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PubMed1996

Epithelial-mesenchymal transformations in early avian heart development.

Cardiac morphogenesis proceeds from a sequential series of epithelial-mesenchymal transitions which begins by establishing bipotential heart-forming cells and later their segregation into endocardial and myocardial lineages. Cells within each lineage integrate to form two concentric epithelia which inductively interact to transform cells of the inner epithelium, the endocardium, into mesenchymal or 'cushion' cells. Noncardiogenic epithelia (dorsal mesocardium, epicardium, neural ectoderm and coelomic mesothelium) undergo transition into populations of extracardiac mesenchyme that combine over time with cushion tissue to remodel the simple tubular heart into a four-chambered organ. Model systems are described for studying the mechanisms of cardiac-related transformations including primary cultures of precardiac epithelia and a differentiation-inducible, avian stem cell line called QCE-6. Focus is centered on the molecular mechanism by which endocardial epithelium transforms into cushion mesenchyme. Experimental findings are reviewed and interpreted in the context of a hypothetical model that seeks to answer why only some cells within an epithelium transform and whether the transformation process is regulated by intrinsic or extrinsic mechanisms. The model proposes that epithelial cells competent to transform to mesenchyme express characteristic markers including receptors for extrinsic signals secreted by stimulator cells (e.g. myocardium). Candidate extrinsic signals include multicomponent complexes called adherons. If applied directly to cultured endocardium, myocardial adherons but not those secreted by L6 myoblasts, induce changes in gene expression within target endocardial cells for proteases and cell:cell and cell:matrix adhesion molecules that accompanied transformation to mesenchyme. A main component of myocardial adherons has been identified as ES antigens, one of which, ES/130, has been cloned, found to have a novel sequence and in culture assays shown to be required for endocardium to transform to mesenchyme. The spatiotemporal pattern of ES protein expression within the embryo suggests that common mechanisms may exist for embryonic epithelial-mesenchymal transformations.

Animals↗

PubMedDate not supplied

Lipid peroxidation and oxidative stress during acute allylamine-induced cardiovascular toxicity.

Allylamine is an aliphatic amine that causes vascular lesions in aorta and medium-sized arteries. This primary amine has been shown to be metabolized to acrolein both in vivo and in vitro. Acrolein may cause allylamine's toxic effects, since it acts as a strong peroxidizing agent itself; in addition, deamination of allylamine is accompanied by production of hydrogen peroxide. To investigate the relative roles of oxidative stress and lipid peroxidation in allylamine intoxication, we conducted an acute in vivo time-course study following administration of allylamine (150 mg/kg) to rats by gavage. Animals were sacrificed at 1, 3 and 5 h after allylamine treatment, and subcellular fractions of aorta, epicardium and endocardium were assayed for enzymes of the oxidant defense system and thiol (-SH) status, capacity for lipid peroxidation, and .OH radical generation. Results suggest that in vivo treatment with allylamine causes preferential damage to aortic mitochondria. A marked depletion of total and free -SH content was found in aorta, epicardium and endocardium, with a striking increase in the formation of thiobarbiturate-reactive substance by aortic mitochondria at all time points. A significant increase in the capacity to generate .OH was found in aorta (with lesser increases in epicardium and endocardium) after allylamine treatment. Levels of defense system enzymes were not consistently altered, however. In a totally in vitro experiment, liposomes incubated with acrolein (0.2-2 mM) showed a proportional increase in lipid peroxidation of liposomal membrane. A likely basis of allylamine's cardiovascular toxicity is acrolein-induced lipid peroxidation, especially in mitochondria.

Allylamine↗

PubMed1983

Recurrent sustained ventricular tachycardia: structure and ultrastructure of subendocardial regions in which tachycardia originates.

