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PubMed1989

Endocardial injury and the pathogenesis of mural thrombosis in the left ventricle.

To define the interactions between blood and endocardium damaged by lactic acid, the left ventricles of 48 isolated continuously perfused and beating hearts were exposed for 0-4 hours to Krebs Henseleit buffer (KHB) with or without 33 mumol.ml-1 of lactic acid (pH 6.4). After excising its apex, the left ventricle was flushed with KHB, followed by 10 ml of lightly heparinised blood, and then by a further 10 ml of KHB. Lactic acid caused endothelial cell membrane rupture, intercellular separation, and exfoliation with exposure of the basal lamina and underlying connective tissue. Whereas multilayered platelet aggregations formed on exposed basal lamina, fibrin deposition and incorporation of blood cells were only observed in the larger thrombi which formed on exposed collagen. These findings indicate that a metabolite which accumulates in ischaemic myocardium can cause endocardial injury which would predispose to the mural thrombosis which can complicate myocardial infarction.

Animals↗

PubMed1991

The contribution of ischaemia to the development of microvascular incompetence in the myocardium.

STUDY OBJECTIVE: The aim was to determine the contribution of ischaemia per se to the development of microvascular incompetence in the myocardium. DESIGN: Isolated, buffer perfused rat hearts were made globally ischaemic for 0-60 min, then fixed with nitrogen bubbled glutaraldehyde and perfused with nuclear track emulsion to identify and quantify competent blood vessels in scanning and transmission electron micrographs. SUBJECTS: Adult Male Wistar rats weighing between 275 and 350 g were used. MEASUREMENTS AND MAIN RESULTS: Thirty or more min ischaemia significantly (p less than 0.05) reduced the density of competent capillaries in the subendocardial third of the myocardium, as did 45 or more min in the subepicardial third and 60 min in the middle third. Following 60 min ischaemia virtually all vessels in the subendocardial third were not perfusable. Severely ischaemic myocardium showed relatively normal, open, unobstructed capillaries and an absence of the endothelial, myocyte and mitochondrial swelling which have previously been attributed to ischaemia. CONCLUSIONS: In severely ischaemic myocardium microvascular incompetence shows a transmural gradient in severity. It develops progressively, starting near the endocardium. These findings suggest that postischaemic reoxygenation may accelerate the development of microvascular incompetence.

Animals↗

PubMed1994

Non-Hodgkin's lymphoma related eosinophilic endomyocardial disease.

Two patients with eosinophilic endomyocardial disease related to peripheral T-cell lymphomas are reported. Both patients were free of cardiac symptoms at presentation and during follow-up. Routine two dimensional echocardiography revealed bi-apical ventricular obliteration, which was also seen on MR imaging. On the T1-weighted sequence, the thickened endocardium appeared with an isointense signal. Gadolinium DOTA provided an enhanced contrast of the internal part of the left ventricular wall. On T2-weighted sequence, a thin hypointense curvilinear structure drew a dividing line between the internal, endocardial, and the external, myocardial area. Left-ventricular systolic and diastolic functions remained unaltered during subsequent follow-up.

Adult↗

PubMed1991

Ventricular tachycardia in an isolated guinea pig ventricular free wall model of ischemia and reperfusion.

Electrical activity from endo- and epicardium was recorded from isolated segments of right ventricular free walls of guinea pigs using standard differential microelectrode techniques and a high-gain electrocardiogram (ECG). Stimulation was applied to the endocardium. Tissues were exposed to ischemic conditions for 10 min and then were reperfused with "normal" Tyrode's solution. Early premature beats or rapid ventricular tachycardia (VT) occurred in 36% of hearts during "ischemia" and 79% of hearts on reperfusion. Endocardial activation was not significantly slowed by ischemic conditions or reperfusion. However, transmural conduction times increased, and muscle action potential durations decreased during ischemic conditions and early reperfusion. Rapid VT began with alternating activation of endo- and epicardium, and continuous low-voltage ECG activity bridging diastole. Activation of epicardium was essential for occurrence of early premature beats and rapid VT. Hyperkalemia during ischemia promoted arrhythmias during "ischemia," but not during reperfusion. Oscillatory afterpotentials (OAP) also occurred during reperfusion (36%), but not during "ischemia". Our study provides an isolated tissue model that reproducibly generates tachycardias, and that permits study of ischemia and reperfusion-induced transmembrane activity and defects in transmural conduction.

