Developmental Errors: Congenital Anomalies: The complex events involved in the embryologic development of the heart and great vessels allow substantial opportunities for congenital anomalies to develop (see Fig. 10-1). The functional significance of these anomalies varies widely. Animals with the most extreme defects are unable to survive in utero, and those with the mildest lesions could have no clinical signs of disease during life. However, animals with defects of intermediate severity are most likely to be presented to a veterinarian because of gradually developing signs of cardiac failure, including poor exercise tolerance, cyanosis, and stunted body growth. Ectopia cordis is a congenital development of the heart at an abnormal site outside of the thoracic cavity. In cattle, cases in healthy adult animals have been described in which the heart was located subcutaneously in the caudoventral neck area. The most frequently observed cardiovascular anomalies in domestic animals are listed in Box 10-11.

The causes of congenital cardiovascular anomalies are varied. Most animal species have a low background frequency of spontaneous cardiac malformations. In many species, especially in dogs, these defects are heritable and can be attributed to either single or multiple gene effects. Under experimental conditions, cardiovascular congenital defects can be elicited by exposure of pregnant dams to various chemicals and drugs, physical agents, toxins, or nutritional deficiencies. Chemical compounds implicated include thalidomide, ethanol, salicylates, griseofulvin, and cortisone. Prenatal exposure to x-irradiation or fetal hypoxia can induce defects. Maternal nutritional deficiencies of vitamin A, pantothenic acid, riboflavin, or zinc and excess intake of vitamin A, retinoic acid, or copper can result in cardiovascular anomalies in newborn animals. Infectious diseases have been incriminated, but not confirmed, in cardiovascular defects; they include bluetongue infections in sheep, bovine virus diarrhea in cattle, and parvoviral infections in dogs and cats.

Sites of the major cardiovascular anomalies in the dog are shown in Fig. 10-46.

Failure of Closure of Fetal Cardiovascular Shunts:

Hypertrophy and Atrophy:

Neoplastic Transformation: Various primary and secondary neoplasms develop either in or near the heart. Primary neoplasms include rhabdomyoma, rhabdomyosarcoma, schwannoma, and hemangiosarcoma. Rhabdomyomas and rhabdomyosarcomas are rare in animals and form white to gray nodules in the myocardium that often project into the cardiac chambers. Congenital rhabdomyomatosis in pigs and guinea pigs is a nonneoplastic hamartoma (i.e., malformation often resembling a neoplasm that is composed of an overgrowth of mature cells and tissues that normally occur in the affected organ). Single or multiple, pale, poorly circumscribed areas are scattered in the myocardium and are composed of large glycogen-laden myocytes.

Malignant lymphoma (lymphosarcoma) is the most common secondary neoplasm occurring in the heart and often causes lesions in the hearts of cattle, which can be severe enough to cause death from cardiac failure. Cardiac lesions may be present in dogs and cats with malignant lymphoma. The neoplastic cell infiltration can be diffuse or nodular and involve the myocardium, endocardium, and pericardium. Lymphomatous tissue appears as white masses that may resemble deposits of fat (Fig. 10-55). Microscopically, extensive infiltrations of neoplastic lymphocytes are present between myocytes (Fig. 10-56). Other neoplasms, such as malignant melanomas, occasionally have metastatic lesions in the heart.

Heart-based tumors are primary neoplasms of extracardiac tissues in dogs and rarely cats. They arise at the base of the heart and can produce vascular obstruction and cardiac failure. The most common neoplasm arising at this location is the aortic body tumor or paraganglioma (chemodectoma), but occasionally, ectopic thyroid or parathyroid tissue gives origin to neoplasms in this area. The aortic body is a chemoreceptor organ. In some cases, aortic body tumors become large, white, firm masses that surround and compress the great vessels and atria (Fig. 10-57). Brachycephalic dog breeds are most frequently affected. Microscopically, the neoplastic cells are polyhedral with vacuolated cytoplasm and are supported by a fine connective tissue stroma (see Fig. 12-55).

