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Chapter 11: Hypertrophic Cardiomyopathy  123


              tric left ventricular hypertrophy (see Chapter 26). Mild   occurs  in  approximately  10–15%  of  people  with  end-
              hepatic enzyme elevations (alanine aminotransferase or   stage HCM, which may lead to decreased renal perfusion
              aspartate  aminotransferase)  commonly  occurred  in   and renal injury (Lee et al. 2007). In this group of chil-
              approximately  70%  of  cats  with  HCM  according  to  a   dren undergoing pediatric heart transplantation, chronic
              large retrospective study of 260 cats (Rush and Freeman   renal insufficiency postcardiac transplantation increased
              2002).  In  this  study,  serum  creatinine  or  blood  urea   risk of mortality by ninefold (Lee et al. 2007). Treatment
              nitrogen concentration was not different between cats   of concurrent renal failure and heart failure secondary
              who were asymptomatic versus cats with heart failure or   to severe HCM can be challenging, with a significantly
              arterial thromboembolism at baseline prior to therapy   poorer  prognosis  than  either  disease  independently.
              (Rush and Freeman 2002). However, diuretic treatment   However,  it  is  the  authors’  clinical  impression  that
              is expected to cause some level of prerenal azotemia due   asymptomatic cats with IRIS stage 1 or 2 chronic kidney
              to dehydration. The sudden rise in serum BUN or cre-  disease  (http://www.iris-kidney.com/)  and  HCM
              atinine concentrations in the face of oliguria or anuria   without congestive heart failure tend to do well for many   Cardiomyopathies
              in a patient with aortic thromboembolism should raise   months to years (see Chapter 24).
              the  suspicion  of  renal  artery  embolization.  A  CBC  is
              important  to  evaluate  for  significant  anemia  (HCT   Routine Cardiovascular Diagnostics
              ≤22%), as this may worsen left ventricular volume over-  Electrocardiogram (see also Chapter 18)
              load and contribute to heart failure and arrhythmogen-
              esis in cats with severe HCM and diastolic dysfunction.
                 When renal dysfunction is present, it should be iden-  Key Points
              tified prior to treatment with heart failure medications
              such as furosemide or angiotensin converting enzyme   •	An	ECG	has	poor	accuracy	for	diagnosis	of	HCM	but	is
              (ACE) inhibitors. Otherwise, abnormalities encountered   the	test	of	choice	to	diagnose	an	arrhythmia	in	cats	with
              later (e.g., elevated BUN or creatinine, or inadequately   HCM.
              concentrated urine) may not be characterized as being   •	The	most	common	arrhythmias	in	cats	with	HCM	include
              caused  by  preexisting  renal  disease,  new-onset  renal   ventricular	premature	complexes	(occurring	in	41%
              disease, or simply an effect of heart failure medications.   of	cats),	ventricular	tachycardia	(10%	of	cats),	atrial
              Baseline blood chemistry and urinalysis are essential in   premature	complexes	(10%	of	cats),	atrial	tachycardia
                                                                     (10%	of	cats),	and	atrial	fibrillation	(10%	of	cats),	based
              cats with severe HCM and heart failure. After starting   on	in-hospital	ECG	evaluation.
              furosemide, the urine specific gravity usually becomes   •	Tachyarrhythmias	worsen	diastolic	dysfunction	and
              isosthenuric,  and  renal  dysfunction  cannot  be  distin-  lead	to	higher	diastolic	filling	pressures	in	HCM,
              guished from prerenal azotemia. In cats with underlying   potentially	precipitating	development	of	heart	failure.
              kidney disease, heart failure therapy may be modified to   Therefore,	whether	through	environmental	adjustments,
              be slightly more cautious, and recheck renal panels may   pharmacologic	control,	or	both,	high	heart	rates	should
              be  done  more  frequently.  Likewise,  fluid  diuresis  for   be	avoided	in	cats	with	HCM.
              treatment of renal failure may involve lower fluid rates   •	A	left	axis	deviation	suggestive	of	left	ventricular
              in cats with underlying severe HCM, with careful moni-  hypertrophy	or	left	anterior	fascicular	block	may	be
              toring of respiratory rate and effort and periodic recheck   present	on	the	ECG	of	in	cats	with	HCM	(10–33%)	but	is
              thoracic  radiographs  (see  Chapter  24).  Monitoring  is   not	specific	for	HCM.	Left	axis	deviation	may	be	present
                                                                     on	the	ECG	in	cats	with	other	heart	diseases,	particularly
              important  because  the  prevalence  of  azotemia  in  cats   hyperthyroidism	(6–8%	of	hyperthyroid	cats).
              with  HCM  is  59%  compared  to  25%  prevalence  in
              normal control cats (Gouni et al. 2008). Twenty percent
              of cats with HCM had congestive heart failure, which
              was  not  statistically  affected  by  plasma  urea  nitrogen   An electrocardiogram is the diagnostic test of choice to
              and plasma creatinine concentrations. Likewise, there is   evaluate an arrhythmia. If an abnormal heart rhythm is
              no effect of plasma urea nitrogen and plasma creatinine   ausculted, an electrocardiogram is essential to define the
              concentrations on conventional echocardiographic vari-  specific arrhythmia present and aid in the decision of
              ables.  Therefore,  this  study  documents  that  cats  with   whether antiarrhythmic therapy is necessary. Since cats
              HCM  also  frequently  are  concurrently  affected  with   have  small  ECG  deflections  and  fast  heart  rates,
              kidney disease. In a human study of children undergo-  the  ECG  paper  speed  should  be  set  at  50 mm/s  and
              ing  pediatric  heart  transplant,  HCM  was  an  indepen-  the amplitude increased to 20 mm/mV to optimize the
              dent  risk  factor  for  development  of  chronic  renal   tracing in most cases. A gallop heart sound, commonly
              insufficiency or end-stage renal disease (Lee et al. 2007).   referred to as a gallop rhythm, is not specifically evalu-
              One  explanation  is  that  systolic  myocardial  failure   ated with an ECG because it does not reflect a change in
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