Page 122 - Feline Cardiology

Chapter 11: Hypertrophic Cardiomyopathy 121

hypertrophy). Increased ventricular wall thickness never arterial blood pressure, and presence of systemic disease
causes systemic hypertension, but rather is caused by likely to cause dehydration/hypovolemia are clues that
systemic hypertension. Aortic stenosis (typically subaor- should prompt the clinician to consider that a “thick”
tic, rarely valvular or supravalvular) is a congenital heart left ventricle on the echocardiogram may in fact repre-
defect that increases afterload and likewise leads to a sent only pseudohypertrophy. The pseudohypertrophy
secondary concentric left ventricular hypertrophy. normalizes upon restitution of normal circulating blood
Acromegaly causes concentric left ventricular hypertro- volume, as does the ventricular size.
phy as a result of the direct stimulatory effect of growth Infiltrative neoplastic diseases such as lymphoma or
hormone on the cardiomyocytes, which increases repli- rhabdomyosarcoma can cause asymmetrical concentric
cation of the sarcomeres (Peterson et al. 1990). Secondary hypertrophy (see Chapter 16). Typically the affected
causes of concentric hypertrophy usually lead to only myocardium has a different echogenicity than the
mild left ventricular hypertrophy, with end-diastolic wall normal myocardium and is hypokinetic. The infiltration
thickness usually less than 7 mm. All of these secondary and functional defects may improve with chemothera- Cardiomyopathies
causes of left ventricular hypertrophy have one point in peutic treatment, which has been well documented in a
common, which is that they represent an adaptive few cases including a cat with renal lymphoma and met-
response to a disturbance (i.e., increased blood pressure astatic infiltrative cardiomyopathy (Brummer and Moïse
or increased thyroxine level). This is in contrast to HCM, 1989). Infiltrative neoplastic myocardial diseases are
which is a spontaneous and maladaptive increase in uncommon in cats, whereas asymmetrical, segmental
myocardial mass independent of any concurrent illness HCM is quite common.
or defect. The therapeutic implication is that elimination Cardiac amyloidosis has been thoroughly described in
of the abnormality causing secondary left ventricular people, but antemortem evaluation in cats is lacking. In
hypertrophy may lead to its regression, whereas HCM is people, concentric left ventricular hypertrophy and
an irreversible disorder. Secondary causes of HCM do severe diastolic heart failure may occur in end-stage
not usually cause severe concentric hypertrophy or con- amyloidosis. Histologic evidence of amyloid deposition
gestive heart failure. in small vessels within the myocardium was seen in most
If a secondary cause of left ventricular hypertrophy is (86%) Abyssinian cats with amyloidosis, but was classi-
identified and successfully treated, the left ventricular fied as mild in a majority of cases and did not cause
hypertrophy should markedly regress or resolve over concentric hypertrophy of the ventricle (DiBartola et al.
several months. To illustrate this, left ventricular wall 1986).
thickness of 91 hyperthyroid cats decreased from a mean SAM of the mitral valve is a unique abnormality
of 4.7 mm to 4.2 mm when pretreatment echocardio- present in some cats with HCM, and may uncommonly
grams were compared to posttreatment echocardio- occur in secondary causes of left ventricular hypertro-
grams performed 2 to 3 months following radioiodine phy, or rarely in catecholamine-driven volume under-
treatment (Weichselbaum et al. 2005). The maximal loaded patients (Luckie and Khattar 2008; Sakurai et al.
end-diastolic septal and free wall thicknesses (from an 1985; Yang et al. 2008). Presence of SAM of the mitral
observed range) decreased from 7.2 and 8.9 mm to valve raises suspicion of HCM, alone or in addition to
5.5 mm and 5.9 mm, respectively, showing significant other secondary causes of left ventricular hypertrophy.
regression of hypertrophy in those cats with increased Although there has long been the dogma that SAM is a
end-diastolic ventricular septal or wall thickness at unique feature of HCM, it is now recognized that other
baseline. Likewise, cardiac troponin-I levels (which forms of heart disease may uncommonly cause SAM in
may be measured by a benchtop cartridge analyzer (I- people (Luckie and Khattar 2008). This may be the case
Stat; http://www.abbottpointofcare.com) decrease over in cats, too. SAM is seen in <1% of people with hyper-
time in hyperthyroid cats after successful treatment, tensive heart disease (Luckie and Khattar 2008). The
possibly indicating resolved cardiomyocyte injury once term “pseudo-SAM” is used in people with SAM caused
a euthyroid state is achieved (Connolly et al. 2005). In by cardiac disease other than HCM, and there are several
patients with persistent left ventricular hypertrophy distinguishing features compared to “true-SAM” seen in
despite normalization of blood pressure or thyroid patients with HCM. Pseudo-SAM was identified in 12
levels, HCM is likely a concurrent disease. Marked dehy- of 37 people with hypertensive heart disease, and
dration decreases left ventricular chamber size and leads occurred in those patients with a smaller left ventricular
to the appearance of increased wall thickness, which is cavity size (Doi et al. 1983). Pseudo-SAM was found to
termed “pseudohypertrophy,” and which may be con- occur at end-systole coincident with the peak contrac-
fused with HCM (Campbell and Kittleson 2007). Overt tion of the left ventricular posterior wall, compared to
clinical signs of hypoperfusion or dehydration, a low an earlier onset of true-SAM in patients with HCM that