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  • 1
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Pathology of Intra-Hisian Block. Introduction: The length of the His bundle and the precise location of injury responsible for split His potentials have not been fully established in patients with intra–Hisian block. We conducted an autopsy study comparing histologic findings in intra-Hisian block versus control hearts. Methods and Results: We studied hearts from 4 intra-Hisian block patients (age 66 to 93 years, mean 79.5) and hearts from 14 patients without AV conduction abnormalities (control). All intra-Hisian block patients underwent electrophysiologic evaluation; 3 patients demonstrated intra-Hisian block and 1 showed no His potential. Autopsies were performed when each patient died. After the heart was fixed in formaldehyde, the AV septal junctional area was removed en bloc and serially sectioned into 7-μm thick slices. For study purposes, we considered the three segments of the His bundle separately: the penetrating bundle, the nonbranching bundle, and the branching bundle. The actual length of each segment was calculated from the number of respective serial sections, and the lesion was reconstructed within the conduction axis. Intra-Hisian block hearts were heavier than control hearts (mean weight 389 vs 301 g; P 〈 0.05). The lesion was situated in the nonbranching bundle in 3 hearts and in the penetrating bundle in 1 heart. Mean compact node length was 3.8 mm in intra-Hisian block hearts and 3.3 mm in control hearts. The penetrating bundle was 2.1 and 2.1 mm, the nonbranching bundle was 3.5 and 1.9 mm, and the branching bundle was 4.5 and 4.6 mm in intra-Hisian block and control hearts, respectively. Conclusion: Most lesions were observed in the nonbranching bundle adjacent to the junction between the central fibrous body and ventricular septum. This segment was longer in intra-Hisian block hearts than in control hearts.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Flutter Isthmus Anatomy Revisited. Introduction: The “flutter isthmus.” the part of the lower right atrium between the eustachian valve and the tricuspid annulus inferior to the coronary sinus os, is considered the crucial zone for conduction delay necessary for the genesis of atrial flutter. However, the underlying mechanism remains unclear. Methods and Results: We studied the “flutter isthmus” in 50 hearts obtained at autopsy from patients without atrial tachyarrhythmias. The muscular trabecular arrangement was dissected carefully by peeling off the endocardium. Documentation of the trabecular arrangement focused, in particular, on the question of whether there was a uniform pattern of well-aligned muscle trabeculae or a nonuniform architecture. It appeared that a nonuniform trabecular pattern prevailed (37/50 [74%]). In these hearts, the muscular arrangement showed abundant cross-overs and interlacing traheculae, particularly in the zone immediately inferior to the coronary sinus os. Connections also occurred along the Inferior rim of the os. Conclusion: The normal anatomy of the lower right atrium favors nonuniform muscular trabeculation, with Interlacing bundles and a multitude of cross-overs. The potential for conduction delay is present in the vast majority of normal hearts. This raises the question as to what has changed in the hearts of patients with atrial flutter such that the potential for conduction delay and reentry has become effective.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 16 (2005), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Anatomy of Pulmonary Veins. Introduction: Electrophysiologic studies have shown that spontaneous initiation of atrial fibrillation (AF) by ectopic heats may originate from within pulmonary veins. The extensions of left atrial myocardium are considered to play a role, but there is little detailed anatomic information available. particularly in humans. Methods and Results: Thirty-nine human autopsy hearts were studied; 22 with AF and 17 without atrial arrhythmias. The muscle fiber arrangement of the left atrial wall and pulmonary veins was dissected. In 18 hearts, myocardial sleeves were studied microscopically; in five hearts, three-dimensional reconstruction of the fiber arrangement in the myocardial sleeves was performed. Of 99 pulmonary veins examined, 96 contained a myocardial sleeve. The length of the sleeves was largest in the superior pulmonary veins (P 〈 0.01). There were no statistically significant differences between uniform and nonuniform muscle fiber arrangements. Microscopic evaluation revealed myocardial sleeves positioned on the adventitial side of the pulmonary vein, separated from the muscular media by a fibrofatty tissue plane. The most distal zone of the myocardial sleeves showed increasing fibrosis with encapsulation of small groups of myocardial cells and eventually with total disappearance of atrophic cells within fibrous tissue. Node-like structures were not encountered. There was no relationship with presence or absence of AF. Conclusion: The observation that the peripheral zones of myocardial sleeves are associated with increasing connective tissue deposition between myocardial muscle groups suggests a degenerative change that, from the histologic viewpoint, fits with progressive ischemia. These changes could provide a basis for microreentry and, hence, for atrial arrhythmias.
    Type of Medium: Electronic Resource
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