Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.
BackgroundThe benefit of pimobendan in delaying the progression of preclinical dilated cardiomyopathy (DCM) in Dobermans is not reported.HypothesisThat chronic oral administration of pimobendan to Dobermans with preclinical DCM will delay the onset of CHF or sudden death and improve survival.AnimalsSeventy-six client-owned Dobermans recruited at 10 centers in the UK and North America.MethodsThe trial was a randomized, blinded, placebo-controlled, parallel group multicenter study. Dogs were allocated in a 1:1 ratio to receive pimobendan (Vetmedin capsules) or visually identical placebo.The composite primary endpoint was prospectively defined as either onset of CHF or sudden death. Time to death from all causes was a secondary endpoint.ResultsThe proportion of dogs reaching the primary endpoint was not significantly different between groups (P = .1). The median time to the primary endpoint (onset of CHF or sudden death) was significantly longer in the pimobendan (718 days, IQR 441–1152 days) versus the placebo group (441 days, IQR 151–641 days) (log-rank P = 0.0088). The median survival time was significantly longer in the pimobendan (623 days, IQR 491–1531 days) versus the placebo group (466 days, IQR 236–710 days) (log-rank P = .034).Conclusion and Clinical ImportanceThe administration of pimobendan to Dobermans with preclinical DCM prolongs the time to the onset of clinical signs and extends survival. Treatment of dogs in the preclinical phase of this common cardiovascular disorder with pimobendan can lead to improved outcome.
Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.
Background: English Bulldogs (EB) with pulmonic stenosis (PS) sometimes have an aberrant coronary artery (CA) type R2A encircling the pulmonary artery (PA). Balloon valvuloplasty (BV) is treatment of choice for severe PS, but is considered to be contraindicated in dogs with aberrant CA.Hypothesis: Conservative BV in EB with aberrant CA is safe and improves clinical signs and quality of life. Animals: Four client-owned EB with severe PS were retrospectively reviewed/analysed. Methods: Retrospective study: Case records, echocardiography, BV, and follow-up investigations of EB diagnosed with severe PS and treated with BV were reviewed. The ratios of PA to aortic (Ao) velocity time integral (VTI) were calculated to assess progression/improvement of PS.Results: An aberrant CA was confirmed on angiography in all EB. Conservative BV was performed, using a balloon of the size of the PA annulus or smaller (0.6-1 Â PA annulus size). All dogs survived the procedure, but only a mild reduction in pressure gradient was achieved. There was an improvement in PA to Ao VTI in 3 of 4 dogs (P .017), which were free of evidence of congestive heart failure (CHF) 5, 10, and 15 months after BV. One dog that had right-sided CHF when BV was performed died due to progressive right-sided CHF within 3 months.Conclusions: Conservative BV in EB might be safe and might improve quality and quantity of life.
An 8-year-old sexually intact male Golden Retriever with a history of collapse during exercise underwent an examination during which tachydysrhythmia was identified. At another institution, a 12.5-year-old spayed female Lhasa Apso was referred because of a cough and for evaluation of a heart murmur. In the Golden Retriever, radiographic examination revealed bulging of the craniodorsal aspect of the cardiac silhouette and echocardiography revealed right atrial dilatation. In the Lhasa Apso, a cranial mediastinal mass was suspected on the basis of radiographic findings, but no abnormalities were detected echocardiographically. In both dogs, nonselective angiography and contrast-enhanced computed tomography revealed a markedly enlarged, thin-walled right auricle. Exploratory thoracotomy in the Golden Retriever revealed a defect in the pericardium through which the right auricle and part of the atrium had herniated. In dogs, a right auricular aneurysm should be considered in differential diagnoses of a cranial mediastinal mass (detected radiographically) adjacent to the cardiac silhouette.
An unusual vascular ring anomaly consisting of a persistent right aortic arch and a left ligamentum arteriosum extending from the main pulmonary artery to an aberrant left subclavian artery and left aortic arch remnant complex was identified in a German shepherd dog and a great Dane. The left subclavian artery and left aortic arch remnant complex originated at the junction between the right distal aortic arch and the descending aorta and coursed dorsal to the oesophagus in a cranial direction. The attachment of the ligamentum arteriosum to the aberrant left subclavian artery was approximately 5 cm cranial to the point of origin of the aberrant left subclavian artery and left aortic arch remnant complex from the descending aorta in both dogs. This anomaly observed in both dogs is similar to an anomaly reported in humans, in which a persistent right aortic arch is found in conjunction with an aberrant left subclavian artery and a left aortic arch remnant (Kommerell's diverticulum). Surgical ligation and division of the left ligamentum arteriosum in both dogs, along with division of the left subclavian artery in the great Dane, resulted in resolution of clinical signs in both of the dogs in this report.
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