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Myocardial bundles working as accessory pathways in Wolff-Parkinson-White (WPW) syndrome are generally tiny tissues, so elucidating the culprit histology of atrioventricular (AV) myocardial connections requires careful serial sectioning of the AV junction. We performed a postmortem examination of accessory AV myocardial connections in an 84-year-old man who died from pneumonia 20 years after surgical cryoablation for WPW syndrome. Three-dimensional reconstruction images of serial histologic sections revealed accessory AV connections between the atrial and ventricular myocardium in the vicinity of the cryoablation scar. The remnant myocardial bridge was 4 mm wide and made up of multiple discontinuous fibers. This case was informative in that it provided for visualization of the histologic morphology of a remnant bundle of Kent.

A highly sensitive method was developed for the analysis of alendronate in human plasma and dialysate using MonoSpin™ SAX® extraction and metal-free high-performance liquid chromatography (HPLC)-tandem mass spectrometry (MS/MS) following methylation with trimethylsilyldiazomethane. The chromatographic separation of the derivatives for alendronate and alendronate-d6 was achieved on an L-column2 ODS metal-free column (50 mm × 2 mm i.d., particle size 3 µm) with a linear gradient elution system composed of 10 mM ammonium acetate (pH 6.8) and acetonitrile at a flow rate of 0.3 ml/min. Quantification was performed by multiple reaction monitoring (MRM) with positive-ion electrospray ionization (ESI). Distinct peaks were observed for alendronate and for the internal standard on each channel within 1 min. The regression equations showed good linearity within the ranges of 2.0-100 ng/0.5 ml for the plasma and 1.0-100 ng/0.5 ml for the dialysate, with the limits of detection at 1.0 ng/0.5 ml for the plasma and 0.5 ng/0.5 ml for the dialysate. Extraction efficiencies for alendronate for the plasma and dialysate were 41.1-51.2% and 63.6-73.4%, respectively. The coefficient of variation (CV) was ≤8.5%. The method was successfully applied to the analyses of real plasma and dialysate samples derived after intravenous administration of alendronate.

Loeffler endocarditis is a fibrous restrictive cardiomyopathy thought to be caused by persistent eosinophilia. It is difficult to diagnose, and the prognosis is often poor if the underlying eosinophilia is not promptly recognized and treated. We describe the case of a middle-aged woman treated for hypertrophic cardiomyopathy first detected during a routine check-up at age 35 years but whose symptoms gradually progressed over the next 14 years. Right ventricular biopsy showed extensive fibrosis of the endocardial tissue, and right heart catheterization revealed right heart failure and a low cardiac output state. Ultimately, she became reliant on inotropic and mechanical cardiovascular support, but we were not able to bridge her to transplant. Autopsy findings were typical of endocardial fibroelastosis, but she had not suffered from any tropical disease or traveled to high-risk areas. The presence of abnormal capillary proliferation suggested a diagnosis of Loeffler endocarditis. Nonetheless, apart from a 6-month period of eosinophilia 7 years before her death, a history of well-controlled asthma and several drug sensitivities, we were unable to definitively identify the disease trigger. It is critical to diagnose and treat the underlying eosinophilia of Loeffler endocarditis to avoid a poor prognosis. This case highlights the importance of considering the diagnosis of eosinophilic endomyocarditis in patients with an unusual pattern of apical hypertrophic cardiomyopathy (or myocardial fibrosis of unknown etiology), even when there is no apparent history of eosinophilia.

The Fontan procedure is an open heart procedure performed in pediatric patients with a particular congenital cardiac anomaly known as a univentricular heart. The procedure is used to reroute the systemic venous blood from the inferior vena cava directly to the pulmonary artery. It improves patients' prognoses, but various late-phase extracardiac complications that manifest when patients reach adolescence have been recognized. These complications, pulmonary arteriovenous fistula and protein losing gastroenteropathy, for example, present significant challenges in the management of adults with Fontan circulation. Liver fibrosis is another possible late-phase complication and one of the most serious. Development of a neoplasm, usually a hepatocellular carcinoma, is sometimes reported. We encountered a young patient in whom Fontan circulation led to the development of a histologically unusual liver cancer that resembled the poorly differentiated hepatocellular carcinoma or the combined hepatocellular-cholangiocarcinoma with stem-cell features described in the latest WHO classification.

