The following mechanisms can result in abnormalities of the cardiovascular system: 1) the cardiac valves fail to close or open properly (valvular disease); 2) the heart muscle pumps too feebly or relaxes inadequately (myocardial disease); 3) the heart beats too slowly, too rapidly, or too irregularly (arrhythmia); 4) the systemic vessels offer too great an interference to blood flow (vascular disease); 5) there may be holes between chambers of the left side and right side of the heart (cardiac shunts); 6) there is too little or too much blood compared with the ability of the blood vessels to store that blood; and 7) there is parasitism of the cardiovascular system (eg, heartworm disease). The diseases of greatest importance, due to their prevalence, are mitral regurgitation in dogs, hypertrophic cardiomyopathy in cats, dilated cardiomyopathy in dogs, arrhythmic cardiomyopathy in Boxers, and heartworm disease.
Inadequate closure of valves leads to regurgitation, which occurs most commonly as mitral regurgitation, or mitral and tricuspid regurgitation. Regurgitation through the mitral and/or tricuspid valves constitutes >75% of all heart disease in dogs. As blood regurgitates through either set of AV valves, a typical systolic murmur is heard between the first and second heart sounds. When blood regurgitates through the mitral or tricuspid valves, an excessive amount of blood moves back and forth between the ventricle and atrium. Thus with mitral regurgitation, it is common to see dilation of the left atrium and left ventricle. The degree of left atrial enlargement, documented by either radiography or echocardiography, may be predictive of disease severity. Mitral or tricuspid regurgitation is most common in older small-breed dogs and older horses that have valve leaflets thickened and gnarled by infiltration with glycosaminoglycans. Mitral regurgitation occurs more often in Cavalier King Charles Spaniels, and at a younger age, than in any other breed.
Aortic regurgitation occurs most often in large-breed dogs and in older horses after developing infections (dogs) or noninflammatory degeneration of the aortic valve. The left ventricle can become dilated due to the aortic regurgitation, but this is proportional to the degree of regurgitation. The murmur produced by blood regurgitating from the aorta into the left ventricle is always a diastolic murmur, heard immediately after the second heart sound. In horses, the murmur of aortic regurgitation can be described as “blowing” due to the regurgitant blood flow, or as “buzzing” due to the aortic leaflets vibrating as the blood flows past. The buzzing murmur is almost always associated with a relatively small amount of regurgitant flow. A similar relationship can be seen in dogs with mitral regurgitation.
Inadequate opening of valves is termed stenosis. Pulmonic stenosis is most prevalent, while valvular aortic stenosis is uncommon, and mitral or tricuspid stenosis is rare. However, subaortic stenosis, produced by a fibrous or fibromuscular band of tissue just beneath the aortic valves, is prevalent, especially in certain breeds (eg, Newfoundlands, Golden Retrievers, Boxers, Rottweilers, and German Shepherds). If a valve opens inadequately, a greater pressure must be generated to maintain the normal volume of blood flowing through it. The ventricle responsible for pumping blood through the stenotic valve hypertrophies (thickens) proportionally to the degree of tightness of the stenosis. The systolic murmurs produced by pulmonic or subaortic stenosis are heard between the first and second heart sound; typically, they are shorter in duration than the systolic murmur of mitral regurgitation and are heard best over the left heart base. The severity of stenosis can usually be predicted by the intensity of the murmur. In general, the louder the murmur, the greater the stenosis. The velocity of blood flowing through a stenosis correlates with the severity of the stenosis, which can be estimated by spectral Doppler echocardiography.
Impaired force of contraction is termed reduced systolic function, which occurs most commonly with dilated cardiomyopathy (in large-breed dogs and in cats that are typically taurine deficient) and in longstanding mitral regurgitation. When this occurs, the cardiac muscle is said to be in a reduced inotropic state, or to have reduced contractility. In large-breed dogs, this is usually termed idiopathic dilated cardiomyopathy, because the origin is unknown.
Impaired ventricular relaxation is termed reduced diastolic function, which occurs most commonly when the cardiac muscle suffers oxygen debt and the consequent lack of energy to fuel relaxation. Ventricular muscles also relax poorly in hypertrophic cardiomyopathy (ie, when the muscle is too thick), or with pericardial disease when either the thickened pericardium or fluid contained within the pericardial sac interfere with relaxation. Hypertrophic cardiomyopathy is most common in cats. Probably >85% of cats with heart disease have hypertrophic cardiomyopathy. A smaller number of cats will have so-called restrictive car-diomyopathy, in which the heart fills poorly because the walls are stiffer than normal. Pericardial disease is most common in older, large-breed dogs with tumors bleeding into the pericardial sac.
Any cardiac rhythm falling outside of normal sinus rhythm is termed an arrhythmia. An arrhythmia that is too fast, too slow, or too irregular can result in reduced cardiac output, thereby causing clinical signs that could include exercise intolerance, syncope, or exacerbation of congestive heart failure (CHF). The most common arrhythmias are atrial fibrillation (seen commonly in horses and in large-breed dogs with an enlarged left atrium), ventricular premature depolarizations (seen most commonly in Boxers and Doberman Pinschers), sick sinus syndrome (seen mainly in aged Miniature Schnauzers), and third-degree AV block.
