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The primary function of the Cardiovascular System is to maintain the circulation of blood so that normal exchange of fluids, electrolytes, oxygen, etc., can be made between the vascular system and tissues. The heart and blood vessels are the two functional units of this system, and either one may fail independently of the other. In heart failure, the inadequacy is due to involvement of the heart itself; the clinical syndrome known as "congestive heart failure" is the consequence of most serious forms of heart diseases. In peripheral circulatory failure, the deficiency is in the vascular system which fails to return blood to the heart. Vessels are affected most commonly secondarily by lesions in adjacent and/or surrounding structures. Remember, cardiovascular diseases are definitely important in veterinary medicine, but such diseases in animals are not the dominating cause of death and disability as recorded in man.
In this section, a discussion of the heart and its associated structures is followed by a discussion of diseases and/or conditions affecting the cardiovascular system.
At the conclusion of this section, each student should be able to perform the following tasks:
The student should be able to define, spell correctly, and use the following terms:
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1.4.1.1 GENERAL:
The heart has an enormous capacity to deal with transient increases in workload, as long as adequate intervals are provided for the recovery of nutritive and electrolyte levels. However, if the heart is forced to work against a sustained overload, it eventually becomes unable to deliver a normal output of blood. This leads to cardiac enlargement (dilatation and hypertrophy) which is the cardinal sign of heart disease. The onset of myocardial fatigue is characterized by slight acute dilatation of the heart which is due primarily to stretching of individual myocardial fibers subsequent to overfilling with blood during diastole. Eventually, the myocardium responds to sustained overload by undergoing hypertrophy and chronic dilatation. Cardiac hypertrophy and dilatation are compensatory in nature and they usually occur together. However, in order for cardiac hypertrophy to develop, a healthy myocardium and adequate nutrition (blood supply) are required. If these factors are lacking, dilatation in the absence of hypertrophy occurs.
1.4.1.2 HEART FAILURE
Heart failure occurs when the myocardium is no longer able to compensate for increases in workload. "Congestive Heart Failure" is the clinical syndrome resulting from the inability of cardiac output to keep pace with venous return. It is characterized by pulmonary and/or generalized venous congestion and low cardiac output. Congestive heart failure is the final pathway of several important types of heart diseases. Subsequent to a failing heart, there is retention of sodium and water by the body (apparently from decreased renal blood flow and adrenal cortical mechanisms). This further distends the venous bed so that the heart cannot keep up with the amount of blood delivered. The clinical signs of congestive heart failure are the secondary effects of a failing circulation. Lesions are most prominent and extensive in the lungs and liver.
The normal cardiac output can be broadly defined as the output necessary to meet the needs of the organism at rest. The ability of the heart to respond to circulatory demands over and above those of the animal at rest is referred to as the cardiac reserve. Any cardiac lesion which impairs the efficiency of the heart reduces the cardiac reserve. Therefore, when the cardiac reserve is exhausted and the circulatory requirements of the animal at rest can no longer be met,"congestive heart failure" follows.
The components of the cardiac reserve are increased of rate of contraction and increased stroke volume; however, there are limits to the effectiveness of each. Increased stroke volume is the most effective of the two components.
In cardiac failure (decompensation), many circulatory reflexes become active. The net effect is that of a coordinated sympathetic nervous system stimulation with reciprocal parasympathetic inhibition. The strong sympathetic stimulation increases the force of myocardial contractions and increases the tone in most of the blood vessels of the body.
When one side of the heart fails. the ensuing sequence of events usually makes the opposite side fail as well. However, it is convenient to discuss the manifestations of left and right-sided heart failure separately.
Remember, the manifestations of left and right heart failure apply to many of the diseases and conditions to be discussed later in this section.
1.4.1.3 LEFT-SIDED HEART FAILURE:
The clinical signs of left heart failure are primarily pulmonary (lungs), and include dyspnea on exertion, cough, and orthopnea. Common causes of left heart failure include:
Regardless of the cause, there is progressive dilatation of the left ventricle and atrium which may be followed by left ventricular and atrial hypertrophy. If the heart is unable to maintain a state of compensation, blood accumulates in the pulmonary veins and lung capillaries. Pulmonary (lung) congestion, edema, and induration ensue. The reduction in pulmonary vital capacity and impaired gaseous exchange result in hypoxic stimulation of the carotid sinus. Eventually, right heart failure develops subsequent to increased pulmonary resistance and increased pressure in the pulmonary artery (refer to the manifestations of right heart failure).
It should be noted that coughing is usually the most distinctive and alarming feature of left heart failure in the dog. The productive cough is explained by the increased production of mucous, stimulated by severe lung congestion.
Clinical signs of right heart failure are the manifestations of generalized venous congestion, and include distention of the jugular and other superficial veins, liver and spleen enlargement, and an accumulation of fluid in serous cavities and in tissues (generalized edema). Common causes of right-heart failure include:
Regardless of the causes, there is progressive dilatation of the right ventricle and atrium which may be followed by right ventricular and atrial hypertrophy. As the heart fails, blood accumulates in the vena cava leading to generalized venous congestion. Centrilobular congestion, degeneration, necrosis, and fibrosis of the liver ensue. The splenic red pulp becomes engorged, and there is generalized edema (ascites, etc.). Eventually, the effects of right heart failure are reflected in the left heart and lungs (if the animal lives long enough).
Generalized edema is a prominent feature of right heart failure and there are some species differences in the location of the edematous fluid. In the horse and cow, a dependent subcutaneous edema is expected (subcutaneous edema is scant or absent in other species). In the dog, the predominant accumulation of fluid is in the peritoneal cavity (ascites); whereas in the cat, fluid is most commonly encountered in the thorax (hydrothorax).
