECAM, MHC class I--and, to a lesser extent, VCAM-1 and DR antigen--are expressed on arterioles and venules, whereas ELAM-1 and Pal-E are restricted to venules. Expression of Pal-E, VCAM-1, ICAM-1, and DR antigen was increased during rejection. Capillary endothelium normally expresses EN4, ICAM-1, PECAM, MHC class I, and DR antigen but little, if any, VCAM-1 or ELAM-1. During rejection, however, there is an increased expression of all adhesion molecules. This is paralleled by an increased expression of vWF by capillary endothelium. In addition, ICAM-1 like MHC class I antigen is induced on the myocardial membrane and intercalating discs. Endocardium from donor heart expresses EN4, vWF, PECAM, MHC class I, and sometimes Pal-E and ICAM-1, but very little VCAM-1, ELAM-1 or DR antigen. There is an increased expression of Pal-E, ICAM-1, VCAM-1, and DR antigen on endocardium from rejecting heart biopsies. Proliferating Ki-67+ cells and activated T cells expressing the receptor for IL-2 were also found in biopsies during rejection episodes.

Adolescent↗
PubMed1997

The role of nitric oxide and cytokines in heart failure.

Heart failure is a common problem associated with considerable mortality and morbidity. The mechanisms underlying the heart failure syndrome, which remain poorly understood, may involve an inflammatory process. Nitric oxide (NO) and various cytokines could play an important role in this inflammatory process. Recent evidence has emerged in both animal models and humans suggesting that both of these mediators may play an important role in heart failure. NO is synthesized by the NO synthase family of enzymes. Two of these enzymes are constitutive, endothelial NO synthase and neuronal NO synthase. The third enzyme, inducible NO synthase, is capable of producing large amounts of NO once induced by mediators such as interleukin (IL)-1, IL-2, IL-6, tumour necrosis factor (TNF)-alpha, and interferon-gamma. Endothelial NO synthase is present in the heart in the endocardium, cardiac myocytes, and cardiac conduction tissue. Inducible NO synthase is present in cardiac myocytes, endocardium, vascular smooth muscle cells, and infiltrating inflammatory cells. Evidence from both animal models and patients suggests that NO exerts a negative inotropic effect. Increased inducible NO synthase, TNF-alpha, and IL-6 have been found in patients with heart failure in several studies. In other studies, decreased endothelial NO synthase was found in patients with heart failure. TNF-alpha and IL-6 may be produced in heart failure and may induce inducible NO synthase, resulting in NO production, which acts as a negative inotrope. Endothelial NO synthase may be decreased as a result of downregulation by TNF-alpha or inducible NO synthase. The possible role of these mediators in heart failure needs further evaluation because these findings could have novel therapeutic implications.

Animals↗
PubMed1982

Intrinsic sympathomimetic activity and coronary blood flow.

1 The effects of four beta-adrenoceptor blocking agents, propranolol, pindolol, practolol and atenolol, used in doses inducing the same degree of beta 1-adrenoceptor blockade, have been investigated on regional myocardial blood flow (microspheres) and coronary vascular resistance in the normal and ischaemic myocardium of the anaesthetized dog. 2 In the ischaemic and non-ischaemic myocardial areas, transmural blood flow was significantly reduced by propranolol and atenolol which are devoid of intrinsic sympathomimetic activity (ISA) while it remained unaffected by beta-adrenoceptor blocking drugs endowed with ISA, whether cardioselective (practolol) or not (pindolol). In non-ischaemic areas, only propranolol and atenolol increased coronary vascular resistance. 3 Regarding coronary blood flow distribution between the epicardium and endocardium, only propranolol and pindolol induced a favourable redistribution towards the endocardium increasing the endo/epi flow ratio, while practolol and atenolol were ineffective. 4 These results suggest that ISA is of major importance in maintaining coronary flow especially in the ischaemic myocardium but that it is not involved in the mechanisms underlying coronary blood flow redistribution between the different myocardial layers.

