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PubMed1980

Mitral valve prolapse: jet stream causing mural endocarditis.

A 53 year old man died of cerebral hemorrhage while being treated for Streptococcus mutans endocarditis. At autopsy the only endocarditic lesion was on the left atrial mural endocardium. The noninfected mitral valve demonstrated prolapse and mucinous degeneration. The latter had led to rupture of several chordae tendineae, with the resultant jet stream predisposing to endocarditis at its point of atrial impact. The case provides confirmation of current concepts of the pathogenesis of endocarditis and has important therapeutic implications.

Arteriosclerosis↗
PubMed1983

Long-term echocardiographic assessment of dilated cardiomyopathy in children.

Left ventricular (LV) dimensions and function were assessed by echocardiography in 22 children with dilated cardiomyopathy. They had survived an initial episode of congestive heart failure in infancy for greater than or equal to 2 years. At the time of echocardiography, when they were 3 to 16 years old, 8 patients (Group 1) still had signs of dilated cardiomyopathy and 14 (Group 2) had lost all roentgenographic and electrocardiographic evidence of heart disease. All 8 patients in Group 1 (average follow-up 4.5 years) had significantly increased LV dimensions. The end-diastolic dimension averaged 144 +/- 18% of the normal value. Fractional LV shortening with systole was significantly reduced and averaged 23 +/- 3%. The E point-septal separation ranged from 7 to 17 mm (mean 12 +/- 4) and was far above the normal limit in all. Of the 14 patients in Group 2, seven (average follow-up 7 years) had normal ventricular dimensions and 7 (average follow-up 10 years) had LV dimensions larger than the upper range of the 95% prediction limit. In 6 of the latter patients the fractional LV shortening with systole was less than or equal to 31% and the E point-septal separation in excess of the upper limit of normal. These findings indicate that about half of the patients who had apparently recovered still had residual lesions as judged from the echocardiogram. In 6 patients in group 1, two-dimensional echo-cardiography allowed the visualization of a thickened endocardium. One of these 6 patients died. The echocardiographic image correlated well with the process of LV endocardial fibroelastosis found at necropsy.

Adolescent↗
PubMed1985

Development of an endocardial-epicardial gradient of activation rate during electrically induced, sustained ventricular fibrillation in dogs.

Electrograms recorded with currently available electrodes become indistinct soon after the onset of ventricular fibrillation (VF), thus, little is known about transmural myocardial depolarization during VF. A plunge electrode system (plunge) was developed that registers discrete deflections during VF. These plunges were used to record for 20 minutes after inducing VF with a single premature shock in 20 open-chest dogs. In the first 6 dogs the epicardium was exposed to room temperature and in 14 dogs transmural temperature was maintained at 38 degrees C. Electrograms recorded with the transmural plunges contained sharp, discrete deflections during early VF in all dogs. Over the next 20 minutes of VF, the rate, regularity of cycle length and discreteness of the deflections in the electrograms decreased with time, first at the epicardial level, then deeper toward the endocardium. In all dogs, however, discrete, regular, rapid deflections persisted in the most subendocardial electrogram throughout the recording period. In 8 dogs, transmural myocardial biopsy samples were taken before fibrillation, and at intervals after the onset of fibrillation. The high-energy phosphate content of the myocardium decreased during VF, with comparable decreases in the epicardial and endocardial halves. Coronary perfusion was maintained during the first 20 minutes of VF in 6 additional dogs by cardiopulmonary bypass. A gradient of activation rates did not develop on bypass, but did develop within 1 minute of halting bypass. Thus, the endocardial-epicardial gradient of activation rates during VF is caused by ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1993

Acute electrical stimulation increases extramyocardial collateral blood flow after a cardiomyoplasty.

