scholarly journals Right ventricular hypertrophy with heart failure in Holstein heifers at elevation of 1,600 meters

2012 ◽  
Vol 24 (5) ◽  
pp. 867-877 ◽  
Author(s):  
Christopher R. Malherbe ◽  
Jana Marquard ◽  
David E. Legg ◽  
Kristi M. Cammack ◽  
Donal O’Toole
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Clinical Signs ◽  
Histological Change ◽  
Ventricular Myocardium ◽  
Colorado Front Range ◽  
Ultrastructural Changes ◽  
Front Range ◽  
Jugular Veins ◽  
Right Atria

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.

scholarly journals Arrhythmogenic right ventricular cardiomyopathy in a dog : case report

2000 ◽  
Vol 71 (2) ◽  
Author(s):  
A.J. Möhr ◽  
R.M. Kirberger
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Clinical Signs ◽  
Right Heart Failure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Ventricular Enlargement ◽  
Ventricular Cardiomyopathy ◽  
Right Heart

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.

Myocardial protein aggregates in pet guinea pigs

2021 ◽  
pp. 030098582110425
Author(s):  
Teresa Southard ◽  
Kathleen Kelly ◽  
Anibal G. Armien
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Guinea Pigs ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Body Burden ◽  
Ventricular Myocardium ◽  
Right Ventricular Free Wall ◽  
Periodic Acid Schiff ◽  
The Right

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.

Evidence-based management of arrhythmogenic right ventricular cardiomyopathy in pregnancy

2020 ◽  
Author(s):  
Jagjit Khosla ◽  
Reshma Golamari ◽  
Alice Cai ◽  
Jamal Benson ◽  
Wilbert S Aronow ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Retrospective Studies ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Genetic Disorder ◽  
Ventricular Myocardium ◽  
Evidence Based ◽  
Ventricular Cardiomyopathy ◽  
Genes Encoding ◽  
In Pregnancy

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.

Abstract 1247: Heart Function is Transiently Sustained Despite a Near Loss of SERCA2 Protein in Cardiomyocyte-specific Serca2 null Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Kristin B Andersson ◽  
Alexandra V Finsen ◽  
Ivar Sjaastad ◽  
Yibin Wang ◽  
Ju Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Clinical Signs ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Lung Weight ◽  
Adult Mice

The SERCA2 Ca 2+ ATPase is of central importance for refilling of the sarcoplasmic reticulum (SR) Ca 2+ store and cardiac contractility. Reduced SERCA2 function is associated with heart failure. We hypothesized that loss of SERCA2 would result in immediate severe myocardial contractile dysfunction and death. Transgenic mice were generated with a Cre-loxP strategy in which tamoxifen induces Serca2 ( Atp2a2 ) gene excision in the cardiomyocytes (SERCA2KO) of adult mice. In SERCA2KO mice, SERCA2 protein was rapidly reduced in left ventricular myocardium with a half-life < 3 days. After 4 weeks, SERCA2 protein was reduced to < 5% of control values. In isolated cardiomyocytes, SERCA2a, SERCA2b, SERCA1 and SERCA3 proteins were not detectable. Strikingly, SERCA2KO mice did not present clinical signs of circulatory failure at 4 weeks. Fractional shortening was preserved, and cardiac output was reduced to 80% of control values. The left atrial diameter, lung weight and left ventricular end-diastolic pressure (LVEDP) were slightly increased in SERCA2KO mice compared with controls, and the maximal rates of pressure development and decline in the left ventricle were affected with a prolongation of the ventricular relaxation time. After seven weeks, SERCA2KO mice developed severe congestive heart failure with dilated chambers, elevated LVEDP and pronounced increases in lung and atrial weights. Cardiac output was reduced to 70% of control values. There were no indications of major cardiomyocyte disarray in the myocardium at the 4 or 7 week timepoints. The abundance of Na + ,Ca 2+ exchanger, L-type Ca 2+ channel 1c and alpha2delta1 subunit proteins and Pmca1 mRNA were all increased at 4 and 7 weeks. The expression of calsequestrin protein and Ryr2 mRNA were unchanged. L-type Ca 2+ channel alpha2delta1 subunit and PMCA1 expression were further enhanced at 7 weeks in SERCA2KO mice. Thus, cardiac function is supported in SERCA2KO mice for several weeks despite the near absence of SERCA2 protein. Alterations in the expression of Ca 2+ transporting proteins suggest that Ca 2+ transients are generated over the plasma membrane rather than the SR. However, the adaptations induced by loss of SERCA2 are not sufficient for long-term support of heart function in adult mice.

