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224    PART I   Cardiovascular System Disorders


            corticosteroid therapy in pathologic thrombosis is unclear.   heart. Hyperthyroidism could be a risk factor for ATE in cats
            However, TE disease is relatively common in animals receiv-  independent of its cardiac effects. A rare cause of ATE could
  VetBooks.ir  ing exogenous corticosteroids and in those with hyperadre-  occur in cats with atrial septal defect, if a venous embolus
                                                                 crossed from RA to LA. In some cases of feline ATE, no
            nocorticism (see next paragraph). Other predisposing factors
            usually coexist in these cases as well.
                                                                   Systemic arterial emboli usually lodge at the aortic trifur-
              TE disease occurs in some dogs with spontaneous hyper-  predisposing condition is identified.
            adrenocorticism. This endocrinopathy has been associated   cation (so-called “saddle thrombus” or, more correctly,
            with decreased fibrinolysis (resulting from increased PAI   “saddle embolus”; Fig. 12.1), but iliac, femoral, renal, bra-
            activity) and high levels of several coagulation factors.   chial, and other arteries can be affected depending on
            Corticosteroids result in hypercoagulable thromboelastogra-  embolus size and flow path. Besides obstructing flow in the
            phy (TEG) tracings in normal dogs. Diabetes mellitus is   affected artery, thromboemboli release vasoactive substances
            occasionally associated with TE disease in dogs. Platelet   that induce vasoconstriction and compromise collateral
            hyperaggregability and possibly hypofibrinolysis are thought   blood  flow  around  the  obstructed  vessel.  Tissue  ischemia
            to be involved. Greyhounds appear to be predisposed to TE   results and causes further damage and inflammation, includ-
            disease despite lack of detectable hemostatic or cardiovascu-  ing ischemia-reperfusion injury after blood flow to the area
            lar abnormalities; one proposed mechanism is abnormalities   is  restored.  An  ischemic  neuromyopathy  occurs  in  the
            of homocysteine metabolism (hyperhomocysteinemia).   affected limb(s), with peripheral nerve dysfunction and
            Occasionally, a patient with clinically relevant TE disease   degeneration, as well as pathologic  changes in associated
            does not have any detectable abnormality that can result in   muscle tissue. Coronary thromboembolism with myocardial
            hypercoagulability.                                  necrosis has occurred in cats with cardiac disease, especially
                                                                 severe HCM or infective endocarditis, as well as from carci-
                                                                 noma emboli.
            PULMONARY THROMBOEMBOLISM
                                                                 Clinical Features
            Pulmonary thromboemboli (PTE) in dogs are associated   Arterial TE in cats usually causes acute and dramatic clinical
            with HWD, IMHA, neoplasia, DIC, sepsis, hyperadrenocor-  signs secondary to tissue ischemia (Fig. 12.2). Male cats
            ticism, protein-losing nephropathy, pancreatitis, trauma,   appear to be at higher risk for ATE, but this gender bias
            hypothyroidism, and right atrial (RA) thrombi related to   appears to be related to the prevalence of HCM. Common
            infection or neoplasia.                              physical examination findings of cats with ATE can be sum-
              Pulmonary TE disease appears to be rare in cats com-  marized with the mnemonic “5 Ps”: pain, pallor (pale color-
            pared with dogs, except in those with HWD (see Chapter   ation of affected pawpad[s]), paresis or plegia (of affected
            10). Nevertheless, PTE have been associated with a variety   limb[s]), pulselessness (weak or absent pulse in affected
            of systemic and inflammatory disorders in cats, including   limb[s]), and poikilothermia (decreased temperature of
            neoplasia, HWD, anemia (probably immune-mediated),   affected compared with unaffected limb[s]). Additional clin-
            pancreatitis,  glomerulonephritis,  encephalitis,  pneumonia,   ical abnormalities are summarized in Box 12.2.
            heart disease, sepsis, glucocorticoid administration, protein-
            losing enteropathy, and hepatic lipidosis.
              Pulmonary TE disease is an important cause of precapil-
            lary pulmonary hypertension, and can lead to right ven-
            tricular hypertrophy and even right-sided congestive heart
            failure (CHF). See Chapters 19 and 25 for further informa-
            tion about pulmonary thromboembolism and pulmonary
            hypertension.


            SYSTEMIC ARTERIAL
            THROMBOEMBOLISM IN CATS

            Cardiomyopathy, mainly HCM, is the most common under-
            lying disease in cats with arterial thromboembolism (ATE)
            (see  Chapter  8).  Thrombi  initially  form  in  the  left  heart,
            usually in an enlarged LA or auricle, and can become quite
            large. Neoplastic and systemic inflammatory disease occa-  FIG 12.1
            sionally are associated with systemic thromboemboli in cats.   Postmortem image with opened distal aorta, from a cat with
            Pulmonary carcinoma is the most common neoplasm to   cardiomyopathy. A thromboembolus (just left of the forceps
            cause ATE, potentially because tumor emboli from the lungs   tip) is lodged at the aortic trifurcation. The rear limbs are to
            have direct access to pulmonary veins and, thereby, the left   the left in the image; cranial is to the right.
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