We hypothesized that acute electrical stimulation of a latissimus dorsi cardiomyoplasty would augment the collateral blood flow delivered by the skeletal muscle to the heart. This hypothesis was tested in an animal model (13 goats) of coronary artery disease. Six weeks after a cardiomyoplasty was performed, myocardial collateral blood flow derived from the latissimus dorsi muscle was measured with colored microspheres when the muscle was at rest and during electrical stimulation of the thoracodorsal nerve at 1.25 Hz. The area at risk for ischemia averaged 13.37 +/- 2.08 g (mean +/- standard error), or 18.4% of left ventricular mass (n = 13). At rest, significant skeletal muscle-derived collaterals developed in 9 animals, and formed predominantly to chronic ischemic myocardium (mean +/- standard error, 0.07 +/- 0.02 mL.g-1 x min-1; n = 9), rather than infarct (0.03 +/- 0.02 mL.g-1 x min-1; n = 5), or normal myocardium (0.0005 +/- 0.0001 mL.g-1 x min-1; n = 9). Stimulation increased skeletal muscle-derived collateral blood flow to chronic ischemic areas to 0.38 +/- 0.09 mL.g-1 x min-1 (n = 9) (p < 0.05). During stimulation, the collateral flow was greater in the epicardium (0.46 +/- 0.11 mL.g-1 x min-1) than in endocardium (0.14 +/- 0.09 mL.g-1.min-1) (p < 0.05). This study demonstrates that electrical stimulation of a latissimus dorsi cardiomyoplasty increases extramyocardial collateral blood flow to chronic ischemic myocardium.

Animals↗
PubMed1984

An indirect immunofluorescence study of the distribution of fibronectin during the formation of the cushion tissue mesenchyme in the embryonic heart.

Indirect immunofluorescence studies have localized fibronectin (FN) within the trunco-conal ridges of the chick embryo heart during the formation of the cushion tissue mesenchyme. Prior to cell migration into the endocardial pads, fluorescence for FN is demonstrated almost entirely in association with the basal surfaces of endocardium and myocardium. Scattered spots and thin dotted-strands of fluorescent material can be demonstrated in the cardiac jelly. Cushion tissue (CT) cells migrating into the cardiac jelly have patches of fluorescent material associated with their surfaces. Filopodial processes always show intense fluorescence. The close association between the fluorescence and the surface of the CT cells suggests that FN may be implicated in the interaction of these cells with the matrical components of the cardiac jelly and, therefore, in the process of cell migration into the endocardial pads. The intensity and amount of FN staining decreased concomitantly with the progressive accumulation of cells in the cushion areas. After the completion of CT cell migration only reduced amounts of faint fluorescence remained in the endocardial pad areas. The possible significance of the changes observed in the distribution of FN during the formation of the cushion tissue mesenchyme is discussed.

Animals↗
PubMed1991

Expression of adhesion molecules during the formation and differentiation of the avian endocardial cushion tissue.

The expression of cytotactin, the cytotactin-binding (CTB) proteoglycan, and the neural cell adhesion molecule, N-CAM, was examined during the development of the avian endocardial cushion tissue (ECT). N-CAM was present in the cardiac mesoderm from its earliest time of development. At the time when endothelial cells converted to mesenchyme and began to migrate, they ceased their expression of N-CAM. Cytotactin and CTB proteoglycan were present in the cardiac jelly (into which the ECT cells migrate) in patterns that were correlated with cell migration. At early times of migration (stage 18), the region of the cardiac jelly near the endocardium contained cytotactin in the vicinity of the migrating cells. During later migration (stage 22), cytotactin remained associated with the leading zone of cell migration, but its expression began to decrease in areas where cells had accumulated. After ECT cell migration had ceased, cytotactin expression decreased, remaining high only in the peripheral portion of the aorticopulmonary septum and absent from its ridges. CTB proteoglycan was expressed during early migration at high levels in and adjacent to the myocardium. By stage 22, its distribution had become more uniform throughout the ECT regions and in the myocardium. The combined results of this study suggest that cytotactin, CTB proteoglycan, and N-CAM each play a distinct, critical role in pattern formation in the early heart.

Animals↗
PubMed1992

Endothelium-derived relaxing factor inhibits platelet adhesion to cultured porcine endocardial endothelium.

