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PubMedDate not supplied

Case report of a Quilty lesion within a coronary artery.

The Quilty lesion is the moniker of a lymphoid proliferation that resides predominantly in the endocardium and underlying myocardium within transplanted hearts. It has been described in the endocardium, myocardium, and epicardium. Although its pathogenesis is not understood, it is generally considered that the Quilty lesion is not a manifestation of acute rejection. However, its clinical significance and relation to acute rejection, such as its pathogenesis, are still not completely understood. Immunohistochemical studies distinguish between the cellular infiltrates of Quilty lesions and those associated with acute rejection. We describe, what we believe to be, the first case of a Quilty lesion in an epicardial coronary artery from an 8-year-old girl with congenital heart disease who required retransplantation 25 months after her cardiac transplantation for severe graft coronary artery disease. The lesion consisted of an intramural nodular aggregate of numerous T and B lymphocytes, with fewer macrophages, characteristic of a Quilty lesion.

Child↗

PubMed2004

A field of myocardial-endocardial NFAT signaling underlies heart valve morphogenesis.

The delicate leaflets that make up vertebrate heart valves are essential for our moment-to-moment existence. Abnormalities of valve formation are the most common serious human congenital defect. Despite their importance, relatively little is known about valve development. We show that the initiation of heart valve morphogenesis in mice requires calcineurin/NFAT to repress VEGF expression in the myocardium underlying the site of prospective valve formation. This repression of VEGF at E9 is essential for endocardial cells to transform into mesenchymal cells. Later, at E11, a second wave of calcineurin/NFAT signaling is required in the endocardium, adjacent to the earlier myocardial site of NFAT action, to direct valvular elongation and refinement. Thus, NFAT signaling functions sequentially from myocardium to endocardium within a valvular morphogenetic field to initiate and perpetuate embryonic valve formation. This mechanism also operates in zebrafish, indicating a conserved role for calcineurin/NFAT signaling in vertebrate heart valve morphogenesis.

Animals↗

PubMed2005

The architecture of the ventricular mass and its functional implications for organ-preserving surgery.

It has generally been accepted that the myocardial fibres within the ventricular mass are arranged in syncytial fashion, precluding the identification of discrete and isolated muscular pathways. Recently, however, an entire hypothesis for surgical treatment has been proposed on the basis of the existence of a 'ventricular myocardial band', suggesting that this arrangement in itself points to detrimental results following partial ventriculectomy. In this review, we re-state the evidence supporting the accepted concept of the ventricular mass being made up of an undefined number of wedge-shaped functional units, each of them exerting its individually programmed contribution to the global activity of the ventricular walls. The wedge-shaped units consist of bundles of individual fibres which are arranged tangentially. An important subset of fibres intrudes into the ventricular wall, thus creating oblique pathways. Their angle of intrusion varies, and can be measured at up to 30 degrees . The steeper the angle of their intrusion, the more efficiently do the fibres counteract the systolic mural thickening. The network of supporting connective tissue, nonetheless, provides the necessary steep angulation towards the endocardium. This fibrous matrix serves as continuous chain for the transmission of forces, including that in the direction from the epicardium towards the endocardium, resulting in a dilating force. We have shown, using needle force probes, that in the hypertrophic heart the dynamic equilibrium of dilating and constricting forces acts at elevated diastolic and systolic levels, because the obliquity of the fibres increases due to the thickening of the wall, and there is a concomitant increase in connective tissue, causing an increase in the forces opposing systolic mural thickening. Then, in a vicious cycle, both populations of myocardial fibres stimulate each other to hypertrophy. Eventually, coronary perfusion becomes critically impaired, with still further deposition of connective tissue. Ultimately, the vector of the dilating force comes to dominate the constricting force, and the ventricle dilates. In this setting, partial left ventriculectomy remains a functionally sound intervention, since it is capable of improving global ventricular function by improving the geometrical state of the remaining anatomic myocardial units.

Biomechanical Phenomena↗

PubMed2005

Surgical treatment of atrial fibrillation with diathermy: an in vitro study.

