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[Recording of monophasic action potentials using a contact catheter in humans. Preliminary report].

Investigations of a monophasic action potential (MAP) at a cellular level in experiments provided basic findings on the course of the electric activity in cells in various cardiac compartments and tissues under physiological conditions and various pathological states and has become an indispensible part of the evaluation of electrophysiological properties of various cardiovascular drugs, in particular antiarrhythmic drugs. A record corresponding to the MAP can be obtained also from the surface of the human endocardium during catheterization by means of a Franz contact catheter. MAP is induced by pressure depolarization after applying the catheter to the endocardium of different cardiac compartments. The objective of the author's preliminary communication is to present the initial experience with the MAP record from right-sided cardiac compartments during a routine electrophysiological examination in five patients at rest, during increasing stimulation of the atria and ventricles and after administration of some antiarrhythmic drugs. The authors evaluated the duration of MAP, the duration of 10%, 50% and 90% repolarization, the MAP amplitude, the activation time, repolarization time and the incidence of spontaneous diastolic depolarization. The recording and evaluation of MAP during the routine electrophysiological examination can contribute to the understanding of the development of arrhythmias, the action of antiarrhythmic drugs and to the evaluation of ischaemic changes of the myocardium. The clinical impact of MAP records is not clear so far and its assessment will call for further experience with this method.

Action Potentials↗

A case of solanum malacoxylon toxicity in pigs.

The postmortem and histological changes seen in the kidneys, lungs and vascular system in spontaneous Solanum malacoxylon poisoning on a pig farm in Buenos Aires Province, Argentina, are reported. Macroscopic calcified plaques in the endocardium, aorta, and pulmonary artery and mineralization in renal pelvis were observed. Microscopic examinations revealed tubulonephrosis and calcification of the elastic fibers of kidney vessels. Severe calcinosis of the endocardium and elastic fibers of arteries (aorta, pulmonary, renal) were seen. In the lung, calcification of the elastic fibers of the alveolar wall and the lamina propia of the bronchia were also noted.

Animals↗

[Detection and localization of the ventricular septum defect using color Doppler echocardiography. Sensitivity, specificity, limitations].

In part 1 of this study 50 healthy children and 56 patients with known VSD were examined by color-Doppler-echocardiography to derive criteria for the diagnosis of a VSD by this technique. Using a defined Nyquist velocity the healthy children showed a monochrome ventricular bloodflow pattern. In patients with VSD and an interventricular pressure gradient greater than 15 mm Hg a turquois-yellow jet could be seen additionally in the ventricle with the lower pressure. The same pattern could be observed within the defect itself, except for four patients, in whom the VSD could not be visualized by two-dimensional echocardiography. In these patients, however, the VSD could be localized by tracing the jet to the septal endocardium. In patients with equal left and right ventricular pressures a monochrome transseptal bloodflow could be seen. Its color pattern was not significantly different from the normal bloodflow pattern. In these cases it was difficult to diagnose a small VSD, if the defect itself could not be visualized. Thus, the following criteria for the diagnosis of a VSD by color-Doppler-echocardiography were derived depending on the interventricular pressure gradient: 1) Interventricular pressure gradient greater than 15 mm Hg: visualization of the VSD-jet including its origin at the septal endocardium. 2) Equal left and right ventricular pressures: visualization of the VSD as echo drop-out as well as a transseptal bloodflow. Using these criteria, sensitivity and specificity of color-Doppler-echocardiography in the detection of VSD were evaluated in part II; 234 consecutive patients, of which 119 had a VSD, were examined. All had undergone cardiac catheterisation. A high sensitivity of 98.3% and a specificity of 99.1% were found. Diagnostic problems remain in patients with a small VSD and also in patients with equal left and right ventricular pressures. In particular, multiple VSD with equal left and right ventricular pressures are difficult to visualize completely, as compared to cases with significant interventricular pressure gradients.

