Use of an Implantable Loop Recorder in a Chimpanzee (Pan troglodytes) to Monitor Cardiac Arrhythmias and Assess the Effects of Acupuncture and Laser Therapy

Cardiovascular disease is a leading cause of death in captive chimpanzees and is often associated with myocardial fibrosis, which increases the risk of cardiac arrhythmias. In this case report, we present a 36-y-old male chimpanzee (Pan troglodytes) diagnosed with frequent ventricular premature complexes (VPC). We placed a subcutaneous implantable loop recorder for continual ECG monitoring to assess his arrhythmias without the confounding effects of anesthetics. During his initial treatment with the antiarrhythmia medication amiodarone, he developed thrombocytopenia, and the drug was discontinued. After reviewing other potential therapies for the treatment of cardiac arrhythmias, we elected to try acupuncture and laser therapy in view of the positive results and the lack of adverse side effects reported in humans. We used 2 well-known cardiac acupuncture sites on the wrist, PC6 (pericardium 6) and HT7 (heart 7), and evaluated the results of the therapy by using the ECG recordings from the implantable loop recorder. Although periodic increases in the animal''s excitement level introduced confounding variables that caused some variation in the data, acupuncture and laser therapy appeared to decrease the mean number of VPC/min in this chimpanzee.Abbreviations: HT7, acupuncture site heart 7; ILR: implantable loop recorder; PC6: acupuncture site pericardium 6; VPC, ventricular premature complexesCardiovascular disease is one of the leading causes of death in captive chimpanzees (Pan troglodytes).^9,15 This incidence represents a similarity to humans, in whom cardiovascular disease is also the leading cause of death,⁸ although the pathologic processes differ between these species. Although human heart disease generally results from coronary artery atherosclerosis, heart disease in chimpanzees is associated with a diffuse interstitial myocardial fibrosis;³¹ however, both processes can be fatal. A survey of 87 deceased adult chimpanzees found evidence of cardiac disease in 68% of the cases, among which it was the primary cause of death in 34%.²⁶ At another NHP facility, 38% (n = 13) of all deaths reported in a 6-y period were associated with sudden cardiac death.¹⁴ All of these animals had been diagnosed with various degrees of cardiomyopathy prior to death, and 12 of the 13 cases were diagnosed with interstitial myocardial fibrosis according to histology.¹⁴Myocardial fibrosis is correlated with an increased risk of cardiac arrhythmias^2,7 and is a common cause of sudden cardiac death in chimpanzees, occurring much more frequently in male than in female chimps.^12,29,31 In chimpanzees, interstitial myocardial fibrosis has a random distribution throughout the myocardium. As the fibrosis progresses, it is thought to disrupt cardiac electrical signals, potentially leading to a fatal arrhythmia that presents as a sudden cardiac death.³¹ The mechanism underlying interstitial myocardial fibrosis is not entirely understood but might be related to age-associated activation of fibroblasts and diminished reparative stimuli.¹ In addition, inflammation might play a role in the development of interstitial myocardial fibrosis, given that cardiac fibrosis and remodeling are common sequelae to inflammation.¹¹ Other factors that increase the risk of developing cardiac arrhythmias in chimpanzees include age (older than 30 y), male sex, and structural heart disease.^4,12Given the high rate of mortality caused by cardiovascular disease in chimpanzees, detecting the disease early and beginning appropriate therapeutics are important. Electrocardiography is a simple diagnostic test that can detect cardiac rhythm abnormalities. However, anesthesia can serve as a confounding variable during ECG analysis of sedated chimpanzees. For the safety of both people and animals during physical examinations, chimpanzees are sedated by using tiletamine–zolazepam; anesthesia is then maintained with isoflurane. These anesthetic agents can cause decreases in heart rate, blood pressure, and cardiac output, as well as respiratory depression.²⁰ In humans, the inhalant agent isoflurane prolongs the QT interval, and this prolonged cardiac repolarization can cause ventricular arrhythmias.²⁸ Given the limited application of tiletamine–zolazepam, which primarily is used as a veterinary drug, no information regarding the association of tiletamine–zolazepam with cardiac arrhythmias in humans is available. However, cardiac arrhythmias are not uncommon in sedated chimpanzees, in which the most common arrhythmia is ventricular premature complexes (VPC).^4,27 Although VPC can occur in sedated chimpanzees with no apparent adverse effects, multiform VPC are associated with the highest risk of mortality.⁴Acknowledging the confounding effects of anesthesia in evaluation of ECG and cardiac arrhythmias, assessing ECG data from a nonsedated chimpanzee likely would be beneficial. In this report, we present a case in which we subcutaneously implanted a cardiac loop recorder to obtain ECG data longitudinally from a nonsedated chimpanzee. This technique was used successfully previously to investigate cardiac arrhythmias in 4 adult chimpanzees.¹³ Here we present the ECG findings from a male chimpanzee with cardiac arrhythmia and describe the effects of both antiarrhythmic pharmaceutical agents and the use of integrative medicine in treating the arrhythmia.     