OBJECTIVE: The utilization of diathermy (electrocautery) as an energy source in the treatment of chronic atrial fibrillation has generated positive early clinical results. Although this technology is available and affordable, it has not been well studied for this indication. The objectives of this study were: (1) to characterize atrial lesions created by diathermy, (2) to determine relationships between power setting, tissue contact time, and lesion depth and (3) to histologically compare diathermy and unipolar radiofrequency lesions. METHODS: Fresh bovine atrial tissue samples were used to create endocardial lesions using a unipolar diathermy system with a blade tip. A total of 120 lesions were created at varying power settings and tissue contact times. Subendocardial temperatures were recorded. All lesions were examined grossly, then fixed, sectioned and evaluated histologically by a blinded pathologist. Comparisons were made with saline irrigated unipolar radiofrequency lesions. RESULTS: Gross examination revealed extensive tissue destruction of the endocardial surface at the point of contact. Histological examination showed minimal penetrance of the lesions beyond the destroyed tissue margin of the endocardium. This was corroborated by the finding of minimal thermal penetration beyond the endocardium and superficial myocardium. There was a linear relationship between the power setting (15-55 watts), depth of penetrance (2-15 mm) at varying contact times (1-5s/cm). CONCLUSIONS: In this in vitro model, lesions created by diathermy were not transmural, even with high power settings and prolonged contact times. At these settings, significant tissue destruction was observed that may predispose to atrial perforation without achieving penetration. Diathermy did not constitute an effective energy source in the creation of transmural lesions for atrial fibrillation ablation.

Animals↗

PubMed2006

Regional variation in mRNA transcript abundance within the ventricular wall.

Previous studies have shown that regional variation in ion channel gene expression contributes to electrical heterogeneity within the walls of the cardiac ventricles. To map the extent of regional variation in gene expression in the ventricular walls and to begin to understand its genesis we have performed a microarray analysis of gene expression in the epicardial and endocardial tissues of the rat adult left ventricle. While the vast majority of the genes are expressed at uniform levels across the ventricular wall, a total of 36 transcripts (representing less than 0.1% of the genes expressed in the ventricle) are expressed more abundantly in either epicardium or endocardium. One of these differentially expressed genes is the sodium channel gene Scn5a, which is expressed at higher levels in the endocardium than in the epicardium of rat heart. The transcription factor genes Irx3, Irx5 and Etv1 were found to be expressed in transmural gradients across the ventricular wall of rat heart and also of canine heart. The Irx3 and Irx5 genes were expressed in an inverse pattern to that of the Kcnd2 (Kv4.2) gene in rat heart, suggesting that these transcription factors may act as negative regulators of Kcnd2 expression in vivo.

Animals↗

PubMed2003

Intra-atrial temperatures in radiofrequency endocardial ablation: histologic evaluation of lesions.

BACKGROUND: Because of the limited information on the effects of ablation in human tissues, we studied intra-atrial temperatures during endocardial radiofrequency applications. We correlated the intra-tissue temperatures with the tissue thickness and with the histologic appearance of the lesions. METHODS: Radiofrequency currents were delivered to human atrial tissue, simulating conditions in endocardial ablation during surgery at set temperature of 70 degrees and 80 degrees C, and intra-tissue temperatures were measured with thermocouples. Radiofrequency applications at 70 degrees C were performed in patients undergoing mitral valve surgery and biopsy specimens were obtained. Samples from in vitro studies and from patients were assessed histologically. RESULTS: The subepicardial temperatures were usually over 60 degrees C in applications in vitro at 70 degrees C and over 70 degrees C in applications at 80 degrees C. Values were higher when the interior of the tissue was warmer than its surface as a result of consecutive radiofrequency applications over the same area. Histologic examination of 12 in vitro samples showed that 10 had transmural lesions. Five of 10 samples from patients with mitral valve surgery had lesions confined to the endocardium, 3 had damaged variable portions of the myocardium, and 2 had transmural lesions. CONCLUSIONS: Although it is possible to obtain transmural lesions in vitro and in vivo with endocardial applications at 70 degrees C, it is significantly more difficult to achieve transmural lesions in patients with mitral valve disease than in normal atrial tissue in vitro. Consecutive applications can raise the intra-tissue temperatures to values significantly higher than those used for application. Our findings suggest that the composition of the endocardium and of the myocardium is a major determinant in lesion formation.

Aged↗

PubMed2000

Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions.