Action Potentials↗

PubMed1992

Role of endocardial endothelium in the positive inotropic effect of cholic acid in isolated myocardium.

In isolated feline right ventricular papillary muscles, with intact or damaged (exposure to dry air for 30 s) endocardium, the effects of cholic acid were studied. At 35 degrees C and a [Ca2+] of 1.25 mM, isometric twitches and the maximal unloaded velocity of shortening (Vmax) were registered. Endocardial endothelium (EE) and myocardial ultrastructure were evaluated on scanning and transmission electron microscopy. In muscles with intact EE, low concentrations of cholic acid (3 x 10(-9) to 3 x 10(-7) M) or short incubation (30 min) with 3 x 10(-8) M induced a mild positive inotropic response, manifested as an increased peak isometric twitch tension (TT) and shortened twitch duration, without changes in Vmax. This inotropic response was abolished by damaging the EE. It was also absent after the addition of propranolol to muscles with intact EE. Higher concentrations (3 x 10(-6) to 3 x 10(-4) M) or prolonged incubation at 3 x 10(-8) M caused extensive morphologic damage of the EE, without detectable impairment of subjacent myocardium. This was accompanied by a progressive decrease in the TT and further twitch abbreviation, without changes in Vmax, resembling twitches obtained from muscles with experimentally damaged EE. These observations suggest that cholic acid induces an EE-dependent and beta-receptor-mediated positive inotropic effect, while simultaneously causing damage to EE cells.

Animals↗

PubMed2000

Spatial regularization of the electrocardiographic inverse problem and its application to endocardial mapping.

Numeric regularization methods for solving the inverse problem of electrocardiography in realistic volume conductor models have been mostly limited to uniform regularization in the spatial domain. A method of spatial regularization (SR) was developed and tested in canine, where each spatial spectral component of the volume conductor model was considered separately, and a SR operator was selected based on explicit a posteriori criterion at each time instant through the heartbeat. The inverse problem was solved in the left ventricle by reconstructing endocardial surface electrograms based on cavitary electrograms measured with the use of a noncontact, multielectrode probe. The results were validated based on electrograms measured in situ at the same endocardial locations using an integrated, multielectrode basket-catheter. A probe-endocardium three-dimensional model was determined from multiplane fluoroscopic images. The boundary element method was applied to solve the boundary value problem and derive the relationship between endocardial and probe potentials. Endocardial electrograms were reconstructed during both normal and paced rhythms using SR as well as standard, uniform, zeroth-order Tikhonov (ZOT) regularization. Compared to endocardial electrograms measured by the basket, electrograms reconstructed using SR [relative error (RE) = 0.32, correlation coefficient (CC) = 0.97, activation error = 3.3 ms] were superior to electrograms reconstructed using ZOT regularization (RE = 0.59, CC = 0.79, activation error = 4.9 ms). Therefore, regularization based on spatial spectral components of the model improves the solution of the inverse problem of electrocardiography compared to uniform regularization.

Animals↗

PubMed2004

Solving the inverse problem of electrocardiography using a Duncan and Horn formulation of the Kalman filter.

Numeric regularization methods most often used to solve the ill-posed inverse problem of electrocardiography are spatial and ignore the temporal nature of the problem. In this paper, a Kalman filter reformulation incorporated temporal information to regularize the inverse problem, and was applied to reconstruct left ventricular endocardial electrograms based on cavitary electrograms measured by a noncontact, multielectrode probe. These results were validated against in situ electrograms measured with an integrated, multielectrode basket-catheter. A three-dimensional, probe-endocardium model was determined from multiplane fluoroscopic images. The boundary element method was applied to solve the boundary value problem and determine a linear relationship between endocardial and probe potentials. The Duncan and Horn formulation of the Kalman filter was employed and was compared to the commonly used zero- and first-order Tikhonov spatial regularization as well as the Twomey temporal regularization method. Endocardial electrograms were reconstructed during both sinus and paced rhythms. The Paige and Saunders solution of the Duncan and Horn formulation reconstructed endocardial electrograms at an amplitude relative error of 13% (potential amplitude) which was superior to solutions obtained with zero-order Tikhonov (relative error, 31%), first-order Tikhonov (relative error, 19%), and Twomey regularization (relative error, 44%). Likewise, activation time error in the inverse solution using the Duncan and Horn formulation (2.9 ms) was smaller than that of zero-order Tikhonov (4.8 ms), first-order Tikhonov (5.4 ms), and Twomey regularization (5.8 ms). Therefore, temporal regularization based on the Duncan and Horn formulation of the Kalman filter improves the solution of the inverse problem of electrocardiography.