Adrenergic beta-Antagonists↗
PubMed1999

Prejunctional effects of angiotensin II and bradykinin in the heart and blood vessels.

1. Angiotensin and bradykinin facilitate the release of noradrenaline from sympathetic nerve terminals and cause positive inotropy in rat isolated atria and ventricles. The effect of bradykinin was enhanced by the ACE inhibitor, ramiprilat. 2. The facilitated release of noradrenaline in rat ventricle by bradykinin was blocked by the beta2-receptor antagonist HOE-140. This response is also reduced by removing the endocardium, suggesting the release of a mediator from the endocardium. 3. The facilitated noradrenaline release by angiotensin II and bradykinin was blocked by the angiotensin receptor antagonist saralasin to the same extent. In contrast, losartan caused only minor blockade in a range of vascular and cardiac tissues. This suggests that angiotensin and bradykinin exert these responses by interacting with a prejunctional receptor different from the established AT1 subtype. 4. These results suggest that bradykinin mediates facilitation of noradrenaline release via the local release of angiotensin onto an atypical AT1 receptor.

Angiotensin II↗
PubMed1993

Perfusion pressure and transmural flow distribution in the left ventricles of isolated rat hearts.

1. The influence of perfusion pressure on flow distribution in the left ventricular wall was investigated with a newly developed microsphere method in Langendorff preparations of the rat heart. 2. Microspheres with a diameter of 10 microns stained with the fluorescent dye yellow-green were infused into the perfusion medium. The hearts were then relaxed with a calcium-chelator, fixed with formaldehyde and cut transversally with a freezing microtome. Photographs were taken of the 52 microns slices with a fluorescence photomacroscope. The ventricular wall was subdivided into four zones, evaluated planimetrically and the beads were counted for calculation of microsphere density. 3. Perfusion of groups of hearts, paced at 5 Hz, with Tyrode's solution at pressures of 30, 50, 80 or 120 cmH2O for 30 min revealed an increase of left ventricular pressure amplitude, coronary flow, myocardial oxygen consumption and flow redistribution towards the endocardium of the left ventricular wall with increasing perfusion pressure. 4. The quotient of the sphere densities in the inner endocardium over that in the outer epicardium, however, was already maximal at a pressure of 80 cmH2O and amounted to 1.59 +/- 0.15. This quotient was only 0.52 +/- 0.11 at a perfusion pressure of 30 cmH2O, thus indicating massive change in flow distribution upon hypoperfusion. 5. These results indicate that transmural left ventricular flow redistribution in response to hypoperfusion in the isolated rat heart is similar to that in hearts of much larger species.

Animals↗
PubMed1985

Right-sided infective endocarditis combined with mitral involvement in a patient with ventricular septal defect.

An autopsy case of right-sided infective endocarditis combined with mitral valvular involvement in a 20-year-old male Japanese with ventricular septal defect (VSD) was reported. The vegetations were found on the endocardium bordering VSD, tricuspid valve, mural endocardium of the right ventricular outflow tract, and even the pulmonic valve, resulting in forming infective aneurysm of the pulmonary trunk. Streptococcus was morphologically identified in the vegetations obtained at autopsy. On the other hand, smaller vegetations were also noted on the mitral valve. The mechanisms of the mitral extending were discussed when right-sided infective endocarditis associated with VSD preceded that on the mitral valve. The authors think that mitral regurgitation in relation to VSD and right to left shunt through VSD which occur even temporarily may be the most important mechanism responsible for the mitral valvular involvement. Several differences between right-sided and left-sided infective endocarditis were also reviewed.

Adult↗
PubMed1990

Evaluation of the effect of azapropazone on neutrophil migration in regional myocardial ischaemia/reperfusion injury in rabbits.

