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 901 records · Page 50Linked to original sources
PubMed2006

Increased coronary flow may prolong transmural ventricular repolarisation.

An increase in spatial dispersion of ventricular refractory periods reflects inhomogeneity of ventricular refractoriness and is associated with an increased risk of life-threatening ventricular arrhythmias. Spatial dispersion in ventricular refractoriness is determined by the differences in refractory periods of myocytes in epicardium, mid-myocardium and endocardium. Prolongation of ventricular repolarisation with drugs or physical means may reduce the spatial dispersion and the risk of arrhythmia. An increase in coronary flow has been shown to prolong the duration of ventricular repolarisation measured from epicardium in the intact animal heart. We hypothesised that an increase in coronary flow may also prolong ventricular repolarisation cross the three layers of ventricular myocardium through the release of nitric oxide. The simultaneously prolongation of transmural repolarisation may reduce the spatial dispersion of ventricular repolarisation and hence, the risk of life-threatening ventricular arrhythmias.

Action Potentials↗
PubMed2005

Convergent proliferative response and divergent morphogenic pathways induced by epicardial and endocardial signaling in fetal heart development.

Heart development requires cardiomyocyte proliferation, coupled with morphogenic differentiation of the inner trabecular myocardium and the outer compact zone myocardium. In mouse embryos lacking the retinoic acid receptor RXRalpha, proliferation and morphogenesis of the compact zone fails. We demonstrated previously that epicardial cells, in response to retinoic acid, secrete an activity that promotes cell proliferation. In this study, we have investigated downstream signaling pathways that are elicited in response to this factor. We find that cells treated in culture activate PI3 kinase and Erk pathways, and that these are required for a proliferative response. In vivo, phosphorylation of Akt and GSK3beta (PI3K pathway) and of Erk1/2 and p90rsk (Erk pathway) is substantially reduced in RXRalpha-deficient heart tissue. Neuregulin, a mitogen secreted from the endocardium which promotes cardiomyocyte proliferation and trabecular differentiation, also activates proliferation via PI3K and Erk pathways. However, the epicardial factor is not neuregulin, and does not function via the neuregulin receptor. Gene markers known to be selectively expressed in trabecular or compact myocardium in vivo are differentially activated in cell culture by treatment with neuregulin or epicardial factor, and are misexpressed in RXRalpha(-/-) heart tissue. We therefore conclude that epicardial and endocardial signals converge on common proliferative components, but diverge in downstream pathways that lead to compact vs. trabecular morphogenic differentiation.

Animals↗
PubMed2006

NFATc1 expression in the developing heart valves is responsive to the RANKL pathway and is required for endocardial expression of cathepsin K.

NFATc1 is necessary for remodeling endocardial cushions into mature heart valve leaflets and is also an essential effector of receptor activator of NFkappaB ligand (RANKL) signaling required for transcriptional activation of bone matrix remodeling enzymes during osteoclast differentiation. Therefore, developing heart valves were examined to determine if NFATc1 functions in the RANKL pathway during leaflet remodeling. Key components of RANKL signal transduction including RANKL, its receptor RANK, and the downstream remodeling enzyme cathepsin K (Ctsk) are expressed in the heart during valve remodeling and colocalize with NFATc1 in developing valve endocardium. However, the absence of tartrate-resistant acid phosphatase (TRAP) activity and the lack of F4/80-positive macrophage lineage contribution to the remodeling valves demonstrate that certain aspects of osteoclast RANKL function are not shared during valve formation. Analysis of NFATc1-/- mouse embryos shows that NFATc1 is specifically required for endocardial expression of RANKL and Ctsk during valve formation. In addition, RANKL treatment augments expression of NFATc1 and Ctsk in embryonic heart cultures, and the RANKL-mediated increase in Ctsk expression is dependent on NFATc1. Together, these results support a role for RANKL signaling during heart valve development and suggest that valve leaflet morphogenesis involves NFATc1-dependent expression of remodeling enzymes including Ctsk.