Toxicoses: The mechanisms of cardiotoxicities include (1) exaggerated pharmacologic action of drugs acting on cardiovascular tissues, (2) exposure to substances that depress myocardial function, (3) direct injury of cardiac muscle cells by chemicals, and (4) hypersensitivity reactions.

Myocardial Necrosis and Mineralization: Myocardial necrosis and mineralization can result from a number of causes, including nutritional deficiencies, chemical and plant toxins, ischemia, metabolic disorders, heritable diseases, and physical injuries (see Box 10-5). From this large list of causes of myocardial injury, some of the most frequently observed current examples are ionophore toxicity in horses and ruminants, vitamin E–selenium deficiency in the young of all species, “heart-brain syndrome” of dogs (see Fig. 10-83), anthracycline toxicity in dogs, and gossypol toxicosis in pigs. In various localized areas throughout the world, numerous deaths in ruminants have resulted from consumption of poisonous plants such as Acacia georginae and Dichapetalum cymosum.

Myocarditis: See the discussion on inflammation in the section on Myocardium, Responses to Injury.

Bacterial Septicemias: See the discussion on bacterial septicemias in Chapter 4.

Neoplastic Transformation:

Developmental Errors: Congenital Anomalies:

Uremic Endocarditis: Uremic endocarditis is most commonly a disorder in dogs that follows acute or repeated episodes of uremia. These episodes cause ulcerative endocarditis (injury of the endothelium) of the left atrium that is resolved via healing characterized by fibrosis, with or without mineralization and chronically dilated atria (Fig. 10-61).

Myxomatous Valvular Degeneration (Valvular Endocardiosis): Degenerative changes in the valves are frequently seen in older dogs and the process that leads to this lesion is termed myxomatous valvular degeneration (valvular endocardiosis). Also see the section on Disorders of Dogs; also see Fig. 10-84).

Endocardial Mineralization: Endocardial mineralization occurs from intake of excessive amounts of vitamin D and from intoxication by calcinogenic plants (Cestrum diurnum, Trisetum flavescens, Solanum malacoxylon, Solanum torvum) that contain vitamin D analogs. These plant-induced syndromes of cattle have been called by different names in various areas of the world, such as “Manchester wasting disease” in Jamaica, “enzootic calcinosis” in Europe, “Naalehu disease” in Hawaii, “enteque seco” in Argentina, and “espichamento” in Brazil. Multiple, large, white, rough, firm plaques of mineralized fibroelastic tissue are present in the endocardium and intima of large elastic arteries. Fibrosis, with or without mineralization, occurs in chronically dilated hearts, in hearts of debilitated cattle with Johne’s disease (see Figs. 10-32 and 10-39), in dogs with healed lesions of left atrial ulcerative endocarditis associated with a prior uremic episode (see Fig. 10-61), and in the so-called jet lesions produced by the trauma of refluxed blood in valvular insufficiencies.

Valvular Endocarditis: See the discussion on vegetative valvular and mural endocarditis in the section on Inflammation, Endocardium, Responses to Injury, as well as the discussion on valvular endocarditis in Chapter 3.

Disturbances of Circulation:

Disturbances of Growth:

Cell Degeneration and Death: Toxicants that affect vessels are listed in Web Box 10-1.

Inflammation:

Disturbances of Circulation:

Disturbances of Growth:

Inflammation: The most common diseases with thrombosis and embolism are listed in Box 10-14.

Equine Viral Arteritis: Equine viral arteritis is a systemic viral infection with a tropism for vascular endothelial cells. In this disease, affected small muscular arteries have lesions of fibrinoid necrosis, extensive edema, and leukocytic infiltration (Fig. 10-70). Grossly the vascular injury is reflected by hemorrhage and severe edema of the intestinal wall and mesentery accompanied by notable accumulation of serous fluids in body cavities and pulmonary edema (see Chapter 14).

