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Feline NT- proBNP as a cardiac biomarker

Maigan Espinili Maruquin

  1. Feline NT- proBNP

The atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are hormones released into the circulation in response to stimuli. These Natriuretic peptides (NP) are synthesized by cardiomyocytes which regulates body fluid homeostasis and blood pressure (Wilkins, Redondo et al. 1997, Connolly 2010)( Martinez RA, et al., 2009). From preprohormones, NP are processed to prohormones (Blake 2018). The proANP and proBNP, once released, quickly cleaves into separate inactive N-terminal (NT-proANP, NT-proBNP) and active C-terminal (C-ANP, C-BNP) fragments (Oyama 2013, Blake 2018).

In humans, ANP has shorter half- life than the BNP (Suga, Nakao et al. 1992, Blake 2018). On the other hand, while C-terminal provides counterbalance to those of the renin-angiotensin-aldosterone system, it has shorter half-life than that of the N-terminal, making NT-proBNP more stable for assay detection (Potter 2011, Oyama 2013, Blake 2018).

  1. Hypertrophic Cardiomyopathy (HCM)

The HCM has a prevalence of around 15% among cats wherein this disease of the myocardium causes abnormal thickening of the walls of the left ventricle (LV) (Paige, Abbott et al. 2009, Abbott 2010, Wagner, Fuentes et al. 2010, Payne, Brodbelt et al. 2015, Luis Fuentes and Wilkie 2017). Some cats experiencing HCM develop congestive heart failure (CHF), arterial thromboembolism (ATE), or sudden cardiac death (SCD) (Payne, Borgeat et al. 2013, Payne, Borgeat et al. 2015, Luis Fuentes and Wilkie 2017).

Usually, HCM in felines is detected incidentally on routine veterinary examinations through auscultatory findings including arrhythmias, gallop sounds, or murmurs, while sometimes, detection is from heart failure clinical signs or embolism (Atkins, Gallo et al. 1992, Rush, Freeman et al. 2002, Abbott 2010). Moreover, HCM is considered the most prevalent myocardial disorder in cats (Fox, Liu et al. 1995, Fox, Basso et al. 2007, Paige, Abbott et al. 2009, Fox, Rush et al. 2011).

Due to limited sensitivity and specificity of physical examination, electrocardiography (ECG) and thoracic radiography, diagnosing cardiomyopathy has been a challenge (Côté, Manning et al. 2004, Wood and Picard 2004, Schober, Maerz et al. 2007, Harris, Estrada et al. 2017), whereas, the current clinical gold standard used in cats is echocardiography (Harris, Estrada et al. 2017). Although echocardiography has high specificity in diagnosing myocardial disease (Wood and Picard 2004, Fox, Rush et al. 2011), its sensitivity is sometimes limited in detecting HCM (Fox, Rush et al. 2011).

The efficacy of treatments for the HCM has limited knowledge. Some agents were suspected to slow the progression of HCM in other breeds of cats, considering the probable existence of genetic heterogeneity in feline HCM. Interventions to speed myocardial relaxation or slow heart rate were also observed in attempt to improve diastolic function. (Abbott 2010).

  • Feline NT- proBNP Assay

 

 

 

Table 1. Plasma Levels of Feline NT-proBNP and their indications

 

(https://www.cliniciansbrief.com/article/cardiac-n-terminal-pro-b-type-natriuretic-peptide-assay)

 

There is an increase of interest in the usefulness of cardiac biomarker measurement in veterinary practice (Oyama 2013). In cats, there are available, inexpensive, not requiring advance training cardiac biomarkers for initial screening cardiomyopathy (Luis Fuentes and Wilkie 2017)( Charron P., et al., 2003). The echocardiography has a huge role in feline diagnosis of structural heart disease, however, due to its availability and appropriateness in in emergent circumstances, the use of NT-proBNP assays have been stimulated in differentiating CHF and non- cardiac causes of respiratory distress (Oyama, Boswood et al. 2013).

A biomarker is considered clinically useful if it provides information on diagnosis, prognosis, or response to treatment (Oyama 2013). The NT-proBNP in cats can be measured by conducting feline-specific NT-proBNP assay (Singletary, Rush et al. 2012). It has been reported that low NT-proBNP concentration is mostly non- cardiac cause (Oyama 2013) while cats with increased NT-proBNP were reported to have clinically relevant structural heart and elevated concentration suggests CHF (Connolly, Magalhaes et al. 2008, Fox, Oyama et al. 2009, Fox, Rush et al. 2011, Singletary, Rush et al. 2012, Oyama 2013).  The NT-proBNP test appears to be not useful for breeding examination (Hsu, Kittleson et al. 2009, Singh, Cocchiaro et al. 2010, Hassdenteufel, Henrich et al. 2013).

 

 

References:

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Charron P, Forissier JF, Amara ME, et al. Accuracy of European diagnostic criteria for familial hypertrophic cardiomyopathy in a genotyped population. Int J Cardiol 2003; 90:33–38

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