Animals↗
PubMed2006

Evidence for cystic fibrosis transmembrane conductance regulator chloride current in swine ventricular myocytes.

The present study investigated whether cAMP-dependent cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel current (i.e., I(Cl.CFTR) or I(Cl.cAMP)) would be expressed in pig cardiac myocytes using whole-cell patch technique and reverse transcription polymerase chain reaction (RT-PCR). It was found that the beta-adrenoceptor agonist isoproterenol activated a time-independent current in myocytes from the ventricle, but not the atrium of pig heart. Histamine and forskolin (an adenylate cyclase activator) induced a similar current in pig ventricular cells. The current induced by isoproterenol was blocked by the PKA inhibitor H-7, reduced by the replacement of external Cl(-) ion, and inhibited by the application of 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), but not 4'-diisothiocynatostilbene-2,2'-disulfonic acid (DIDS), typical of I(Cl.CFTR). I(Cl.CFTR) showed a small difference in regional myocytes across the left ventricular wall from epicardium to endocardium. Isoproterenol-induced current was 3.1+/-0.2 (n=33), 2.8+/-0.2 (n=25) and 2.3+/-0.2 pA/pF (n=31) respectively in subepicardial, midmyocardial, and subendocardial myocytes (P<0.05, subepicardium vs. subendocardium). RT-PCR and Western blotting analysis revealed that significant differences in CFTR channel mRNA and protein levels were present in atrial and ventricular cells, but not in regional ventricular cells across the ventricular wall from subepicardium to subendocardium. These results indicate that the functional CFTR channel (i.e., I(Cl.CFTR)) is present in ventricular myocytes, but not in atrial cells of pig heart.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1976

Vascular and cardiac contractile reserve in the dog heart with chronic multiple coronary occlusions.

Nineteen mongrel dogs survived chronic occlusion of the left circumflex and of the right coronary artery without infarction due to the timely development of a collateral circulation. Only 38 per cent of the conductance of the arteries before occlusion was restored by collateral vessels. In these animals and in 15 control dogs with normal coronary arteries myocardial contractility, contractility reserve, and myocardial blood flow were studied. The same was done in dogs with chronic coronary artery occlusion after aortocoronary bypass. Myocardial blood flow was determined woth the tracer microsphere technique. Contractility reserve was tested and defined as isovolumetric left ventricular pressure and dp/dt max with norepinephrine infusion and cross-clamping of the aorta. Contractile reserve was not significantly different between normal dogs and dogs with chronic coronary artery occlusion before and after aortocoronary bypass. Myocardial blood flow during control conditions was homogenously distributed in all three groups studied. The ratio of blood flow to the endocardium and the epicardium was not significantly different from inity. Coronary reserve was determined at peak reactive hyperemia following a 20 second period of coronary artery occlusion, with ongoing norepinephrine infusion. Under these conditions subendocardial fow in normal dogs rose by a factor of 7.9 while subepicardial flow increased 7.4 times. In dogs with chronic occlusion of two coronary arteries the increase of myocardial flow was nonnomogenous; subendocardial flow to areas supplied by a normal coronary artery rose by a factor of 7.0 while subepicardial flow increased 5.7 times control. Subendocardial collateral flow rose by a factor of 2.4 and subepicardial collateral flow increased 3.5 times control. In normal dogs norepinephrine alone did not result in maximal coronary flow but only 57 per cent thereof. Dogs with chronic coronary occlusion, however, required the entire coronary reserve in areas that were supplied by a normal coronary artery, whereas areas supplied by collaterals became ischemic. Opening of an aortocoronary bypass restored normal flow to previously ischemic areas, and reduced the flow to areas supplied by a normal artery. With the bypass open no differences existed between normal dogs and those with two occluded coronary arteries. We conclude that the norepinephrine-stimulated contractile reserve of hearts with chronic coronary occlusion was comparable to that of normal hearts; however, norepinephrine forced these hearts to spend the entire flow reserve of the remaining normal artery while producing ischemia in collateral-dependent areas. The same dose of norepinephrine did not require the entire flow reserve of normal dogs.