African Horse Sickness: Subacute Cardiac Form: African horse sickness is an insect-borne (Culicoides spp.) viral disease of Equidae that is endemic in Africa, the Middle East, India, and Spain. The occurrence is seasonal because the insect vectors thrive in hot wet conditions. The febrile disease may produce high mortality (up to 95%) and appears in several clinical forms, including the subacute cardiac form described here, as well as an acute respiratory form with massive pulmonary edema. The pathogenesis is initiated by the introduction of the virus by bites of the insect vector. The virus proliferates in local lymph node, and viremia ensues. The virus has a tropism for endothelial cells, monocytes, and macrophages and increased vascular permeability, edema, hemorrhage, and microthrombosis are produced. The gross lesions are extensive subcutaneous and intermuscular edematous swelling of the head and neck. Massive hydropericardium is present with accompanying epicardial and endocardial ecchymotic hemorrhages. Histopathologically, endothelial degeneration and necrosis occur with the edema. In the myocardium, hemorrhage, edema, and focal myocardial necrosis with inflammatory cell infiltrates are present (see Chapter 4 and Fig. 4-44).

Cranial Mesenteric Arteritis and Thrombosis: Cranial mesenteric arteritis and thrombosis results from fourth stage larval migration from Strongylus vulgaris (Fig. 10-71). Infection of horses by Strongylus vulgaris is now less common because of widespread use of highly efficacious antiparasitic drugs. During its larval development, the parasite migrates through the intestinal arteries, and the most severe lesions are generally found in the cranial mesenteric artery near its origin. The affected vessel is enlarged, and its wall is firm and fibrotic. The intimal surface often has an adhering thrombus admixed with larvae. Microscopically, the affected vessel has extensive infiltration of inflammatory cells and proliferation of fibroblasts throughout the wall. As a consequence, thromboembolism of the intestinal arteries frequently occurs and can produce colic, but the abundant collateral circulation to the equine intestinal tract makes intestinal infarction an unusual event.

Aortoiliac Thrombosis: Aortoiliac thrombosis is thought to be caused by migration of fourth stage larval migration from Strongylus vulgaris. See the previous section on cranial mesenteric arteritis and thrombosis.

Jugular Thrombophlebitis: See the discussion on jugular thrombophlebitis in the section on Inflammation, Blood and Lymphatic Vessels, Disorders of Domestic Animals.

Arterial Intimal Calcification: Arterial intimal calcification (intimal bodies) are distinctively small, mineralized masses within the subendothelium in small muscular arteries and arterioles of horses (Web Fig. 10-21). They have no deleterious effect.

Glanders Disease (Farcy): Cutaneous Form: Glanders disease (Farcy) is a contagious disease of horses caused by infection with Burkholderia (Pseudomonas) mallei. Once worldwide in distribution, it is now seen in Eastern Europe, Asia, and northern Africa. The disease occurs in several clinical forms, and the cutaneous form with involvement of lymphatic vessels is described here. The pathogenesis is initiated by ingestion of contaminated food and water. The organisms enter through the pharynx and are disseminated to the skin hematogenously. The gross lesions of the skin appear as multiple ulcerated nodules that follow infected lymphatic vessels. Most frequent in the limbs, the ulcerated lesions discharge suppurative exudate onto the skin surface. Swollen tortuous cutaneous lymphatic vessels are visible between the ulcerative lesions. Microscopically, the skin nodules represent pyogranulomatous inflammation extending from cutaneous lymphatic vessels with suppurative lymphangitis (see Fig. 4-24).

Miscellaneous Cutaneous Lymphangitides (See Box 10-8): The cutaneous lesions affecting lymphatic vessels in the diseases are as follows:

These lesions mimic those of Glanders disease, and differentiation occurs by impression smears and microbiologic cultures and analyses. The skin of the legs, head, neck, and/or flanks has raised firm nodules (≈1 to 2 cm in diameter), draining nodules, and draining fistulous tracts, often arranged in linear bands (beaded appearance) that follow the flow of lymphatic vessels. These lesions contain or drain pus, which is often thick and white-yellow in color. Microscopically, lesions are characterized by suppurative to pyogranulomatous inflammation. Infectious microorganisms are often present in the exudate (see Fig. 4-24).

