Myocardial protein aggregates in pet guinea pigs

2021 ◽  
pp. 030098582110425
Author(s):  
Teresa Southard ◽  
Kathleen Kelly ◽  
Anibal G. Armien

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.

2007 ◽  
Vol 117 (3) ◽  
pp. e104-e106 ◽  
Author(s):  
Yoshitaka Sakai ◽  
Yuichi Sato ◽  
Shinro Matsuo ◽  
Shinobu Imai ◽  
Taeko Kunimasa ◽  
...  

Author(s):  
A.J. Möhr ◽  
R.M. Kirberger

An 8-month-old Labrador retriever bitch was evaluated for sudden-onset, progressive abdominal distension. Physical examination revealed an exaggerated inspiratory effort, severe ascites, bilateral jugular vein distension, and hypokinetic femoral arterial pulses. Thoracic auscultation detected tachycardia with muffled heart sounds, without audible cardiac murmurs. Thoracic radiographs identified severe right ventricular enlargement and pleural effusion. The electrocardiogram was consistent with incomplete right bundle branch block or right ventricular enlargement. Echocardiography demonstrated severe right ventricular and atrial dilation, secondary tricuspid regurgitation, and thinning and hypocontractility of the right ventricular myocardium. Left heart chamber sizes were slightly decreased, with normal left ventricular contractility. Adiagnosis of arrhythmogenic right ventricular cardiomyopathy was reached, based on the characteristic clinical, electrocardiographic, radiographic and echocardiographic findings, and the exclusion of other causes of isolated right ventricular failure. Treatment effected good control of clinical signs, until acutely decompensated congestive right heart failure led to euthanasia after 4 months. Arrhythmogenic right ventricular cardiomyopathy is a well-described clinical entity in humans, and has previously been documented in 3 male dogs. The condition is characterised by progressive fibro-adipose replacement of right ventricular myocardium, while the left ventricle usually remains unaffected. It should be considered a differential diagnosis in any young dog presented with isolated right heart failure, syncope, or unexplained ventricular tachyarrhythmias. This article reports the 1st case of arrhythmogenic right ventricular cardiomyopathy in a female dog, and highlights its echocardiographic features.


2004 ◽  
Vol 26 (4) ◽  
pp. 452-454 ◽  
Author(s):  
J. Hruda ◽  
M.A. Sobotka-Plojhar ◽  
W.P.F. Fetter

2005 ◽  
Vol 15 (4) ◽  
pp. 434-436 ◽  
Author(s):  
Dursun Alehan ◽  
Omer Faruk Dogan

Ventricular noncompaction is a rare unclassified cardiomyopathy occurring because of arrest of the normal intrauterine compaction of the loose luminal component of the ventricular myocardium. There is limited data regarding its diagnosis and outcome in children. It is recognised, however, that right ventricular involvement is extremely rare. We report a case in which only the right ventricular myocardium was noncompacted, a situation which led to heart failure soon after birth.


2012 ◽  
Vol 24 (5) ◽  
pp. 867-877 ◽  
Author(s):  
Christopher R. Malherbe ◽  
Jana Marquard ◽  
David E. Legg ◽  
Kristi M. Cammack ◽  
Donal O’Toole

A syndrome of progressive right-sided heart failure occurred among yearling Holsteins at a heifer-raising facility and 2 dairies on the Colorado Front Range between 2007 and 2011. Most cases were seen at the heifer-raising facility, where the disease ranked second only to pneumonia as a major cause of death in animals aged <1.5 years. The disease resulted in the death or premature sale of 55 animals over the 5-year period. Affected heifers were 4–15 months old when they developed dyspnea, tachycardia, distention and pulsation of jugular veins, lethargy, and weight loss. Clinical progression in most was rapid (2 days to 2 weeks). Ten cattle with typical clinical signs were examined postmortem between 2008 and 2010. Seven developed clinical signs after transportation 57–238 days earlier from Wisconsin (elevation: < 275 m); the remaining 3 animals were born and raised at an altitude of 1,600 m. At necropsy, the 10 cattle had marked hypertrophy of right ventricular myocardium, dilated right atria, right ventricles, and pulmonary trunks, as well as hepatomegaly, ascites, and serous atrophy of fat. The principal histological change in lungs was hypertrophied tunicae adventitia and media of muscular arteries. Hepatic changes were typical of chronic passive congestion. Ultrastructural changes in heart were consistent with uncomplicated hypertrophy of cardiocytes with no evidence of primary cardiomyopathy. The syndrome most likely represents brisket disease due to pulmonary hypertension at the modest elevation of 1,600 m.


2019 ◽  
Vol 72 (8) ◽  
pp. 1491-1493
Author(s):  
Viktor P. Boriak ◽  
Svitlana V. Shut’ ◽  
Tetiana A. Trybrat ◽  
Olena V. Filatova

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.


2020 ◽  
pp. 13-17
Author(s):  
Dmitrii Aleksandrovich Lopyn ◽  
Stanislav Valerevich Rybchynskyi ◽  
Dmitrii Evgenevich Volkov

Currently the electrophysiological treatment options have been considered to be the most effective for many patients with arrhythmogenic cardiomyopathies, as well as in those with arrhythmias on the background of heart failure. Currently, the dependence of efficiency of the pacemakers on the location of the electrodes has been proven. In order to study the effect of a myocardial dysynchrony on the effectiveness of pacing depending on the location of the right ventricular electrode, an investigation has been performed. This study comprised the patients with a complete atrioventricular block, preserved ejection fraction of the left ventricle (more than 50 %), with no history of myocardial infarction, who were implanted with the two−chamber pacemaker. It has been established that the best results were achieved with a stimulation of the middle and lower septal zone of the right ventricle, the worst ones were obtained with a stimulation of its apex. It has been found that the dynamics of the magnitude of segmental strains and a global longitudinal strain coincided with the dynamics of other parameters of the pacemaker effectiveness, which indicated the pathogenetic value of myocardial dysynchrony in the progression of heart failure after implantation of the pacemaker. Therefore it could be concluded that the studying of myocardial mobility by determining a longitudinal strain for assessing the functional state of the myocardium and the effectiveness of pacing is highly advisable. It is emphasized that the use of the latest strains−dependent techniques for cardiac performance evaluation in the patients with bradyarrhythmia have a great potential to predict the development of chronic heart failure and to choose the optimal method of physiological stimulation of the heart. Key words: right ventricular lead, cardiac stimulation, myocardial dyssynchrony.


2020 ◽  
Author(s):  
Jagjit Khosla ◽  
Reshma Golamari ◽  
Alice Cai ◽  
Jamal Benson ◽  
Wilbert S Aronow ◽  
...  

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disorder resulting in fibrofatty replacement of the myocardium. Genetic mutations in genes encoding for desmosome proteins result in a ventricular myocardium prone to arrhythmias and heart failure. Although ARVC is known for a few decades, most of the outcomes in pregnancy are reported recently. Pregnancy leads to significant physiological changes with excess mechanical stress on the myocardium. All the retrospective studies suggest that pregnancy is well tolerated in these patients despite the high risk of arrhythmias and heart failure. Our review focuses on the most up-to-date evidence on the management of ARVC patients during the antepartum and postpartum period.


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