Animals↗
PubMed1977

Cardiac pathology of transvenous pacemakers in dogs.

Transvenous right ventricular pacemaker catheters were implanted in 18 mongrel dogs for periods of 2 to 18 months (average 4.9 months). Heart block was produced in 15 of these dogs by injection of 37 per cent formaldehyde into the interatrial septum. In the other three dogs which served as controls, no heart block was produced and no electrical stimulation was applied to the implanted catheters. After the animals had been put to death, gross and microscopic examination of the hearts revealed four categories of morphological changes: (1) connective tissue sheath formation around the catheters, (2) endocardial papillary thickening, (3) interatrial septal changes, and (4) myocardial damage. Changes 1, 2, and 4 occurred in one or more intracardiac locations in all 18 dogs. Change 3 occurred only in the 15 dogs in which heart block was produced. The most striking histologic findings were areas of cartilagenous metaplasia in endocardium an underlying myocardium and areas of marked cellular proliferation of the endocardial cells both in the endothelium and underlying stroma. Chronic implantation of transvenous intracardiac pacemaker catheters in dogs consistently produces morphologic changes which may interfere with cardiac and pacemaker function and may hinder attempts to remove nonfunctional or unneeded catheter electrodes. The changes observed appear to be related to the presence of foreign material per se and not external electrical stimulation of the heart.

Animals↗
PubMed1983

Topographic changes in the left ventricle after experimentally induced myocardial infarction in the rat.

The factors that determine the thickness of transmural myocardial infarcts are unknown. Therefore, the relation between the size and thickness of transmural infarcts in 67 rats 21 days after occlusion of the left main coronary artery was studied. On examination of histologic sections, infarct size was determined by planimetry and expressed as a percentage of the left ventricular (LV) area, and thickness was expressed as a percentage of noninfarcted ventricular septal wall thickness. The circumferential length of the infarcted ventricle was measured in millimeters, as well as the circumferential length of the noninfarcted ventricular septum. Septal wall thickness was similar in rats with transmural infarcts and in sham-operated rats. No significant correlation was observed between infarct size and thickness (r = 0.10) or between circumferential length of the infarct and infarct thickness (r = 0.17). However, large (greater than or equal to 20% of the left ventricle, n = 37) and small (less than 20% of the left ventricle, n = 30) infarcts which were similarly thin (37 +/- 1% and 34 +/- 2% of septal wall thickness, respectively) affected LV topography differently. Large infarcts resulted in a 23% greater loss of myocardium (p less than 0.001), greater expansion of the LV cavity (18 +/- 9 mm2 compared with 14 +/- 1 mm2 in small infarcts, p less than 0.005), and lengthening of the septal wall (7.2 +/- 1.1 mm and 6.7 +/- 1.0 mm in large and small infarcts, respectively [p less than 0.05], and 6.3 +/- 0.1 mm in shams). Increase in cavity area and septal length in infarcted ventricles suggested a volume overload hypertrophy, which at 3 weeks was nonetheless inadequate to provide as much normal muscle as was present in sham-operated rats. In an additional 9 rats with subendocardial infarctions (involving less than 75% of the LV wall from endocardium to epicardium), the LV walls were thicker (94 +/- 5% of septal wall thickness, compared with 35 +/- 1% for transmural infarcts, p less than 0.001) and an inverse correlation was observed between infarct size and thickness. In conclusion, neither the size of a transmural infarct in rat nor the circumferential length of infarction determines the thickness of the infarct; however, infarct size does affect LV topography by increasing LV cavity area and the length of the noninfarcted septal wall. Subendocardial infarcts result in less myocardial thinning than do transmural infarcts.

Animals↗
PubMed1980

Endomyocardial fibrosis: report of 6 patients and review of the surgical literature.