Adolescent↗

[Hypereosinophilic syndrome with Löffler's endomyocarditis: report of an autopsy case].

Hypereosinophilic syndrome (HES) with Löffler's endomyocarditis is a rare disease with poor prognosis. Clinically, it mainly affects young adults, characterized by prolonged idiopathic blood eosinophilia, cardiopulmonary symptoms and hepatosplenomegaly. Pathological features consist of ventricular mural thrombi, marked fibrotic thickening of endocardium with scarring of myocardium, and multiorgan eosinophilic infiltration. We report a 2-year-old girl with idiopathic HES associated with Löffler's endomyocarditis. The girl was noted to have constitutional symptoms, cardiomegaly, and hepatosplenomegaly. Her total eosinophil count reached 150,000/microliters. She had no history of allergic diseases. The microbiological studies were negative. Echocardiography suggested thickened endocardium, mitral stenosis and regurgitation. In spite of intensive medical management, the girl died of refractory congestive heart failure. Autopsy revealed thick fresh mural thrombi involving the biventricular inflow tracts, inflammation and fibrosis of the endomyocardium, systemic thromboembolism and multiorgan eosinophilic infiltration. The pathology and pathogenesis of the disease are discussed and the literature is reviewed.

Child, Preschool↗

Fetal echocardiographic signs of congenital endocardial fibroelastosis.

Endocardial fibroelastosis is characterized by a porcelain-like thickening of the endocardium, resulting in a marked increase in echodensity of the endocardium, as well as ventricular dilatation and aortic atresia. With improvement in prenatal ultrasound, this condition can be suspected in utero on the basis of ventricular enlargement, poor ventricular contractility, and marked echodensity of the endocardial surface. We present two cases in which such conditions were found on prenatal M-mode echocardiography and two-dimensional directed pulsed Doppler. Ventriculomegaly and hypocontractility of the ventricle are, however, nonspecific for such conditions; the diagnosis can be made accurately only by pathology. When such findings appear on ultrasound, all efforts should be made to deliver the patient in a perinatal center for optimal neonatal surgery to improve the survival of the newborn.

Adult↗

Septicemia secondary to impacted infected pacemaker wire. Successful treatment by removal with cardiopulmonary bypass.

Infection of an intravenous pacemaker electrode developed in a 78-year-old man after multiple replacements and revisions of the pulse generator and the pacemaker lead. Spread of the infective process to the endocardium was followed by septicemia with Serratia marcescens and Staphyloccus epidermids. Failure of medical treatment and external traction on the pacemaker electrode led to thoracotomy and removal of the pacemaker electrode wires with the use of extracorporeal circulation. The tip of one of the pacemaker electrodes was found imbedded in the wall of the right ventricle and attached to the base of the tricuspid valve. Cultures from the endocardium removed with the electrode rendered the same organisms as cultured preoperatively. There has been no recurrence after 2 years following the removal of the infected electrodes. Although the problem described herein is not frequently found, radical treatment becomes necessary whenever infection and septicemia develop.

Aged↗

Scanning electron microscopy of Thebesian ostia (microdissection by ultrasonication: enzymatic digestion).

Thebesian vasculature provides for communication between the coronary system and the chambers of the heart. Anatomic, embryologic, physiologic, and therapeutic investigations have involved this component of cardiac anatomy from the early 18th century to the present time. The scanning electron microscope (SEM) now affords an innovative approach to the study of the ostia of these veins as they open into the chambers of the heart. The surface of the intact endocardium is continuous, whether it is treated with boric acid or not, as long as it remains intact. Enzymatic microdissection of tissues with trypsin, hyaluronidase and pronase, followed by similar treatment with boric acid, reveals continuity of successive component layers of the endocardium extending into Thebesian substructure. Thebesian tributaries are easily visualized from the ostia but the deeper capillary network of the Thebesian system is not demonstrable by this approach. Valvular structures such as might prevent retroflow during the cardiac cycle are not present. Our observations with SEM support anatomic relationships indicated by previously published work.