Thrombotic Meningoencephalitis: Histophilus somni (formerly Haemophilus somnus) causes a systemic vasculitis in cattle resulting in meningoencephalitis. Mural thrombi from local vascular injury rather than thromboemboli from distal sites of vascular injury, such as the lungs, are the major type of thrombus in this disease. Gross lesions in the central nervous system (CNS) are characteristic of infarcts (see Fig. 14-89, A). Microscopic lesions are initially vasculitis and vascular necrosis, which are followed by thrombosis and infarction (see Fig. 14-89, B). Septic vasculitis, the initial event, is followed by edema and an influx of neutrophils and macrophages in and around vessel walls and adjacent parenchyma. Colonies of small Gram-negative bacilli are frequent in thrombi, in and around affected vessels, and in areas of necrosis. Histophilus somni can also cause a necrotizing myocarditis.

Thrombosis of the Caudal Vena Cava: Thrombosis of the caudal vena cava occurs in association with rupture of hepatic abscesses into either the hepatic vein or the caudal vena cava. The hepatic abscess inflammation extends into the adjacent large hepatic veins and results in formation of a septic thrombus in the caudal vena cava. Rupture and release of the contents of the abscess into the lumen can cause multiple septic emboli in the pulmonary capillaries and unexpected death of the affected animal, often preceded by severe hemoptysis.

Foreign Parasitic Diseases: Foreign parasitic diseases important in tropical regions of the world are characterized by presence of parasites in the lumens of veins. These diseases in cattle include schistosomiasis (blood fluke infection—Schistosoma spp.) in which adult parasites are present in the mesenteric and portal veins, and the resulting phlebitis is characterized by intimal proliferation and thrombosis.

Omphalophlebitis (“Navel Ill”): See the discussion on omphalophlebitis (“navel ill”) in the section on Inflammation, Blood and Lymphatic Vessels, Disorders of Domestic Animals, and also Chapters 8 and 16.

Johne’s Disease: Lesions of Johne’s disease affecting blood and lymphatic vessels and characterized by intimal mineralization and granulomatous lymphangitis, respectively, are discussed in greater detail in Chapters 4, 7, and 13.

Anthrax: Anthrax in herbivores often occurs as an acute febrile highly fatal septicemic disease. Although global in distribution, the disease is enzootic in certain areas. The etiology is Bacillus anthracis, a large rod-shaped spore-forming bacterium. The pathogenesis of the disease in affected herbivores is exposure by ingestion of contaminated food (especially bone meal) and water. The organisms produce a variety of lethal toxins that provoke local edema and tissue necrosis and increased vascular permeability associated with lymphangitis and lymphadenitis. Herbivores that die from septicemic anthrax have dark thick unclotted blood oozing from body orifices. These cases should NOT be subjected to necropsy to avoid massive contamination of the environment by the spores of the organism. Instead, a blood smear should be collected and examined for the presence of the diagnostic bacilli. If a case is necropsied by mistake, the diagnostic findings are massive splenomegaly (so-called blackberry jam spleen), disseminated serosal hemorrhages, and swollen edematous lymph nodes. Microscopic findings (histopathologic evaluation is NOT recommended) include massive numbers of typical large rod-shaped organisms in the blood, congestion, hemorrhage, lymphangitis, and lymphadenitis (see Chapter 4, Fig. 4-23, and Chapter 7, Fig. 7-135).

Neospora caninum: See the discussion on Neospora caninum in Chapter 4.

Malignant Catarrhal Fever: See the discussion on malignant catarrhal fever in Chapter 4.

Bovine Virus Diarrhea: See the discussion on bovine virus diarrhea in Chapters 4 and 7.

Bluetongue: See the discussion on bluetongue in Chapters 4 and 7.

Dietary Microangiopathy: Mulberry Heart Disease: Dietary microangiopathy of pigs or “mulberry heart disease” is produced by a deficiency of vitamin E and/or selenium and the resultant effect on the microvasculature, which is characterized by fibrinoid necrosis, and thromboses of small vessels resulting in microhemorrhages. The hemorrhage results in major discoloration of the epicardial surface of the heart, particularly the right atrium said to resemble a mulberry (Figs. 10-77 and 10-78). In addition to the epicardial hemorrhages, hydropericardium often ensues. Massive hemorrhagic hepatic necrosis (hepatosis dietetica) is also produced with vitamin E and/or selenium deficiency (see Fig. 8-69). With either form of the disease, fibrinoid necrosis of small muscular arteries and arterioles is widespread and is accompanied by endothelial damage and fibrin thrombi in capillaries, especially capillaries of the myocardium (Fig. 10-79; Web Fig. 10-23). This complex of vascular lesions has been termed dietary microangiopathy.