Transient Postnatal Heart Failure Caused by Noncompaction of the Right Ventricular Myocardium

2004 ◽  
Vol 26 (4) ◽  
pp. 452-454 ◽  
Author(s):  
J. Hruda ◽  
M.A. Sobotka-Plojhar ◽  
W.P.F. Fetter
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Ventricular Myocardium ◽  
The Right

Right ventricular noncompaction in a neonate with complex congenital heart disease

2005 ◽  
Vol 15 (4) ◽  
pp. 434-436 ◽  
Author(s):  
Dursun Alehan ◽  
Omer Faruk Dogan
Keyword(s):  
Heart Failure ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Right Ventricular ◽  
Congenital Heart ◽  
Ventricular Myocardium ◽  
Complex Congenital Heart Disease ◽  
Limited Data ◽  
Ventricular Noncompaction ◽  
The Right

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.

METABOLIC SIGNATURE OF HUMAN RIGHT VENTRICULAR MYOCARDIUM IN END STAGE HEART FAILURE

2020 ◽  
Vol 75 (11) ◽  
pp. 1043
Author(s):  
Giovanni Davogustto ◽  
Jean Wassenaar ◽  
Fan Run ◽  
Haocan Song ◽  
Fei Ye ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Ventricular Myocardium ◽  
Human Right ◽  
Metabolic Signature ◽  
End Stage Heart Failure ◽  
End Stage

Myocyte cytoskeletal disorganization and right heart failure in hypoxia-induced neonatal pulmonary hypertension

2000 ◽  
Vol 279 (3) ◽  
pp. H1365-H1376 ◽  
Author(s):  
Matthew S. Lemler ◽  
Roger D. Bies ◽  
Maria G. Frid ◽  
Amornrate Sastravaha ◽  
Lawrence S. Zisman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Total Content ◽  
Immunohistochemical Analysis ◽  
Right Heart Failure ◽  
Barometric Pressure ◽  
Ventricular Myocardium ◽  
Cytoskeletal Proteins ◽  
Right Heart

Previous studies have demonstrated that environmentally or genetically induced changes in the intracellular proteins that compose the cytoskeleton can contribute to heart failure. Because neonatal right ventricular myocytes are immature and are in the process of significant cytoskeletal change, we hypothesized that they may be particularly susceptible to pressure stress. Newborn calves exposed to hypobaric hypoxia (barometric pressure = 430 mmHg) for 14 days developed severe pulmonary hypertension (pulmonary arterial pressure = 101 ± 6 vs. 27 ± 1 mmHg) and right heart failure compared with age-matched controls. Light microscopy showed partial loss of myocardial striations in the failing neonatal right but not left ventricles and in neither ventricle of adolescent cattle dying of altitude-induced right heart failure. In neonatal calves, immunohistochemical analysis of the cytoskeletal proteins (vinculin, metavinculin, desmin, vimentin, and cadherin) showed selectively, within the failing right ventricles, patchy areas characterized by loss and disorganization of costameres and intercalated discs. Within myocytes from the failing ventricles, vinculin and desmin were observed to redistribute diffusely within the cytosol, metavinculin appeared in disorganized clumps, and vimentin immunoreactivity was markedly decreased. Western blot analysis of the failing right ventricular myocardium showed, compared with control, vinculin and desmin to be little changed in total content but redistributed from insoluble (structural) to soluble (cytosolic) fractions; metavinculin total content was markedly decreased, tubulin content increased, particularly in the structural fraction, and cadherin total content and distribution were unchanged. We conclude that hypoxic pulmonary hypertensive-induced neonatal right ventricular failure is associated with disorganization of the cytoskeletal architecture.

Clinical Features of English Bulldogs with Presumed Arrhythmogenic Right Ventricular Cardiomyopathy: 31 Cases (2001–2013)

2018 ◽  
Vol 54 (2) ◽  
pp. 95-102 ◽  
Author(s):  
Suzanne M. Cunningham ◽  
Joseph T. Sweeney ◽  
John MacGregor ◽  
Bruce A. Barton ◽  
John E. Rush
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sudden Death ◽  
Right Ventricular ◽  
Clinical Features ◽  
Clinical Characteristics ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Clinical Signs ◽  
Ventricular Cardiomyopathy ◽  
Kaplan Meier

ABSTRACT Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an important cause of sudden death in people and boxer dogs that has recently been described in English bulldogs. The objective of this retrospective study was to describe the clinical characteristics of English bulldogs with presumed ARVC. The medical records were searched for English bulldogs examined between 2001 and 2013 with a clinical diagnosis of ARVC. The average age of the 31 dogs identified was 9.2 ± 1.6 yr (range 7–13 yr). Males were overrepresented by a factor of 2.9 to 1. At initial presentation, 5 dogs had subclinical arrhythmia, 10 dogs had clinical signs attributable to arrhythmia, and 16 dogs had congestive heart failure. Eighteen dogs (58%) had ventricular tachycardia and five (16%) also had supraventricular arrhythmias. Four dogs experienced sudden death, 2 dogs died from congestive heart failure, 11 dogs were euthanized for cardiac causes, and 2 dogs died or were euthanized for noncardiac causes. Kaplan-Meier analysis showed a median survival time of 8.3 mo. This is the first study to describe the clinical characteristics of a population of English bulldogs with presumed ARVC. Further studies are needed to better characterize the clinical features of the disease in this breed.

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