Surgical resection of the endocardium and subendocardium often abolishes chronic recurrent sustained ventricular tachycardia in patients with healed myocardial infarcts or ventricular aneurysms, presumably by interrupting the reentrant pathway. To define the morphologic characteristics of cells in the reentrant pathway, we studied the histology and ultrastructure of the endocardial resections of 23 patients who underwent this procedure. Bundles of apparently viable myocardial fibers embedded in dense fibrous tissue were identified throughout the endocardial resections from all patients. These bundles of cells were separated from one another by fibrous tissue but extended uninterrupted to the margins of the surgical resection. In 14 patients Purkinje fibers were identified beneath the thickened endocardium whereas the remaining bundles were composed of ventricular muscle. The Purkinje fibers appeared to have normal ultrastructure and ventricular cells with both normal and abnormal ultrastructures were present. The abnormal muscle cells were characterized by loss of contractile elements, aggregates of dilated sarcoplasmic reticulum, and osmiophilic dense bodies. The sarcolemma was intact and the nuclear chromatin was evenly dispersed suggesting that these cells were still viable. The abnormal structure and arrangement of the surviving cardiac fibers in the endocardium may cause the abnormal electrophysiologic function that results in ventricular tachycardia.

Adult↗

PubMed1993

Simultaneous epicardial and endocardial activation sequence mapping in the isolated canine right atrium.

BACKGROUND: Since the atria are thin-walled structures, most studies that have examined the spread of activation in the atria have assumed that they behave electrophysiologically as a two-dimensional surface. It was the objective of this study to determine whether or not this assumption is true by simultaneously mapping the epicardial and endocardial activation sequences in the right atrium. METHODS AND RESULTS: Identical precisely superpositioned epicardial and endocardial electrode templates with 250 unipolar electrodes each were used to map the isolated canine right atrium (n = 8) during continuous perfusion and superfusion with Krebs-Henseleit buffer. Data were recorded during control conditions (normal sinus rhythm), continuous pacing (S1S1 = 300 msec), and premature stimulation (S1S2 = effective refractory period + 5 msec). Pacing was performed at two sites, one located on the inferior crista terminalis and one lateral to the crista terminalis on a pectinate muscle. Tachyarrhythmias were induced by a single extrastimulus during the continuous perfusion of acetylcholine (10(-3.5) mol/L). Individual electrode sites were correlated with the gross anatomy and histology. Activation time differences were calculated between each two corresponding epicardial and endocardial sites. There were differences in the activation times between the epicardium and endocardium during all experimental conditions. However, the average difference for each condition was < 1 msec, suggesting that overall activation did not spread faster on either the epicardium or the endocardium, even though in certain regions one surface could lead the other. The dispersion of time differences was smallest during normal sinus rhythm and continuous pacing (SD = 5.6-5.8 msec) and largest after premature stimulation (SD = 6.3 msec for crista pacing, p < 0.05; SD = 8.1 msec for pacing lateral to the crista, p < 0.001). Differences in the activation sequence correlated with the underlying anatomic architecture. The largest differences in activation times between the epicardium and endocardium were associated with those regions of the atrium where pectinate muscles ran below the epicardial surface. The pectinate muscles in those areas were often discontinuous with the epicardial surface and facilitated the discordant epicardial-endocardial activation. The discordant activation was also found in regions where the atrial wall thickness was < 0.5 mm and correlated with transmural differences in fiber orientation. A tachyarrhythmia induced in the presence of acetylcholine, which demonstrated a focal activation pattern, was shown to have a reentrant loop that used free-running muscle bundles connecting the epicardial and endocardial surfaces, resulting in a three-dimensional pathway. CONCLUSIONS: The findings of this study demonstrate that epicardial and endocardial activation can be discordant in specific regions and that discordance increases with abnormal activation sequences. Many of the differences in the epicardial and endocardial activation can be correlated with the heterogeneity of the anatomic architecture of the right atrium. The study also demonstrates that reentry can occur in a three-dimensional plane using the epicardial and endocardial surfaces connected by transmural muscle fibers.

Animals↗

PubMed2005

Cellular mechanism of calcium-mediated triggered activity in the heart.