An Isoprene Lipid-Binding Protein Promotes Eukaryotic Coenzyme Q Biosynthesis

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Sphingosine-1-phosphate signaling in vasculogenesis and angiogenesis

Blood vessels either form de novo through the process of vasculogenesis or through angiogenesis that involves the sprouting and proliferation of endothelial cells in pre-existing blood vessels. A complex interactive network of signaling cascades downstream from at least three of the nine known G-protein-coupled sphingosine-1-phosphate (S1P) receptors act as a prime effector of neovascularization that occurs in embryonic development and in association with various pathologies. This review focuses on the current knowledge of the roles of S1P signaling in vasculogenesis and angiogenesis, with particular emphasis on vascular cell adhesion and motility responses.     

Invasive plants in conservation linkages: a conceptual model that addresses an underappreciated conservation issue

Conservationists have frequently touted the merits of increased landscape connectivity, usually focusing on the efficacy of conservation linkages (corridors) for maintaining viable populations of target species. An often‐mentioned, but still greatly understudied, concern is that increased landscape connectivity via linkages may also aid the movement of undesired species. This paper provides conceptual guidance for research on one major aspect of this gap: invasive plants in conservation linkages. To guide research goals and methods, I develop a conceptual model describing eight interaction types between invasive plants and linkages, i.e. the ways that invasive plants can exist in and move into, through, and out of conservation linkages. Each interaction type within the model has three main components: linkage, matrix, and focal species. I discuss several aspects of these components, including a) differentiating among matrix types, b) understanding edge effects within the linkages, and c) incorporating relevant invasive species’ ecology (primarily dispersal ecology). Spatially‐explicit documentation of invasive plant distribution is essential to understanding these interactions. By focusing on landscape‐scale patterns in real‐world systems, this model will enhance landscape‐level knowledge of invasion ecology and aid land managers in identifying and prioritizing research and management decisions regarding invasive plants in conservation linkages.     

Evolution of mitochondrial and ribosomal gene sequences in anophelinae (Diptera: Culicidae): implications for phylogeny reconstruction

In this study, two mitochondrial genes, cyt b and ND5, and the D2 expansion segment of the 28S nuclear ribosomal gene were used to reconstruct a phylogeny of the mosquito subfamily Anophelinae. The ingroup consisted of all three genera of Anophelinae and five of six subgenera of Anopheles. Six genera of Culicinae were used as the outgroup. Extreme conservation at the protein level coupled with rapid saturation of synonymous positions probably accounted for the lack of meaningful phylogenetic signal in the cyt b gene. In contrast, abundant variation at all codon positions of the ND5 gene allowed recovery of the basal and most of the recent relationships. Phylogenetic analysis of D2 produced results consistent with those of ND5. Combined analysis indicated well-supported monophyletic Anophelinae (with Chagasia basal), Anopheles + Bironella, and subgeneric clades within the genus Anopheles. Moreover, subgenera Nyssorhynchus and Kerteszia were supported as a monophyletic lineage. The Kishino-Hasegawa test could not reject the monophyly of Anopheles, whereas the recently proposed hypothesis of close affinity of Bironella to the subgenus Anopheles was rejected by the analyses of ND5 and combined data sets. The lack of resolution of Bironella and Anopheles clades, or basal relationships among subgeneric clades within Anopheles, suggests their rapid diversification. Recovery of relationships consistent with morphology and previous molecular studies provides evidence of substantial phylogenetic signal in D2 and ND5 genes at levels of divergence from closely related species to subfamily in mosquitoes.     

Disability and <Emphasis Type="Italic">Depression</Emphasis>

Here, Ann Cvetkovich, interviewed by Abby Wilkerson, brings Cvetkovich’s influential cultural studies analysis of depression explicitly into conversation with disability studies. Cvetkovich understands “feeling bad” (a term she prefers to “depression”) as a defining affective state under neoliberalism. Drawing on a distinctive historical/cultural archive, she challenges the atomism of the neoliberal medical model that frames depression and affective distress more generally as the result of faulty brain chemistry—individual organisms gone awry. Instead, she traces these common experiences to sociopolitical phenomena ranging from current neoliberal demands for productivity as exemplified in university life, to histories of colonization, slavery, and displacement. The conversation considers the value of disability frameworks for understanding mental health diagnoses and the intersections of social institutions, bodily practices, and everyday affective life.