Stress cardiomyopathy in stranded cetaceans: a histological, histochemical and immunohistochemical study

2019 ◽  
Vol 185 (22) ◽  
pp. 694-694 ◽  
Author(s):  
Nakita Câmara ◽  
Eva Sierra ◽  
Carolina Fernández-Maldonado ◽  
Antonio Espinosa de los Monteros ◽  
Manuel Arbelo ◽  
...  

BackgroundFree-living cetaceans are exposed to a wide variety of stressful situations, including live stranding and interaction with human beings (capture myopathy), vessel strikes, and fishing activities (bycatch), which affect their wellbeing and potentially lead to stress cardiomyopathy (SCMP).MethodsHere, the authors aimed to characterise SCMP of stranded cetaceans as an injury resulting from extreme stress responses, based on pathological analyses (histological, histochemical and immunohistochemical). Specifically, the authors examined heart samples from 67 cetaceans found ashore (48 live strandings, seven dead from ship collision and 12 dead from bycatch) on the coast of Spain, more specifically in the Canary Islands from 2000 to 2016 and Andalusia from 2011 to 2014.ResultsThe microscopic findings were characterised by vascular changes, acute or subacute cardiac degenerative necrotic lesions, interstitial myoglobin globules, and infiltration of inflammatory cells. Immunohistochemically, cardiac troponin I, cardiac troponin C and myoglobin were depleted, along with fibrinogen being expressed in the degenerated/necrotic cardiomyocytes. A perivascular pattern was also identified and described in the damaged cardiomyocytes.ConclusionsThis study advances current knowledge about the pathologies of cetaceans and their implications on conserving this group of animals by reducing mortality and enhancing their treatment and subsequent rehabilitation to the marine environment.

Animals ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 220
Author(s):  
Nakita Câmara ◽  
Eva Sierra ◽  
Antonio Fernández ◽  
Manuel Arbelo ◽  
Yara Bernaldo de Quirós ◽  
...  

Capture myopathy (CM) is described in wild animals as a metabolic syndrome resulting from the extreme stress suffered during and after capture, handling, restraint, and transport. Although CM has been characterized in many species of cetaceans, descriptions of cardiac injury—an important component of this syndrome, and, according to previous authors, comparable to the existing human pathology so-called stress cardiomyopathy (SCMP)—are still rare. Therefore, the main aim of this report is to illustrate, for the first time, the biochemical analysis, and gross, histopathological, histochemical and immunohistochemical features of CM, and more specifically of the SCMP involved in this syndrome, caused by the live-stranding and consequent rehabilitation attempt, for a certain period of time, in a juvenile male Risso’s dolphin (Grampus griseus). The animal presented elevated values of creatine kinase, cardiac troponin I and blood urea nitrogen, with some variations during the rehabilitation period. Histologically, we detected vascular changes and acute degenerative lesions analogous to the ones observed in humans with SCMP. We consider this study to be an important contribution to the study of cetaceans since it could help in decision-making and treatment procedures during live-strandings and improve conservation efforts by reducing the mortality of these animals.


VASA ◽  
2008 ◽  
Vol 37 (4) ◽  
pp. 327-332 ◽  
Author(s):  
Koutouzis ◽  
Sfyroeras ◽  
Moulakakis ◽  
Kontaras ◽  
Nikolaou ◽  
...  

Background: The aim of this study was to investigate the presence, etiology and clinical significance of elevated troponin I in patients with acute upper or lower limb ischemia. The high sensitivity and specificity of cardiac troponin for the diagnosis of myocardial cell damage suggested a significant role for troponin in the patients investigated for this condition. The initial enthusiasm for the diagnostic potential of troponin was limited by the discovery that elevated cardiac troponin levels are also observed in conditions other than acute myocardial infarction, even conditions without obvious cardiac involvement. Patients and Methods: 71 consecutive patients participated in this study. 31 (44%) of them were men and mean age was 75.4 ± 10.3 years (range 44–92 years). 60 (85%) patients had acute lower limb ischemia and the remaining (11; 15%) had acute upper limb ischemia. Serial creatine kinase (CK), isoenzyme MB (CK-MB) and troponin I measurements were performed in all patients. Results: 33 (46%) patients had elevated peak troponin I (> 0.2 ng/ml) levels, all from the lower limb ischemia group (33/60 vs. 0/11 from the acute upper limb ischemia group; p = 0.04). Patients with lower limb ischemia had higher peak troponin I values than patients with upper limb ischemia (0.97 ± 2.3 [range 0.01–12.1] ng/ml vs. 0.04 ± 0.04 [0.01–0.14] ng/ml respectively; p = 0.003), higher peak CK values (2504 ± 7409 [range 42–45 940] U/ml vs. 340 ± 775 [range 34–2403] U/ml, p = 0.002, respectively, in the two groups) and peak CK-MB values (59.4 ± 84.5 [range 12–480] U/ml vs. 21.2 ± 9.1 [range 12–39] U/ml, respectively, in the two groups; p = 0.04). Peak cardiac troponin I levels were correlated with peak CK and CK-MB values. Conclusions: Patients with lower limb ischemia often have elevated troponin I without a primary cardiac source; this was not observed in patients presenting with acute upper limb ischemia. It is very important for these critically ill patients to focus on the main problem of acute limb ischemia and to attempt to treat the patient rather than the troponin elevation per se. Cardiac troponin elevation should not prevent physicians from providing immediate treatment for limb ischaemia to these patients, espescially when signs, symptoms and electrocardiographic findings preclude acute cardiac involvement.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1461-P
Author(s):  
PAUL WELSH ◽  
DAVID PREISS ◽  
ARCHIE CAMPBELL ◽  
DAVID J. PORTEOUS ◽  
NICHOLAS L. MILLS ◽  
...  

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