Calcium overload due to enhanced calcium entry is a mechanism for spontaneous calcium release (SCR) from the sarcoplasmic reticulum, delayed-afterdepolarizations (DAD), and triggered activity. However, the exact mechanistic relationship between elevated intracellular calcium levels and triggered activity originating from a specific location remains unclear. We hypothesize that under conditions of enhanced calcium entry, elevation of intracellular calcium will result in multiple calcium release events of which only one is more likely to initiate a triggered beat. We used optical mapping of action potentials and ratiometric calcium transients in an electromechanically-uncoupled canine wedge model of enhanced calcium entry, using I(Ks) blockade with beta-adrenergic stimulation. Under conditions of enhanced calcium entry, the rate of calcium uptake was faster compared with control conditions; however, during rapid pacing, cytoplasmic calcium elevation at the endocardium was significantly increased (15+/-4%) compared with control (10+/-3, P<0.04). Rapid pacing induced multiple simultaneous SCR events with largest amplitude and earliest onset near the endocardium compared with the epicardium. Furthermore, SCR events with largest amplitude and earliest onset served as a focus for DAD-mediated triggered activity. Interestingly, polymorphic VT occurred in some experiments when multiple SCR events occurred. In conclusion, multiple, simultaneous SCR events occur over a broad region of relatively slower calcium uptake and elevated diastolic calcium levels. However, SCR events closer to the endocardium have the largest amplitude and earliest onset and are, thereby, more likely to initiate DAD-mediated triggered activity. Finally, multiple SCR events may be a mechanism of polymorphic VT under calcium overload conditions.

Action Potentials↗

PubMed1978

The role of canine superficial ventricular muscle fibers in endocardial impulse distribution.

Thin sections of canine right and left ventricular endocardium and myocardium were studied in a tissue bath to compare conduction properties of intraventricular specialized conducting tissue [Purkinje fibers (PF)], the superficial layers of subendocardial ventricular muscle (SVM), and the deeper ventricular muscle (DVM) below this level. The study was carried out because of observations that some areas of the endocardium, which are devoid of either specialized conducting tissue or of PF-VM junctions between specialized conducting tissue and ventricular muscle, conduct relatively rapidly, favoring specific orientations of propagation. Preparations containing PF, SVM, and DVM were studied electrophysiologically and histologically. A technique of stripping limited areas of endocardium was used to expose DVM in order to determine its intrinsic calculated conduction velocity. In 12 preparations, the average calculated conduction velocity in PF was 1.62 m/sec, and the average in DVM was 0.26 m/sec. The SVM conduction velocity was intermediate between the two, averaging 0.98 m/sec when propagation was parallel to SVM fiber orientation. Conduction velocity transverse to SVM fiber orientation was not significantly different from DVM conduction velocity. Histologically, the most superficial layers of VM were oriented uniformly in the direction of rapid subendocardial conduction, in contrast to DVM fibers in which orientation varied. It is concluded that the geometric arrangement of SVM fibers may provide a means for rapid subendocardial conduction and impulse distribution at a conduction velocity intermediate between PF and DVM in areas devoid of specialized conducting tissue.

Animals↗

PubMed1988

Effects of damaging the endocardial surface on the mechanical performance of isolated cardiac muscle.

The mechanical properties of mammalian ventricular cardiac muscle have been studied in the presence and in the absence of an intact endocardial surface. Isotonic and isometric twitch contractions were obtained from papillary muscles of the right ventricle of cat at 29 degrees and 37 degrees C, at different extracellular calcium concentrations ([Ca2+]o), and at different initial muscle lengths. The endocardial surface was damaged by gentle abrasion of the muscle surface with a plastic blade or by brief immersion for 1 second with 1% Triton X-100. Although there was no evidence of damage to myocardial cells, damaging the endocardial surface resulted in an immediate and irreversible abbreviation of the twitch contractions with, except at the highest ([Ca2+]o, a decrease in peak isometric twitch tension. These changes induced 1) an asymmetrical shift of the tension-[Ca2+]o relation towards increasing [Ca2+]o but with no effect at the highest [Ca2+]o, and 2) a rightward and downward shift of the length-tension relation. Both shifts were significantly more pronounced at 37 degrees C than at 29 degrees C; they were not accompanied by significant changes in Vmax. The asymmetrical shift of the tension-[Ca2+]o relation suggests that the endocardium-mediated chain of events may be mediated by changes in the sensitivity of the contractile proteins to Ca2+. This hypothesis is also supported by the similar pattern of changes (i.e., modulation of the onset of early tension decline) induced by decreasing length at each [Ca2+]o and by the removal of a functional endocardium. Accordingly, the endocardium may help to control the performance of the heart by modulating peak contractile performance and relaxation of the underlying myocardium.