In atrial fibrillation, depolarization of the atria is not coordinated, stimulation of the AV node is frequent but random, and the heart rate is rapid and irregular. Ventricular premature depolarizations (also called ventricular premature beats or complexes) arise from irritated regions of the ventricles. Such irritations commonly result from chronic stretch of the fibers, as well as from oxygen debt or drug effects. A single premature beat causes no trouble, but premature beats may evolve into short or long bursts that lead to hemodynamic impairment and syncope, or even to a complicated ventricular spasm (ventricular fibrillation) leading to sudden death. This commonly occurs in Boxers with arrhyth-mogenic right ventricular cardiomyopathy (previously termed Boxer cardiomyopathy). With either sick sinus syndrome (ie, transient arrest of discharge of the SA node) or complete heart block (in which no atrial depolarization enters the ventricles), the ventricular rate is exceptionally slow and may lead to hemodynamic impairment and exercise intolerance or syncope.
Interference to blood flow through arterioles often leads to hypertension, which is most common in aging animals with impaired renal function (dogs and cats), hyperadrenocorticism (dogs), or hyperthyroidism (cats). The exact underlying cause is usually unknown, but suspected causes include sodium retention and plasma volume expansion, hyperaldosteronism, increased sympathetic tone, and possibly increased angiotensin II. Regardless of the cause, a loss in arteriolar compliance may persist even with adequate treatment of the associated clinical condition. Arterial vasodilators are a mainstay of antihypertensive therapy.
Abnormal communications between the left and right side of the circulation are termed cardiovascular shunts. These take the form of (in decreasing prevalence) patent ductus arteriosus (between the aorta and pulmonary trunk), ventricular septal defect (between the left and right ventricles), or atrial septal defect (between the left and right atria). When blood crosses these defects from the left side to the right side, which is most common, these defects are termed left-to-right shunts. They result in overcirculation of the lungs and dilatation of the cardiac chambers required to pump or to carry the shunted blood. Chronic dilatation ultimately leads to myocardial failure.
Tetralogy of Fallot (see Congenital and Inherited Anomalies of the Cardiovascular System: Tetralogy of Fallot) is a complex congenital anomaly that consists of a hypoplastic right ventricular outflow tract and/or pulmonary trunk, an aorta that overrides the interventricular septum (therefore arising from both ventricles), ventricular septal defect, and right ventricular hypertrophy. Poorly oxygenated blood enters the systemic circulation and produces a bluish tinge (cyanosis) to the mucous membranes and increased numbers of RBC (polycythemia). Tetralogy of Fallot is the most common form of a right-to-left shunt.
Heartworm disease (see Heartworm Disease) is another important heart disease seen predominantly in dogs but also in cats that is transmitted via mosquitoes. In heartworm disease, adult heartworms in the pulmonary vessels impede flow through the lungs, and blood dams up in the right side of the heart and systemic veins. The disease progresses at a varying rate in dogs, but usually lasts <2 yr in cats. Both species may die from pulmonary hypertension arising from partial obstruction to the flow of blood through the diseased pulmonary vessels.
Common Endpoints of Heart Disease
Signs associated with any of the above diseases are due either to inadequate organ perfusion (eg, exercise intolerance, weakness, syncope) or to blood damming up in organs in which the venous effluent is emptied inadequately (eg, pulmonary edema, ascites, pitting edema, effusions). An animal showing signs due to relative inadequacy of the cardiovascular system to deliver enough blood to sustain normal function is said to be in heart failure. An animal showing signs caused by blood damming up in poorly drained organs is said to be in CHF. When inadequate amounts of oxygen are present in systemic arterial blood and there is too much unoxygenated Hgb, the mucous membranes appear cyanotic, and often there is polycythemia.
Animals with heart disease may deteriorate gradually, due most often to pulmonary edema, or they may die suddenly, due to arrhythmias, chordal rupture, or left atrial tear.
Heart Failure, Congestive Heart Failure, and the Failing Heart
Myocardial failure is described as reduced myocardial contractility, which can be determined by a reduced force of contraction from any given preload. More objectively, a failing heart can be described as one with a reduced rate of liberation of energy from the breakdown of ATP, or with a reduced velocity of fiber shortening when the heart contracts during the imaginary situation of contracting against no load. It is difficult to directly measure myocardial contractility and to identify myocardial failure. Almost any animal with heart disease leading to chamber enlargement or increased wall thickness has a failing heart, but such animals have usually compensated and do not manifest symptoms; therefore, they are not in heart failure or CHF.
Heart failure and CHF (see Heart Disease and Heart Failure) are clinical syndromes in which an animal manifests signs referable to a complex interaction between a failing heart and the blood vessels. In heart failure, cardiac output is insufficient to perfuse organs with enough oxygenated blood for the organs to function properly either at rest (termed functional class IV heart failure), during mild exertion (class III), during moderate exercise (class II), or during extreme exercise (class I). In CHF, blood dams up in organs—usually the lungs but occasionally in the systemic organs—and causes the congested organs to function abnormally, become edematous, or both. The functional classification of heart failure is expressed when, during graded exercise, the animal shows signs (eg, dyspnea, cough, collapse) due to the heart disease.
Last full review/revision March 2012 by Daniel F. Hogan, DVM, DACVIM (Cardiology)