The kinetics of cytosolic calcium in the right ventricular myocardium of guinea pigs and rats

A retrospective study of guinea pigs submitted for necropsy revealed intracytoplasmic inclusions in the cardiomyocytes of 26 of 30 animals. The inclusions were found with approximately the same frequency in male and female guinea pigs and were slightly more common in older animals. In most cases, the animals did not have clinical signs or necropsy findings suggestive of heart failure, and the cause of death or reason for euthanasia was attributed to concurrent disease processes. However, the 4 guinea pigs with the highest inclusion body burden all had pulmonary edema, sometimes with intra-alveolar hemosiderin-laden macrophages, suggestive of heart failure. The inclusions were found in both the left and right ventricular myocardium, mainly in the papillary muscles, but were most common in the right ventricular free wall. No inclusions were detected in the atrial myocardium or in skeletal muscle. The inclusions did not stain with Congo red or periodic acid–Schiff. Electron microscopy revealed dense aggregates of disorganized myofilaments and microtubules that displaced and compressed the adjacent organelles. By immunohistochemistry, there was some scattered immunoreactivity for desmin and actin at the periphery of the inclusions and punctate actin reactivity within the aggregates. The inclusions did not react with antibodies to ubiquitin or cardiac myosin, but were variably reactive for alpha B crystallin, a small heat shock chaperone protein. The inclusions were interpreted as evidence of impaired proteostasis.

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CONDITION OF HEMODYNAMICS IN THE PULMONARY CIRCULATION OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) CONCURRENT WITH METABOLIC SYNDROME WITH HYPERTROPHY AND ATROPHY OF THE MYOCARDIUM

Wiadomości Lekarskie ◽

10.36740/wlek201908114 ◽

2019 ◽

Vol 72 (8) ◽

pp. 1491-1493

Author(s):

Viktor P. Boriak ◽

Svitlana V. Shut’ ◽

Tetiana A. Trybrat ◽

Olena V. Filatova

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Metabolic Syndrome ◽

Right Ventricular ◽

Pulmonary Disease ◽

Pulmonary Circulation ◽

Contractile Function ◽

Ventricular Myocardium ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

The Right

Introduction: In recent years, COPD is observed as not an isolated, but an associated pathology, in particular, concurrent with metabolic syndrome. The aim of the research is to identify the differences in changes of the rheopulmonography parameters (RPG) depending on the presence of hypertrophy or atrophy of the right ventricular myocardium in patients with COPD concurrent with metabolic syndrome.. Materials and methods: We studied changes in rheopulmonography (RPG) in 145 patients with chronic obstructive pulmonary disease (COPD) concurrent with metabolic syndrome. Results: We detected precapillary hypertension of the pulmonary circulation in patients with right ventricular myocardial hypertrophy: anacrotism serration; flattened peak of the systolic wave; decreased Vcp; high placement of incisura; horizontal course of catacrotism; decreased amplitude of the systolic wave (in this case, due to a greater increase in the resistance of the blood flow in the pulmonary vessels than the decreased impact volume of the right ventricle); prolonged Q-a (in this group of patients, it depends more on hypertension of the pulmonary circulation than on the reduction of contractile function of the myocardium). In atrophy of the right ventricular myocardium, the following changes in the RPG were revealed: decreased systolic wave at its dramatic rise; prolonged Q-a (in this case, due to the weakened heart contraction); Vmax reduction (it reflects the reduction of myocardial contractility); in hypertrophy of the myocardium, Vcp., unlike RPG, does not decrease, which is explained by the decrease in the pressure of the pulmonary circulation. Conclusions: We believe that these changes in RPG allow differentiating hypertrophy and right ventricular myocardial atrophy along with established diagnostic criteria, and can be used as markers for the diagnosis and treatment of COPD concurrent with metabolic syndrome.

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Stress-induced ischemia in the right ventricular myocardium on 99mTc-MIBI myocardial perfusion scintigraphy in a rare case of double-chambered right ventricle

Journal of Nuclear Cardiology ◽

10.1007/s12350-018-01528-4 ◽

2018 ◽

Vol 26 (6) ◽

pp. 2148-2150

Author(s):

Shelvin Kumar Vadi ◽

Palanivel Rajan ◽

Ashwani Sood ◽

Manoj Kumar Rohit ◽

Madan Parmar ◽

...

Keyword(s):

Myocardial Perfusion ◽

Right Ventricle ◽

Right Ventricular ◽

Rare Case ◽

Myocardial Perfusion Scintigraphy ◽

Ventricular Myocardium ◽

Perfusion Scintigraphy ◽

99Mtc Mibi ◽

The Right

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Myocyte Transdifferentiation

Archives of Pathology & Laboratory Medicine ◽

10.5858/2000-124-0287-mt ◽

2000 ◽

Vol 124 (2) ◽

pp. 287-290 ◽

Cited By ~ 3

Author(s):

Giulia d'Amati ◽

Cira R. T. di Gioia ◽

Carla Giordano ◽

Pietro Gallo

Keyword(s):

Right Ventricular ◽

Transplant Patient ◽

Arrhythmogenic Right Ventricular Cardiomyopathy ◽

Ventricular Myocardium ◽

Ventricular Cardiomyopathy ◽

Familial Dilated Cardiomyopathy ◽

Familial Cardiomyopathy ◽

New Type ◽

The Right ◽

Gross Examination

Abstract Adipose substitution of ventricular myocardium is characteristic of arrhythmogenic right ventricular cardiomyopathy, but is also found in other heart conditions. It is thought to be a consequence of myocyte loss due to myocarditis or other noxious stimuli. We describe a unique case of cardiomyopathy with a morphologic pattern suggestive of transdifferentiation from myocytes to mature adipocytes. Gross, histologic, and ultrastructural examination were performed on the heart of a female transplant patient with a clinical diagnosis of familial dilated cardiomyopathy. Gross examination showed fibroadipose substitution of the left ventricle and adipose replacement of the right. Histology, immunohistochemistry, and ultrastructure were highly suggestive of transdifferentiation from cardiac muscle to adipose tissue. Myocyte transdifferentiation could represent an alternative pathogenetic pathway to the myocyte-loss and adipose-replacement mechanism in arrhythmogenic right ventricular cardiomyopathy, or it could be the basis of a new type of familial cardiomyopathy.

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