Adenosine Triphosphate↗

PubMed1993

Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle.

Recent studies from our laboratory involving syncytial preparations have delineated electrophysiological distinctions between epicardium, endocardium, and a unique population of cells in the deep subepicardial to midmyocardial layers (M region) of the canine ventricle. In the present study, we used standard microelectrode, single microelectrode switch voltage-clamp, and whole-cell patch-clamp techniques to examine transmembrane action potentials, steady-state current-voltage relations, and the 4-aminopyridine-sensitive transient outward current (Ito1) in myocytes enzymatically dissociated from discrete layers of the free wall of the canine left ventricle. Action potential characteristics of myocytes isolated from the epicardium, M region, and endocardium were very similar to those previously observed in syncytial preparations isolated from the respective regions of the ventricular wall. A prominent spike and dome was apparent in myocytes from epicardium and the M region but not in myocytes from endocardium. Action potential duration-rate relations were considerably more pronounced in cells isolated from the M region. Current-voltage relations recorded from cells of epicardial, M region, and endocardial origin all displayed an N-shaped configuration with a prominent negative slope-conductance region. The magnitude of the inward rectifier K+ current (IK1) was 392 +/- 86, 289 +/- 65, and 348 +/- 115 pA in epicardial, M region, and endocardial myocytes, respectively, when defined as steady-state current blocked by 10 mM Cs+. Similar levels were obtained when IK1 was defined as the steady-state difference current measured in the presence (6 mM) and absence of extracellular K+. Ito1 was significantly greater in epicardial and M region myocytes than in endocardial myocytes. At a test potential of +70 mV (holding potential, -80 mV), Ito1 amplitude was 4,203 +/- 2,370, 3,638 +/- 1,135, and 714 +/- 286 pA in epicardial, M region, and endocardial cells, respectively. No significant differences were observed in the voltage dependence of inactivation of Ito1 in the three cell types. The time course of reactivation of Ito1 was slower in cells from the M region compared with either epicardial or endocardial cells. Our data suggest that prominent heterogeneity exists in the electrophysiology of cells spanning the canine ventricular wall and that differences in the intensity of the transient outward current contribute importantly, but not exclusively, to this heterogeneity. These findings should advance our understanding of basic heart function and the ionic bases for the electrocardiographic J wave, T wave, U wave, and long QT intervals as well as improve our understanding of some of the complex factors contributing to the development of cardiac arrhythmias.

Action Potentials↗

PubMed1993

Endocardial versus epicardial differences of intracellular free calcium under normal and ischemic conditions in perfused rat hearts.

Transmural heterogeneity of myocardial metabolism and function are present in the left ventricle under normal and ischemic conditions. To determine if endocardial versus epicardial differences of [Ca2+]i are also present, perfused rat heart studies using indo-1 fluorescence as an index of [Ca2+]i were performed in the left ventricular epicardium and endocardium. Hearts were studied during control conditions and low-flow ischemia. Results demonstrated the following: 1) At a pacing rate of 1.5 Hz, endocardial levels of diastolic and systolic [Ca2+]i (470 +/- 40 and 1,240 +/- 170 nM) were higher than epicardial levels (290 +/- 30 and 920 +/- 150 nM). 2) At a more physiological pacing rate of 5 Hz, endocardial levels of diastolic and systolic [Ca2+]i (680 +/- 50 and 1,230 +/- 70 nM) were also higher than epicardial levels (390 +/- 20 and 950 +/- 60 nM. 3) During low-flow ischemia, endocardial levels of diastolic [Ca2+]i rose to a greater degree (from 680 +/- 50 to 1,050 +/- 70 nM at 10% of control coronary flow) compared with epicardial levels (from 390 +/- 20 to 580 +/- 40 nM at 10% of control flow), suggesting that the endocardium is more susceptible to low-flow ischemia. 4) The amplitude of the [Ca2+]i transient was the same at the endocardium (540 +/- 50 nM) and epicardium (560 +/- 50 nM) and did not change during low-flow ischemia, despite marked contractile dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Effects of the renin-angiotensin system on the current I(to) in epicardial and endocardial ventricular myocytes from the canine heart.