1. The purpose of the present study was to determine the myocardial cytoprotective efficacy of azapropazone (AZA) and its potential site of action on neutrophil infiltration into reperfused/ischaemic myocardium with or without in vivo activation of neutrophils in rabbits. 2. AZA, 100 mg kg-1, was administered i.v. 10 min after occlusion of the left circumflex (LCX) artery in rabbits with and without pretreatment with phorbol myristate acetate ester (PMA). The LCX occlusion was then released at 10 min after AZA administration. Haemodynamic parameters (heart rate, LV pressure, mean arterial blood pressure and dp/dt) were monitored throughout the experiment. After 60 min reperfusion, the area at risk was delineated and the heart was then excised and divided into epi- and endocardial pieces for analysis of myeloperoxidase activity. 3. AZA inhibited neutrophil infiltration into the reperfused/ischaemic rabbit myocardium with and without PMA treatment. The inhibition of neutrophil infiltration was more apparent in the epicardium than in the endocardium. Additionally, AZA inhibited to a similar extent the in vivo PMA-stimulated neutrophil migration into the epicardium and endocardium area at risk. AZA had no significant effect on the haemodynamic parameters as compared to control. 4. AZA administered in an anaesthetized rabbit model of LCX occlusion/reperfusion resulted in the reduction of infarct size. 5. It is concluded that AZA has significant inhibitory effects on neutrophil migration which might contribute to its myocardial cytoprotective effect.

Animals↗
PubMed1993

The Dotter retriever and pigtail catheter: efficacy in extraction of chronic transvenous pacemaker leads.

Several techniques exist for percutaneous extraction of chronic pacemaker leads. To establish the efficacy of the Dotter retriever and pigtail catheter, we reviewed the removal of 59 endocardial pacemaker leads in 42 patients (mean age 71 years). The mean duration of lead implantation was 44 months (range 1-169 months). Thirty-two leads were withdrawn with simple traction alone, and five leads were abandoned when traction failed. The remaining 22 leads were manipulated with a Dotter retriever or pigtail catheter, or both. Twelve leads were dislodged from the endocardium with simple traction (10) or with traction transmitted through an entwining pigtail catheter (2), but they could not be fully withdrawn. Eleven of these leads (92%) were then successfully extracted with the Dotter retriever. Seven of the remaining 10 leads were successfully dislodged and removed by the Dotter retriever. Overall, 9 of 12 leads (75%) that could not be dislodged from the endocardium with simple traction were removed with a Dotter retriever or pigtail catheter, or both. Three patients in whom no catheter method worked required thoracotomy for removal of infected leads. No complications resulted from use of the Dotter retriever or pigtail catheter. We conclude that the Dotter retriever and pigtail catheter have moderate efficacy for dislodging chronic endocardial leads. Once mobilized, however, the leads can be withdrawn with great success with the Dotter retriever. Newer technology should not result in the abandonment of this proven technique.

Adolescent↗
PubMed1994

Why is catheter ablation less successful than surgery for treating ventricular tachycardia that results from coronary artery disease?

Nearly 80% of patients with coronary artery disease who have map-directed surgery for control of ventricular tachycardias require no drug therapy to prevent recurrences, while fewer than 50% of patients undergoing catheter ablation have similar outcomes. Catheter ablation will fail if arrhythmogenic sites are incompletely ablated by lesions that are too small or too far away from the reentrant pathway or if all arrhythmogenic sites are not identified. The underlying assumptions used to guide site selection are that: (a) ventricular tachycardias arise from reentrant mechanisms; (b) monomorphic ventricular tachycardias with similar QRS morphologies arise from the same pathway; (c) the ventricular tachycardia initiated during the procedure represents the patient's spontaneous arrhythmia; (d) the endocardial site that should be ablated can be identified from cardiac activation maps produced during induced ventricular tachycardia or from ancillary techniques; and (e) the patient has only one or two reentrant pathways. Relying on incorrect assumptions may account for the difference in success rates. Patients may have similar appearing ventricular tachycardias that arise from different pathways, and the entire thin layer of viable tissue between the infarct and the endocardium may contain many reentrant pathways. Some ventricular tachycardias may arise from the myocardium away from the endocardium, while others may arise from the epicardium. Small lesions may not be large enough to eliminate all possible reentrant pathways. Catheter ablation may be less successful because the lesions are inadequate, the assumptions guiding the selection of arrhythmogenic tissue are incorrect, or all arrhythmogenic sites are not identified. The primary reason catheter ablation is less successful than surgery in the treatment of ventricular tachycardias is that catheter ablation does not ablate as much tissue as is removed by surgery. The success rate of catheter ablation probably can be improved if the amount of tissue ablated is increased.