Remember, Cor pulmonale is the clinical term applied to right ventricular strain produced by diffuse pulmonary diseases (chronic emphysema, etc.).
Remember, cardiac enlargement is the "cardinal sign" of heart disease. Myocardial hypertrophy is an increase in bulk of cardiac muscle due to an increase in size of component fibers. There are three descriptive types of hypertrophy:
Is the term used when hypertrophy occurs in the absence of dilatation.
Is the term used when there is both hypertrophy and dilatation of the heart.
Is the term used when hypertrophy results in a decrease in size of the heart chambers.
Hypertrophy affects the left heart more frequently than the right and the ventricles more frequently than the atria. Hypertrophy of the right heart makes the heart broader at the base; whereas hypertrophy of the left heart increases the organ length. Bilateral hypertrophy results in a more rounded shape than normal. Grossly, increased thickness and a rubbery firmness are the best indices of cardiac hypertrophy.
Cardiac dilatation may involve one or both chambers of the heart. Grossly, the dilated heart is globose shaped, the walls are soft, pliable, and thin. The endocardium is usually diffusely thickened and opaque.
Anomalies or malformations of the heart and vessels occur with frequency in domestic animals. In order to detect such anomalies at necropsy, the heart must be opened correctly and the circulation of blood traced carefully through the chambers. The heart and vessels should be examined in situ since relationships are difficult to establish once the structures are removed.
Cardiovascular anomalies are usually compatible with intrauterine life since the fetus depends on the placental blood for its oxygen supply. However, most anomalies do become apparent shortly after birth. Some may permit survival to maturity before decompensation occurs. Relatively little is known of the causative mechanisms of cardiovascular anomalies. Only a few have been shown to follow a clear pattern of inheritance.
There are apparent differences in the relative frequency of cardiovascular anomalies between animal species. In the dog, patent ductus arteriosus, subaortic stenosis, and persistent right aortic arch are most frequently diagnosed; whereas in cattle, atrial and ventricular septal defects, and transposition of the major vessels are most commonly encountered. The most common anomaly in pigs is subaortic stenosis.
Early recognition of congenital cardiovascular disease is important since the pet owner may be able to reclaim his investment, or the livestock producer can avoid attempting to raise an animal which is destined to die at an early age.
If the cardiovascular anomaly is severe enough to impair cardiac function, signs of "congestive heart failure" (generalized venous congestion, hepatomegaly, ascites, etc.) ensue.
In this section, some of the more common cardiovascular anomalies are discussed. To understand the origin of these defects, the student may wish to review briefly the embryonic development of the heart
Refer to Principles of Veterinary Pathology; Runnells, Monlux, and Monlux, 7th edition, page #30).
The ductus arteriosus arises from the left sixth aortic arch. In fetal life, it is an important communication between the aorta and pulmonary artery (takes blood from the pulmonary artery to the aorta). Functional closure of the ductus arteriosus occurs within minutes or hours after birth. Anatomical closure may not occur until the 6th or 7th day after birth. Failure of the ductus arteriosus to close leads to an anomaly known as a "persistent or patent ductus arteriosus." After closure, a nonpatent fibrous cord known as the ligamentum arteriosum persist.
If the ductus arteriosus remains patent after birth, a part of the arterial (aortic) blood is pumped during systole through the patent duct into the pulmonary artery. This left-to-right shunting of blood is due to the existence of higher pressure in the aorta than in the pulmonary artery. In addition, blood reaching the systemic circulation is decreased in amount. This pattern persists if pulmonary vascular resistance remains low. However, if pulmonary vascular resistance is high, right ventricular hypertrophy and pulmonary hypertension occurs and a part of the venous blood is pumped through the patent duct into the aorta (right-to-left shunt).
Large patencies may result in right and/or left heart failure within a few weeks or months of life (smaller patencies may permit survival until maturity). Significant clinical signs include cyanosis, fatigue, lack of stamina, dyspnea, hindleg weakness, and weight loss. A "continuous'' or ''machine-like" murmur is considered to be pathognomonic for patent ductus arteriosus when there is a left-to-right (arteriovenous) shunting of blood. Necropsy findings include those changes described for congestive heart failure (generalized venous congestion, hepatomegaly. ascites, etc.).
In dogs, a persistent right aortic arch is a common vascular anomaly. The right fourth embryonal aortic arch persists, resulting in displacement of the esophagus and trachea to the left. Both the trachea and esophagus become incarcerated in a vascular ring formed by the arch of the aorta. the pulmonary artery, the base of the heart, and the ligamentum arteriosum (or ductus arteriosus). Persistent right aortic arch has been reported in dogs, cats, cattle, and horses. In the German Shepherd dog, the condition is considered to be hereditary.
Significant clinical signs include dysphagia and regurgitation since the vascular ring encircles and compress the esophagus and trachea. At necropsy, the portion of the esophagus anterior to the obstruction is usually dilated.
Defects in the atrial septum may be three types:
Results from the persistence of the opening that serves as a circulatory pathway between the right andleft atria during fetal life. Functional closure occurs normally at birth due to increased left atrial pressure (a valve-like structure prevents the shunting of blood). Anatomical closure of the foramen ovale is complete within a week after birth in the dog, but may not be completed for several months in cattle and horses (the defect is not significant as long as left atrial pressure exceeds right atrial pressure).