The Ca(2+)-independent portion of transient outward K(+) current (I(to)) exhibits a transmural gradient in ventricle. To investigate control mechanisms for this gradient, we studied canine epicardial and endocardial ventricular myocytes with use of the whole-cell patch-clamp technique. I(to) was larger in amplitude, had a more negative voltage threshold for activation, and had a more negative midpoint of inactivation in epicardium. Recovery from inactivation was >10-fold slower in endocardium. Incubation of epicardial myocytes with angiotensin II for 2 to 52 hours altered I(to) to resemble unincubated endocardium and reduced the amplitude of the phase 1 notch of the action potential. In contrast, incubation of endocardial myocytes with losartan for 2 to 52 hours altered I(to) to resemble unincubated epicardium and induced a phase 1 notch in the action potential. With RNase protection assays, we determined that incubations with angiotensin II or losartan did not alter mRNA levels for either Kv4.3 or Kv1.4; thus, a change in the alpha subunit for I(to) is unlikely to be responsible. To test whether posttranslational modification produced the effects of angiotensin II, we coexpressed Kv4.3 and the angiotensin II type 1a receptor in Xenopus oocytes. Incubation with angiotensin II increased the time constant for recovery from inactivation of the expressed current by 2-fold with an incubation time constant of 3.7 hours. No effect on activation or inactivation voltage dependence was observed. These results demonstrate that the properties of I(to) in endocardium and epicardium are plastic and likely under the tonic-differing influence of the renin-angiotensin system.

Action Potentials↗

PubMed1981

The surface morphology of the infundibular muscle in patients with tetralogy of fallot.

The surface morphology of the infundibular muscles obtained from open heart surgery was investigated in 10 patients with tetralogy of Fallot. Various degrees of abnormal surface morphological changes were observed from the endocardium to the myocardium. In the endocardium striking proliferation of the endothelial cells was usually accompanied by focal loss of the endothelium with fibrotic change. Based on the characteristic alterations of the surface morphology 4 different groups of myocardial cells could be identified: normal myocytes, defective myocytes, sclerotic myocytes, and necrotic myocytes. Because intact surface morphology is responsible for integrated cellular function these pathological findings observed on the surface morphology of the endocardium and myocardium can provide a valuable reference to further understanding of functional disorders of the infundibular muscle in patients with tetralogy of Fallot.

Adolescent↗

PubMed1976

Aging and hydroxproline content in human heart muscle.

Hydroxproline content was chemically determined in 45 human hearts obtained at autopsy, in order to know possible correlations between aging and hydroxyproline content in the heart muscle. There were no significant differences in the mean total hydroxyproline content between the epicardium and the endocardium, between left and right ventricles, nor between young, middle and old age groups. The hydroxyproline content in NaCl-soluble fraction decreased, and that in TCA-soluble fraction and in residue fraction increased with age. There were significant differences in the mean hydroxyproline content in NaCl-soluble fraction between middle and old age groups, and in residue fraction between young and old age groups in the endocardium of the left ventricle. Accordingly, the ratio of the content in NaCl-soluble fraction to that in TCA-soluble fraction decreases with age. This tendency was more evident in the epicardium than in the endocardium on the left ventricle. These results indicate that total hydroxyproline content per 1 mg of lyophilized material does not show any quantitative changes, but does show qualitative changes with age.

Adolescent↗

PubMed1990

[Unusual location of mural thrombi in the right atrium caused by pathological changes in the sinoatrial node].