Catheter Ablation↗
PubMed1998

Histological examination of the topography of the atrioventricular nodal artery within the triangle of Koch.

UNLABELLED: The treatment of choice in patients with drug-resistant atrioventricular nodal reentry tachycardia is radiofrequency fast or slow pathway ablation. Ablation of the reentrant circuit in the region of the His bundle, when approached from the anterior-superior region (fast pathway); can result in complete AV block. This is less likely if the posterior-inferior (in the region of coronary sinus ostium) approach is used (slow pathway ablation). The possibility that radiofrequency energy may damage the vascular supply to the AV node must be considered. In order to confirm this hypothesis observation was conducted on the autopsy material of 50 human hearts (20 F, 30 M) from 18 to 81 years of age. Specimens were taken containing the triangle of Koch (the apex- right fibrous trigone, the base- coronary sinus ostium). These histological blocks were sectioned in the frontal plane and stained using Masson's method. Koch's triangle was divided in the sagittal plane into 3 parts: inferior (between the base and the attachment of the tricuspid valve), central (between the base and the apex of the right fibrous trigone) and superior (between this trigone and the tendon of Todaro). It was observed that the AVN artery at the coronary sinus ostium level (the base of the triangle of Koch) was positioned in 68% in the central and in 32% in the inferior part of Koch's triangle. The AVN artery in the central part was removed from the endocardium 1 mm (18%), 2 mm (42%), 3 mm (22%), 4 mm (18%). In the inferior part 1 mm (26%), 2 mm (37%), 3 mm (37%). No statistically significant relationship was observed between those groups. CONCLUSIONS: 1) in 20% of examined hearts the AVN artery lay just beneath the endocardium near the coronary sinus ostium 2) there is a risk of the AVN artery coagulation during radiofrequency ablation in the slow pathway region.

Adult↗
PubMed2004

Deep myocardial ablation lesions can be created with a retractable needle-tipped catheter.

RF catheter ablation of ventricular tachycardia is sometimes limited by inadequate lesion depth. This study investigated the use of a retractable needle-tipped catheter to create deep RF lesions in vivo in porcine myocardium. An 8 Fr electrode catheter with an extendable 27-gauge needle at the tip was modified for RF ablation by embedding a thermocouple and attaching a pin connector. In three swine (32-58 kg) the left ventricle was entered via the femoral artery and endocardial contact was made. The needle was advanced 10 mm and 13 RF applications were made under a controlled temperature (90 degrees C x 120 s). Nine control lesions were made using a standard 4-mm tip catheter (60 degrees C x 120 s). The lesions were fixed, serially sectioned from the endocardium, digitally imaged, and quantified. Needle ablation lesions were deeper (10.15 +/- 0.77 vs 5.67 +/- 0.37 mm, P < 0.001) and more likely to be transmural (77 vs 11%, P = 0.008) than control lesions. The volume of control lesions, however, was larger (358.4 +/- 56.2 vs 174.7 +/- 18.6 mm(3), P = 0.002) due to a significantly larger cross-sectional area at the endocardium (0.548 +/- 0.04 vs 0.151 +/- 0.01 cm(2), P < 0.001). At depths > 6 mm, the needle electrode lesions had a greater cross-sectional area (0.136 +/- 0.01 vs 0.005 +/- 0.004 cm(2), P < 0.001). Catheter-based needle ablation is feasible and allows creation of deeper lesions that can be transmural. Although deep, the lesions had a small cross-sectional area such that precise targeting would be required for success.