Cerebrospinal Angiopathy (Edema Disease): Cerebrospinal angiopathy in pigs is characteristically sporadic in pigs with signs of nervous system disease. Fibrinoid necrosis is consistently present in arteries of the CNS. Similar lesions occur in the arteries of the gastric submucosa of pigs with edema disease, a form of colibacillosis, and many researchers believe that cerebrospinal angiopathy represents a subacute form of edema disease (Fig. 10-80; Web Fig. 10-24; also see Fig. 10-42; Chapters 4, 7, and 11; and Figs. 7-126 and 7-127).

Fibrinoid Necrosis of Blood Vessels: Fibrinoid necrosis of arteries and veins (see Fig. 10-42) is particularly frequent in pigs and is an important diagnostic feature in cases of vitamin E–selenium deficiency (heart), edema disease (gastric submucosa), cerebrospinal angiopathy, porcine circovirus II vasculopathy, and organic mercury toxicosis (meninges). See the previous section on Dietary Microangiopathy: Mulberry Heart Disease.

Erysipelosis (Erysipelelothrix rhusiopathiae): Cutaneous lesions in erysipelosis are caused by Erysipelothrix rhusiopathiae and are the result of bacterial embolization to the skin during sepsis. Lesions consist of square to rhomboidal, firm, raised, pink to dark purple areas (Fig. 10-81, see Fig. 17-51) caused by vasculitis, thrombosis, and ischemia (infarction). The rhomboidal shape likely represents an area of skin supplied by a thrombosed vessel (see Chapter 17).

Porcine Polyserositis (Streptococcus suis II): Streptococcus suis II is one of several bacteria that can cause the disease porcine polyserositis. Gross lesions include vasculitis leading to variable quantities of a gray-white friable material (fibrin) on serosal surfaces (fibrinous polyserositis) of the lungs (fibrinous pleuritis), heart (fibrinous pericarditis [see Fig. 10-75]), and abdominal cavity (fibrinous peritonitis). The bacterium gains access to and spreads systemically through the blood vascular system. Lesions suggest this bacterium may have a tropism for vascular endothelial cells of serosae and bacterial endotoxins may contribute to vascular injury and permeability changes leading to the leakage of fibrinogen and its polymerization to fibrin on serosal surfaces and in some cases to microthrombus formation and disseminated intravascular coagulation (DIC) in other organ systems (see Chapters 4, 7, and 9).

African Swine Fever (Wart Hog Disease, African Pig Disease): African swine fever (ASF) is a highly contagious febrile hemorrhagic disease of pigs associated with a DNA virus. The clinical and pathologic features are very similar to those of classic swine fever (hog cholera). The disease is enzootic in Africa, and outbreaks have occurred in Europe, South America, and the Caribbean region. The pathogenesis of the disease is via entry in the upper respiratory tract. The virus proliferates in the tonsils and lymph nodes of the head and neck with subsequent viremia and dissemination to the entire body. Transmission to domestic swine is via ingestion of infected tissues of warthogs and bush pigs, which develop an inapparent infection, or by the bite of infected soft ticks (Ornithodoros moubata). The distinctive hemorrhagic lesions are attributed to disruption of the clotting mechanism and thrombocytopenia. The gross lesions are characterized by widespread congestion, edema, and hemorrhage. Hemorrhagic visceral lymph nodes and splenomegaly are present along with petechial hemorrhages of the renal cortices, epicardium, and other serosal surfaces. Pulmonary edema and hydrothorax also occur. Microscopically, viral-induced vascular alterations include congestion, hemorrhage, and edema with fibrin microthrombi (Web Fig. 10-25). The virus produces widespread necrosis of lymphocytes and macrophages (see Fig. 4-42).