Animals↗

Endocardial fibroelastosis and tricuspid valve insufficiency in a calf.

A 5-month-old Holstein heifer had clinical signs of tricuspid valve insufficiency and histopathologic evidence of endocardial fibroelastosis. The calf had a 3-week history of weight loss, abdominal distention, dyspnea, and decreased appetite. Physical examination revealed signs of right-sided heart failure, and a systolic murmur (II/VI) was heard best over the right heart base. Results of cardiac catheterization and echocardiography indicated tricuspid valve insufficiency and right-sided heart failure. The calf was euthanatized after not responding to treatment with penicillin, furosemide, and removal of fluid from the thorax and abdomen. Necropsy findings included multifocal areas of thickening and opacification of the endocardium of the left and right ventricles. Excessive elastic fibers, consistent with fibroelastosis, were seen by use of special stains applied to sections of endocardium.

Animals↗

Regional coronary blood flow in canine hemorrhagic shock.

This study examined circumferential, apex-to-base, and transmural distribution of coronary blood flow at rest and in hemorrhagic shock in a canine model. In addition, animals subjected to identical anesthesia and instrumentation were not hemorrhaged and served as controls. Regional coronary blood flow was measured by the radioactive microsphere technique, using 15-microns diameter microspheres in both control and shocked dogs. Circumferential variation in flow occurred at rest with the left ventricular free wall blood flow higher than septal flow and the anterior region better perfused than the posterior region. In addition, the endocardium was favored over epicardium as indicated by an endocardial-epicardial flow ratio greater than one. Early shock altered the regional distribution of coronary flow, resulting in better perfusion in some areas of the heart than in others. Two hours of sustained shock (mean arterial blood pressure at 30 mm Hg) oblated differences in circumferential as well as apex-to-base distribution of flow, resulting in global hypoperfusion. Transmural distribution of flow was also altered with a significantly greater fall in endocardial compared to epicardial flow. The greater vulnerability of the endocardium to low-flow injury in shock was confirmed by the presence of hypercontraction lesions and necrosis in the papillary muscle and endocardial regions, but not in the epicardial region. Injury was homogenous, as indicated by the uniformed distribution of lesions and necrosis across the anterior and posterior regions, as well as the free wall and septum of the left ventricle. Two hours of anesthesia alone did not significantly alter the transmural or circumferential distribution of coronary blood flow. While there was a tendency for total coronary flow to fall over the experimental period, this did not achieve statistical difference. Our study confirms a significant relationship between reduced coronary perfusion and hypercontraction injury in canine hemorrhagic shock.

Animals↗

[2-dimensional echocardiographic analysis of the volume and function of the right ventricle in the apical and subcostal 4 chamber image].

To determine the diagnostic accuracy of two-dimensional echocardiography in the evaluation of RV dimensions and function, biplane angiography of the right ventricle and 2-D echo was performed in 60 consecutive patients and analyzed by two independent investigators. In 42 of 60 patients (group A) the RV could be visualized in the rotated apical 4 chamber view and in 18 patients in the subcostal 4 chamber view with good quality, which made it possible to define the right ventricular endocardium in the real-time proceeding. In 20 of these 42 patients the RV could be registered in the apical 4 chamber view with complete definition of the endocardium also in the stop frame (group B). Quantitative analysis was performed in the end-diastolic and end-systolic stop frame, using the area-length method. The correlation of echocardiography and angiography for the end-diastolic volumes was poor in group A (r = 0.62) and superior in group B (r = 0.73). The correlation coefficient for end-systolic volumes was r = 0.70 in group A and r = 0.92 in group B. End-diastolic and end-systolic volumes were systematically underestimated by echocardiography. RV ejection fraction did not correlate between both methods. The subcostal 4 chamber view was not sufficient in determining RV volumes and function. The results demonstrate that the right ventricle can be visualized in 70% of patients with sufficient quality. RV dimensions and volumes can be determined with high accuracy in these patients.