Algorithms↗

PubMed2004

Instantaneous quantitative video intensity heterogeneity: evaluation with low mechanical index contrast echocardiography.

BACKGROUND: Instantaneous video intensity of myocardium has been poorly characterized. Myocardial video intensity is usually displayed in the fitted curve from the exponential equation, y = a(1 - e (-bt)). However, information from the fitted curve will be as accurate as the original video intensity data from the perfusion image. Therefore, we sought to characterize the intramyocardial instantaneous video intensity from low mechanical index (MI) contrast echo imaging for variation. METHOD: Low-MI imaging using a nonlinear cancellation technique was performed on 10 subjects with normal myocardium. Quantitative video intensity was analyzed in five segments in the epicardium and subendocardium, as well as in systole and diastole. RESULTS: Video intensity varied between the epicardium and endocardium in each of the region that was analyzed, with the greatest variation in the inferior region (P < 0.0001). Diastolic and systolic differences were also present. CONCLUSION: Instantaneous video intensity is heterogeneous within the myocardium. Differences can result from attenuation, myocardial fiber structure, and even isotropic effects of the contrast agent, and should be taken into account when data are fitted into an exponential function.

Aged↗

PubMed2005

Endocardial schwannomas in the Wistar rat.

Endocardial neoplasms were observed in 13 Wistar rats, 15-30 months old, from a 30-month inhalation study. Eight of the rats were dissected at 30 months and the other five between 15 and 29 months. Histologically, the lesions in the heart were diagnosed as endocardial schwannomas. Two of the 13 schwannomas were malignant, while the rest were benign. One malignant schwannoma metastasized to the thymus and the other metastasized to the aorta, oesophagus, liver and spleen. Some schwannomas appeared as early lesions limited to the endocardium consisting of round to ovoid cells interspersed with spindle cells, while other schwannomas appeared as advanced lesions consisting of a thin superficial layer of round to ovoid cells and a deeper layer of spindle cells characteristic of endocardial schwannomas. The histological appearance of the metastases was identical to that of the primary tumour. The diagnosis was confirmed by positive immunostaining for S-100 protein. The incidence of endocardial schwannomas in the Wistar rat strain was 1.8%.

Animals↗

PubMed1997

Acute vascular embolus resulting from metastatic endocardial involvement with synovial sarcoma: report of a case and review of the literature.

A rare case of metastatic soft tissue sarcoma (STS) involving the endocardium of the left ventricle of the heart is described. A 57-year-old man with a previously resected synovial sarcoma of the anterior abdominal wall presented 5 years later with an acute ischaemic arm resulting from tumour embolus. The treatment and outcome of the patient are outlined. Metastatic STS cardiac involvement and management of this complication are reviewed.

Abdominal Muscles↗

PubMed2006

Gene expression of stretch-activated channels and mechanoelectric feedback in the heart.