Six patients with endomyocardial fibrosis were treated by endocardium decortication and atrioventricular valve replacement. There were 5 female patients and 1 male patient ranging from 14 to 48 years old (mean, 30 years). Four patients had involvement of the right ventricle, 1 patient had involvement of the left ventricle, and 1 patient had biventricular disease. There was 1 operative death due to low cardiac output state (the patient with biventricular endomyocardial fibrosis), and there was 1 late noncardiac death. The surgical literature, which describes 19 previously reported cases, was reviewed. On the basis of the results of this series and those of the reported cases, it is concluded that surgical treatment of endomyocardial fibrosis is feasible and provides good clinical improvement.

Adolescent↗
PubMed2001

Spatial alterations of Kv channels expression and K(+) currents in post-MI remodeled rat heart.

OBJECTIVE: The hypothesis being tested in the present study is that increased anisotropic properties occurs in the remodeled post-infarction heart due to spatial alterations in Kv channels expression and K(+) currents of the remodeled myocardium. METHODS: Three to 4 weeks post myocardial infarction (MI) in the rat, we measured the two components of the outward K(+) current, I(to-fast (f)) and I(to-slow(s)) in the epicardium (epi) and endocardium (endo) of noninfarcted remodeled left ventricle (LV) using patch clamp techniques. Alterations in mRNA and/or protein levels of potassium channel genes Kv1.4, Kv1.5, Kv2.1, Kv4.2 and Kv4.3 were measured in epi, midmyocardium (mid), and endo regions of LV and in the right ventricle (RV). RESULTS: In sham operated rat heart, the density of I(to-f) was 2.3 times greater in epi compared to endo myocytes. In post-MI heart, the density of I(to-f) and I(to-s) decreased to a similar degree in LV epi and endo but the difference in I(to-f) density between epi and endo persisted. The mRNA and/or protein levels of Kv1.4, Kv2.1, Kv4.2 and Kv4.3 but not Kv1.5 decreased to a varying extent in different regions of LV but not in RV of post-MI heart. CONCLUSIONS: Our results suggest that regional downregulation of Kv channels expression and density of K(+) currents can be a significant determinant of increased spatial electrophysiological heterogeneity and contribute to increased electrical instability of the post-MI heart.

Analysis of Variance↗
PubMed2002

Effects of gonadal steroids on gender-related differences in transmural dispersion of L-type calcium current.

OBJECTIVES: Repolarization-prolonging drugs induce torsades de pointes (TdP) in females more than males. The action potential plateau and the early afterdepolarizations that induce TdP are determined, in part, by L-type calcium current (I(Ca,L)). Therefore, we studied gender- and hormone-related differences in I(Ca,L) in age-, and weight-matched normal male, female and hormonally-treated, castrated rabbits. METHODS: Oophorectomized (OVX) or orchiectomized (ORCH) 50- to 60-day-old rabbits were subcutaneously implanted with pellets impregnated with placebo (PLA), 5 alpha-dihydroxytestosterone (DHT), or 17 beta-estradiol (EST). Four to five weeks later, epicardial and endocardial myocytes were isolated from the left ventricle. Patch clamp technique was performed to assess I(Ca,L). RESULTS: I(Ca,L) density (measured as peak current density [pA/pF] at +15 mV, V(h)= -40 mV), was greater in female epicardium (-7.4 +/- 0.9) than endocardium (-5.6 +/- 0.7, P<0.05), while male epicardial I(Ca,L) density (-6.5 +/- 0.7) did not differ from endocardial (-5.9 +/- 1.0, P>0.05). OVX-female, DHT and EST-treated groups had epicardial I(Ca,L) density (-5.6 +/- 0.6, and -5.9 +/- 0.7, respectively) greater than endocardial (-4.3 +/- 0.3, and -3.6 +/- 0.4, P<0.05). However, OVX-females had hormone levels not significantly different from female controls and EST-treated females had non-physiological levels of estradiol. There were no differences between endocardial and epicardial I(Ca,L) activation and inactivation. In contrast, epicardial-endocardial differences in I(Ca,L) density in EST-treated OVX-females were associated with epicardial-endocardial differences in I(Ca,L) activation and conductance; in DHT-treated OVX-females only epicardial-endocardial activation differed. The other groups, showed no I(Ca,L) transmural gradient, or differences in activation, inactivation or conductance. CONCLUSIONS: The greater dispersion in I(Ca,L) density of OVX-DHT and OVX-EST than OVX-PLA suggests both hormones can modulate I(Ca,L) density in females. That gonadal steroids had no effect on I(Ca,L) dispersion in males suggests gender differences in mechanism of action of both hormones. The greater I(Ca,L) dispersion in females may contribute to gender differences in repolarization.