Occur in the dorsal or middle portions of the interatrial septum. OSTIUM (SEPTUM) PRIMUM DEFECTS are situated in the lower or ventral portion of the interatrial septum and usually involve the atrioventricular valves as well.
If large interatrial defects are present. blood passes from the left to the right atrium through the defects. This additional blood must be pumped as an "extra load" by the right side of the heart. In time, right ventricular dilatation and hypertrophy occurs and pulmonary hypertension may ensue, followed by congestive heart failure. The flow of blood from the right atrium to the left atrium through a defect can occur but it is usually secondary to increased right atrial pressure (due to pulmonary stenosis, tricuspid stenosis, etc.).
Interventricular septal defects may occur in the muscular and/or membranous portion of the wall that separate the left and right ventricles. However, the majority of these defects occur in the upper membranous portion (high septal defects), providing an opening from beneath the aortic valves to a site beneath the base of the tricuspid valves. Such defects are commonly referred to as "subaortic septal defects".
In the presence of a large ventricular septal defect, the direction of blood flow depends on the relative resistance to flow through the pulmonary vascular bed as compared with that of the systemic vascular bed. In young animals, the blood flow is entirely from left to right since resistance in the pulmonary vascular bed is lower than that in the systemic vascular bed. Thus, the right ventricle is over-loaded leading to right ventricular dilatation and hypertrophy, and subsequent "congestive heart failure". However, if resistance in the intrapulmonary vascular bed exceeds that in the systemic circulation, blood flow is shunted from right to left through the defect. Small interventricular septal defects may be asymptomatic. Subaortic septal defects are commonly associated with microphthalmia in cattle.
Stenosis of the pulmonary valve obstructs the normal flow of blood from the right ventricle to the pulmonary artery. The stenosis may involve the valve directly (valvular) or it may be subvalvular. Valvular stenosis is one of the most frequently diagnosed congenital cardiac anomaly in dogs. In both forms, blood accumulates in the right ventricle leading to ventricular dilatation and hypertrophy. Subsequently, congestive heart failure may ensue. In addition, poststenotic dilatation of the pulmonary artery may occur, producing a rounded enlargement of the vessel resembling an aneurysm.
Stenosis of the aortic valve obstructs the flow of blood from the left ventricle into the aorta. The involvement may be valvular or subvalvular in location. Subvalvular aortic stenosis is most common. Aortic stenosis leads to an accumulation of blood in the left ventricle with left ventricular dilatation and hypertrophy. Subsequently, signs of congestive heart failure ensue (pulmonary congestion, edema, etc.). Oftentimes, there is poststenotic dilatation of the ascending aorta.
The aorta and pulmonary artery may be transposed with the aorta arising from the right ventricle and the pulmonary artery from the left ventricle. If this is simply a shift in position with the arterial side of the heart on the right and the venous side on the left, no significant clinical signs are encountered. However, if the aorta originates from the venous side and the pulmonary artery from the arterial side, death ensues.
Tetralogy of fallot consists of several individual anomalies occurring together. These include:
An overriding, dextropositioned aorta (that receives blood from both the left and right ventricles).
Right ventricular hypertrophy (which is secondary to the other defects).
It should be noted that the aorta may arise form the right ventricle or from both ventricles. Tetralogy of fallot has been reported in dogs, cats, horses, and cattle. The condition is inherited in the Keeshond breed.
The pulmonary stenosis results in an accumulation of blood and increased pressure in the right ventricle. Therefore, blood flow is shunted from right to left through the ventricular septal defect, with mixing of arterial and venous blood. Since the aorta receives blood from both ventricles, venous blood is mixed with arterial blood. Thus, cyanosis is a prominent clinical sign. At necropsy, those changes associated with right-sided heart failure are encountered.
The Eisenmenger complex is similar to tetralogy of fallot but pulmonary stenosis is not present. Therefore. the Eisenmenger complex consist of:
Congenital endocardial fibroelastosis is a developmental anomaly characterized by focal or diffuse thickening of the endocardium by layers of fibrous and elastic tissue. The left heart is involved primarily, but in severe cases the right ventricle may be involved. The thickened endocardium is always more severe adjacent to, and involving the valves. The involved heart valves are puckered and distorted. The chordae tendineae of the atrioventricular valves are shortened and taut. Necrosis and calcification of the papillary muscles may occur.
Congenital hematomas may occur on the margins of the atrioventricular valves. They are especially common in young calves. Congenital hematomas are actually blood-filled cysts, lined by endothelium. The size may range up to 1.0 cm in diameter. They do not persist and no clinical signs ensue.
In this condition, the entire heart lies outside the thoracic cavity.
The pericardium is the fibro-serous sac which encloses the heart. The fibrous or outer layer is rather thin but strong and inelastic. The serous layer is an enclosed sac surrounded by the fibrous layer and invaginated by the heart. It is smooth and glistening and normally contains a small amount of clear serous fluid. The parietal part of the serous layer lines the fibrous layer, to which it is closely attached; whereas the visceral part of the serous layer covers the heart and parts of the great vessels. This portion is referred to as the epicardium.
Most diseases of the pericardium are secondary to disease processes in the heart, lungs, pleura, and other sites in the body. Usually, pericardial diseases are detected clinically only when they cause an accumulation of fluid within the pericardial sac.
Hydropericardium refers to the accumulation of fluid (transudate) within the pericardial sac (remember, a small amount of clear fluid is found normally in the sac). Hydropericardium is caused by those factors responsible for generalized and/or local edema.