Cardiac Catheterization↗

[Effects of nicardipine on regional coronary deficit and the ST segment of the healthy and ischemic myocardium in dogs].

The effects of nicardipine, a phenyldihydropyridine calcium-channel antagonist agent, have been investigated on regional blood flow and epicardial ST-segment elevation in the nonischemic and ischemic myocardial zones after either intermittent, or permanent coronary artery occlusion in dogs. Whichever the experimental model used, nicardipine reduced heart rate and arterial blood pressure and increased regional myocardial blood flows (50 to 100% of control flow values). All these effects were dose-dependent. During intermittent coronary occlusion (a model that mimics angina pectoris), the nicardipine-induced myocardial vasodilation was homogeneous between the endocardium and the epicardium of the ischemic and nonischemic zones. During permanent coronary occlusion (a model that mimics myocardial infarction), the nicardipine-induced myocardial vasodilation mainly developed within the endocardium of the ischemic zone, leading thus to a beneficial transmural blood flow redistribution in that zone. Finally, and whichever the experimental model used, nicardipine did not reduce the ischemic injury as assessed by epicardial ST-segment elevation.

Animals↗

Transmural distribution of metabolites and blood flow in the canine left ventricle following isoproterenol infusions.

The effects of intravenous infusions of isoproterenol (0.1, 1.0 or 2.5 micrograms/kg/min for 1 hr) on the transmural distribution of myocardial high-energy phosphates and glycolytic intermediates were determined in anesthetized, open chested dogs. The transmural distribution of blood flow across the left ventricular wall was determined after serial injections of 15 mu radioactively labeled microspheres. A biopsy of the posterolateral wall was frozen in liquid nitrogen, divided into epicardial, midmyocardial and endocardial thirds, and assayed for metabolites. The remainder of the heart was processed for light and electron microscopy. At the infusion rate of 2.5 micrograms/kg/min, isoproterenol caused nonuniform reductions in ATP, phosphocreatine, total adenine nucleotides and glycogen, which were particularly depleted in the endocardium. Isoproterenol also caused nonuniform increases above baseline in blood flow (epicardial, 492%; midmyocardial, 197%; and endocardial, 131%). The endocardial/epicardial blood flow ratios, however, were reduced. Evidence of cellular damage was demonstrated by the presence of numerous contraction band lesions along with mitochondrial swelling and the appearance of electron-dense deposits. It is concluded that necrogenic infusions of isoproterenol impair myocardial energy production in all myocardial layers despite an overall increase in blood flow. There appears to be a link between the gradients in metabolites and the distribution of blood flow such that the endocardium becomes more vulnerable to injury.

Animals↗

[Significance of immunologic effector mechanisms in infectious endocarditis].

Whereas a number of investigations deals with extracardiac manifestations of immune reactions in infective endocarditis (e.g. circulating immune complexes), immunological effector mechanisms directed against the heart itself have not yet been analyzed. In 72 patients with infective endocarditis (41 patients with defined pathogen, 31 no pathogen isolated) humoral und cellular immunological effector mechanisms were investigated. Antibodies directed against the cytoskeleton of myocardial cells and against the endocardium were demonstrated in 60% to 100% depending on the infective pathogen and the clinical course. Whereas the antibodies were found in subacute and chronic courses regularly, they were found less frequently in acute lethal cases. Antibodies directed against connective tissue, endocardium and sarcolemma were indicative of, but not specific for the endocardial affection. Those antibodies which were directed against the inner parts of the sarcolemma, the myolemma, appear to be indicators of an additional myocardial affection, if they are cytolytic against vital cardiocytes in vitro. Circulating immune complexes are non-specific markers of an increased immunoreactivity. They were detected in 35 out of 41 patients with defined bacterial pathogen in the early phase of the disease. Both, their incidence and serum concentrations decreased significantly after antibiotic treatment. Cellular immune reactions directed against vital heart cells (e.g. cytotoxic reactions) can most likely be attributed to K- or NK-lymphocytes and were found in 48% of patients. Serum factors such as circulating immune complexes and/or antimyolemmal antibodies may enhance or block this cytotoxic reaction.

