Page 173 - Small Animal Internal Medicine, 6th Edition

CHAPTER 7 Myocardial Diseases of the Dog 145

Other clinicopathologic findings are noncontributory reduce risk of sudden death. Common first-line ventricular
in most cases, although prerenal azotemia from poor renal antiarrhythmic medications used in DCM include sotalol
VetBooks.ir perfusion or mildly increased liver enzyme activities from and/or mexiletine. Amiodarone or procainamide sometimes
are used in refractory cases (see Chapter 4).
passive hepatic congestion often occur in advanced disease.
Severe CHF can be associated with hypoproteinemia, hypo-
natremia, and hyperkalemia. Hypothyroidism, with associ- STAGE C (CLINICALLY EVIDENT)
ated hypercholesterolemia, occurs in some dogs with DCM. DILATED CARDIOMYOPATHY
Others have a low serum T 4 hormone concentration without Therapy is aimed at improving the patient’s quality of life
hypothyroidism (euthyroid sick syndrome); normal thyroid- and prolonging survival to the extent possible by control-
stimulating hormone (TSH) and free T 4 concentrations are ling signs of CHF, optimizing cardiac output, and managing
common. Increased circulating neurohormones (e.g., nor- arrhythmias. Pimobendan, an ACEI, and furosemide (dosed
epinephrine, aldosterone, endothelin, in addition to the as needed) are used for most dogs (Box 7.1). Spironolactone
natriuretic peptides) occur mainly in DCM dogs with overt is advocated as well. Antiarrhythmic drugs are used based
CHF. on individual need.
Acute therapy
STAGE B (OCCULT) DILATED Dogs with acute CHF are treated as outlined in Box 3.1,
CARDIOMYOPATHY with parenteral furosemide, supplemental oxygen, inotropic
support, cautious use of a vasodilator, and other medications
Treatment according to individual patient needs. Thoracocentesis is
Pimobendan has been shown to delay progression to CHF indicated if pleural effusion is suspected or identified.
or sudden death in Doberman Pinschers with echocardio- Dogs with poor myocardial contractility, persistent hypo-
graphic evidence of occult DCM. In a randomized, blinded, tension, or fulminant CHF can benefit from additional ino-
placebo-controlled study, pimobendan prolonged the pre- tropic support provided by intravenous (IV) infusion of
clinical period by approximately 9 months compared with dobutamine (or dopamine) for 1 to 3 days. Long-term use
placebo. It is unclear whether pimobendan would also be of strong positive inotropic drugs is thought to have detri-
beneficial in Doberman Pinschers with ventricular arrhyth- mental effects on the myocardium. During infusion of these
mias only (before echocardiographic changes). Pimoben- drugs, the patient must be observed closely for worsening
dan also has been shown to delay progression to CHF or tachycardia or arrhythmias (especially VPCs). If ventricular
sudden death in Irish Wolfhounds with AF and/or echo- arrhythmias develop, the drug is discontinued or infused at
cardiographic evidence of occult DCM. Compared with up to half the original rate. In dogs with AF, catecholamine
benazepril or digoxin, pimobendan delayed the preclinical infusion is likely to increase the ventricular response rate
period in Irish Wolfhounds by approximately 2 years. It because of enhanced AV conduction.
remains unknown whether the benefits of pimobendan in Rapid AF is treated with drugs to slow ventricular
occult disease extend to other dog breeds commonly affected response rate. Diltiazem and digoxin are options for rate
by DCM. control in this setting; although both are available in IV and
An angiotensin-converting enzyme inhibitor (ACEI) also oral formulations, IV digoxin is avoided in most circum-
is generally recommended for dogs with LV dilation or stances. Diltiazem is more effective at lowering heart rate,
reduced LV systolic function. Preliminary evidence in but its negative inotropic properties can further compromise
Doberman Pinschers suggests this may delay the onset of systolic function in patients with advanced DCM; if the dog
CHF. Other therapy aimed at modulating early neurohor- is not already receiving pimobendan, this drug should be
monal responses and ventricular remodeling processes have administered as soon as possible. Digoxin is less potent for
theoretical appeal, but their clinical usefulness is not clear. rate reduction, with slower onset of action, but has the
In particular, certain β-blockers have proven beneficial in benefit of being a mild positive inotrope. For long-term rate
humans with cardiomyopathy, but clinical trials demonstrat- control, a combination of oral diltiazem and oral digoxin is
ing benefit in canine DCM are lacking. Carvedilol, a com- preferred. Strategies for acute rate control include (see p. 84):
bined β-blocker and α-blocker with antioxidant properties, (1) diltiazem loading (either PO or with small IV boluses, if
has largely fallen out of favor due to limited and unpredict- necessary followed by cautious continuous rate infusion
able oral bioavailability in dogs. [CRI]), with transition to oral maintenance diltiazem and
The decision to use antiarrhythmic drug therapy in dogs addition of oral digoxin; or (2) digoxin loading (PO loading
with ventricular tachyarrhythmias is influenced by arrhyth- with double the oral maintenance dose, or possibly cautious
mia frequency and complexity seen on Holter recording, as IV loading using small boluses hourly over 4 hours), with
well as presence or absence of clinical signs (episodic weak- subsequent initiation of oral maintenance digoxin and addi-
ness, syncope). Various antiarrhythmic agents have been tion of oral diltiazem. During an acute episode of CHF, the
used, but the most effective regimen(s) and when to institute goal is to reduce ventricular response rate to 150 to 160 beats
therapy remain unclear. A regimen that decreases arrhyth- per minute to maximize cardiac output; more aggressive rate
mia frequency and severity and increases ventricular fibril- reduction is counterproductive and can lead to worsened
lation threshold is desirable to decrease clinical signs and cardiogenic shock.