Samar Elsharkawy

Calanus oil, an oil extracted from the marine crustacean Calanus finmarchicus, is one of the richest sources of omega-3 and poly-unsaturated fatty acids. Although calanus oil has been shown to have a significant anti-hypertensive, anti-inflammatory, anti-fibrotic and anti-obesity effects in various cardiovascular diseases, but little is known about its effect on pathological cardiac hypertrophy. Thus, the present study was carried out to evaluate the therapeutic effect of calanus oil on cardiac hypertrophy. Cardiac hypertrophy was induced by subcutaneous injections with isoproterenol (5 mg/kg b.w) for 14 consecutive days. Calanus oil (400 mg/kg) was given orally for 4 weeks. Cardiac pathological remodeling was evaluated by echocardiography, after which morphometric, biochemical, histological and ultrastructural analyses were performed. Calanus oil treatment significantly ameliorated isoproterenol-induced structural and functional alterations in echocardiography. Calanus oil also reduced the relative heart weight, significantly decreased the elevated cardiac enzymes (LDH and CK-MB) and the lipid peroxidation marker (MDA), augmented the myocardial antioxidant status (TAC), and ameliorated the histopathological and ultrastructural changes in cardiac tissues and prevented interstitial collagen deposition. The present study, for the first time, provided morphometric, biochemical, histological and ultrastructural evidences supporting the promising anti-hypertrophic effect of calanus oil against ISO-induced cardiac hypertrophy. This anti-hypertrophic effect of calanus oil is via regulating myocardial remodeling and oxidative stress. Therefore, it could be used as potential pharmacological intervention in the management of cardiac hypertrophy.

INTRODUCTION: Dilated cardiomyopathy (DCM) is common in Great Danes (GDs) but screening for this condition can be challenging. We hypothesised that cardiac troponin-I (cTnI) concentration is elevated in GDs with DCM and/or ventricular arrhythmias (VAs), and is associated with reduced survival time in GDs.

ANIMALS: One hundred and twenty-four client-owned GDs assigned echocardiographically as normal (n = 53), equivocal (n = 37), preclinical DCM (n = 21), or clinical DCM (n = 13).

MATERIALS AND METHODS: A retrospective epidemiological study. Echocardiographic diagnosis, VAs, and contemporaneous cTnI concentrations were recorded. Diagnostic accuracy and cTnI cut-offs were determined with receiver operating characteristic analyses. Effects of the cTnI concentration and disease status on survival and cause of death were explored.

RESULTS: Median cTnI was greater in clinical DCM (0.6 ng/mL [25th-75th percentiles: 0.41-1.71 ng/mL]) and GDs with VAs (0.5 ng/mL [0.27-0.80 ng/mL], P<0.001). Elevated cTnI detected these dogs with good accuracy (area under the curve: 0.78-0.85; cut-offs 0.199-0.34 ng/mL). Thirty-eight GDs (30.6%) suffered a cardiac death (CD); GDs suffering CD (0.25 ng/mL [0.21-0.53 ng/mL]) and specifically sudden cardiac death (SCD) (0.51 ng/mL [0.23-0.72 ng/mL]) had higher cTnI than GDs dying of other causes (0.20 ng/mL [0.14-0.35 ng/mL]; P<0.001). Elevated cTnI (>0.199 ng/mL) was associated with shorter long-term survival (1.25 years) and increased risk of SCD. Great Danes with VAs had shorter survival times (0.97 years).

CONCLUSIONS: A cardiac troponin-I concentration is a useful adjunctive screening tool. Elevated cTnI is a negative prognostic indicator.

A 10-year-old female Griffon dog was presented for evaluation due to a 5-month history of hematuria and systemic hypertension. Thoracic auscultation detected a grade II/VI left apical systolic murmur. Abdominal ultrasound revealed the presence of a heterogeneous mass at the trigonal area of the urinary bladder, extending to the left ureter cranially and caudally toward the bladder's neck. Marked left hydronephrosis and hydroureter were detected as well as mild right hydronephrosis. Cytological examination of urine sediment confirmed the presence of transitional cell carcinoma. Echocardiography disclosed marked left ventricular concentric hypertrophy, which likely developed as a consequence of systemic hypertension induced by the bilateral hydronephrosis due to bladder transitional cell carcinoma.