Although percutaneous coronary intervention (PCI) routinely achieves good angiographic success, 5% to 30% of patients experience periprocedural myocardial injury (pMI), which is associated with long-term adverse outcomes and immediate adverse events [(1)][1]. Because coronary high-intensity

Background Although the pulmonary veins are accepted as preferential trigger sites for paroxysmal atrial fibrillation/flutter (AF/AFL), the intrinsic basis for reentrant excitation is undetermined in persistent AF/AFL. Objective To identify histoanatomic substrates for reentrant AF/AFL in rats. Methods Spatiotemporal patterns of impulse propagation were visualized optically on the posterior surface of the atria in di-4-ANEPPS-stained Langendorff-perfused rat heart/lung preparations. The relevant histology was also analyzed. Results Burst (S1-S2) pacing at the right atrium provoked AF/AFL in 15 of 19 hearts, and most cases developed by organized reentrant excitation through the coronary sinus (CS) and left atrial (LA) roof, with nonorganized irregular propagation in 3 cases. The reentrant circuit developed along 2 pathways of propagation: a slower pathway at the LA roof (conduction velocity, 42.4 ± 16.6 cm/s) and a faster pathway along the CS (conduction velocity, 53.3 ± 9.2 cm/s). Upon extra stimulus (S2) after consecutive S1 pacing, the impulse at the roof propagated retrogradely from the CS, resulting in reentrant propagation anchored by the atrial septum and posterior LA. Histologic quantification revealed significantly lower myocardial density in the posterior LA and the septum than elsewhere in the atria. Moreover, myocytes in the LA roof, than in the CS, were of lower density, more randomly arranged in the direction of conduction, and characterized by more disorganized distribution of connexin 43 over the entire cell membrane, which is consistent with the slower impulse propagation there. Conclusion The intrinsic histoanatomic heterogeneity in the LA would constitute a pro-reentrant substrate responsible for perpetuating AF/AFL.

Dilated cardiomyopathy (DCM) is a major cause of end-stage heart failure. Myocardial infiltrative inflammatory cells are considered to play some role in ongoing myocardial damage and tissue remodeling. Tenascin-C (TN-C), an extracellular matrix glycoprotein, becomes expressed in myocardium under the

Introduction: Imbalanced autonomic activity in the area of the pulmonary veins (PVs) can result in spontaneous atrial fibrillation (AF). Histologic characteristics of the PV sleeve musculature and associated autonomic nerve are not fully understood. We investigated the arrangement of autonomic nerve fibers around PV-left atrium (LA) junctional musculature. Methods: Thirteen autopsied adult hearts (9 men and 4 women; mean age at death, 66.2 years were studied. The atria were removed from each heart, along with all PV stalks, and cut longitudinally to each PV myocardial sleeve. After treatment with azan-Mallory stain and immunohistochemical staining for S-100 and tyrosine hydroxylase (TH), autonomic nerve distribution was assessed by counting the numbers of TH-positive (adrenergic and -negative (non-adrenergic) fibers within S-100-positive fibers (>50 mm in diameter) in the anterior, posterior, and septal junctions. Results: TH-positive adrenergic fibers, consisting of sympathetic nerves, were most predominant in the anterior and septal junctions. In the anterior junction, these fibers were packed tightly among myocardial sleeve fascicles. In the posterior junction, the numbers of adrenergic and non-adrenergic fibers were fewer. In the septal junction, the number of THnegative non-adrenergic fibers (predominantly parasympathetic nerves) was greater, concomitant diffuse ganglionic nodule distribution in the interatrial fat pad. Conclusions: In each PV-LA junction, autonomic nerves were localized on the anterior and septal walls. Heterogeneous distribution of TH-positive and TH-negative fibers and ganglion nodules around each PV opening appears to represent the major histologic characteristic in these areas.

Segmental arterial mediolysis is an unusual arterial lesion for which pathogenesis has remained controversial. We report on a 47-year-old Japanese woman who underwent surgery for an abdominal aortic aneurysm that was 10.5 cm in diameter and contiguous with a left common iliac aneurysm that was 2.3 cm in diameter; the aneurysms were considered to have progressed rapidly in size. Pathologic examinations of the respective aneurysms showed cystic medial necrosis in the aortic and segmental arterial mediolysis in the iliac aneurysm. Coexistence of these two pathologic findings indicates that there may be a strong relation between these two disease entities.

