Atherosclerosis denotes inner arterial wall thickening in association with lipid deposition. Affected large coronary arteries often appear grossly thickened, yellow-white, and may have narrowed lumina. Histologically, deposits of plaque containing cholesterol, lipoid material, focal calcification, and lipophages thicken the inner sections of arterial wall (intima and inner media). There can be widespread involvement of arteries from many organs. Unlike the disease in humans, canine atherosclerosis is uncommonly associated with extensive plaque formation, arterial calcification, or thrombosis. Atherosclerosis has not been described in cats.
Atheromas are lipoid arterial plaques and they are rare features of canine atherosclerosis. Atheromas are sometimes referred to as xanthomatosis. Atherothrombosis results when a localized atheroma forms on an atherosclerotic plaque, resulting in disruption of blood flow and subsequent ischemia, infarction, or both. Atherothrombosis is most severe in both extramural and intramural coronary arteries, carotid arteries, and renal arteries.
Atherosclerosis has been detected in older dogs as a consequence of the hypercholesterolemia and lipidemia associated with thyroid atrophy. A predisposition for spontaneous atherosclerosis was reported in old, obese dogs with atrophied thyroid glands and hypothyroidism. This observation is in accordance with experiments in which atherosclerosis could be induced in thyroidectomized dogs fed large quantities of cholesterol or cholic acids. The spontaneous disease mainly affects male and spayed female dogs. An increased prevalence in miniature schnauzers, Doberman pinchers, and Labrador retrievers has been reported. The distribution and severity of arterial lesions and thyroid atrophy are typically associated with clinical signs of lethargy, anorexia, weakness, dyspnea, collapse, heart failure, vomiting, disorientation, blindness, circling, and coma. Recorded ECG abnormalities included atrial fibrillation, notched QRS complexes, and ST segment elevation. Laboratory abnormalities included hypercholesterolemia, lipidemia, low serum triiodothyronine (T3) and thyroxine (T4) concentrations, elevated blood urea nitrogen (BUM) (often associated with renal infarction) and liver enzyme concentrations, and high alpha2 and beta fractions in the protein electrophoresis.
Clinical diagnosis of atherosclerosis is difficult, and the prognosis for dogs with clinical signs related to stenosing atherosclerosis is poor. Potential treatments include thyroid replacement drugs, antihypertensive medication, blood cholesterol-reducing agents, or a low-cholesterol diet. Treatment strategies have not been tested in dogs, and severe lesions are essentially irreversible. Not all dogs with hypothyroidism develop atherosclerosis. Only those with increased levels of very low-density beta lipoproteins tend to be prone to develop atherosclerosis and plaques. Blood levels of low-density lipoproteins may be increased in these dogs because lipoprotein receptors are reduced and lipoid removal by the tissues is decreased. The elevated lipoprotein concentrations account for arterial lipoid deposits.
Atherosclerosis is strongly suspected as being an inflammatory disease developing in response to injury in the vessel wall in humans. Infiltration of the mononuclear lymphocytes into the intima, local expansion of vascular smooth muscle cells, and accumulation of extracellular matrix is believed to be the pathogenesis of the inflammation. Previously determined risk factors including hyperlipidemia and hypercholesterolemia are believed to enhance leukocyte adhesion to damaged endothelium and reduce local immune response. The role of inflammation in the development of canine atherosclerosis has yet to be determined.
Traumatic and Functional Arterial Disease
Trauma from direct accidental injury or iatrogenic trauma (e.g. surgery or vascular interventional procedures) is a common cause of vascular disease. Direct trauma may result in direct vascular wounds, or it can result in mural contusions leading to delayed thrombosis, necrosis, late hemorrhage, and false aneurysm formation. Vascular wounds can also occur from fractures because adjacent vessels are relatively fixed and vulnerable. Clinical features of traumatic arterial injuries may include diminished or absent pulse, enlarging hematoma, pulsatile arterial bleeding, symptoms of ischemia distal to the wound, injury of anatomically related nerves, and hypotension with major hemorrhage. Compressive forces from local tissue trauma (compartment syndrome) and vascular stenosis may delay or inhibit return to normal function of the affected area. Accurate diagnosis and extent of traumatic vascular injuries can be accomplished by direct examination, arteriography, ultrasound, and magnetic resonance imaging (MRI).
Vasospasm refers to reversible localized or diffuse vasocon-striction of arteries or small blood vessels. If short lived, the ischemia is reversible and permanent damage does not result. However, prolonged vasospasm with ischemia may lead to tissue damage and ulceration. Vasospasm is a common response to blunt and perforating vascular trauma and may also result from perivascular injection of irritating substances. When this occurs, tissue injury and vasospasm can be minimized by local infiltration with procaine hydrochloride or lidocaine. Uncommonly, vasospasm occurs in association with spontaneous arterial rupture (e.g. ruptured cerebral aneurysm, stroke). Angiography is usually required for confirmation. Vasospasm may be elicited by exotoxins. The best-known example is ergotism that produces intense vasospasm of the digits and large vessels by stimulation of the alpha-adrenoceptor. The differential diagnosis of vasospasm includes polycythemia, cold agglutinins, thrombosis, arteriosclerosis, and vasculitis.