The volume of fluid that accumulates in the pericardial sac varies greatly, and is of lesser significance than the rate at which fluid accumulates. If fluid accumulates rapidly, the pericardium is placed under considerable tension and this is reflected in the pooling of venous blood (generalized venous congestion). However, when fluid accumulates slowly, there is time for the pericardium to stretch and adapt. Thus, large amounts of fluid can accumulate before there is significant impediment to blood flow in the large veins and in the right side of the heart.
Remember, a small increase in pericardial fluid occurs by transudation after death which is soon reddened by the products of postmortem hemolysis.
Hemopericardium refers to an accumulation of pure blood in the pericardial sac. The condition is uncommon in animals except in the following instances;
Remember, the term cardiac tamponade refers to compression of the heart subsequent to the accumulation of any fluid within the pericardial sac.
Pericarditis refers to inflammation of both the parietal and visceral surfaces of the pericardium. A true pericarditis is nearly always infectious with an accumulation of exudate within the sac. Infectious agents usually reach the pericardium by extension from surrounding structures and/or by way of the blood stream (hematogenous route). The hematogenous route of infection is most common and the exudate tends to-be of the fibrinous or sero-fibrinous type. It should be noted that infection involving the pericardial (epicardial) surface seldom shows an appreciable spread into the underlying myocardium.
1.6.3.1 FIBRINOUS PERICARDITIS
is a characterized by an accumulation of fibrin within the pericardial sac. Exudation of fluid is not a prominent feature. Grossly, the fluid is grayish to yellow, and flecks of blood may be present. In cattle. it is commonly a part of blackleg, pasteurellosis, contagious bovine pleuropneumonia, sporatic bovine encephalomyelitis, and some forms of neonatal coliform infections. In swine, fibrinous pericarditis is frequently associated with Glasser's disease, pasteurellosis, and salmonellosis. In the horse, streptococci are usually present.
1.6.3.2 PURULENT PERICARDITIS
is characterized by the accumulation of pus in the pericardial sac (due to pyogenic bacteria). It occurs most commonly as a result of traumatic perforation by a foreign body originating from the reticulum (traumatic pericarditis). Also, in traumatic pericarditis the exudate may be fibrinous or fibrino-purulent in nature.
Pus within the pericardial sac may appear as a thin cloudy exudate, as frank creamy exudate, or as a mixture of purulent exudate and masses of pus. The accumulation of pus in the sac places tension on the pericardium which may be reflected in pooling of venous blood (congestive heart failure).
In both fibrinous and purulent pericarditis, healing is usually by organization.
Ultimately, the organizing fibrous connective tissue joins the two surfaces of the serous pericardium resulting in an adhesive pericarditis. Thus, considerable pressure is exerted, and the heart muscles become more or less rigid (constrictive pericarditis). This pressure on the myocardium and large vessels causes compensatory ventricular dilatation and hypertrophy. Subsequently, generalized venous congestion occurs and death may ensue from "congestive heart failure."
1.6.3.3 TRAUMATIC PERICARDITIS
This condition occurs in cattle as a result of traumatic perforation of the pericardium by a foreign body originating in the reticulum (traumatic reticulitis). Ingested foreign bodies enter the reticulum; pierce the wall of the reticulum, overlying peritoneum and diaphragm and enter the thoracic cavity. Subsequently the foreign body may enter the pericardial sac (as well as the myocardium and endocardium) resulting in an exudative pericarditis).
1.6.3.4 SEROUS ATROPHY OF PERICARDIAL FAT
In any cachexia and/or debilitating condition, there is progressive mobilization of depot fat, including that beneath the epicardium. As normal lipid vacuoles are reduced in size, they are replaced by a proteinaceous fluid; subsequently, normal fat is converted to grayish-brown gelatinous masses.
The endocardium lines the cavities of the heart, and is continuous with the intima of vessels which enter and leave the organ. Its free surface is smooth and glistening and is formed by a layer of endothelial cells. This endothelial layer rest on a thin layer of fibroelastic tissue which is connected to the myocardium by subendothelial elastic tissue containing nerves and vessels.
Endocarditis refers to inflammation of the endocardium which may be valvular or mural. In domestic animals, valvular endocarditis occurs more frequently than mural.
Endocarditis is usually caused by bacterial agents, but occasionally parasites and mycotic agents may serve as causative factors. A large number of bacteria are capable of causing endocarditis; however, the manner by which these bacteria localize on a valve is not clear. Apparently, endocarditis occurs subsequent to a substained or recurrent bacteremia. In the dog and horse, streptococci and staphylococci are most commonly isolated from valvular lesions: whereas Corynebacterium pyogenes is most frequently recovered in cattle. In swine, streptococci are common.
The location of endocarditis varies with the animal species involved. In cattle, lesions are most common in the right heart; whereas in the horse. dog, and pig, endocarditis occurs most frequently in the left heart. In cattle, the tricuspid valve is most commonly affected followed by the mitral, pulmonary, and aortic valve. In the horse, the aortic valve is most frequently involved, followed by the mitral and finally the pulmonary valve. In the pig and dog, lesions are most commonly observed in the mitral valve, followed by the aortic, tricuspid, and the pulmonary valve.
Acute ulcerative mural endocarditis is commonly encountered in dogs suffering from acute renal insufficiency (uremia). The lesions (ulcers and thrombi) occur primarily in the left atrium, but may be found in the left ventricle and large elastic arteries. Experimentally, lesions occur more commonly in dogs fed diets high in fat prior to the onset of renal failure. Also, ulcerative mural endocarditis occurs frequently in the left atrium of calves with blackleg.