OBJECTIVES: Left ventricular hypertrophy (LVH) has been reported to produce differential electrophysiological effects in isolated epicardial and endocardial cells. This study aimed to examine regional electrophysiological effects of LVH in normal and ischaemic conditions in the whole heart. METHODS: LVH was secondary to perinephritis-induced hypertension. Monophasic action potential duration (MAPD(90)), effective refractory period (ERP) and conduction delay were measured in paced, isolated working rabbit hearts either at one right ventricular and two left ventricular sites (apical and basal epicardium) or at three left ventricular sites (apical and basal epicardium, apical endocardium). The hearts were subjected to 30 min of regional ischaemia and 15 min of reperfusion. RESULTS: In non-ischaemic conditions, LVH produced uniform prolongation of MAPD(90) and ERP in the left ventricular epicardium, but not in the endocardium. After coronary artery occlusion, LVH significantly increased ischaemia-induced transepicardial dispersion of repolarisation, but not refractoriness. LVH did not affect arrhythmogenesis in either non-ischaemic or ischaemic conditions. CONCLUSIONS: Differential effects of LVH on epicardial and endocardial electrophysiological parameters are also observed in the whole heart. In addition, the sensitivity of hypertrophied myocardium to ischaemia is increased and leads to an increase in ischaemia-induced dispersion of repolarisation. However, neither dispersion of refractoriness nor arrhythmogenesis are affected by LVH in non-ischaemic or ischaemic conditions in this experimental model.

Action Potentials↗

PubMed1983

Effects of hyperkalemia on local changes of repolarization duration in canine left ventricle.

The effect of hyperkalemia on the distribution of ventricular repolarization properties was investigated using the interval between minimum QRS and maximum T derivatives of multiple electrograms as a measure of local repolarization duration. Local repolarization duration decreased, with more marked reduction at the epicardium than endocardium near the base, and greater decrease at the endocardium than epicardium near the apex. The nonhomogeneous reduction of repolarization duration helps account for T waveform changes due to hyperkalemia and may be a factor in the occurrence of re-entrant ventricular arrhythmias.

Animals↗

PubMed1987

Influence of the mesenchymal microenvironment on myocardial and endocardial cell behaviour in experimental interaction with chick limb mesenchyme.

In an attempt to clarify the possible influence of the mesenchymal microenvironment in the differentiation of myocardial and endocardial cells, an "in vivo" transplantation experiment was performed in which the ventricular region of the heart (chick or quail) was placed in close association to the mesenchyme of the anterior chick limb to create an experimental interaction between myocardium and foreign mesenchyme. The results showed that after 48 h of tissue interactions the ventricular myocardium is incorporated into the mesenchyme of the anterior chick limb, changing its organization and cytological appearance. The myocytes tend to dissociate, exhibiting a less organized myofibrillar pattern. In addition, abundant extracellular matrix components made up of granular and fibrillar material were observed associated with the myocardial and the mesenchymal cell membranes as well as distributed in their surrounding microenvironment. The endocardium became discontinuous, due to detachment of the cells and emitted multiple pseudopodia and filopodia. These observations indicate that the mesenchyme from the anterior chick limb modifies the cellular behaviour and organization of the neighbouring myocardium and endocardium with which it interacts. We suggest that this might occur through participation of extracellular matrix components such as glycosaminoglycans, fibronectin and collagen which are known to act as macromolecular mediators in cell to cell interactions, cell migration and differentiation.

Animals↗

PubMed1990

Histomorphologic characteristics of endomyocardial fibrosis: an endomyocardial biopsy study.

Endomyocardial biopsies from right, left, or both ventricles were performed in 13 angiographically documented cases of endomyocardial fibrosis. The endocardium was appreciably thickened due to acellular hyalinized collagen tissue in all cases. Variable amounts of elastic tissue intimately admixed with fibrous tissue were recognized. A "zonal layering" pattern of the endocardium was absent. Thrombus, inflammatory cells, and granulation tissue at the endomyocardial interphase, and eosinophils within the biopsy were not seen. In addition, lymphomononuclear interstitial inflammatory infiltrates were seen in five cases.

Adolescent↗

PubMed1997

Expression of fibrinolytic antigens in redistributed cardiac mast cells in auricular thrombosis.

Recent data suggest that auricular thrombosis is associated with an increase and accumulation of mast cells (MC) in the subendothelial region of the upper endocardium. However, the molecular basis and the functional role of MC in this process are not known. In the current study, expression of fibrinolytic and antifibrinolytic antigens in human cardiac MC was analyzed by immunohistochemistry. MC were found to react with antibodies against tissue-type plasminogen activator (tPA) and urokinase receptor (uPAR/CD87), but not with antibodies against urokinase (uPA) or plasminogen activator inhibitors (PAI-1, PAI-2). Significant changes were observed when the phenotype of accumulated MC in the upper endocardium in patients with auricular thrombosis was compared with the phenotype of myocardial MC in the same patients or with MC in normal hearts. These redistributed MC stained less intensely with antibodies against tPA and chymase but retained their staining for tryptase and uPAR. Together, these data indicate that cardiac MC are a source of fibrinolytic antigens and that accumulation of MC in auricular thrombosis is associated with phenotypic changes of MC and loss of cellular tPA. It is hypothesized that MC and their products may play a role in endogenous fibrinolysis in auricular thrombosis.

