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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