Regardless of the cause, thrombi are formed in those areas where the endothelium is damaged (valvular or mural). The terms "vegetative" or "cauliflower" are commonly used to describe the gross appearance of these thrombi. The surfaces of the thrombi are friable and embolism may occur. Organization proceeds from the base by the usual process of granulation. Remember, valvular thrombi are almost always serious since they tend to obstruct the normal flow of blood, prevent perfect closure of the valves, and/or result in embolism.
This condition is also referred to as "verrucous endocardiosis" or "nodular fibrosis'', and it is characterized by fibrous thickening of the heart valves. Valvular endocardiosis occurs primarily in dogs and the mitral valve is most frequently and severely affected. The nodular areas of fibrosis develop on the valve leaflets subsequent to proliferation of fibroelastic tissue in which there is abundant mucinous ground substance. The valve cusps are shortened and thickened. The nodular areas of fibrosis are apparently the result of constant mechanical injury to the edges of the valves as they strike against each other (the lesions are not preceded by endocarditis). The incidence of valvular endocardiosis increases with age, and congestive heart failure may develop subsequent to the distorted valves.
The results of valvular lesions depend upon the valve involved and the extent of the valvular injury (the student should refer to the section on "congestive heart failure").
1.7.3.1 INSUFFICIENCY OF THE TRICUSPID VALVE:
Leads to an accumulation of blood in the right atrium -> right atrial dilatation and hypertrophy -> generalized venous congestion (congestion of the vena cava and liver, hepatic cirrhosis, hydroperitoneum, hydrothorax, hydropericardium, etc.).
1.7.3.2 STENOSIS OF THE TRICUSPID VALVE:
Leads to incomplete filling of the right ventricle -> blood accumulates in the right atrium (with the same results as in insufficiency of this valve).
1.7.3.3 INSUFFICIENCY OF THE PULMONARY VALVE:
Leads to a return flow of blood from the pulmonary artery into the right ventricle -> blood accumulates in the right ventricle -> right ventricular dilatation and hypertrophy -> blood accumulates in the right atrium -> generalized venous congestion ensues.
1.7.3.4 STENOSIS OF THE PULMONARY VALVE:
Leads to an accumulation of blood in the right ventricle -> right ventricular dilatation and hypertrophy (with subsequently the same results as in insufficiency of this valve).
1.7.3.5 INSUFFICIENCY OF THE MITRAL VALVE:
Leads to an accumulation of blood in the left atrium -> left atrial dilatation and hypertrophy -> congestion of the pulmonary veins -> congestion, edema, and induration of the lungs -> eventually, congestion of the pulmonary artery occurs which leads to an accumulation of blood in the right ventricle -> right ventricular dilatation and hypertrophy -> an accumulation of blood in the right atrium with dilatation and hypertrophy -> generalized venous congestion.
1.7.3.6 STENOSIS OF THE MITRAL VALVE:
Leads to incomplete filling of the left ventricle -> an accumulation of blood in the left atrium (with subsequently the same results as in insufficiency of this valve).
1.7.3.7 INSUFFICIENCY OF THE AORTIC VALVE:
Leads to a return flow of blood from the aorta into the left ventricle during diastole -> Left ventricular dilatation and hypertrophy (with subsequently the same results as in insufficiency of the mitral valve).
1.7.3.8 STENOSIS OF THE AORTIC VALVE
Leads to an accumulation of blood in the left ventricle -> left ventricular dilatation and hypertrophy (with the same results as in insufficiency of the mitral valve).
In cats, (less commonly in dogs) left atrial thrombosis develops in the absence of a pre-existing endocardial lesion. The etiologic mechanism of these thrombi is unclear. They usually reveal themselves as one or more episodes of secondary thrombosis of the terminal aorta with lameness of the hindlimbs.
Calcification of the elastic fibers of the endocardium is encountered in dogs, cattle, sheep, and horses. In dogs, endocardial calcification occurs most commonly in those which have recovered from acute ulcerative endocarditis of renal insufficiency. It occurs in calves and lambs with vitamin E and selenium deficiency (white muscle disease), and in older cattle with hypomagnesemia. Also, endocardial calcification may be associated with any debilitating disease.
Manchester wasting disease of cattle (Jamaica), Naalehu disease of cattle (Hawaii), and enteque seco of cattle (Argentina), are all characterized by severe calcification (mineralization) of a variety of fibroelastic tissues, including the endocardium. Enteque seco is caused by the ingestion of leaves from a woody plant called Solanum malacoxylox. The unknown toxic principle from the leaves produces rapid weight loss and elevation of blood calcium and phosphorus levels. The cause(s) of Manchester wasting disease and Naalehu is/are unknown, but plant intoxication seems a likely possibility.
Myocarditis refers to inflammation of the myocardium, which is usually secondary to a wide variety of systemic diseases. The causative agents may reach the myocardium by extension or by the hematogenous route. The lesions are usually focal and may be overlooked on causal gross inspection.
1.8.1.1 SUPPURATIVE MYOCARDITIS
Is associated with the presence of pyogenic organisms, and abscess formation is common.
1.8.1.2 EOSINOPHILIC MYOCARDITIS
Is characterized by an infiltration of eosinophils in the myocardium. The condition is occasionally observed in cattle, and the cause is unknown. In addition, an eosinophilic myocarditis is observed in animals given excessive amounts of sulfonamides and occasionally in penicillin hypersensitivity.
1.8.1.3 PARASITIC MYOCARDITIS
May be caused by a variety of parasites (to be discussed in your parasitology course).
Cardiac muscle is subject to the same type of degenerative changes as skeletal muscle. However, there is a greater tendency for heart muscle to undergo degenerative changes as a response to non-specific causes.