Hog Cholera/Classic Swine Fever (Swine Fever, Swine Plague, Schweinpest): Hog cholera (also termed classic swine fever) is a highly contagious febrile hemorrhagic disease of swine produced by an RNA virus. The disease is enzootic in South America, Central America, Caribbean countries, Asia, and Europe. The pathogenesis of the disease is initiated by inhalation of the virus from direct contact with infected pigs or by ingestion of uncooked infected pork. The virus traverses the oral mucosa, replicates in the tonsils, and initiates viremia. The virus selectively damages endothelial cells, cells of the immune system (lymphoreticular cells and macrophages) and epithelial cells. The characteristic hemorrhagic lesions are associated with increased vascular permeability, thrombocytopenia, and DIC (see Web Fig. 10-25). The gross lesions are characterized by widespread petechial hemorrhages, especially of the renal cortices, urinary bladder, larynx, gastric mucosa, and epicardium with accompanying hemorrhage in lymph nodes and skin. A distinctive finding is hemorrhagic infarction of the spleen and “button ulcers” of the colonic mucosa. Microscopically, endothelial damage is evident as hydropic degeneration and cellular proliferation. Affected vessels may have fibrinoid necrosis with fibrin deposition in the media and intima. Circulatory alterations include congestion, hemorrhage, thrombosis, and infarction. The brain has a diffuse nonsuppurative encephalitis (see Fig. 4-43).

Porcine Anthrax: See the discussion on anthrax in the section on Blood and Lymphatic Vascular Systems, Disorders of Ruminants, and also Chapter 4.

Dilated (Congestive) Cardiomyopathy: Dilated or congestive cardiomyopathy is an important cause of congestive heart failure in dogs. Some affected dogs have low tissue concentrations of taurine, but supplementation has not proved beneficial. Affected dogs often are males of large breeds, such as Doberman pinschers, Portuguese water dogs, dalmatians, Scottish deerhounds, Irish wolfhounds, Saint Bernards, Afghan hounds, Newfoundland dogs, Old English sheepdogs, Great Danes, and Boxers, although smaller breeds, such as English cocker spaniels, may be affected. The disease often has a familial pattern in the affected breeds and appears to be inherited as an autosomal recessive or X-linked recessive trait. At necropsy, lesions of congestive heart failure are present and the hearts are rounded because of biventricular dilation (see Figs. 10-52 and 10-53). The dilated cardiac chambers often have a diffusely white, thickened endocardium. Microscopic and ultrastructural alterations are nonspecific, can be either mild or absent, and may include interstitial fibrosis and fatty infiltration and changes of myocyte degeneration, including the occurrence of so-called attenuated wavy fibers. See the discussion on cardiomyopathies in the section on Disturbances of Growth, Myocardium, Disorders of Domestic Animals.

Arrhythmogenic Right Ventricular Cardiomyopathy: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an important cardiac disease of Boxer dogs, and rare cases are seen in cats. Other names for the disease include Boxer cardiomyopathy and familial ventricular arrhythmias of Boxers. Inherited as an autosomal dominant trait in Boxers, most dogs present with arrhythmias and enlargement of the right ventricular chamber. The distinctive histopathologic findings are similar to those of the disease in humans and include thinning of the right ventricular free wall with fibrofatty replacement of cardiac muscle cells.

Developmental Errors: Congenital Anomalies:

Medial Necrosis and Hemorrhage: Medial necrosis and hemorrhage is a distinctive lesion produced in muscular arteries and arterioles of dogs and rats by a wide variety of vasoactive drugs. These vascular lesions, detected during evaluations of new compounds, produce grossly apparent hemorrhage, especially in the epicardium. Microscopically, acute damage is evident as necrosis of smooth muscle cells in the tunica media with surrounding erythrocytes. Healing lesions have fibrosis of the vessel wall and perivascularly.