Animals↗
PubMed1995

Electrophysiologic characteristics of M cells in the canine left ventricular free wall.

INTRODUCTION: Recent studies have described the existence of M cells in the deep structures of the canine and human ventricle. The present study was designed to further characterize the M cell with respect to its distribution across the canine left ventricular free wall and the dependence of its action potential on [K+]o. METHODS AND RESULTS: We used standard microelectrode techniques to record transmembrane activity from deep subepicardial or transmural strips isolated from the canine left ventricular free wall near the base as well as subendocardial Purkinje fibers. M cells behavior (steep APD-rate relation) was observed at depths of 1 to 7 mm from the epicardial surface (deep subepicardium to mid-myocardium). M cells were found to be distributed uniformly in the deep subepicardium and did not appear in discrete bundles. We observed transitional behavior throughout the wall. The maximum rate of rise of the action potential upstroke, Vmax, increased sharply between epicardium and deep subepicardium (176 +/- 13 to 332 +/- 61 V/sec), remained high throughout the mid-myocardium and deep subendocardium, and returned to lower values only in the superficial layers of the endocardium (205 +/- 21 V/sec). The relationship between Vmax and takeoff potential in the M cell was fit by a Boltzmann equation with a V0.5 of -68.6 +/- 1.5 mV and k of 3.4 +/- 0.5. The relationship between resting membrane potential (RMP) and [K+]o in the M cell was exponential from 8 to 20 mmol/L (58 mV change in RMP per 10-fold change in [K+]o), deviating from K+ electrode behavior at [K+]o < 8 mmol/L. RMP in M cells continued to hyperpolarize at [K+]o < 2.5 mmol/L, reaching potentials of approximately -110 mV at [K+]o of 1 mmol/L. In contrast, subendocardial Purkinje fibers depolarized at these low levels of [K+]o. Unlike endocardium and epicardium, M cells developed early afterdepolarizations at low [K+]o and slow rates. CONCLUSIONS: Our data indicate that the M cells are widely distributed in the intramural layers of the canine left ventricular free wall. M cells and transitional cells occupy 30% to 40% of the left ventricular wall and an estimated 20% to 40% of the mass of the ventricles of the normal canine heart. They display characteristics common to both myocardial and specialized conducting cells. Like Purkinje fibers, M cells exhibit a relatively large Vmax and steep APD-rate relations that are modulated by [K+]o. Unlike Purkinje fibers, M cells do not appear in bundles, they do not depolarize at [K+]o < 2.5 mmol/L, nor do they exhibit phase 4 depolarization.

Action Potentials↗
PubMed2006

Substrate in the interventricular septum for left ventricular and right ventricular outflow tract tachycardia: ablation from the right side of the septum.

Simultaneous epicardial and endocardial mapping demonstrated that in a substantial number of ventricular tachycardias (VTs) endocardial, intramural, and epicardial structures are involved in the substrate of the reentrant circuits. Both right and left ventricular breakthrough has also been described during VT originating in the interventricular septum. We report the case of a patient with a nonischemic left ventricular aneurysm presenting with a left ventricular outflow tract (LVOT) tachycardia and a right ventricular outflow tract (RVOT) tachycardia. Mapping from the anterior interventricular vein and the endocardium of the RVOT revealed mid-diastolic potentials at the epicardium of the LVOT and the endocardium of RVOT, where the criteria of central isthmus sites could be demonstrated. Ablation targeting an isolated late potential during sinus rhythm in RVOT eliminated both the LVOT tachycardia and the RVOT tachycardia. In this patient with a nonischemic left ventricular aneurysm, the substrate of a LVOT tachycardia and RVOT tachycardia is described, and successful catheter ablation of the right and left ventricular tachycardia from the septal wall of RVOT is reported.

Adult↗