HYALINE CHANGES (and necrosis) of the myocardium occurs as a part of "white muscle disease syndrome" and gossypol poisoning. Calcification of the myocardium is usually dystrophic in type, and it occurs whenever there are dead or dying myocytes. In organomercurial poisoning of cattle, calcium salts are selectively deposited in the purkinje network.
Myocardial infarction precipitated by arteriosclerosis of the coronary artery is a burden of aging humans, but is rare in domesticated animals. In animals however, acute obstruction of the coronary arteries due to emboli occurs with some frequency, with the development of infarction. If the coronary obstruction is chronic, the end result is diffuse scarring of the myocardium and markedly altered function. Coagulative necrosis of the myocardium is a lesion commonly associated with vitamin E and selenium deficiency (white muscle disease) in lambs, calves, and pigs.
Petechial, ecchymotic, and larger hemorrhages occur beneath the epicardium and endocardium as agonal changes. Agonal hemorrhages are due to anoxia and rupture of small vessels that occur during the process of dying. Also, subendocardial and subepicardial hemorrhages are commonly associated with septicemias, bacteremias, toxemias, and hypoxic conditions.
(also referred to as "High Mountain Disease" "Brisket Disease", and "Pulmonary Hypertensive Heart Disease")
High altitude disease of cattle develops subsequent to chronic hypoxia of a high altitude environment which causes increased pulmonary vascular resistance and increased pulmonary arterial pressure. The disease is characterized by dilatation and hypertrophy of the right ventricle and atrium with the ultimate development of cardiac decompensation and signs related to "congestive heart failure." Affected cattle reside in mountainous altitudes (usually above 7,000 feet). There is a failure of the cardiorespiratory system to adjust to the chronic anoxia.
The disease usually develops slowly and generalized edema is a prominent feature. Edematous swelling in the ventral pectoral region is responsible for the term "brisket disease." Due to chronic venous congestion, liver lesions may vary from early "nutmeg" appearance to severe centrilobular fibrosis. The lungs exhibit varying degrees of atelectasis and emphysema. Microscopically, hypertrophy of the media of small pulmonary arteries may be observed.
Young cattle are more susceptible than adults and the morbidity rate is highest in animals exposed to high altitudes for the first time. In animals transported from low altitudes to about 10,000 feet, the incidence of severe pulmonary hypertension may not affect more than 2%.
(Also referred to as Dietetic Microangiopathy)
Mulberry heart disease occurs primarily in pigs from 3-4 months of age and the cause has not been clearly elucidated. Grossly, the disease is characterized by extensive hemorrhages throughout the myocardium, as well as subepicardial and subendocardial hemorrhages. The pericardial sac is usually distended with straw-colored fluid and flakes of fibrin. Microscopically, the walls of arterioles and capillaries oftentime contain an amorphous material of glycoprotein nature (microangiopathy). Myocardial necrosis together with thrombi within capillaries may be noted. Although the cause of mulberry heart disease is not fully understood, it is widely felt that a deficiency of vitamin E and selenium plays a prime role.
The encephalomyocarditis virus is capable of producing an encephalomye1itis as well as a myocarditis, depending on host susceptibility and the virus strain. It appears to be primarily a disease of rodents and natural infection is probably unapparent. However, under experimental conditions, the virus is capable of producing both an encephalomyelitis and myocarditis in mice, rats, and hamsters. The encephalomyelitis virus is of greatest importance in swine and non-human primates where it produces a fatal myocarditis (without encephalitis).
In swine, gross findings include cardiac dilatation and an accumulation of fluid in the peritoneal cavity and pericardial sac (the lesions described for "congestive heart failure" may be observed). Microscopically, the principal lesion is an interstitial myocarditis, which is characterized by necrosis of myocardial fibers and a rather intense infiltration of mononuclear cells with fewer leukocytes. The virus is reported to induce myelitis in horses and myocarditis in cattle. Neutralizing antibodies have been found in human sera.
Parvovirus infection in pups is characterized by a severe non-suppurative myocarditis which causes sudden death in the 4 to 6-week age range. The viral myocarditis is apparently a new disease entity in the dog.
Clinically, severe depression may be observed just prior to death, but affected pups usually are found dead without premonitory signs. Grossly, pulmonary edema is the most prominent lesion; the myocardium is grossly normal. Microscopically, there is a rather intense infiltration of the myocardium with mononuclear cells. Basophilic intranuclear inclusion bodies are found within cardiac myofibrils in association with the myocarditis (the nuclear inclusion bodies must be differentiated from the nuclear material of Aschoff cells). Ultrastructurally, the intranuclear inclusion bodies contain parvoviruses. The virus has been reported to induce a fatal enteritis in pups which closely mimic the lesions of feline panleukopenia.
Feline idopathic cardiomyopathy is an acquired disease of obscure cause which develops at all ages beyond adulthood. Pathologically, the disease is associated with endomyocardial fibrosis, ventricular hypertrophy, atrial dilatation, and in many cases, secondary thromboemboli involving the left atrium, aorta, and major arteries and organs.
Feline idopathic cardiomyopathy has been described as occurring in three broad categories. In the younger cat (averaging 1.3 years of age), there is a non-suppurative endocarditis and myocarditis; In cats averaging 7.3 years of age, focal endocardial and myocardial fibrosis, left ventricular hypertrophy, and left atrial dilatation are prominent features. In those cats averaging 10.3 years of age, there is diffuse myocardial and endocardial fibrosis with dilatation of both the left and right ventricles. It has been postulated that endocarditis and myocarditis which occur at an early age heal with fibrosis. The degenerating cardiac tissue induces hypertrophy which is followed later by left and right ventricular dilatation.