By using a simple platelet binding assay, we investigated whether endothelium-derived relaxing factor (EDRF) released from endocardial endothelium influences the adhesion of unstimulated platelets to these cells. Under basal conditions 8.0 +/- 0.32% of total platelets added adhered. The nitric oxide (NO) synthase inhibitor, i.e. NG-nitro L-arginine methyl ester (L-NAME), and the EDRF inhibitor haemoglobin (Hb) increased this adhesion, but another NO synthase inhibitor, NG-monomethyl L-arginine (L-NMMA), did not. The EDRF releasing agent substance P (SP) decreased adhesion, L-NMMA reversed this inhibition, whereas L-NAME and Hb did so only partially. Superoxide dismutase (SOD) caused a marked decrease in adhesion which was fully reversed by L-NMMA, L-NAME and Hb. SOD and SP together showed a cumulative effect on platelet adhesion; this inhibition was significantly reversed by all the EDRF inhibitors, although the levels of adhesion did not return to those seen under basal conditions. These results indicate that EDRF release can inhibit the adhesion of unstimulated platelets to cultured porcine endocardium and that NO synthase inhibitors have differential effects on basal and stimulated EDRF release by these cells.

Animals↗
PubMed1996

Mechanics of ventricular torsion.

Recent research suggests that left ventricular torsion is an important indicator of cardiac function. We used two theoretical models to study the mechanics of this phenomenon: a compressible cylinder and an incompressible ellipsoid of revolution. The analyses of both models account for large- strain passive and active material behavior, with a muscle fiber angle that varies linearly from endocardium to epicardium. Relative to the end- diastolic configuration, the predicted torsion exhibits several experimentally observed features, including a peak near end systole, rapid untwisting during isovolumic relaxation, and increased twist near the apex. The magnitude of the twist is sensitive to the fiber architecture, the ventricular geometry, and the compressibility and contractility of the myocardium. In particular, the model predicts that the systolic twist increases with increasing compressibility, contractility, and wall thickness, while it decreases with increasing cavity volume. The peak twist approximately doubles (from about 0.02 to 0.04 rad cm(-1)) with a doubling of myocardial compressibility or with a change in the endocardial/epicardial muscle fiber angles from 90/ -90 degrees to 60/ -60 degrees. The twist is less sensitive to changes in contractility and ventricular geometry. These findings provide a basis for interpreting measurements of ventricular torsion in the clinical setting.

Animals↗
PubMed1984

Left ventricular wall motion: its dynamic transmural characteristics.

Cardiac wall motion has been studied extensively. It is usually determined by indirect two-dimensional measurements for the true three-dimensional (3D) motion with its specific speed and direction. Errors are also introduced by using internally fixed reference systems and by the inability to identify precise points on the heart wall during the cardiac cycle. Because of these limitations, the endocardial and epicardial wall motion and their relationship are still unclear. This study was designed to assess endocardial and epicardial wall motion by measuring the direction and speed of implanted markers in an externally fixed 3D coordinate system. Fifty-seven pairs of endocardial and epicardial metallic markers were placed at anterior, lateral, posterior, basal, and apical regions of the left ventricles of 14 normal mongrel dogs. Biplane cineradiographs were performed at 50 frames/sec, and the 3D motions of the markers were analyzed using a specially designed computer system. It was found that the speeds, directions, displacements, and phases of the movements of corresponding endocardial and epicardial points were highly correlated. The correlation coefficients were 0.77 to 0.95 for the mean directions, 0.61 to 0.96 for the mean speeds, and 0.59 to 0.96 for the mean displacements at various regions of the heart, and the periodic movements of the endocardium and epicardium were always in phase. The mean epicardial speeds and displacements are fixed proportions (approximately 70%) of the mean endocardial speeds and displacements despite the differences in absolute values between regions in the same dog and the same regions in different dogs. The correlation coefficients for endocardial and epicardial instantaneous speeds, directions, and velocities ranged from 0.68 to 0.83, 0.81 to 0.88, and 0.77 to 0.86, respectively, for different regions of the heart. The correlation coefficients were significant for both the mean values and the instantaneous values. Thus, when only fixed epicardial points are accessible for wall motion measurements in clinical situations, it is possible to infer the endocardial motion from the epicardial motion.