Analysis of Variance↗
PubMed1999

Differences in the electrophysiologic response of four canine ventricular cell types to alpha 1-adrenergic agonists.

OBJECTIVE: The present study was designed to examine regional differences in the response of alpha 1 adrenoceptor stimulation in the canine ventricle. METHODS: Standard microelectrode techniques were used to record transmembrane action potentials from epicardial, M cell, and endocardial as well as Purkinje fiber preparations isolated from the canine left ventricle. RESULTS: Phenylephrine (0.1-10 microM+ propranolol 0.2 microM) and methoxamine (1-10 microM) produced dose- and rate-dependent prolongation of action potential duration (APD90) in Purkinje fibers (P < 0.05, at 0.1-10 microM, BCL = 0.5-2 s), but an abbreviation of APD90 in tissues from the M region (P < 0.05, at 10 microM, BCL = 0.5-2 s). At slow pacing rates (> or = 2 s), phenylephrine (1 microM) exerted a small, significant (P < 0.05) prolongation of APD90 in epicardium and endocardium which returned to control values when the concentration was increased to 10 microM. The amplitude of phase 1 of the action potential in M and epicardial cells was significantly increased by phenylephrine at concentrations of 10 microM (P < 0.05). Prazosin (1 microM), a nonspecific alpha 1 antagonist, reversed these effects of phenylephrine (10 microM) and methoxamine (10 microM) on APD90 and the action potential notch. The alpha 1b-antagonist, chloroethylclonidine (0.1-1.0 microM), but not the alpha 1a-antagonist, WB-4101 (0.1-1.0 microM), reversed the APD-abbreviating effect of methoxamine in the M cell. CONCLUSION: Our results demonstrate striking regional differences in the electrophysiological response of the four canine ventricular cell types to alpha 1 adrenergic agonists. Our data provide support for the hypothesis that different adrenoceptor subtypes underlie the opposite response of M cells (alpha 1b-APD abbreviation) and Purkinje fibers (alpha 1a-APD prolongation) to alpha 1-adrenoceptor activation.

Action Potentials↗
PubMed2000

M cells and transmural heterogeneity of action potential configuration in myocytes from the left ventricular wall of the pig heart.

OBJECTIVE: Heterogeneity of action potential configuration in the left ventricle (LV), and the contribution of M cells to it, has been observed in the human heart and is important for arrhythmogenesis. Whether the pig heart has similar properties remains a controversial but important issue as the pig heart is currently under study for use in xenotransplantation. METHODS: Single myocytes were enzymatically isolated from the epicardium (EPI, ncells = 29), midmyocardium (MID, ncells = 38), and endocardium (ENDO, ncells = 13) of the free LV wall (npigs = 26, 14-22 weeks old, 55-80 kg), and studied at different stimulation rates during whole-cell recording (normal Tyrode's solution, K(+)-aspartate-based pipette solution, 50 microM K5fluo-3 as [Ca2+]i indicator, 37 degrees C). Standard six-lead ECGs were recorded from anesthetized pigs. RESULTS: The action potential duration (APD) was not significantly different at 0.25 Hz vs. 2 Hz for the majority of cells in all three layers. However, a subpopulation of cells behaved like M cells and had a very steep frequency response (APD90 at 0.25 Hz 538 +/- 30 ms, vs. 337 +/- 9 ms at 2 Hz, P < 0.05, n = 22). These cells were found predominantly in the MID layer (34% of cells), but also (24%) in EPI. M cells had a more pronounced spike-and-dome configuration, with a significantly larger phase 1 magnitude and plateau voltage. The frequency response of these parameters was different from the other cell types. [Ca2+]i transients tended to be larger in M cells. For the in vivo ECG of anesthetized pigs, the QT time was close to the APD90 of M cells, and J waves were seen in 7/12 recordings. CONCLUSIONS: In young adult pigs, M cells can be identified by a steep frequency response of the APD and by a spike-and-dome configuration. These cells are mostly, but not exclusively, found in the midmyocardium, and could contribute to the ECG characteristics. Their properties may however be different from those of other species, including humans.

