Page 360 - Feline Cardiology

Chapter 24: Comorbidities 375

0.81% for the dry kibble formulation (Purina Guide prognosis in feline congestive heart failure. While several
2010). Therefore, the clinician treating a cat that has mechanisms could explain this phenomenon (Tobias
both lower urinary tract disease and heart disease should et al. 2005), subsequent data identified hyperglycemia-
recommend a specific diet that is suitably sodium bal- associated hypervolemia as the most likely pathway
anced: mild or no sodium restriction is likely appropri- (Ployngam et al. 2006). In a study of 12 cats given a
ate for cats with mild cardiovascular changes (e.g., no standard injection (5 mg/kg IM) of methylprednisolone
overt signs of heart failure, no diuretic treatment needed, acetate, blood glucose levels rose from a mean of
no atrial enlargement, and normal arterial blood pres- 136 ± 46 mg/dl to 187 ± 51 mg/dl (p = 0.002) (Ployngam
sure) whereas moderate or marked sodium restriction et al. 2006). These cats’ plasma volumes also increased
should be considered for cats with advanced heart (median 13%; up to 49% in one cat) 3–6 days after injec-
disease, particularly if they have experienced congestive tion, but simultaneously calculated total body water
heart failure and are receiving diuretics (Table 24.2). content was unchanged or slightly lower. This interest-
ing series of findings suggests that methylprednisolone
injections cause a substantial shift in body fluid from the
CARDIAC DISEASE AND FELINE ASTHMA
extravascular space (interstitium, intracellular) into the
Glucocorticoids have beneficial effects for inflammatory vascular space, likely as an osmotic shift due to hyper-
disorders such as feline lower airway disease (asthma) glycemia triggered by the corticosteroid (Ployngam et al.
and are recommended as a mainstay of treatment when 2006). The clinical implications are that cats’ responses
environmental modification alone is insufficient to to glucocorticoid administration are highly variable,
control respiratory signs (Reneiro 2011). However, glu- that in some cats glucocorticoids may cause an excessive
cocorticoids are also recognized to have deleterious volume expansion that leads to congestive heart failure
effects in cats with cardiac disease. Specifically, an asso- whereas other cats may tolerate a similar treatment, and
ciation between glucocorticoid administration and the that oral glucocorticoids may produce such events later
subsequent onset of congestive heart failure has been after initiation of treatment than repositol injections.
documented in some cats with heart disease (Smith et There are several alternatives to oral or injectable glu-
al. 2002). In this retrospective study of 29 cats, most cocorticoids for cats with asthma. The most commonly
(19/29, 68%) had echocardiographically identified left used include inhaled beta-agonists (e.g., albuterol, ter-
ventricular concentric hypertrophy (i.e. increased ven- butaline) and inhaled glucocorticoids (e.g., fluticasone)
tricular wall or septal thickness). Interestingly, follow-up (Padrid 2008). These beta-agonists are beta-2 receptor
echocardiography in 11 cats identified resolution of the selective and thus have minimal or no cardiac effect in
ventricular hypertrophy in most (9/11; 82%) cases, sug- aerosol form. There may be a crossover effect and some
gesting pseudohypertrophy or a transient cause of ven- degree of beta-1 agonism with terbutaline (and other
tricular hypertrophy. Most cats (22/29, 76%) had beta-2 agonists) when administered orally or by injec- Comorbidities
received long-acting repositol injections such as meth- tion, likely as a function of dosage given, interindividual
ylprednisolone acetate (Depo-Medrol) or triamcinolone variation (such as beta-receptor polymorphisms
acetonide, but 8 had received oral forms (prednisone, observed in the cat) (Maran et al. 2010) and other
n = 7; methylprednisolone, n = 1; some cats received factors. Fluticasone, similarly, does not undergo appre-
both injectable and oral forms). Generally, the injectable ciable systemic absorption when administered by
forms were associated with congestive heart failure signs aerosol, and systemic glucocorticoid effects such as those
much sooner after administration (mean = 4.4 ± 2.7 described above are not expected. Recommendations
days) in contrast to the onset of signs after beginning typically include initiation with parenteral (short-acting
oral administration (mean = 34.4 ± 30.7 days). The injectable, or oral) glucocorticoids for a few days to one
prognosis for survival was markedly, and favorably, week, to allow systemic drug levels to reach the airways,
influenced by glucocorticoid administration: compared followed by transition to aerosol administration (fluti-
to cats with spontaneously occurring congestive heart casone one 110 mcg actuation [“puff”]/cat q 12–24 h
failure and no recent glucocorticoid administration PRN; 44 mcg actuations may be sufficient for some cats)
history (median survival time = 65 days), cats with con- (Reneiro 2011). In the acute setting, aerosol delivery is
gestive heart failure that was associated with glucocorti- discouraged because the drug may not reach the target
coid administration had a median survival time of 439 airways in acceptable concentrations during acute small
days (p = 0.0006). These findings suggest that glucocor- airway narrowing or obstruction. Administration by
ticoids can trigger congestive heart failure in cats with aerosol at home is tolerated by most cats: 65% of cats
clinically silent/occult heart disease, and that recovery accept this form of treatment from the very beginning,
from the acute episode can lead to a better-than-expected and an additional 15% can be coaxed to accept it over a