Antifibrinolytic Agents↗

PubMed1998

New concept in echocardiography: harmonic imaging of tissue without use of contrast agent.

BACKGROUND: Endocardial border detection is important for echocardiographic assessment of left-ventricular function. Second harmonic imaging of contrast agents enhances this border detection. We discovered that harmonic imaging improves tissue visualisation even before contrast injection. We therefore sought objectively to demonstrate the degree of enhancement of endocardial and myocardial visualisation. METHODS: An ATL HDI-3000 scanner with software for contrast harmonic imaging was used to record short-axis images of the left ventricle in 27 patients with possible myocardial disease and 22 controls, in the fundamental mode and with harmonic imaging. A computer program measured the relative grey-scale values within six segments of the endocardium and myocardium. An Acuson Sequoia scanner equipped with software for tissue harmonic imaging was used to investigate the reproducibility of ejection-fraction calculations in 22 patients with ischaemic heart disease. FINDINGS: Harmonic imaging produced brighter endocardium within each segment. Relative to the mean grey value of the total imaging sector, the values for harmonic and fundamental imaging were 171.5 vs 85.6% (p<0.0001) in end diastole and 194.1 vs 106.7% (p<0.0001) in end systole. Results for the myocardial segments were also significantly better for harmonic imaging. Structure enhancement of similar magnitude was seen among patients and healthy controls. Use of harmonic imaging reduced the proportion of unacceptable images by 14-46% in different views and improved the reproducibility of biplane ejection-fraction measurements. INTERPRETATION: In comparison with fundamental imaging, the relative endocardial and myocardial brightness is enhanced by harmonic imaging.

Aged↗

PubMed2002

Midwall myocardial shortening in athletic left ventricular hypertrophy.

BACKGROUND: Patients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown. METHODS: Forty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects. RESULTS: Left ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P<0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P<0.05 compared with groups 1 and 2). CONCLUSION: Subjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.

Adult↗

PubMed1984

Endocardial fibroelastosis. Clinico-pathological study of 38 cases.

A clinico-pathological study was carried out based on 38 autopsies of patients with endocardial fibroelastosis ( EFE ): 82% of the cases were below the age of one year. The primary EFE was established in 21 (55%) of the cases, and in the last 17 (44%) it was associated with different congenital heart malformations (secondary EFE ). Different pathological conditions during pregnancy were present in 24% of the cases. Most often the left ventricle and atrium were involved, but in most of the cases the endocardium of the right cardiac chambers appeared by histological examination to be also affected. The varying morphological pictures of the heart suggest that EFE is a reaction of endocardium to different damaging factors.

Adult↗

PubMed2002

Endocardial wave front organization during ventricular fibrillation in humans.

OBJECTIVES: This study was designed to characterize the organization of ventricular fibrillation (VF) on the endocardium of humans. BACKGROUND: Most proposed mechanisms for the maintenance of VF postulate the propagation of a number of activation wave fronts that reenter to maintain the arrhythmia. We tested the hypothesis that, in patients undergoing internal cardioverter-defibrillator implantation, VF consists primarily of a few large wave fronts on the endocardium. METHODS: Electrograms were recorded from a 36-electrode catheter in the left ventricle of 16 patients during VF. Activation times were chosen for a 2-s epoch for each fibrillation episode, and a two-dimensional Kolmogorov-Smirnov test was performed to determine if activation occurred randomly along the catheter over that time interval. The maximum cross-correlation was found for all possible pairs of electrodes on the catheter, and these values were plotted relative to the distance between the two electrodes. An exponential curve was then fit to the data, and a length constant was determined. Activation times were grouped into wave fronts along the catheter, and the lengths of the wave fronts were estimated. RESULTS: The Kolmogorov-Smirnov test showed that activation was not random along the catheter in any of the patients studied. The correlation length determined was 9 +/- 2 cm. The number of wave fronts recorded by the catheter was 9.2 +/- 2.9 wave fronts/s. The length of the pathway of each wave front along the catheter was 6.5 +/- 4.5 cm. CONCLUSIONS: Ventricular fibrillation is well organized on the endocardial surface of humans, consisting primarily of a few large wave fronts on the order of 6 to 9 cm.