Background Dendritic cells ( DC ) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post‐infarction healing process after experimental myocardial infarction ( MI ). However, its clinical significance has not been determined. Methods and Results The degree of DC infiltration and its correlation with the post‐infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST ‐elevation MI . Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD 68 + macrophage infiltration was increased and CD 209 + DC , and CD 11c + DC infiltration and the extent of reparative fibrosis were decreased compared with the non‐rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD 209 + DC , and CD 11c + DC and the extent of reparative fibrosis. Conclusions Decreased number of DC in human‐infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI . These findings suggest a protective role of DC in post‐ MI inflammation and the subsequent healing process.

Neopterin, a GTP metabolite produced by activated macrophages, has been regarded as a pro-inflammatory agent. However, the modulatory effect of neopterin on atherosclerosis has not yet been reported. We investigated the atheroprotective effects of neopterin on HUVECs, human monocyte-derived

Kisspeptin-10 (KP-10), a potent vasoconstrictor and inhibitor of angiogenesis expressed in vascular endothelial cells (ECs), has currently received much attention as a potential regulator in cardiovascular diseases. However, it still remains unknown whether KP-10 could affect atherogenesis. We

s / Placenta 36 (2015) A1eA14 A8 pointed out severe fetal growth restriction and placental enlargement by ultrasonography in 22 gestational weeks. At the time of her hospitalization with PIH, ultrasonography revealed a placental hyperplasia with low echoic area at the site of retroplacental space. 3 weeks later, regular uterine contractions and abnormal laboratory date such as low levels of fibrinogen and hemoglobin were observed. By ultrasonography, intrauterine fetal death (IUFD) and increase in retroplacental structure were confirmed. Pathologically, inetrvillous thrombus and massive perivillous fibrinoid deposition were observed. Clinically, we guessed that placental dysfunction by retroplacental and intraplacental hematomas were the cause of FGR and IUFD. We concluded that chronic placental dysfunction was the cause of IUFD. JPA2015-29. NOVEL PATHOLOGICAL FINDINGS OF PLACENTA WITH FETAL HEART FAILURE ASSOCIATED WITH CONGENITAL HEART DISEASE Takekazu Miyoshi , Taka-aki Matsuyama, Atsushi Daimon , Chi-ichiro Kuwazuru , Masami Sawada , Hiroshi Sato , Chinami Horiuchi , Mitsuhiro Tsuritani , Naoko Iwanaga , Jun Yoshimatsu , Hatsue Ueda-Ishibashi . Department of Perinatology and Gynecology, National Cerebral and Cardiovascular Center, Japan; Department of Pathology, National Cerebral and Cardiovascular Center, Japan Objective: We investigated the pathological findings of placenta with fetal heart failure associated with congenital heart disease (CHD). Methods: A retrospective evaluation in single-center was performed in 123 placentas of fetuses with CHD between 2011 and 2014. The same pathologist evaluated presence and degree of the following items in placenta under blinded clinical information. 1) dysplastic villi, 2) edema of villi, 3) lymphatic duct-like vessels, 4) fibrosis of villi, 5) chorioamnionitis, 6) chorangiosis, 7) perivillous fibrin deposition, 8) subchorionic hematoma, 9) infarction, 10) nucleated erythrocyte, 11) single umbilical artery. Fetal heart failure was evaluated by cardiovascular profile score (CVPS) using echocardiography. CHD was categorized as 6 physiologies; isomerism (n1⁄419), hypoplastic left heart syndrome (n1⁄410), hypoplastic right ventricle (n1⁄415), cyanotic heart defects with biventricular (n1⁄431), acyanotic heart defects (n1⁄424) and arrhythmia (n1⁄424). Results: Of 123 placentas, dysplastic villi (n1⁄412), advanced edema of villi (n1⁄44), fibrosis of villi (n1⁄424) and nucleated erythrocyte (n1⁄420) were confirmed, which were associated with low CVPS, respectively (p

Background Takaytasu aortitis (TA) is an inflammatory large-vessel vasculitis of unknown origin. In rare cases, isolated aortitis (IA) is usually diagnosed by its incidental microscopic findings after ascending aortic surgery. Some of isolated aortitis are thought to be IgG-4 related disease. Methods We compared 52 TA patients and 7 IA patients who underwent aortic surgery to investigate clinical and histopathological features. Results Patients with TA were older than IA patients (M/F; 3/4) (median 56 vs 78 years; p Conclusions In comparison to IA, TA tends to show poor clinical outcome because of its multiple vascular damage. Clinically, isolated aortitis may be a distinct disease of TA. IA was also considered in case of ascending aortic aneurysm.