Adult↗

Cardiac infections in the immunocompromised host.

Bacterial infections of the heart in compromised patients are uncommon but may be increasing in relative frequency. They are associated with near-equal frequencies in patients who have pre-existing or simultaneous infections at other sites, patients with neoplasms (usually solid tumors), those who have undergone cardiac surgery, and intravenous drug or ethanol abusers. Staphylococcus aureus is the bacteria most often identified, in contrast to a preponderance of Streptococcus isolated in the pre- and early antibiotic era. Gram-negative bacilli are the causative organisms in a significant number of cases. The endocardium remains the most common site of infection, and left-sided valves are most commonly involved, especially the mitral valve, often in the absence of pre-existing valvular damage. The majority of cases are associated with involvement at other sites, and premortem blood cultures are positive in approximately two thirds of patients who undergo autopsy. Fungal infections involving the heart do not occur as often as bacterial infections. The frequency, however, is increasing. Fungal infections usually occur in patients who have received treatment with antineoplastic agents, antibiotics, or corticosteroids, alone or in combination, or who have had abdominal or cardiac surgery. Candida is the organism found most frequently and usually causes myocarditis or endocarditis, whereas Aspergillus involves the myocardium but may be invasive to the endocardium or pericardium. Other fungi that occasionally infect the heart include Phycomycetes and Cryptococcus. Dissemination is usually present and involves the lungs, kidneys, brain, or gastrointestinal tract. The diagnosis may be difficult prior to death, because blood cultures are positive in only one third of patients who come to autopsy. Precipitin tests and antibody titers for specific organisms may be helpful in providing early diagnosis. Survival rates can be improved by early diagnosis and the institution of aggressive antifungal treatment.

Adolescent↗

[Myocardium-cardiac jelly dissociation and conal torsion. A study on the chick embryo heart].

Conal twisting seems to result from dissociation between the cardiac jelly and the deep myocardial interface like the lining in the sleeve of a jacket. The conal ridges are the natural markers of the jelly and endocardium. They are responsible for septation of the conus and enable the twisting to be observed and measured. The myocardium is marked artificially by cauterisation. This marks the armature of the wall and leaves behind a zone of reduced resistance in the form of a hernia or false diverticulum. The conal ridges and marked myocardium dissociate. In the mid segment the myocardium does not play any role in twisting. In the proximal and distal segments it is only partially involved. This dissociation is observed even in the structure of the conal wall; the jelly, which is dense near the endocardium, is loose near the myocardium and adheres to the deep surface by dispersed fibres. Perfusion under pressure of the investigated specimens induces a detachment between the jelly and the myocardium and there only. This fragility only lasts during the twisting period. It is not found at the end of cardiac embryogenesis. This zone would allow not only a sliding--due to its fragility--but also a controlled sliding--by its fibres. In addition to twisting there is also conal migration. This takes place in the same direction as proximal twisting and determines myocardial rotation, which is less marked however, than that of the corresponding ridges. Experimentation may exaggerate this dissociation by preventing migration. It may also reduce or even suppress it by the formation of adhesions between the two layers. Although this mechanism is not univocal, a myocardial-jelly adhesion could stop distal twisting for example and explain malposition or transposition of the great vessels. This dissociation is no unique to superior vertebrates as it has also been found in the first living animals in whom conal twisting occurs, the dipneustes.

Animals↗

Regional abnormalities of left ventricular wall movement during isovolumic relaxation in patients with ischemic heart disease.

In order to study events during isovolumic relaxation, left ventricular angiograms of 120 patients with ischemic heart disease were digitized frame by frame, and compared with those of 15 normal subjects. In patients with ischemic heart disease, abnormal inward movement of endocardium occurred in areas supplied by narrowed coronary arteries. When these involved the free wall, they were due to abnormal wall thickening rather than to inward movement of epicardium. Since the volume of the ventricle was constant, they were accompanied by compensatory outward movement of endocardium elsewhere, due to premature thinning. Identical abnormalities were demonstrated in 80 patients by M-mode echocardiography, and in individual patients, agreement with angiography was good. These abnormalities were aggravated by TNT administration, and were unaffected by isometric stress. In approximately half, they were associated with abnormalities of isovolumic contraction. They appear to represent the behavior of regions of the left ventricle with partial loss of function due to previous ischemic injury.

Cineangiography↗

Calcification of implanted xenograft pericardium. Influence of site and function.

In a series of 23 dogs, glutaraldehyde-fixed xenograft pericardium was implanted as a left atrial wall patch (Group I, 11 dogs), as a substitute for the mitral valve chordae (Group II, 12 dogs), and as an external pericardial patch (Group III, five dogs, in which one of the two former procedures was associated). All dogs of Group I survived and were put to death after 12 months. The atrial patch appeared thickened and shrunken in all, with intense fibrous reaction, calcification, and even bone formation. The structural changes were minimal in the external aspect of the patch, not in contact with the host's endocardium and blood. Eight dogs of Group II survived from 7 months to 3 years. In all, the pericardial chordae were thickened and calcified with good healing at the suture lines; that their original length was retained, however, allowed for good valve function. In the dogs of Group III the pericardial substitute appeared well preserved after 12 months, not calcified, and without noteworthy degenerative changes. Minimal or absent epicardial adhesions were noted. We conclude that (1) the tendency for xenograft pericardial tissue to calcify is strongly influenced by the site of implantation and function and by contact with host blood and endocardium; (2) heterologous pericardium may be considered suitable for closure of pericardial defects after open cardiac operations, and (3) studies on calcification of biological tissue should be carried out by long-term evaluation of such tissues inside the heart.

Animals↗

[Effect of catecholamine on reperfused myocardium following hypothermic global ischemia].

This study was aimed to evaluate the effect of catecholamine on the myocardium reperfused after hypothermic global ischemia, by changes of hemodynamics, biochemistry and ultrastructure. Under cardiopulmonary bypass (CPB) at flow rate 80 ml/kg/min., the aorta was clamped for 60 min. at 28 degrees C of myocardial temperature and reperfused for 60 min. in 26 mongrel dogs. They were divided into 4 groups by infusion of physical saline solution (control), epinephrine 1 microgram/kg/min. (group 1), epinephrine 0.1 microgram/kg/min. (group 2) and dobutamine 5 micrograms/kg/min. (group 3) during reperfusion. The hemodynamic parameters and myocardial isoenzyme (m-AST, MB-CPK) of coronary sinus venous blood were measured before CPB, 30 and 60 min. after declamp. The myocardial adenosine triphosphate (ATP), creatine phosphate (CP), water content, tissue Ca content and fine structure with score of mitochondrial membrane and cristae were examined in epicardium and endocardium at the end of experiment. Hemodynamic parameters after declamp were higher in group 1, 2 and 3 than control (p less than 0.05). The water content and tissue Ca content in group 1 were higher than control. The ATP of endocardium was lowest but CP was no significant difference among four groups. The mitochondrial score in group 1 was lower than control. These data suggest that epinephrine and dobutamine increase hemodynamics and tissue Ca content on the reperfused myocardium following 60 min. of hypothermic global ischemia, but they do not improve depletion of ATP and disruption of myocardial ultrastructure. High dose of epinephrine accentuates ischemic damage of reperfused myocardium after hypothermic global ischemia.

Adenosine Triphosphate↗