Adult↗

PubMed1986

Thermal effects of laser and electrical discharge on cardiovascular tissue: implications for coronary artery recanalization and endocardial ablation.

To determine the thermal responses of cardiovascular tissues to laser and electrical ablation, and to characterize the effects of different superfusing media and temperatures on target tissue temperatures and resulting extent of tissue injury, 184 laser and 15 electrical discharges were delivered to segments of human and canine aorta and canine ventricular endocardium. Tissue temperatures were measured 2 mm from the point of contact of laser fiber tip and tissue. When superfusing media consisted of whole blood or plasma at room temperature, a standard 40 J laser discharge caused peak arterial temperatures to rise 29.2 +/- 1.6 degrees C and 30 +/- 1.4 degrees C, respectively; however, tissue cooling was significantly slower in blood than in plasma. When saline solution was superfused, tissue temperatures rose by 11.4 +/- 2.2 degrees C, and tissue cooling occurred significantly faster than with either plasma or blood. The dimensions of the resulting aortic lesions were larger when blood (1.69 +/- 0.26 mm) was superfused than when plasma (1.39 +/- 0.04 mm) or saline (0.77 +/- 0.13 mm) was superfused (p less than 0.0001). Similar findings were observed with ventricular endocardium using blood or saline as the superfusing medium. In arterial tissue, superfusion with cold blood or saline solution resulted in lower peak temperature elevations (22 +/- 3.8 degrees C and 13.5 +/- 1.3 degrees C, respectively) and faster tissue cooling after laser discharge. Corresponding aortic lesion sizes were significantly smaller (1.4 +/- 0.03 and 0.5 +/- 0.02 mm, respectively) than when blood or saline medium was superfused at room temperature (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

A nonflow basis for the vulnerability of the subendocardium.

The functional consequences of a transmural gradient of metabolism in the heart were studied in 19 dogs. The technique of retrograde blood flow diversion after coronary occlusion was used to deplete the ischemic myocardium of blood flow. Blood flow was uniformly and equally depleted in all layers, averaging 0.044 ml/min per g. With oxygen supply a controlled variable, transmural differences in metabolic demand can be addressed. In groups of dogs severe myocardial ischemia was induced for periods of 20 to 90 minutes. No necrosis was noted after 20 minutes of ischemia. Beginning at 30 minutes of blood flow depletion, necrosis progressed from the endocardium toward the epicardium in a "wave front" pattern. At 90 minutes of ischemia, approximately 70% of the area at risk was necrotic. Thus, the relative vulnerability of the endocardium as compared with the epicardium is due to nonflow factors, and probably dictated by transmural differences in metabolic activity. It would appear that myocardial metabolism as compared with blood flow occupies a primary and overriding role during the first 20 minutes of ischemia. Furthermore, differences in transmural metabolism also dictate subendocardial vulnerability for ischemic periods greater than 20 minutes, irrespective of blood flow. The role of blood flow in these events may be to modulate the rate of the transmural wave front of progressing necrosis after 20 minutes of ischemia.

Animals↗

PubMedDate not supplied

The histopathology of endocardial sclerosis.

This histological study of endocardial thickening in human hearts revealed that as in adult hearts, the proliferation in fetal, neonatal, and infant hearts consisted of collagen, elastin, and smooth muscle cells. Variation in severity from chamber to chamber and site to site indicated that severity is not an aging phenomenon and that predominantly local blood flow conditions determine localization and progression of proliferation. The similarity to endocardial thickening of cardiac valves and to intimal proliferation in blood vessels was remarkable. In old age and in chronic rheumatic heart disease the proliferation exhibited hyalinization, cell depletion, loss and fragmentation of elastin, lipid accumulation, and thrombosis, indicative of a similar pathogenesis to atherosclerotic changes in valvular endocardium and blood vessels. It was concluded that these chronic hemodynamically induced degenerative changes in the endocardium, including cardiac valves, should be classified as endocardial atherosclerosis analogous to that in arteries and veins and that severity is aggravated by high blood pressure, cardiac malformations, and dysfunction or damage caused by other disease processes.

Adolescent↗