We present a post-mortem examination of two hearts in which we found organized mural thrombi attached to the right atrial endocardium in the recess called antrum atrii dextri. This region is a place where the sinus node is situated very close to the endocardium of right atrium. Any pathological process involving the node (inflammation, degeneration) may reach this part of endocardium by continuity, this in turn creates convenient conditions for mural thrombi formation. The first case--a 52-year old man who died of severe congestive heart failure caused by rheumatic disease with mitral and aortic stenosis. Atrial fibrillation had developed several years before his death. Apart from typical changes of mitral and aortic valves a post-mortem examination revealed an organized, globular thrombus in antrum atrii dextri. In the microscopical findings of the sino-atrial region the fatty degeneration of the sinus node with multiple mononuclear cell infiltration was the most striking feature. The sinus node artery was narrowed due to fibro-muscular dysplasia of its wall. The second case--a 74-years old man who suffered from arterial hypertension and chronic pyelonephritis with a history of heart infarct in the past. The ECG recording showed multifocal atrial rythm with variable P wave morphology and P-Q distance. At necropsy the whole heart was significantly enlarged with no scars or any other signs of healed infarct. The microscopical findings revealed the heart muscle to be infiltrated by amyloid deposits particularly apparent in the sinus node. Similar thrombus of 1.5 cm in diameter was found in antrum of the right atrium.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1990

[Intraorganic lymphatic bed of the cattle heart].

Lymphomicrocirculatory networks of endocardium, myocardium and epicardium, as well as lymphatic vessels of four orders represent the intraorganic lymphatic bed of the cattle heart. In the endocardium there is a lymphatic network with close loops and a small amount of blindly beginning capillaries. The capillary lymphatic bed of the endocardial trabeculae carneae is much more dense than that in the other part of the endocardial surface. The spatial lymphatic network of the myocardium is joined with the lymphomicrocirculatory networks of the endocardium and epicardium by means of a large amount of connections. The epicardial lymphatic bed is formed by blindly beginning lymphatic capillaries, which situate in close and nonclose loops of the lymphatic network. In the epicardium there is only one lymphatic network. The size of the loops and the diameter of the lymphatic capillaries is directly proportional to the age of the animals.

Animals↗

PubMed1995

Morphoregulatory interactions of endocardial endothelium and extracellular material in the heart.

The endocardium forms the inner lining of the cavities of the heart. The luminal surface of the cardiac wall is subjected to considerable cyclical physico-chemical forces. These forces can have structural and physiological consequences both for the endocardial endothelium and for the subjacent interstitial tissue. In the latter tissue space, the extracellular matrix (ECM) plays a dominant role during cardiogenesis. For example, this role becomes evident from the influence of fibronectin in the directional migration of proendocardial cells and in the formation of a trabeculated heart. In particular, the complex processes occurring in the valves of the developing heart illustrate a spatiotemporally regulated expression of ECM components and adhesion molecules. In the adult heart, the endocardial interstitial tissue consists of a thin basal lamina, a reticular lamina and a fibroelastic layer which contains some fibroblasts, smooth muscle cells and a heterogeneous population of nerve fibers. Unlike in arteries, elastic fiber in the fibroelastic layer of ventricular endocardium do not constitute an elastic lamina. Differences in thickness of the endocardium between atria and ventricles, as well as the diffuse and focal endocardial fibrosis during ageing have been related to mechanical stress and local turbulence of flow. Although endocardial fibrosis is a common pathological finding in various cardiomyopathies, our knowledge on the structural organization and on the pathogenetic role of ECM is very limited, mainly by the lack of suitable experimental models.

Age Factors↗

PubMed1994

Differential effects of D-sotalol on endocardial and epicardial action potentials of human ventricular myocardium in dilated cardiomyopathy.

The frequency- and concentration-dependent electrophysiologic effects of D-sotalol (3 x 10(-5)-10(-3) M) were evaluated in human epicardial and endocardial left ventricular (LV) myocardium. Intracellular action potentials (AP) were obtained from explanted hearts of 5 patients with dilated cardiomyopathy in whom orthotopic heart transplantation was performed. The following parameters were recorded: AP amplitude (APA), resting membrane potential (RMP), AP duration at 95 and 50% repolarization (APD95, APD50), maximal upstroke velocity (Vmax), and effective refractory period (ERP) at cycle lengths (CL) of 0.5, 1 Hz, and 1.5 Hz. APD50, APD95, and ERP were significantly prolonged in endocardium at D-sotalol concentration > or = 10(-4) M at all CL. In epicardium, APD50, APD95, and ERP were significantly prolonged at lower D-sotalol concentrations (starting at 3 x 10(-5) M). In contrast to parameters in endocardium, APD50, APD95, and ERP were shortened in epicardial cells at D-sotalol concentrations > or = 3 x 10(-4) M at drive CL of 0.5 and 1 Hz with no effect on Vmax and APA. In endocardium, the prolongation of APD95 and ERP was less at a CL of 1.5 Hz compared with 0.5 Hz at a concentration of 10(-4) M. This frequency-dependent effect was not observed in epicardium. No effects were observed on RMP, APA, or Vmax. These data indicate a differential effect of D-sotalol in endo- and epicardial human ventricular myocardium, which may be an important mechanism of action of D-sotalol.