1. Mechanoelectric feedback (MEF) in the heart is the process by which mechanical forces on the myocardium can change its electrical properties. Mechanoelectric feedback has been demonstrated in many animal models, ranging from isolated cells, through isolated hearts to whole animals. In humans, MEF has been demonstrated directly in both the atria and the ventricles. It seems likely that MEF provides either the trigger or the substrate for some types of clinically important arrhythmias. 2. Mechanoelectric feedback may arise because of the presence of stretch-sensitive (or mechano-sensitive) ion channels in the cell membrane of the cardiac myocytes. Two types have been demonstrated: (i) a non-specific cation channel (stretch-activated channel (SAC); conductance of approximately 25 pS); and (ii) a potassium channel with a conductance of approximately 100 pS. The gene coding for the SAC has not yet been identified. The gene for the potassium channel is likely to be TREK, a member of the tandem pore potassium channel gene family. We have recorded stretch-sensitive potassium channels in rat isolated myocytes that have the properties of TREK channels expressed in heterologous systems. 3. It has been shown that TREK mRNA is expressed heterogeneously in the rat ventricular wall, with 17-fold more expression in endocardial compared with epicardial cells. This difference is reflected in the TREK currents recorded from endocardial and epicardial cells using whole-cell patch-clamp techniques, although the difference in current density was less pronounced (approximately threefold). Consistent with this, we show here that when the ventricle is stretched by inflation of an intraventricular balloon in a Langendorff perfused rat isolated heart, action potential shortening was more pronounced in the endocardium (30% shortening at 40 mmHg) compared with that in the epicardium (10% shortening at the same pressure). 4. Computer models of the mechanics of the (pig) heart show pronounced spatial variations in strain in the myocardium with large transmural differences (in the left ventricle in particular) and also large differences between the base and apex of the ventricle. 5. The importance of MEF and the non-homogeneous gene expression and strain distribution for arrhythmias is discussed.

Animals↗

PubMed2000

The effects of [K+]o on regional differences in electrical characteristics of ventricular myocytes in guinea-pig.

Altering [K+]o might have different effects on action potential duration (APD) in myocytes from different regions. Therefore, the effects of [K+]o on regional differences in action potential characteristics were investigated in sub-endocardial, mid-myocardial and sub-epicardial myocytes isolated from the base of guinea-pig left ventricular free wall using three different [K+]o (2.7, 5.4 and 8.1 mM KCl). Action potentials were recorded using the switch-clamp technique at 0.5 Hz. Increasing [K+]o from 2.7 to 8.1 mM shortened the action potential duration to 90 % repolarization (APD90; mean APD90 values in sub-endocardial, mid-myocardial and sub-epicardial myocytes were, respectively, 295 +/- 9, 286 +/- 9 and 266 +/- 8 ms in 2.7 mM [K+]o, 270 +/- 7, 255 +/- 7 and 215 +/- 7 ms in 5.4 mM [K+]o, 234 + 7, 212 +/- 10 and 155 +/- 8 ms in 8.1 mM [K+]o), depolarized the resting potential, and reduced the amplitude of the action potential. The effect of increasing [K+]o on action potential characteristics was more pronounced in sub-epicardial myocytes than in sub-endocardial and mid-myocardial myocytes. The regional differences in APD90 in 5.4 mM [K+]o were increased in 8.1 mM [K+]o and abolished in 2.7 mM [K+]o. In conclusion, changing [K+]o produces more pronounced effects on action potentials in sub-epicardial myocytes than in sub-endocardial myocytes, modifying the normal heterogeneity of action potentials. The differences in the response of sub-epicardium and sub-endocardium to [K+]o may contribute to the flattening or inversion of the T wave commonly seen in patients presenting with hypokalaemia and the upright and tall T waves observed in electrocardiograms recorded during hyperkalaemia, although the underlying ionic currents remain to be determined.

Action Potentials↗

PubMed2001

Regulation of KChIP2 potassium channel beta subunit gene expression underlies the gradient of transient outward current in canine and human ventricle.

Expression of four members of the KChIP family of potassium channel beta subunits was examined in canine heart. Only one member of the gene family, KChIP2, was expressed in heart. There was a steep gradient of KChIP2 mRNA expression across the canine ventricular free wall. KChIP2 mRNA was 25-fold more abundant in the epicardium than in the endocardium, and this gradient paralleled the gradient in transient outward current (Ito) expression. In contrast, Kv4.3 potassium channel alpha subunit mRNA was expressed at equal levels across the ventricular wall. There was no difference in the pharmacological sensitivity of epicardial and endocardial Ito channels to flecainide, suggesting that the current is produced by the same channel in the two tissues. A similar gradient of KChIP2 expression was found across the ventricular wall of human heart, but not rat heart. It is concluded that transcriptional regulation of the KChIP2 beta subunit gene, rather than the Kv4.3 [alpha] subunit gene, is the primary determinant regulating the transmural gradient of Ito expression in the ventricular free wall of canine and human heart.

Animals↗

PubMed2001

Transmural differences in rat ventricular protein kinase C epsilon correlate with its functional regulation of a transient cardiac K+ current.