Fibrocartilaginous Embolism: Fibrocartilaginous embolism of the spinal cord vasculature and resultant infarction of the spinal cord supplied or drained by the obstructed blood vessel lead to posterior paresis or paralysis. Affected dogs are typically middle-aged large or giant breeds, but occurrence in young Irish wolfhounds has been reported. The mechanism of formation of the arterial or venous emboli is still unclear, but movement within the spinal vasculature of fibrocartilaginous fragments from degenerated intervertebral disks is generally considered to underlie the presence of these unusual emboli (Fig. 10-87; Web Fig. 10-26).

Pulmonary Artery Thromboembolism: Pulmonary artery thromboembolism is often life threatening and occurs in dogs and cats (Fig. 10-88). A wide variety of predisposing conditions that may result in altered blood flow, hypercoagulability, or endothelial damage includes sepsis, immune-mediated hemolytic anemia, protein-losing nephropathy or enteropathy, disseminated intravascular coagulation, cardiac disease, neoplastic disease, hyperadrenocorticism, dirofilariasis, amyloidosis, and use of intravenous catheters.

Aortoiliac Thromboembolism and Thrombosis: Aortoiliac thromboembolism and thrombosis occurs in dogs (Fig. 10-89), cats (see Disorders of Cats), and horses (see Disorders of Horses). They arise from injury to vascular endothelium, propagate via the coagulation cascade (see Chapter 2), and ultimately occlude the caudal abdominal aorta and the external iliac arteries at the aortic bifurcation.

Thrombosis of the Femoral Artery: Thrombosis of the femoral artery, with resulting partial to complete occlusion, has been reported in cavalier King Charles spaniels. The condition may share a common etiopathogenesis with myxomatous valvular degeneration (valvular endocardiosis), which is frequent in this breed, through a genetically mediated connective tissue disorder. Affected dogs generally do not develop hindlimb ischemia, in contrast to human patients with this condition, because of extensive collateral circulation.

Heartworm Dirofilariasis (Dirofilaria immitis): In canine dirofilariasis (heartworm infection), maturation of adult parasites occurs in the pulmonary arteries and may extend into the right atrium and ventricle. The pulmonary arteries containing parasites initially have an infiltration of the intima (termed endarteritis) by eosinophils, with subsequent development of an irregular fibromuscular proliferation of the intima visible grossly as a rough granular or shaggy appearance of the luminal surface (Fig. 10-90; Web Figs. 10-27 and 10-28). Live or dead parasites can be present within these vascular lesions and be accompanied by thromboembolism and pulmonary infarction. The presence of a massive number of adult worms may result in filling the right heart extending into venae cavae resulting in venal caval syndrome. This syndrome results in sudden collapse, liver failure, hemolytic anemia, shock, and death if the adult worms are not removed surgically.

Polyarteritis: “Beagle Pain Syndrome”: Polyarteritis is a disease that occurs sporadically in many animal species and is an important disease of aged rats (Web Fig. 10-29). Many recent reports have described the occurrence of polyarteritis in a disease termed idiopathic necrotizing polyarteritis (idiopathic canine polyarteritis, juvenile polyarteritis syndrome) involving multiple arteries including the coronary and meningeal arteries in dogs, most often pet and laboratory beagle dogs (“beagle pain syndrome”). Clinically, affected dogs typically show recurrent episodes of fever, body weight loss, and occasionally cervical pain manifested by a still gait and stiff neck with a hunched body posture. However, some affected dogs do not display clinical signs of disease. The lesions are usually attributed to an immune-mediated vascular injury. Medium-sized muscular arteries in a wide variety of organs, including the heart and meninges, are selectively involved and grossly appear thick and tortuous, have associated focal hemorrhage, and develop aneurysms and thrombosis. Microscopically the early lesions include fibrinoid necrosis and leukocytic invasion of the intima and media (Web Fig. 10-30). In chronic lesions, inflammatory cells and fibrosis involve all layers of the vascular wall.