Action Potentials↗

PubMed1995

Endocardial and epicardial infarct size after preconditioning by a partial coronary artery occlusion without intervening reperfusion. Importance of the degree and duration of flow reduction.

OBJECTIVE: Recently, we reported that a partial coronary artery occlusion immediately preceding a sustained coronary artery occlusion limited infarct size. We now investigated whether the protection by partial coronary artery occlusions (i) depends on the severity and(or) duration of the flow reduction and (ii) varies in the different myocardial layers. METHODS: In 71 open-chest pigs (eight groups) left ventricular area at risk (AR) and infarct area (IA) were determined for the endocardial (IAendo and ARendo) and epicardial halves (IAepi and ARepi). RESULTS: In control animals (60 min total coronary artery occlusion (TCO) followed by 120 min reperfusion (Rep)) there were highly linear relations between IA and AR in the endocardium (r = 0.98, P < 0.01) and epicardium (r = 0.97, P < 0.01), which could be described by IAendo = 1.01 ARendo - 4.5 and by IAepi = 0.88ARepi - 3.6, respectively. In animals that underwent a 10 min TCO + 15 min Rep prior to the 60 min TCO + 120 min Rep, IA in both myocardial layers were again highly linearly related with AR, with less steep slopes for both the endocardium (0.63) and epicardium (0.57) (both P < 0.01). Two groups of pigs were subjected to either a 30 or 90 min 70% reduction in coronary blood flow (FR) immediately preceding the 60 min TCO + 120 min Rep, without intervening reperfusion. A 30 min 70% FR decreased IA to the same degree in the endo- and epicardial half. A 90 min 70% FR resulted in protection in the epicardium (P < 0.01) but not in the endocardium, most likely because 90 min 70% FR without 60 min TCO already caused infarction which was more severe in the endo- than in the epicardium (P < 0.01). Endocardial and epicardial IA after either a 30 or 90 min 30% FR prior to the 60 min TCO was not different from that in the control group, indicating that this mild flow reduction failed to limit irreversible damage. CONCLUSIONS: Thirty or ninety min of severe (70%) but not mild (30%) coronary flow reductions protected against myocardial infarction. The protection by a 70% FR was influenced by the duration of FR as a 30 min 70% FR similarly decreased IA in the endocardial and epicardial halves, while 90 min 70% FR preferentially limited IA in the epicardial half. These findings suggest that perfusion abnormalities immediately preceding an infarction could be an important source of infarct size variability in patients.

Animals↗

PubMed1998

[Clinical expression of papillary fibroelastoma. Apropos of a case].

The authors review the literature of the clinical features of papillary fibroelastomas in the light of a new case. These benign tumours of the endocardium may be distinguished from Lambl's vegetations by their site and size. Some workers suggest that they correspond to giant Lambl's vegetation and could be a form of "aging" of the valvular endocardium. Nevertheless, Lambl's vegetations are always present after 10 years of age but the papillary fibroelastoma is rarely detected by echocardiography and there have been few case reports. They are essentially cardiac valve tumours (73% of valvular tumours) and may give rise to serious clinical symptoms, sudden death by migration or coronary obstruction, systemic embolism, especially from left heart lesions. However, they can be situated at any point of the endocardium. The diagnosis of a valvular or an endocardial tumour is based on echocardiography which, though not always accurate, gives a better aetiological diagnosis. In cases of symptomatic tumours, surgery (usually simple ablation) is indicated with a low operative risk and cure of symptoms. Tumours discovered by chance pose very difficult problems of management and may lead to diagnostic or preventive surgery.

Aged↗