Page 180 - Small Animal Internal Medicine, 6th Edition

152 PART I Cardiovascular System Disorders

arteriosclerosis of small coronary vessels also has been coronary blood flow. Heart rate elevations magnify these
described. These changes in the walls of the small coronary abnormalities.
VetBooks.ir arteries cause luminal narrowing and can impair resting Clinical Features
coronary blood flow, as well as vasodilatory responses. Small
myocardial infarctions and secondary fibrosis lead to reduced
large-breed dogs, often less than 3 years of age, although
myocardial function. Various arrhythmias can occur. Even- HCM is most commonly diagnosed in young to middle-aged
tual CHF is a cause of death in many cases with intramural there is a wide age distribution. Males are more com-
coronary arteriosclerosis. Sudden death is a less common monly affected. Most dogs diagnosed with HCM are pre-
sequela. Larger breeds of dog may be predisposed, although sented for evaluation of an asymptomatic heart murmur.
Cocker Spaniels and Cavalier King Charles Spaniels appear In some dogs, clinical signs of CHF, episodic weakness,
to be commonly affected smaller breeds. and/or syncope might be evident. Sudden death without
premonitory signs can occur. Ventricular arrhythmias sec-
TACHYCARDIA-INDUCED ondary to myocardial ischemia are presumed to cause the
CARDIOMYOPATHY low-output signs and sudden death. A systolic murmur,
The term tachycardia-induced cardiomyopathy (TICM) refers related to either LV outflow obstruction or mitral insuf-
to the progressive myocardial dysfunction, activation of neu- ficiency, can be heard on auscultation. The systolic ejec-
rohormonal compensatory mechanisms, and CHF that tion murmur of ventricular outflow obstruction becomes
result from rapid, incessant tachycardias. The myocardial louder when ventricular contractility is increased (e.g., with
failure may be reversible if the heart rate can be normalized exercise or excitement) or when afterload is reduced (e.g.,
in time. Tachyarrhythmias inducing TICM usually are supra- from vasodilator use). An S 4 gallop sound is heard in some
ventricular in origin, since rapid incessant ventricular affected dogs.
tachyarrhythmias typically lead to more hemodynamic
instability (syncope, sudden cardiac death) before TICM Diagnosis
develops. TICM has been described in several dogs with AV Echocardiography is the best diagnostic tool for HCM. LV
nodal reciprocating tachycardia associated with accessory hypertrophy (more commonly symmetric) and LA enlarge-
conduction pathways that bypass the AV node (e.g., Wolff- ment are characteristic findings. Mitral regurgitation might
Parkinson-White; see p. 44). Labrador Retrievers appear to be evident on Doppler studies. Systolic anterior motion of the
be predisposed to accessory pathway-mediated supraven- mitral valve often is present, indicating dynamic LV outflow
tricular tachycardias and thus TICM; this often is in associa- obstruction. Other causes of LV hypertrophy to be ruled
tion with tricuspid dysplasia. Rapid artificial pacing (e.g., out include congenital subaortic stenosis, systemic hyperten-
>200 beats/min) is a common model for inducing experi- sion, thyrotoxicosis, chronic phenylpropanolamine adminis-
mental myocardial failure that simulates DCM. tration, and pheochromocytoma. Thoracic radiographs can
indicate LA and LV enlargement, with or without pulmo-
nary edema. Some cases appear radiographically normal.
HYPERTROPHIC CARDIOMYOPATHY ECG findings might include ventricular tachyarrhythmias
and conduction abnormalities, such as AV or bundle branch
Etiology and Pathophysiology blocks. Criteria for LV enlargement are variably present.
In contrast to cats, HCM is uncommon in dogs. Other causes
of LV hypertrophy (subaortic stenosis, systemic hyperten- Treatment and Prognosis
sion, or other metabolic diseases) should always be excluded. The general goals of HCM treatment are to enhance myocar-
A genetic basis for HCM is suspected in Pointers, although dial relaxation and ventricular filling, control pulmonary
the disease occurs sporadically in other breeds. The patho- edema, and suppress arrhythmias. A β-blocker such as aten-
physiology is similar to that of HCM in cats (see Chapter 8). olol (see p. 93) commonly is used to lower heart rate, prolong
Abnormal, excessive myocardial hypertrophy increases ven- ventricular filling time, reduce ventricular contractility, and
tricular stiffness and leads to diastolic dysfunction. The LV minimize myocardial oxygen requirement. β-blockers also
hypertrophy usually is symmetric, but regional variation in can reduce dynamic LV outflow obstruction and may sup-
wall or septal thickness can occur. Compromised coronary press arrhythmias induced by heightened sympathetic activ-
++
perfusion is likely with severe ventricular hypertrophy. This ity. A Ca -channel blocker such as diltiazem could also be
leads to myocardial ischemia, which exacerbates arrhyth- considered to decrease heart rate and facilitate myocardial
mias, delays ventricular relaxation, and further impairs relaxation, although such drugs are less commonly chosen
filling. High LV filling pressure predisposes to pulmonary due to their vasodilatory effects. If CHF occurs, furosemide
venous congestion and edema. Besides diastolic dysfunc- and an ACEI are indicated; pimobendan could be consid-
tion, systolic dynamic LV outflow obstruction occurs in the ered, particularly if myocardial failure develops, although
majority of affected dogs. Malposition of the mitral appara- presence of LV outflow obstruction is a relative contraindica-
tus can contribute to systolic anterior mitral valve motion tion to positive inotropic therapy. Exercise restriction is
and LV outflow obstruction, as well as to mitral regurgita- advised in dogs with HCM.
tion. LV outflow obstruction increases ventricular wall stress Prognosis for canine HCM is variable. Although some
and myocardial oxygen requirement while also impairing dogs develop clinical signs and CHF and others experience