The effects of PKC activation on a transient (It) and a sustained (Iss) cardiac K+ current and the subcellular distribution of the epsilon isoform of PKC (PKC(epsilon)) were compared in epicardial and endocardial regions of the rat ventricle. Activation of PKC(epsilon) with a diacylglycerol analogue (di-octanoyl-glycerol (DiC8), 20 (mu)M) leads to differential effects in epicardial and endocardial cells. In epicardial cells (n = 20) It and Iss are attenuated by 17.7 +/- 2.1 % and 11.9 +/- 3.1 %, respectively (means +/- S.E.M.). In endocardial cells It attenuation was significantly smaller (4.6 +/- 1.6 %, n = 14, P < 0.0005). Iss attenuation was similar to that in epicardial cells (10.5 +/- 3.8 %). PKC[epsilon] expression was measured by Western blotting. Calculated endocardial/epicardial ratios showed no regional differences in total protein extracts (1.04 +/- 0.11, mean +/- S.E.M, n = 4), but PKC[epsilon] distribution in the cytosolic fraction showed a marked difference, with significantly (P < 0.05) higher levels in endocardial extracts. The cytosolic endocardial/epicardial PKC[epsilon] ratio was 2.64 +/- 0.24 (n = 4), indicating a reduced amount of PKC[epsilon] in the membrane fraction of the endocardium. This could account for the reduced effect of DiC8 on It in endocardial myocytes. Under both hypothyroid and streptozotocin-induced diabetic conditions the difference in endocardial and epicardial cytosolic PKC[epsilon] levels was absent (ratios of 0.86 +/- 0.21 (n = 4) and 1.09 +/- 0.16 (n = 3), respectively; means +/- S.E.M.). Ratios in the total protein extracts were not significantly different from those in control conditions. The results show transmural differences in the functional effects of PKC(epsilon) activation on a cardiac K+ current, and in the subcellular distribution of PKC(epsilon). These differences are absent in diabetic and hypothyroid conditions.

Animals↗

PubMed1979

Spontaneous termination of reentry ventricular tachycardia in the late myocardial infarction period: an experimental study in the dog.

Forty episodes of induced ventricular tachycardia in the late myocardial infarction period (4-6 days old) were analyzed in 12 dogs in an attempt to identify the possible mechanisms for the termination of reentry tachycardia. Multiple epicardial and endocardial composite electrograms were recorded in and around the central ischemic zone of the infarction. During tachycardia, the earliest site of activation was identified in the epicardial surface of the border or normal zone immediately adjacent to the ischemic zone in 36 of the 40 episodes, suggesting efferent epicardial spread from the site of the activity. In four instances, the efferent pathways were directed to the endocardial surface. Four distinct patterns of activation sequences were observed during spontaneous termination: (a) a shift of the efferent pathways from epicardial to endocardial site (19 instances); (b) a change of the efferent pathways within the endocardium (4 instances); (c) a shift of the earliest site of activation between the left and right ventricles (9 instances); and (d) no apparent change in the epicardial efferent pathways (4 instances). In four other instances, ventricular tachycardia deteriorated into ventricular fibrillation. In patterns (a) and (c), a shift of the efferent pathways resulted in a more rapid and homogeneous activation of the border and normal zone epicardium. These changes were associated with cessation of delayed or continuous activity in the ischemic zone epicardium, resulting in termination of tachycardia.

Animals↗

PubMed1984

Amaurosis fugax in a patient with a left ventricular endocardial pacemaker.

A transvenous left ventricular endocardial pacemaker catheter is a potential source of systemic arterial embolization. The case of a woman who presented with left-eye amaurosis fugax is reported. The patient had a history of contralateral carotid atherosclerosis; however, the digital subtraction angiography of the carotid arteries was not sufficiently abnormal to account for her present symptoms. The patient had a history of two myocardial infarctions and the tachycardia-bradycardia syndrome for which she was treated with a demand ventricular pacemaker. The chest x-ray and electrocardiogram suggested pacemaker catheter malposition. By M-mode and two-dimensional echocardiography, the catheter was shown to cross the atrial septum and the mitral valve to implant in the left ventricular endocardium. The approach to diagnosis and therapy that led to surgical removal of the pacing catheter is presented. The causes of the electrocardiographic right bundle branch block pattern in cardiac pacing and the usefulness of echocardiography in evaluating pacing catheters are discussed.

