Page 117 - Feline Cardiology

116 Section D: Cardiomyopathies

these veins. Curiously, the visceral pleural veins also fulminant clinical signs of heart failure (DeFrancesco
drain into the pulmonary veins in dogs, who do not et al. 2005).
develop pleural effusion secondary to isolated left-sided
CHF (Miller 1907). Like cats, people with left heart Arterial Thromboembolism
disease may develop pleural effusion in the absence of Cats with severe HCM and moderate to severe left atrial
pulmonary hypertension or elevated right atrial pres- enlargement are at risk for developing a thrombus in
sure (Wiener-Kronish et al. 1987). the left atrium/auricle, which often dislodges to the
distal aortic trifurcation. The incidence of arterial
Systolic Anterior Motion of the Mitral Valve thromboembolism (ATE) in cats with HCM is approxi-
Systolic anterior motion of the mitral valve (SAM) is a mately 12–17% (Rush et al. 2002; Atkins et al. 1992;
Cardiomyopathies been reported to occur in 67% of cats with HCM (Fox left atrium was severely enlarged in 57%, moderately
Peterson et al. 1993). In one study of ATE in cats, the
common feature of HCM in cats and humans and has
et al. 1995). The anterior mitral valve leaflet is displaced
enlarged in 14%, and mildly enlarged in 22%, with only
anteriorly into the left ventricular outflow tract (LVOT),
5% having a normal left atrial size (Laste and Harpster
1995). Thrombus formation may occur when there is an
creating a dynamic obstruction to ejection of blood out
the aorta during mid- to late systole. The magnitude of
Virchow’s triangle, which include: hypercoagulability,
LVOT obstruction varies from trivial to severe (pressure abnormality in one or more of the components of
gradients obtained from Doppler echocardiography endothelial disruption, and blood stasis. When the left
may range from 10–100 mm Hg). Mitral regurgitation atrium becomes moderately to severely dilated, the
arising from the displaced mitral leaflet occurs with blood flow velocity is reduced, resulting in red cell
variable severity and may contribute to increased left aggregation, platelet activation, and subsequent throm-
atrial pressure. There was once a debate over the actual bus formation. Blood stasis appears to be an important
pathophysiologic mechanisms that cause SAM (Sherrid factor for red blood cell aggregation in cats with signifi-
2006). The Venturi theory states that an increased blood cant cardiac disease. Left auricular blood flow velocity
flow velocity of the narrowed LVOT lifts the anterior is reduced in cats with echocardiographic evidence of
mitral leaflet into the LVOT and obstructs systolic blood spontaneous contrast and red blood cell aggregation
flow (Sherrid et al. 1988). This theory has been dis- (Schober and Maerz 2006). There are contradicting
proven by proponents of the “displacement” theory, studies regarding whether cats with cardiac disease tend
stating that papillary muscle hypertrophy anteriorly dis- to be hypercoagulable. One study documented that 45%
places the chordae tendinae and the anterior mitral of asymptomatic cats with HCM had evidence of hyper-
leaflet into the LVOT, which obstructs systolic blood coagulability (Bedard et al. 2007). It is debatable whether
flow (Levine et al. 1995; Sherrid et al. 2000). The LVOT there is platelet hyperreactivity in cats with cardiac
is made more narrow by significant basilar septal hyper- disease, because some studies document increased
trophy, which may contribute to development platelet reactivity and others report no change in plate-
of SAM. Increased contractility and increased accelera- let function in cats with heart disease (Helenski and
tion of LV ejection worsens LVOT obstruction (Sherrid Ross 1987; Jandrey et al. 2008; Welles et al. 1994).
et al. 1998). Moderate or severe SAM of the mitral Platelet endothelial cell adhesion molecule-1 and
valve greatly increases systolic left ventricular pressure endothelin–1 were elevated in asymptomatic Maine
and often leads to anginalike pain in people. Although coon cats with familial HCM compared to normal
identification of pain in cats can be challenging, control cats, indicating the potential for a prothrom-
anecdotal experience suggests that cats with moderate botic state (Jandrey et al. 2009). Endothelial damage
or severe SAM may be reluctant to exert themselves and disruption likely occurs in cats with cardiac disease,
vigorously or may demonstrate dyspnea or abrupt ces- and endothelial damage and fibrin adherence to the
sation of activity associated with vigorous play, and subendothelium has been documented on pathologic
some seem to feel better when the SAM is reduced with examination in several cats with congestive heart failure
beta blockade. However, there may be little impact of (Liu 1970). It is likely that a combination of mecha-
SAM on overall survival of asymptomatic cats with nisms leads to development of a left atrial thrombus in
HCM (DeFrancesco et al. 2005). Cats with SAM lived cats with significant cardiac disease.
longer than cats without obstruction, although this may Once the thrombus becomes dislodged from the left
be due to the earlier detection of HCM in cats with atrium, it travels through the arterial blood system and
SAM; a systolic murmur is readily audible in these cats becomes lodged in an artery depending on the size of
and may not be present in cats with more significant the thrombus, with the most common location being
HCM without SAM, who may be missed until there are the aortic trifurcation (71%). More important than the