Animals↗
PubMed1982

The pericardium as a source of prostacyclin in the dog, ox and rat.

Cyclo-oxygenase products of arachidonic acid metabolism formed by the pericardium and epicardial surface of dog heart were identified and quantitated by radioimmunoassay after separation by high-pressure liquid chromatography. Pieces of parietal pericardium, of dog, ox and rat, when incubated in vitro produced mainly 6-keto-PGF1 alpha, with lesser amounts of PGE2, PGF2 alpha and thromboxane B2. Biosynthesis of all prostanoids increased during incubation of the parietal pericardium of each species with arachidonic acid, but 6-keto-PGF1 alpha was still the major metabolite. When slices of dog heart were incubated with arachidonic acid (1 microgram/ml) the rates of 6-keto-PGF1 alpha formation by the parietal pericardium was much greater than that of the myocardium and endocardium. Epicardial slices appeared to be intermediate in 6-keto-PGF1 alpha formation. The hearts of anesthetized dogs were also irrigated in situ with Krebs' solution, and during the first 5 min of epicardial irrigation the pericardial fluid leaving the heart again contained high levels of 6-keto-PGF1 alpha, with lesser amounts of the other prostanoids. Addition of arachidonic acid (3 micrograms/ml) to the irrigating fluid caused an increase in all measured prostanoid levels, although 6-keto-PGF1 alpha remained the predominant metabolite. In contrast, intravenous infusion of isoproterenol selectively increased the release of 6-keto-PGF1 alpha from the irrigated heart. It is concluded that the pericardium and epicardium continuously release prostacyclin into the pericardial fluid, and that the increased release of this substance observed when cardiac workload increases derives mainly from these membranous sources. This raises the interesting possibility that pericardial prostacyclin might influence coronary vascular tone and chemoreflexes which arise from the epicardium during myocardial ischemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

"Intermittent" and transient ST-segment elevation following direct current cardioversion.

Transient ST-segment elevation immediately following direct current cardioversion is a clearly documented occurrence in a small percentage of cases. Two main explanations have been suggested: myocardial injury or coronary vasospasm. We report two cases of "intermittent" and transient ST-segment elevation after cardioversion. Such intermittent elevation of the ST segment has not been reported previously. We hypothesize that this electrocardiographic observation is explained by a timing difference induced by electroshock in the action potential between the epicardium and endocardium.

Action Potentials↗
PubMed1995

Anatomic distribution of nitric oxide synthase in the heart.

Nitric oxide synthase is a useful maker for nitric oxide's scope. Localized by either NADPH-diaphorase histochemistry or immunohistochemical methods, most nitric oxide synthase activity in the normal heart is present in endothelium along the extensive network of arteries, veins and capillaries within myocardium. This endothelial isoform of nitric oxide synthase also exists in the endocardium lining the cavities. Neuronal nitric oxide synthase appears much less prominent, although the exact amount of this isoform in the heart is uncertain. Scattered nerves and ganglion cells are localized by the histochemical methods. While there is no inducible nitric oxide synthase in the normal heart, macrophages associated with repair following various forms of cardiac damage contain this isoform. For all nitric oxide synthases, however, species variation and variability among models underscore the importance of correlative studies of structure and function.

Animals↗
PubMed1996

Arrhythmogenic right ventricular dysplasia.

Right ventricular dysplasia is a primary disorder of the right ventricular myocardium characterised by a progressive replacement by adipose or fibrous tissue, proceeding from the epicardium towards the endocardium. Right ventricular dysplasia with the predominant clinical manifestation of an arrhythmia of right ventricular origin is defined as arrhythmogenic right ventricular dysplasia. There is, however, a wide spectrum of clinical presentation and physical findings owing to the polymorphism of the condition. The aetiology of right ventricular dysplasia remains unknown. Right ventricular angiography is currently regarded as the gold standard for the clinical diagnosis of right ventricular dysplasia Ventricular endomyocardial biopsy can be useful in confirming the diagnosis but a negative biopsy does not exclude the diagnosis of right ventricular dysplasia. There have been few electrophysiological studies and these, in general, have failed to help in risk stratification. Treatment is focused on the prevention of potentially lethal right ventricular electrical instability.