Action Potentials↗
PubMed1999

Isoforms of cytochrome P450 on organic nitrate-derived nitric oxide release in human heart vessels.

Glutathione S-transferases and the cytochrome P450 system have been proposed for the vascular biotransformation systems in the metabolic activation of organic nitrates. The present study was designed to elucidate the role of human cytochrome P450 isoforms on nitric oxide formation from organic nitrates using lymphoblast microsomes transfected with human CYP isoforms cDNA. CYP3A4-transfected microsomes had the most effective potential of nitric oxide formation from isosorbide dinitrate. Anti-CYP3A2 antibody (which cross-reacts with CYP3A4) or ketoconazole (an inhibitor of the CYP3A superfamily) inhibited nitric oxide formation from isosorbide dinitrate in rat heart microsomes. Immunohistochemistry of human heart also showed intense bindings of CYP3A4 antibody in the endothelium of the endocardium and coronary vessels. These results suggest that the CYP3A4-NADPH-cytochrome P450 reductase system specifically participates in nitric oxide formation from isosorbide dinitrate.

Animals↗
PubMed1981

Cardiovascular alterations induced by chronic transvenous implantation of an automatic defibrillator electrode catheter in dogs.

Six dogs (three large, three small) had defibrillator electrode catheters implanted transvenously via the right jugular vein for 17 weeks. The dogs remained healthy throughout the study. At necropsy, the lead-induced cardiovascular alterations were characterized by (1) formation of a thin white fibrous sheath over portions of the lead along its course in the veins, right atrium and right ventricle; (2) adhesion of parts of the sheathed segments of the lead to the adjacent venous intima or endocardium of the right atrium, tricuspid valve and right ventricle; (3) endocardial fibrosis with foci of cartilaginous metaplasia in areas traumatized by the lead; (4) thrombus formation at ends of sheathed segments of the lead but lack of pulmonary embolism; and (5) partial penetration of the myocardium at the apex of the right ventricle by the end of the lead in two of the small dogs. The lead-induced lesions were similar in type and severity to those produced by chronically-implanted pacemaker leads.

Animals↗
PubMed1986

Magnitude and location of a dipole in a circular ring with non-insulating boundaries.

It was shown that the resultant dipole moment of a system of sources and sinks within a region can be found from integrations of potential and potential gradient or normal current over the surfaces bounding the region. The method was applied in two dimensions to the case of a dipole in an infinite medium of one resistivity outside a circle having a different resistivity. The results agree with the Brody theory in that potentials at remote points due to a radial dipole were increased and potentials due to tangential components were decreased. Potentials on and within the circle are more complicated, however. For a radial or oblique dipole, potentials on the "endocardium" are increased in some areas but reduced at others. In addition, the effects are non-linear, depending on the distance of the dipole from the circle. Neglecting the effects of the low resistance circle leads to false values of dipole moment. When the integrations of potential and potential gradient are used, however, accurate values of dipole moment are obtained. The low-resistivity disk makes a radial dipole appear more centric but a tangential dipole appear further away.

