Page 151 - Feline Cardiology
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150  Section D: Cardiomyopathies


              and  83%,  respectively)  (Hsu  et  al.  2009).  Elevated    and  typically  by  also  performing  an  echocardiogram
              plasma [BNP] does not define the type of heart disease   and an electrocardiogram.
              present, nor the presence or absence of secondary cardiac
              changes such as atrial enlargement or SAM of the mitral   Endothelin I
              valve.  Elevated  plasma  [BNP]  is  also  not  specific  for   Endothelin 1 (ET-1) is a potent vasoconstrictor that also
              heart disease, since some normal cats have an elevated   exerts other deleterious effects including cardiomyocyte
              plasma NT-proBNP, but raises the suspicion that heart   hypertrophy and activation of cardiac fibroblasts. ET-1
              disease may be present. A substantial degree of overlap   levels are increased in people with heart failure, and they
              in  plasma  levels  exists  between  normal  and  mildly   increase  with  severity  of  heart  failure.  Increased  ET-1
              abnormal cats, and a plasma NT-proBNP measurement   was associated with a higher 1-year mortality in people
      Cardiomyopathies  evaluation, nor as a stand-alone screening test for HCM   plasma  ET-1  levels  in  cats  with  various  cardiomyopa-
                                                                 with chronic heart failure. Only one study has evaluated
              cannot be considered a substitute for a complete cardiac
                                                                 thies;  most  had  HCM  (Prosek  et  al.  2004).  ET-1  was
              in the cat.
                 Other  pertinent  areas  of  future  research  need  to
                                                                 increased  in  asymptomatic  cats  with  cardiomyopathy
              explore the utility of NT-proBNP for monitoring disease
                                                                 (11/12 cats had HCM) compared to normal cats, and in
              progression,  guidance  of  pharmacologic  therapy,  and
              potential use as a prognostic indicator as it is in humans.   cats with heart failure compared to normal cats, but was
                                                                 not different between asymptomatic cats and symptom-
              NT-proANP appears to be less useful than NT-proBNP   atic cats. No cut-off values or sensitivity and specificity
              for detection of HCM in asymptomatic cats, as plasma   calculations were made. There appeared to be consider-
              levels are not elevated in cats with HCM compared to   able overlap in ET-1 concentrations between individual
              control cats (MacLean et al. 2006).                cats in the normal group and the asymptomatic cardio-
                                                                 myopathy group. Given the lack of ability to distinguish
                                                                 asymptomatic  cardiomyopathic  cats  from  cats  with
              Cardiac troponin I                                 heart  failure  or  arterial  thromboembolism,  it  is  likely
              Cardiac troponin I (cTnI) is released from cardiomyo-  that  other  biomarkers  such  as  NT-proBNP  are  more
              cytes  when  they  are  damaged.  Unlike  ANP  and  BNP,   clinically useful than ET-1 in cats.
              cardiac troponins are not species-specific; the molecular
              structure is the same across mammalian species. Cardiac   Other Laboratory Tests
              troponins are entirely distinct from skeletal troponins,   Serum growth hormone
              and  therefore  skeletal  muscle  injury  or  inflammation
              does not cross-react with cTnI tests. Cardiac troponin-I
              appears to be the more sensitive test (providing greater
              accuracy), compared to the cTn-T test that preceded its   Key Points
              development. Serum cardiac troponin I (cTnI) has been
              studied in cats with cardiomyopathy and heart failure,   •	Serum	growth	hormone	levels	may	be	mildly	increased
              and it has been shown to be a sensitive biomarker for   in	cats	with	HCM,	but	they	are	much	higher	in	cats	with
              heart disease in cats (sensitivity 87%, specificity 84%)   acromegaly.	The	increase	in	growth	hormone	in	HCM	is
              but did not distinguish cats that were symptomatic from   not	likely	a	primary	factor	in	development	of	concentric
                                                                     ventricular	hypertrophy.
              asymptomatic cats (Connolly et al. 2003). Another study   •	Serum	insulin	like	growth	factor-1	±	growth	hormone
              found  contradictory  results,  with  increased  cTnI  in   levels	should	be	measured	in	cats	with	concentric
              asymptomatic cats with cardiomyopathy, and that was    hypertrophy	of	the	left	ventricle	and	clinical
              further increased in symptomatic cats with heart failure   abnormalities	suggestive	of	acromegaly.
              (Herndon et al. 2002). Normal reference ranges are not
              interchangeable  between  the  different  cTnI  sandwich
              assays,  because  the  five  commercially  available  cTnI   Growth hormone exerts an endocrine effect on the heart
              assays evaluate five different areas of the molecule using   by inducing cardiomyocyte growth, which leads to con-
              proprietary technology. Therefore, when interpreting a   centric ventricular hypertrophy in people and cats with
              cTn-I result in any species, the reference range for the   acromegaly.  Growth  hormone  also  increases  calcium
              instrument  used  in  the  analysis  must  be  provided.  A   sensitivity  of  the  cardiac  myofilaments  and  increases
              positive  cTnI  value  obligates  the  clinician  to  identify   calcium content within cardiomyocytes, which increases
              potential  cardiac  disease  by  reviewing  the  history  for   contractility.  Given  the  known  relationship  of  growth
              potential trauma or illness leading to myocarditis and   hormone and insulinlike growth factor-I to hypertrophic
              the history of heart disease in the individual or family,   cardiac remodeling, serum growth hormone was mea-
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