Adipose Tissue↗
PubMed1994

The geometrical relationship between the human esophagus and left ventricle: implications for three-dimensional ultrasonic scanning.

To establish design parameters for a transesophageal ultrasonic probe to image the left ventricle (LV) in three dimensions, the geometrical relationship between the esophagus and the heart was studied in computed tomographic sections of ten humans. Points describing the esophageal centerpoint and the left-ventricular endocardium were digitized. Algorithms were developed to determine from any esophageal viewpoint the ranges of motion required to cover the LV with four modes of scanning; transverse oblique, longitudinal oblique, rotary and linear. Longitudinal oblique scanning was the only single-degree-of-freedom method that allowed complete imaging of the LV in all patients. However, for both conventional and three-dimensional LV imaging, the most promising probe design appears to be a rotary scanning probe with an added degree of freedom to tilt the axis of rotation +/- 29 degrees away from an axis perpendicular to the local esophageal axis.

Adult↗
PubMed1990

Surgery for control of recurrent life-threatening ventricular tachyarrhythmias within 2 months of myocardial infarction.

Twenty-seven patients (mean age 57 +/- 7 years) underwent surgery for control of recurrent drug-refractory ventricular tachyarrhythmias (uniform ventricular tachycardia alone in 9 patients, ventricular tachycardia and ventricular fibrillation in 15 and ventricular fibrillation alone in 3) within 2 months of acute myocardial infarction. The mean number of major arrhythmic episodes per patient was 15 (range 2 to 200) and of drug failures 4 +/- 2. Left ventricular function was severely impaired in the majority (ejection fraction 29%; range 14% to 47%) and 18 patients (66%) had a left ventricular aneurysm. Endocardial resection guided by a combination of endocardial activation mapping during tachycardia and fragmentation mapping during sinus rhythm was performed in all patients. All electrically abnormal left ventricular endocardium was excised. Eight patients (29.6%) died within 30 days of surgery. Death was not related to age, time of surgery after infarction, ventricular function, bypass time or type of arrhythmia. Patients requiring emergency surgery had a higher early postoperative mortality rate than did those undergoing planned surgery (43% versus 15%). During a follow-up period of 32 +/- 20 months, there have been no arrhythmic deaths and only three patients (16%) have required antiarrhythmic drug therapy. When required in the early weeks after infarction, surgery for ventricular arrhythmias offers a high cure rate at a risk related to the patient's preoperative arrhythmia frequency, which in turn relates to the risk of arrhythmic death.

Adult↗
PubMed1992

Endocardial mapping of ventricular tachycardia in the intact human heart. II. Evidence for multiuse reentry in a functional sheet of surviving myocardium.

OBJECTIVE: The purpose of this study was to obtain improved detection and characterization of reentrant circuits in the infarcted human ventricle. BACKGROUND: The return path of reentrant ventricular arrhythmias usually is not manifested in clinical mapping studies but is thought to be formed by isolated bundles of surviving myocytes whose presence is difficult to detect by standard recording techniques. METHODS: We obtained simultaneous unipolar and high gain bipolar recordings using a left ventricular endocardial balloon array in 10 patients with chronic ischemic heart disease undergoing intraoperative mapping of ventricular tachycardia. RESULTS: Three patients demonstrated seven separate ventricular tachycardias that utilized a return tract that was manifested on up to 20% of all left ventricular electrode sites. The recordings suggested an extensive sheet of surviving myocardial fibers with multiple entry and exit points allowing for different reentrant paths at different times all in the same heart. In one patient, five different ventricular tachycardias could be induced, four of which utilized such a sheet. Two of these tachycardias had the same exit point (site of origin) but two different entry points with a long and short return path resulting in long and short tachycardia cycle lengths. The same sheet sustained another tachycardia with one entry and two exit points resulting in two separate "sites of origin" on the endocardium. Such sheets also were seen to insert into the left bundle system. In one patient portions of the sheet could be detected epicardially. CONCLUSION: The existence of such a structure of surviving myocardium with functional pleomorphism may account for unexplained changes in tachycardia cycle length, epicardial entrainment and spontaneous morphologic changes during ventricular tachycardia.