Electrocardiography↗
PubMed1998

A comparison of simulated QRS isointegral maps resulting from pacing at adjacent sites: implications for the spatial resolution of pace mapping using body surface potentials.

The precise localization of ventricular tachycardia (VT) foci is a prerequisite for the successful radiofrequency catheter ablation in patients. The purpose of this study was to systematically quantify over what distance adjacent sites in the right ventricular (RV) and left ventricular (LV) epicardium and LV endocardium could be distinguished by inspecting morphological features of QRS isointegral maps using statistical methods. We investigated the spatial resolution of QRS isointegral maps by means of an anatomically accurate computer model of the human ventricular myocardium that incorporates a bidomain model for simulating the realistic activation sequences and the oblique dipole model in combination with the boundary element method for calculating extracardiac potentials. In this model, we initiated activation sequences at a total of 183 epicardial and 75 LV endocardial pacing sites, positioned in three levels (basal, middle, and apical). For each of the 258 pacing sites, we calculated a set of 10 QRS isointegral maps with added Gaussian noise at 117 leads (covering the anterior and posterior torso) and at 32 leads (covering only the anterior torso), respectively. Sets of maps were then cross correlated and root-mean-square (RMS) values of difference maps were calculated for all possible pairs of pacing sites on the same level. We applied the nonparametric unpaired Kolmogorov-Smirnov test and defined the spatial resolution as the pacing site separation at which the differences in correlation coefficients and RMS differences were significant (level P < .05). We observed significant differences in maps when the distances between pacing sites were on average (+/- SD) greater than 4.3 +/- 1.0 mm. In more than 90% of pacing sites, the significant differences in maps were observed within 4 mm even when using a 32-lead mapping system. The findings of our study provide theoretical evidence that QRS isointegral maps may offer noninvasive means for preinterventional planning of the ablative treatment in localizing both endocardial and epicardial sites of origin of VT.

Body Surface Potential Mapping↗
PubMed1995

Postinfarction ventricular septal rupture: repair by endocardial patch with infarct exclusion.

A novel operative technique for postinfarction ventricular septal defect has been used in 44 consecutive patients. The operation consists of excluding rather than excising the infarcted septum and ventricular walls. This is accomplished by performance of a left ventriculotomy through the infarcted muscle and securing a glutaraldehyde-fixed bovine pericardium patch to the endocardium of the left ventricle all around the infarcted myocardium. The ventriculotomy is simply closed over the pericardial patch. There were 21 men and 23 women whose mean age was 69 +/- 7 years. Twenty-nine patients were in cardiogenic shock at the time of operation. All patients had Doppler echocardiography and coronary angiography before operation. All but two patients were operated on during the acute phase of the myocardial infarction. There were six operative deaths. Postoperative complications included renal failure in 10 patients and respiratory failure in 18. Severe right ventricular dysfunction was the only independent predictor of operative mortality. Patients have been followed up for a mean of 40 +/- 34 months. There have been six late deaths and three of these were because of cardiac problems. The actuarial survival at 6 years was 66% +/- 7%. Only one patient had a small residual ventricular septal defect. Late postoperative assessment of ventricular function by echocardiography revealed that most patients had normal or mild impairment of right ventricular function and mild or moderate impairment of left ventricular function. Repair of acute postinfarction ventricular septal defect by endocardial patch with infarct exclusion of the left ventricule probably avoids additional damage to the right ventricle, remodels the acutely infarcted left ventricle, and enhances survival.

Aged↗
PubMed1975

Pathogenesis of fungal infection on heart valve prosthesis.

Four patients with heart valve prostheses developed Candidate endocarditis. At autopsy the foci of infection were confined to patches of neoendocardium that appeared to have developed as ingrowths of host endocardium onto the sewing cloth of the artificial valve. This suggested that one mechanism of fungal infection is related to the presence of the neoendocardium rather than to the cloth or metallic substances of the valve itself. Future studies might be directed toward inhibiting the development of the neoendocardium or to agents preventing its susceptibility to infection.

Adult↗