Hemangiosarcoma and Hemangioma: Cardiac hemangiosarcoma is an important neoplasm of dogs and can arise either in the heart (primary) or by metastasis (secondary) from sites such as the spleen. This neoplasm is usually seen in the wall of the right atrium and only occasionally involves the right ventricle. Grossly, protruding red to red-black blood-containing masses are located on the epicardial surface (Fig. 10-91) and may also protrude into the atrial lumen. Rupture can produce fatal hemopericardium and cardiac tamponade. Microscopically, the neoplasms are composed of scattered, elongated, plump neoplastic endothelial cells, which may or may not form vascular spaces containing blood (Fig. 10-92). Pulmonary metastases are frequent. Immunohistochemistry staining for Factor VIII-related antigen confirms the tumor cells are endothelial in origin. Hemangiomas are benign neoplasms often found in the skin of dogs (Fig. 10-93). These red, blood-filled masses are well circumscribed.

Heart-Base Tumors: See the discussion on neoplastic transformation in the section on Disturbance of Growth, Myocardium, Disorders of Domestic Animals and also Fig. 10-57.

Intestinal Lymphangiectasia: Intestinal lymphangiectasia is an important disease of dogs in which there is a protein-losing enteropathy. Lacteals in the intestinal villi are prominently dilated, and lymphatic vessels throughout the wall of the bowel and the mesentery are distended (see Fig. 7-121). The role of obstruction of lymphatic vessels in the pathogenesis of this disease is still unclear. Many diseases with severe acute inflammatory alterations accompanied by vascular damage, as with the pneumonia of bovine pasteurellosis, have prominently dilated lymphatic vessels.

Lymphangioma and Lymphangiosarcoma: Lymphangioma represents a rare benign neoplasm composed of lymphatic channels. Lymphangiosarcoma, the malignant counterpart, occurs more often than the benign neoplasm. Endothelial-lined vascular spaces contain lymph rather than the blood. Lymphatic vessels are frequently invaded by primary carcinomas and are a common route of metastasis.

Hypertrophic Cardiomyopathy: Hypertrophic cardiomyopathy occurs frequently in cats (65% of cases), especially in young adult to middle-aged males (1 to 3 years old). Cats usually have congestive heart failure, and approximately 10% to 20% have posterior paresis from concurrent thromboembolism of the caudal abdominal aorta (“saddle thrombosis”) secondary to left atrial thrombosis. Hypertrophic cardiomyopathy is inherited in an autosomal dominant manner in Maine coon cats. The occurrence of clusters of cases in Ragdoll, Norwegian Forest, and sphinx cat breeds suggests heritability of the disease as an autosomal dominant trait. Some cats die unexpectedly, which is the only clinical expression of the disease. This clinical presentation is often seen in humans with the disease. Affected hearts are enlarged and have prominent hypertrophy of the left ventricle and interventricular septum (see Fig. 10-50). The left ventricular cavity is small, and the left atrium is dilated. In a few cases, the interventricular septum is disproportionately hypertrophied in relation to the remainder of the myocardium. Microscopically the lesions of the myocardium are prominent disarray or disorganizations of myocytes, with interweaving rather than parallel arrangement of fibers (see Fig. 10-51). Myocyte hypertrophy, various degenerative alterations in myocytes, and interstitial fibrosis are present. Caudal aortic thromboembolism is seen in 10% of cats with primary hypertrophic cardiomyopathy (see Fig. 10-89). Current research in cats with the inherited disease and in human patients has documented mutated genes that encode for sarcomere proteins. To date, eleven altered genes are described in the human disease and one in cats (cardiac myosin-binding protein C). See the discussion on cardiomyopathies in the section on Disturbances of Growth, Myocardium, Disorders of Domestic Animals.

Dilated (Congestive) Cardiomyopathy: See the discussion on cardiomyopathies in the section on Disturbances of Growth, Myocardium, Disorders of Domestic Animals.

Endomyocarditis: Endomyocarditis is a disease of cats of undetermined cause. The affected areas are thickened and often in the area of the outflow of the left ventricle. Lesions consist of a mixed population of inflammatory cells, which extends into the adjacent myocardium. Chronic lesions have marked, often visible fibrous connective tissue with fewer inflammatory cells within the endocardium.

Valvular Anomalies and Dysplasia: See the discussion on valvular anomalies and dysplasia in the section on Disturbances of Growth, Disorders of Domestic Animals.

Blood Vessels: