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This is a detailed pathological examination of the heart including the conduction system (CS) from a 64-year-old male who had catheter ablation of the atrioventricular (AV) junction for intractable atrial fibrillation. This is the world's first human who had this procedure, and who survived 3 years and 8 months, and later died of congestive heart failure. Pathologically, the heart was hypertrophied and enlarged. Histologically, there were chronic inflammatory cells, marked fatty metamorphosis with fibrosis of the atria, the approaches to the AV node, and the AV node, with almost isolation of the node from the atria, and considerable fibrosis of the bundle and bundle branches. In addition, there was fibrosis of the summit of the ventricular septum with chronic inflammatory cells. These represent the sequelae of the ablation procedures. It is not known how much of the pathological findings contributed to the cardiac hypertrophy and impairment of cardiac function.
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The authors describe their own method of right heart microcatheterization by means of transcutaneous introduction of an original unipolar microcatheter into the left subclavian vein. The method makes possible recording of th His bundle electrogram as well as of spike potentials of the sinus node and atrial conduction pathways. His bundle electrograms were recorded in 237 subjects, of whom 72 had ischaemic heart disease and 115 suffered from other cardiopathies, 50 persons with non-cardiac diseases constituted the control group. The high diagnostic value of His bundle electrogram was confirmed, especially in appraising the degree of A-V block, differentiation between aberrant QRS complexes and ventricular extrasystolia, and in other arrhythmias. Recording of spike potentials of the sinus node, atrial conduction pathways, and His bundle, and determination of the interposed intervals allow selective assessments of the impulse propagation velocities in individual segments of heart conduction system, especially on drug administration, and offer valuable information on the genesis of various types of arrhythmias and conduction disturbances.
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The purpose of this investigation was to differentiate primary cardiac participation in systemic anaphylaxis from a cardiac reaction secondary to respiratory distress. Hemocyaninsensitized guinea pigs were anesthetized with sodium pentobarbital and artifically ventilated. The chest was opened and the left ventricle cannulated. The electrocardiogram, bronchial resistance, arterial blood pressure, and left ventricular pressure and its first derivative were recorded. Following intravenous administration of antigen, the sinus rate increased by about 50-60 beats/min, left ventricular dP/dt increased by a factor of 3, and mean arterial pressure doubled. Conduction disturbances occurred in all of the experiments and ventricular fibrillation in four of six. These changes were concomitant with a 4-fold rise in bronchial resistance. To separate the cardiac and respiratory components, antigen was administered directly into the left ventricle to expose the heart to antigen before the lungs. The intracardiac challenge resulted in increases in sinus rate and left ventricular and arterial pressure quantitatively similar to changes recorded from guinea pigs after the intravenous challenge. However, all these changes preceded the rise in bronchial resistance by 60 seconds. Arrhythmias occurred as frequently as with the intravenous challenge. Our findings show that by use of an appropriate route for administration of antigen, cardiovascular and respiratory components of systemic anaphylaxis can be separated. Our data also indicate that anaphylactic cardiovascular changes can be dissociated temporally into two sets of events: an initial primary cardiac reaction caused by intracardiac release of histamine and a subsequent cardiovascular reaction secondary to systemic release of mediator.
The muscle cells forming the myocardium and the muscle cells forming the intestinal smooth muscle layers, are both derived from the visceral mesoderm. All cardiomyocytes display autorhythmicity, intercellular conduction via gap junctions, and contraction, irrespective whether they are derived from atrium, ventricle, node, or bundles. it is the anatomical arrangement of the distinct components that is responsible for the coordinate contraction wave over the heart. These very basic principles have been insufficiently appreciated in most studies on the development of the conduction system, by which it got unnoticed that the proper anatomical arrangement is, in essence, layed down very early in development in the cardiac tube. In this review we will summarize recent immunohistochemical studies that have permitted this appreciation.
Recent electrophysiological evidence indicates that periodic spontaneous depolarizations occur in the primordial heart of the bird (and presumably mammal) even before the myocardial cells can contract, and these are initiated in the primordial sinoatrial region. As contractions are generated, these then establish a peristaltic wave. From that time on, during ontogenesis, the contractile sequence follows a regular pattern of development. As chambers form they contract sequentially in the direction of blood flow, even though, in the twisted configuration, myocardial continuities suggest the possibility of short-circuiting the electrical conduction pathways from atrium to bulbus. This implies that, even at these early stages, the electrical properties of the myocardium are not isotropic, and that specialized conduction pathways must exist. To the present time, electrophysiological techniques have limited the direct evidence that can be obtained on these delicate electrically specialized pathways. However, microscopical techniques have permitted studies on the morphological development of the tissue and of the cells in the various regions of the myocardium. The present paper traces the development of cell morphology in these regions, including the development of structural nodes and proximal ventricular fibre pathways, and from these observations, the manner in which the electrical conduction pathways are believed to develop is suggested.
Ligation and cannulation of the anterior septal artery in 43 canine hearts caused changes in ST-T segment of the electrocardiogram in all animals. Perfusions of 0.9% NaCl, one to ten micrograms of acetylcholine, isoproterenol, epinephrine and norepinephrine, into the anterior septal artery caused variations in the ECG ranging from exaggerated ST-T changes to PR prolongation, ectopic atrial, nodal and ventricular beats, A-V blocks and dissociations, atrial fibrillation and ventricular fibrillation. The response seemed to be somewhat specific for cholinergic versus adrenergic agents showing more conduction defects by the former against greater changes in automaticity by the latter agents.
In nine patients without clinical or laboratory evidence of heart disease, premature atrial depolarization (PAB) induced a complete block of conduction in the intraventricular conducting system. In these patients the functional refractory period AV (FRPav)) gave short and very similar results to the effective refractory period of the His-Purkinje system (ERPhp), and the effective refractory period AV (ERPAV) was found to be shorter than the ERPhp in all cases. A linear correlation between the ERPhp and the basic cycle length (BCL) was also observed. These special functional properties of the AV node justify the occurrence of intraventricular block after PAB. In fact, the stimulus, rapidly conducted through the AV node, finds a complete or incomplete refractoriness in the ventricular conducting system, and therefore bundle branch or complete intraventricular block occurs. The linear correlation between the ERPHP and the BCL explains why the atrial pacing is not always useful for pointing out intraventricular conducting defects.
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