Cardiac Pacing, Artificial↗
PubMed1993

Recognition and catheter ablation of subepicardial accessory pathways.

OBJECTIVES: The purpose of this study was to characterize left-sided accessory pathways that traverse the atrioventricular (AV) groove subepicardially and to describe results of radiofrequency catheter ablation within the coronary sinus in the patients studied. BACKGROUND: Radiofrequency catheter ablation has proved to be a safe and effective method for treatment of accessory pathways; however, subepicardial accessory pathways may account for some of the failures encountered during endocardial ablation. METHODS: The study group comprised 51 consecutive patients with a left-sided accessory pathway who were undergoing radio-frequency catheter ablation. Initially, the ablation catheter was introduced into a femoral artery and positioned on the ventricular aspect of the mitral annulus. If this endocardial approach was unsuccessful, the ablation catheter was introduced into the coronary sinus and energy applied at sites with shorter activation times than those recorded from the endocardium. RESULTS: Five (10%) of 51 patients with a left-sided accessory pathway could not have accessory pathway conduction interrupted with a median of 18 endocardial radiofrequency energy applications. Accessory pathway potentials were less frequent during endocardial mapping in these 5 patients than in the 46 patients whose accessory pathway was successfully ablated from the endocardial surface. All five of these patients later had successful ablation using one or two applications of radiofrequency energy from within the coronary sinus. Effective target site electrograms in the coronary sinus were characterized by an accessory pathway potential that was larger than the corresponding atrial or ventricular electrogram. There were no complications or recurrences after ablation within the coronary sinus. CONCLUSIONS: Some left-sided accessory pathways may be difficult to ablate from the endocardial surface because they traverse the AV groove subepicardially. The absence of an accessory pathway potential during endocardial mapping in combination with a relatively large accessory pathway potential within the coronary sinus may be a useful marker of a subepicardial pathway. In this select group of patients, radiofrequency catheter ablation from within the coronary sinus appears to enhance efficacy.

Action Potentials↗
PubMed1993

Opacification and border delineation improvement in patients with suboptimal endocardial border definition in routine echocardiography: results of the Phase III Albunex Multicenter Trial.

OBJECTIVES: This study was designed to assess the safety and efficacy of intravenously administered sonicated human serum albumin for enhancing echocardiographic delineation of the left ventricular endocardium and improving assessment of wall motion in patients with incomplete depiction of noncontrast echocardiography. BACKGROUND: Echocardiographic regional wall motion analysis is impaired by incomplete endocardial definition in as many as 10% of patients. Sonicated human serum albumin is a stable contrast material that, unlike other agents, opacifies the left ventricle when administered intravenously. METHODS: One hundred seventy-five patients were enrolled at eight centers on the basis of incomplete echocardiographic endocardial depiction. Sonicated 5% human serum albumin, a stable preparation of air-filled microspheres (size range 1 to 10 microns), was administered intravenously in divided doses: 0.08 ml/kg body weight in all patients, followed by 0.14 and 0.08 ml/kg or a single dose of 0.22 ml/kg, depending on the result of the initial dose. Investigators and independent reviewers blinded to the protocol scored the echocardiograms for degree of left ventricular opacification and improvement of endocardial border depiction. RESULTS: Overall, 81% of patients had at least moderate left ventricular chamber opacification with at least one contrast dose, and endocardial definition was improved in 83%. In the subgroup with inadequate left ventricular opacification from the initial dose, a second, larger dose (0.22 ml/kg) improved endocardial depiction in 64%. No significant side effects occurred. CONCLUSIONS: In patients with incomplete echocardiographic endocardial definition, sonicated human serum albumin is a safe, effective contrast agent that, when administered intravenously, produces left ventricular chamber opacification, improves endocardial depiction and enhances regional wall motion analysis.

Adult↗