Myocardial sleeves of pulmonary veins and atrial fibrillation: a postmortem histopathological study of 100 subjects

Steiner, I; Hájková, Petra; Kvasnička, J; Kholová, Ivana

doi:10.1007/s00428-006-0197-2

Cited by 38 publications

(34 citation statements)

References 47 publications

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“…This striated muscle compartment of pulmonary veins in humans is the subject of special clinical attention because it is the source of ectopic beats initiating atrial fibrillation [10][11][12][13]. Similar myocardial striated sleeves extending near heart chambers into the beginnings of main vessels were found in the aorta, pulmonary artery [14,15], and caval veins [16].…”

Section: Correspondencementioning

confidence: 97%

Striated muscles in visceral organs of vertebrates

Субботин¹

2016

J Histol Histopathol

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Pathologists involved in the examination of small rodent tissues are familiar with the presence of striated muscle in walls of intrapulmonary veins. Because these striated muscles express cardiomyocyte markers and are involved in rhythmical contraction during systole, this morphologic arrangement was named "pulmonary myocardium". Striated cardiac muscles of intrapulmonary veins have also been found in numerous species, including non-human primates. Great attention has been given to animal striated pulmonary veins because in humans, the presence of cardiomyocytes in the pulmonary veins (myocardial sleeves) is a major origin of paroxysmal atrial fibrillation. It is unequivocally suggested that direct extension/migration of cardiomyocytes from the left atrium into pulmonary veins is the origin of "pulmonary myocardium". This model sounds logical in regard to humans and large mammals because in these cases, striated myocytes extend into pulmonary veins only by 10-30 mm from the left atrium. However, the cardiomyocyte direct extension/migration model becomes less parsimonious when applied to the numerous small intrapulmonary veins with striated muscles in their walls in small mammals. In 1972, Alfred Sherwood Romer, renowned for his contributions to the study of vertebrate evolution, suggested that visceral smooth muscle cells developed a striated phenotype due to the need for more efficient musculature. Romer theorized that the primary anatomical division of the vertebrate muscular system should be not into smooth and striated types but into somatic and visceral systems, because the line of division along the gut between striated and smooth musculature is not a fixed point. Romer's work offered a parsimonious model for the presence of striated muscle in the walls of the intrapulmonary veins-visceral smooth muscle cells, which are capable of differentiating into striated muscle cells, are always present; whether they differentiate depends on functional demands. From Romer's hypothesis, it also could be foreseen that striated muscle could appear in visceral compartments other than the blood circulatory system and pharyngeal muscles to facilitate functional needs. Indeed, it was shown that 1) the lymphatic system of many low vertebrates acquired a lymphatic heart with striated muscle cells; 2) some vertebrates also acquire striated muscles in tunica Muscularis of the stomach and intestine. The facts above undoubtedly corroborate Prof. Romer's notion on the evolution of the vertebrate muscular system.

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Section: Correspondencementioning

confidence: 97%

Striated muscles in visceral organs of vertebrates

Субботин¹

2016

J Histol Histopathol

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“…Similar to that noted with fibrosis [4] and certain infiltrative disorders [5], amyloid deposition in the heart results in the interruption of normal cardiac impulse relay [6, 7] and may manifest as interatrial depolarization abnormalities [8]. Such abnormalities in turn are a purported arrhythmogenic substrate for atrial tachyarrhythmias, mainly atrial fibrillation [6, 7]. Using right atrial appendages that had been obtained from 245 patients undergoing open-heart surgery, Röcken et al [6] demonstrated that IAA significantly affected P wave duration and increased the risk of atrial fibrillation.…”

Section: Introductionmentioning

confidence: 99%

The Association of Atrial Tachyarrhythmias with Isolated Atrial Amyloid Disease: Preliminary Observations in Autopsied Heart Specimens

Ariyarajah¹,

Steiner²,

Hájková³

et al. 2008

Cardiology

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Objective: Isolated atrial amyloidosis (IAA) is associated with atrial tachyarrhythmias. However, only a few studies have appraised atrial tachyarrhythmias and atrial depolarization abnormalities in connection with high-grade IAA. We conducted a collaborative retrospective study to assess this association. Methods: One hundred consecutive autopsied hearts were studied histologically for IAA. To increase the specificity for atrial depolarization abnormalities in this preliminary study, we excluded those specimens with intermediate amyloid involvement, i.e. IAA grades 1 and 2 (grade 0 = absent or trivial deposits; grade 1 = small deposits; grade 2 = moderate deposits; grade 3 = dense, large deposits). We then screened for baseline, premortem electrocardiograms (ECGs) to assess rhythm. In those with sinus rhythm, the P wave axis, duration, dispersion and terminal force in V1 were determined under magnification. Results: Of the 27 premortem ECGs corresponding to the autopsy specimens with grades 3 (sample) or 0 (controls) IAA, 9 showed sinus rhythm, 13 showed atrial fibrillation, 1 showed atrial flutter and 4 were uninterpretable. Fourteen autopsied hearts (52%) were positive for grade 3 IAA. Ten of those had atrial tachyarrhythmias (9 atrial fibrillation and 1 atrial flutter) compared to 4 of the 13 hearts with grade 0 IAA (72 vs. 31%, respectively; p = 0.03). Although there was excellent interobserver agreement using intraclass correlation coefficients, there were no significant differences in P wave measurements among the small number of patients with sinus rhythm for grade 3 versus grade 0 IAA. Conclusion: In a collaborative, preliminary, pilot assessment of autopsied hearts for which premortem ECGs were necessarily screened retrospectively, significantly more hearts with high-grade IAA were associated with atrial tachyarrhythmias compared to those with low-grade IAA. A larger study with an appropriately matched autopsy control group is needed to confirm these and previous observations.

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“…In addition, myocytes in PV of AF patients were not uniform and surrounded by fibrous tissues compared with those in controls. Moreover, Steiner et al (2006) reported that amyloid deposition and scarring in myocardial sleeves t e n d e d t o b e o b s e r v e d m o r e f r e q u e n t l y i n AF patients relative to control patients. Interestingly, the incidence of atrial myocardium extending beyond the PV-LA junction up to the PV periphery in all the examined PV specimens is commonly reported to be 88 to 89% (Tagawa et al, 2001;Steiner et al, 2006).…”

Section: Myocardial Sleeves In Pvmentioning

confidence: 99%