Page 298 - Feline Cardiology

306 Section H: Arterial Thromboembolism

contrast (SEC) in cats with cardiomyopathy. In fact, left
auricular velocity <0.20 m/s was the only independent
variable that predicted SEC. SEC is a possible indicator
that a cat is at increased risk for ATE (Schober et al.
2006).
Results regarding hypercoagulability in cats with heart
disease have been variable; however, a hypercoagulable
environment is present in some cats. For example, feline
platelets are particularly reactive and responsive to ade-
nosine diphosphate (ADP) and other agonists of platelet
aggregation. One study showed that platelets from car-
diomyopathic cats required less ADP to induce aggrega-
tion than did platelets from normal cats (Helinski and
Ross 1987), while another demonstrated decreased plate-
let responsiveness to ADP, but increased responsiveness
to collagen (Welles et al. 1994). Another study, which
defined systemic hypercoagulability as two or more labo-
Figure 20.1. The terminal aorta from a cat affected with ATE. ratory abnormalities reflecting coagulation excess, inhib-
Note the saddle embolus in the distal bifurcation of the vessel. itor deficiency, or thrombin generation, noted
Arterial Thromboembolism 1. Abnormalities in the vessel wall were hypercoagulable (Stokol et al. 2008). These results
Photograph courtesy of Dr. John Bonagura.
approximately half of the ATE cats and cats with SEC

were supported by another group as well (Bedard et al.
2007). Neither left atrial size nor congestive heart failure
2. Abnormal blood flow
3. Altered blood coagulability
(CHF) was associated with hypercoagulability in Stokol’s
study, which suggests that a subset of cats with cardio-
These prothrombotic factors are usually present to some
degree in cats with cardiomyopathy, which predisposes
compared to those cardiomyopathic cats that do not
them to embolic events. Endothelial fibrosis and patches myopathy which develop ATE may be hypercoagulable
develop thromboembolic disease irrespective of atrial
of endomyocardial necrosis have been described in the enlargement. Moreover, their results further support the
left atrium and/or left ventricle of cats with heart disease hypothesis that SEC is a risk factor for ATE. Another
(Liu 1977). These lesions present reactive substrates, study that assessed platelet closure time (the time it takes
(i.e., von Willebrand’s factor, tissue factor, and exposed for a platelet plug to form and occlude flow) was unable
collagen) to circulating blood and may trigger a throm- to identify a difference in normal cats versus a group
botic process by inducing platelet adhesion and aggrega- of cats with HCM. However, no cats with ATE were
tion. The intrinsic clotting cascade can be secondarily included in the study (Jandrey et al. 2008). In a study that
activated. measured feline antithrombin activity and D-dimer con-
Blood stasis, the second arm of Virchow’s triad, is also centration (using a chromogenic AT assay and an immu-
often present when significant chamber dilation has noturbidimetric D-dimer assay), mean AT activity was
developed, especially when severe systolic or diastolic increased in cardiomyopathic cats while the D-dimer
dysfunction is present and when cardiac emptying is assay did not appear to effectively measure feline D-dimer
abnormal. Since left atrial dilation occurs when there is (Brazzell 2007). In contrast, D-dimer concentration was
significant systolic or diastolic dysfunction and elevated elevated in 50% of ATE affected cats and 17% of healthy
left ventricular filling pressure, it is no surprise that cats cats in another study (Stokol et al. 2008). These studies
with severe left atrial dilation are more likely to develop used different reagents and assay methods (Stokol et al.
ATE, likely because of blood stasis. Blood flow stasis 2008). Taken together, these studies show that hyperco-
occurs at very low blood flow velocities and may lead to agulability is unlikely to be the primary factor in throm-
red blood cell aggregation. One study showed that peak bus development since it was not present in a large subset
blood flow velocity in the left atrial appendage was lower of the ATE cats.
in cats with cardiomyopathy than in normal cats, and Cats with cardiomyopathy and ATE were shown in
even lower in cats with evidence of ATE (Schober et al. another study to have low plasma B 12 and arginine con-
2003). More recently, the same group linked reduced left centrations, which suggests peripheral vascular disease
atrial appendage peak blood flow velocity to the pres- and endothelial dysfunction may play a role (McMichael
ence of intracardiac spontaneous echocardiographic et al. 2000). Finally, a genetic tendency for thromboge-