Arteritis is characterized by the presence of inflammatory exudate (neutrophils, etc.) within the layers of the vessel wall. Non-specific types of arteritis is a component of all acute inflammatory lesions. The inflammatory reaction occurs in arteries which pass through inflamed areas, or which contain infected thrombi or emboli. It is usually the smaller arteries that are involved and the arteritis is, therefore, of little consequence except in cases of thrombolic infarction or embolism.
In general, non-specific arteritis is secondary to and correlates directly with the inciting cause. Specific types of arteritis occur in a wide variety of systemic infectious diseases. Damage may be due to direct effect of a microbial agent or its toxin on any component of the vascular wall. In pigs, arteritis is commonly associated with septicemic salmonellosis, erysipelas, and hog cholera. The results are reflected in the skin as well as in other organs. In the horse arteritis commonly occurs subsequent to invasion of the anterior mesenteric artery by immature Strongylus vulgaris. Also, arteritis is an important lesion in Newcastle disease of birds, equine viral arteritis, malignant catarrhal fever, renal insufficiency in dogs, dirofilariasis, etc.
Arteritis subsequent to immunologici njury occurs when munecomplexes (antigen/antibody/complement) attach to vascular endothelium. Initially, antigens localize in vascular walls and subsequently complex with circulating precipitating antibodies. The antigen/antibody complexes attract complement. The arteritis is caused by neutrophils for which the complement containing complexes are chemotactic (neutrophils are attacked by terminal complement fragments). Immunologic arteritis occurs in the Arthus reaction, acute serum sickness. Aleutian disease, and in cases of glomurulonephritis. The Arthus reaction is the classical experimental model of immune complex disease and the basic lesion is an intense arteritis.
Equine viral arteritis is an acute contagious disease of horses characterized by extensive necrosis in the media of small muscular arteries of the intestine, lymphoid tissue, and visceral organs. Initially, the virus destroys the endothelium in the vascular supply (vasa vasorum) of small muscular arteries. Subsequently, there is endothelial swelling and necrosis of the media of small muscular arteries. Grossly, the lesions of equine viral arteritis are attributable to the vascular changes and consist principally of extensive hemorrhages and generalized edema. The distribution of edema in the intestine is considered to be characteristic. "Edematous segments of the intestine (1 to 3 feet), alternate with segments of normal thickness." Clinically, the disease is characterized by depression, fever, leukopenia, limb edema, abortion of pregnant mares (up to 80%), enteritis and pneumonic complications.
A mucoarteritis and a myoarteritis have been described in dogs with acute renal insufficiency. In mucoarteritis, the large elastic arteries are characterized by intimal swelling and by a deposition of mucopolysaccharide. The lesions may subsequently involve the media. The condition is associated with mural endocarditis of renal insufficiency. In myoarteritis, the muscle fibers in the media undergo coagulative necrosis with a deposition of "fibrinoid material." The lesions occur primarily in small muscular arteries and arterioles of the gastric mucosa, colon, gallbladder and urinary bladder. Myoarteritis is the most consistently occurring vascular lesion in any form of severe renal injury and may be responsible for the hemorrhage and necrosis of the gastric mucosa in cases of uremia.
Adults of Dirofilaria immitis live in the right heart and pulmonary artery where they interfere with the circulation of blood. The parasites may cause a variety of arterial lesions in the pulmonary circulation. Extensive arteriosclerotic changes including intimal fibrosis and villous proliferations occur in the pulmonary artery. Smaller pulmonary arteries show medial hypertrophy with almost complete obliteration of the lumen. Also. dead parasites may become embolic in the lungs and provoke thrombosis and infarction.
Arterial calcification occurs frequently in animals as a dystrophic or metastatic process. Calcium salts may be deposited in the intima or media. Calcification of the media is commonly associated with chronic renal insufficiency in dogs, vitamin D toxicosis, and a variety of debilitating diseases of cattle.
are mineralized masses that occur in the intima of arterioles of horses. Evidence suggest that the bodies are mineralized, degenerate cellular and intercellular elements derived from subendothelial cells of arterioles.
Hyaline "degeneration" of arteries is an "umbrella term" which includes lesions of various causes. They have in common the histologic features of smudging and loss of cellular detail in the media of arteries. In hyaline changes, smooth muscle cells (myocytes) of the media lose their organized fibrillar character and become dense, amorphous, necrotic masses which stain heavily eosinophilic with eosin. As the affected myocytes degenerate, shrink, and die, plasma proteins exude into the empty spaces, mix with ground substance and collagen and form an eosinophilic hyaline mass called "fibrinoid." In general, so-called hyaline changes of arteries form a spectrum of changes. At one extreme are the acute changes characterized by necrosis and plasma protein infiltration (fibrinoid changes). At the other extreme are chronic lesions which involve recurring episodes of acute damage superimposed upon healing, sclerosing, and poor functioning arteries (hyalinosis).
An aneurysm is a pathological, more-or-less circumscribed, dilatation of an artery (or chamber of the heart). The arterial wall is composed of stretched intima and adventitia with only remnants of media. There is a tendency for aneurysms to enlarge progressively and to ultimately rupture. A false aneurysm is a blood-containing cavity that communicates with the arterial lumen. The wall is formed from surrounding tissues. A dissecting aneurysm is characterized by the presence of blood between the layers of the arterial wall (usually in the media). The blood current gains access to a defect in the media and the resulting blood pressure forces the blood for some distance between the layers.