Aged↗

PubMed1997

Multipolar endocardial mapping of the right heart using a basket catheter: acute and chronic animal studies.

The development of catheter-based ablative techniques for primary atrial and ventricular arrhythmias is likely to be assisted by improved techniques for systematic endocardial activation sequence mapping. RA mapping using a multielectrode basket catheter has been shown to be feasible with minimal acute toxicity in a prior study. The objectives of the current study are to investigate: (1) the utility of the basket catheter for mapping RV activation; and (2) the evolution of acute endocardial lesions produced by basket catheter use in both the RA and RV over 4-8 weeks time. A flexible, 5-spoke basket catheter bearing 25 electrode pairs was placed in the RA (n = 9) or the RV (n = 13) in 22 juvenile sheep (22-56 kg). The catheter was deployed for 0.1-4.1 hr (RA) and 0.3-3.9 hr (RV). In 20 of these 22 animals, 32 recordings were made of filtered (30-250 Hz) bipolar electrograms and surface ECG. Electrograms were timed and used to construct activation sequences based on a schematic of catheter geometry. Hearts were examined either acutely (4 RA and 9 RV studies) or 4-8 weeks after the procedure (5 RA and 4 RV studies). One animal undergoing RA placement had an air embolism resulting in cardiac arrest immediately prior to basket placement; all other animals were stable during placement. RA electrograms of sufficient quality to determine activation time were recorded from 82% of pairs in RA maps, and RV electrograms from 89% of pairs in RV maps. Mean activation sequence duration in RV was 16 ms versus 47 ms in RA (P < 0.0001), making construction of RV maps more difficult. Acute postmortem studies of RV placement revealed a silent apical RV puncture in one animal. Superficial abrasion or ecchymosis of RV endocardium and/or tricuspid valve were noted in six animals. Postmortem exams in both RA and RV chronic studies showed healed endocardial lesions, with only superficial scarring. Rapid RV activation mapping using a basket catheter is feasible, but requires precision recording techniques. Endocardial abrasions produced in lambs both by RA and RV placement of the catheter are healed in < 4-8 weeks, with trivial residua. The multielectrode basket catheter may be applicable to the mapping of tachycardias originating in or involving the right ventricle.

Animals↗

PubMed1999

Localization of precise origin of idiopathic ventricular tachycardia from the right ventricular outflow tract by a 12-lead ECG: a study of pace mapping using a multielectrode "basket" catheter.

Radiofrequency catheter ablation guided by pace-mapping techniques has proven effective in eliminating idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT). A method for rapidly identifying the origin of VT from 12-lead electrocardiogram (ECG) findings would be helpful for the catheter ablation procedure. The purpose of this study is to precisely localize the origin of idiopathic VT from the RVOT by a 12-lead ECG from a study of multipoint pace mapping. In one patient with premature ventricular complex (PVC) and 3 with VT, a "basket" catheter was deployed in the RVOT for bipolar pacing from 56 sites in the endocardium of RVOT. Under fluoroscopy the pacing sites were classified into the septum and free wall. We investigated the QRS morphology in leads, I, II, and III; the depth of the QS wave in leads aVR and aVL; and the height of the initial r wave in leads V1 and V2. Pacing was captured in 30-47 of 56 sites (54%-84%). As the pacing sites changed from the anterior to posterior of the septum, the QS notch (-) type in lead I shifted through rs to R, while a shift from R type to rR' or Rr' was noted in leads II and III. As the pacing sites changed from the anterior to posterior of the free wall, lead I showed a shift from the QS notch (+) type to R, while a shift from rR' to Rr' (or rR' unchanged) was found in leads II and III. The depth of the QS wave in leads aVR and aVL showed a tendency for aVR to be deeper than aVL toward the posterolateral attachment of both the septum and free wall, whereas aVL tended to be deeper than aVR toward the anterior attachment. The initial r waves in V1 and V2 became greater as the pacing site was positioned at a higher or more posterior location. These findings may provide more precise and clinically useful diagnostic information on the site of the origin of idiopathic VT originating from the RVOT by a 12-lead ECG.

Adult↗