Hypertrophy of arteries may affect one or all components of the vascular wall. It occurs in response to the need to carry an extra load. Medial hypertrophy of the pulmonary arteries occurs commonly in the lungs of cats. The condition is characterized by marked hypertrophy of the muscular media so that the lumen is reduced to rather small slits. There are no apparent clinical signs and the cause is unclear.
1.12.6 ARTERIOSCLEROSIS
Arteriosclerosis literally means hardening of the arteries. It includes those degenerative changes characterized by induration (fibrous thickening), loss of elasticity, and narrowing of the lumen. Usually arteriosclerotic lesions develop as multiple or focal sclerotic changes superimposed upon a generalized, age-related increase in connective tissue elements of the vessel wall.
The "hallmark" of arteriosclerosis is the fibrous plaque which appears as a white, firm, glistening elevation on the luminal surface of arteries. The well-developed fibrous plaque consists largely of "modified" smooth muscle cells (myocytes) surrounded by increased amounts of extracellular matrix.
Experimental evidence indicates that smooth muscle cells (myocytes) are of prime importance in the development of arteriosclerotic lesions. Subsequent to injury to endothelial cells of an artery, medial myocytes migrate through the internal elastic membrane into the intima. In the intima, the myocytes undergo hyperplastic changes and deposit connective tissue components (elastin, collagen, ground substance, etc.). The initial damage to vascular endothelium allows fractions of plasma protein to pass into the media. These plasma protein fractions serve as stimuli for myocyte migration from the media into the intima. (Remember, the myocytes is the cell responsible for the synthesis of normal connective tissue components in the media).
Subclassifications within the broad category of arteriosclerosis are atherosclerosis, medial sclerosis, and arteriolosclerosis.
Atherosclerosis is characterized by the accumulation of lipid in larger arteries in the form of elevated, lipid-filled plaques called atheromas. The atheroma begins as an intimal lesion which progressively extends into and affects the media.
The pathogenesis of the atheroma involves the following:
-> Endothelial damage -> Myocyte migration through the internal elastic membrane -> Proliferation of myocytes in foci within the intima -> accumulation of lipid within the cytoplasm of myocytes -> focal clusters of myocytes become distended by cytoplasmic lipid giving these cells the name of "foam cells."
Aggregates of foam cells appear grossly as small elevated fatty streaks in the arterial luminal surface. In progressively expanding lesions, foam cells become necrotic and the liberation of free lipid incites fibrosis and calcification. Advanced atheromas are complicated by hemorrhage, thrombosis, ulceration, and the infiltration of the lesions by plasma proteins.
In animals, atherosclerosis occurs primarily in the aorta and small muscular arteries. In the dog, severe systemic atherosclerosis is associated with advanced age, obesity, and hyperlipoproteinemia. The majority of these dogs have hyperthyroidism which leads to hypercholesterolemia and, indirectly, to atherosclerosis.
Experimentally, atherosclerosis is classically produced by feeding animals on cholesterol and high lipid diets. In diet-induced atherosclerosis, the high plasma levels of cholesterol and lipoproteins give rise to large fat-laden foam cells below the intima. These foam cells represent either macrophages and/or myocytes.
In aged humans, atherosclerosis is an extremely common lesion and disease. The aorta, coronary, iliac, and cerebral arteries are most often affected. Because atherosclerotic lesions can occlude blood vessels, serious consequences such as myocardial infarction and stroke may occur.
1.12.6 Medial Sclerosis of Monkeberg (medial calcification)
Is characterized by hyaline and fatty changes which subsequently lead to necrosis and calcification in the media of medium-sized muscular arteries.
Phlebitis is characterized by the presence of inflammatory exudate in the wall of veins. The condition is less common than arteritis. Acute phlebitis occurs in "naval infection" (omphalophlebitis) of calves, lambs and foals. The resulting bacteremia may lead to acute death or give rise to wide-spread suppurative lesions (abscesses).
Dilated and elongated veins are referred to as varicose veins. Such veins follow an irregular and tortuous course and hold an abnormally large amount of blood. Varicose veins are less common in animals than in man.
Lymphangitis is the term used to refer to inflammation of lymphatic vessels. Inflammatory reactions occur under circumstances similar to those discussed for veins. In most instances, the involved vessels are so small as to have no significance; however, in some cases, the involvement of larger vessels results in serious consequences. Lymphangitis is associated with several specific diseases, including:
of horses is a chronic progressive inflammation of the subcutaneous lymphatics. The condition is caused by Corynebacterium ovis (C. pseudotuberculosis) which is the pathogen responsible for caseous lymphadenitis of sheep and goats.
Infection with C. ovis is initiated in cutaneous wounds, typically in the fetlock region of the hindlimbs. Subsequent to the lymphangitis, there is diffuse swelling in the legs. Later, abscesses which ulcerate and discharge a thick creamy pus develop along the course of involved lymphatics.
1.13.2.1 Dilatation (ectasis)
Of lymph channels usually develops subsequent to some form of obstruction. This lead to the accumulation of excess interstitial fluid in the drainage area (local edema). The more common causes of lymphatic obstruction include infiltrating neoplasms and thrombosis of the channels.
1.13.2.2 Ruptures
Of lymph channels are important only when the thoracic duct or larger vessels are the sites of injury. Leakage of lymph usually occur in the thoracic cavity and the condition is referred to as chylothorax. Chylothorax occurs most frequently in cats.
After completing the Cardiovascular system, each student should be able to provide answers for the following questions. Please review the instructional materials if there is a need.
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