The following mechanisms can result in abnormalities of the cardiovascular system:
the cardiac valves fail to close or open properly (valvular disease)
the heart muscle pumps inefficiently or relaxes inadequately (myocardial disease)
the heart beats too slowly, too rapidly, or irregularly (arrhythmia)
the systemic vessels offer too great an interference to blood flow (vascular disease)
there may be abnormal communications between chambers of the left side and right side of the heart (cardiac shunts) or between the systemic and pulmonary circulations (extracardiac shunts)
there is too little or too much blood compared with the ability of the blood vessels to store that blood
there is parasitism of the cardiovascular system (eg, heartworm disease)
Cardiac diseases can be either congenital defects or acquired in nature. The diseases of greatest importance, because of their prevalence, are mitral regurgitation in dogs (degenerative mitral valve disease), hypertrophic cardiomyopathy in cats, dilated cardiomyopathy (DCM) in dogs, arrhythmogenic right ventricular cardiomyopathy in Boxers and Bulldogs, and heartworm disease.
Auscultation of a cardiac murmur can indicate underlying structural cardiac disease or a physiologic change (eg, elevated cardiac output). A heart murmur is generated by turbulent blood flow that can be auscultated with a stethoscope. The conditions under which turbulence will occur (ie, development of a murmur) can be described by the Reynold's number, which is calculated: Re = (mean velocity of blood flow x vessel diameter x blood density) / blood viscosity. When a critical Reynold's number is exceeded, turbulence and a resultant murmur will occur.
As detailed in the specific cardiac disease sections that follow, the location, timing, and intensity of a heart murmur may correlate with a specific type of cardiac disease or the severity of the disease. Heart murmurs are graded on a scale of I–VI:
Grade I: extremely quiet, focal, and only heard in a quiet environment
Grade II: soft, focal, although consistently auscultated
Grade III: consistent, moderate intensity, and regional (heard throughout hemithorax)
Grade IV: consistent, loud, radiating widely without a palpable thrill
Grade V: consistent,widely radiating, with palpable precordial thrill present
Grade VI: consistent, loud, widely radiating with palpable precordial thrill, and audible with the stethoscope when lifted 1 cm away from the surface of the thorax
Depending on the underlying etiology, the intensity of the murmur may correlate with the severity of the disease, as seen with valvular disease. In dogs with degenerative mitral valve disease, the intensity of the left apical systolic murmur correlates well with the degree of mitral regurgitation. This does not hold true in the face of systolic dysfunction or for myocardial disease such as dilated cardiomyopathy. This principle also cannot be applied to cats.
Inadequate closure (coaptation) of valves leads to regurgitation (back flow of blood), which occurs most commonly as mitral regurgitation, or mitral and tricuspid regurgitation (concurrent tricuspid regurgitation occurs in ~30% of cases with mitral regurgitation). Regurgitation through the mitral and/or tricuspid valves due to myxomatous degeneration of the valve leaflets (degenerative mitral valve disease, DMVD) constitutes >75% of all heart disease in dogs. DMVD is characterized by deposition and infiltration with glycosaminoglycans, disorganization and net destruction of collagen and elastin within the extracellular matrix, and lack of an inflammatory component within valve tissue. As blood regurgitates through either set of AV valves, a typical holosystolic murmur is heard between the first and second heart sounds. A mid-systolic click, secondary to mitral valve prolapse, may precede development of a murmur in the early stages of disease.
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 predict disease severity. Mitral or tricuspid regurgitation is most common in older small-breed dogs and older horses that have valve leaflets thickened by DMVD. DMVD occurs more often in Cavalier King Charles Spaniels, and at a younger age, than in any other breed; however, there is not a significant difference in the timeframe of progression to onset of CHF. The disease affects roughly 10% of dogs 5–8 years old, 20%–25% of those 9–12 years old, and 30%–35% of dogs older than 13 years (additional information regarding cardiac disease in cats and dogs can be found via the Cardiac Education Group website).
Aortic regurgitation occurs most often in older horses due to calcification or noninflammatory degeneration of the aortic valve. It may also develop secondary to aortic endocarditis (infection of the valve leaflets), most often in large-breed dogs. The left ventricle and atrium 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.
Inadequate opening of valves is termed stenosis. Pulmonary valve stenosis is most prevalent, 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 valve leaflets, 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 concentrically hypertrophies (thickens) proportionally to the degree of tightness of the stenosis.
The systolic ejection quality murmurs produced by pulmonic or subaortic stenosis are heard between the first and second heart sound; typically, they are shorter in duration than the holosystolic murmur of mitral regurgitation and are heard best over the left heart base and thoracic inlet (subaortic stenosis). In general, the louder the murmur, the greater the stenosis, although the severity of stenosis is not always predicted by the intensity of the murmur. The velocity of blood flowing through a stenosis correlates with the severity of the stenosis, which can be estimated by spectral Doppler echocardiography or evaluation of the pressure gradient with hemodynamic monitoring during cardiac catheterization.
Medications (beta-blockers) or interventional procedures (balloon valvuloplasty: -conventional, cutting balloon, or high pressure) may be recommended in cases of severe subaortic or pulmonary valve stenosis. Additional interventions for severe pulmonary valve stenosis may include placement of an endovascular stent or conduit.
Impaired force of contraction is termed reduced systolic function (pump failure) or systolic dysfunction, which occurs most commonly with dilated cardiomyopathy (DCM)—primary DCM in large- or giant-breed dogs (Dobermans, Great Danes, Irish Wolfhounds, etc), DCM-phenotype with Boxer cardiomyopathy, and in cats that are typically either taurine deficient or in the end-stages of other types of cardiomyopathy and in longstanding mitral regurgitation. The DCM phenotype can also occur in association with some grain-free diets, tachycardia-induced cardiomyopathy, doxorubicin-induced cardiomyopathy, and myocarditis (inflammation of the heart muscle). When this occurs, the cardiac muscle is said to be in a reduced inotropic state, or to have reduced contractile function. In large-breed dogs, this is usually termed idiopathic DCM, because the origin is unknown.
Impaired ventricular relaxation is termed reduced or impaired diastolic function, which occurs most commonly when the cardiac muscle suffers oxygen debt and the consequent lack of energy to fuel relaxation. Diastolic dysfunction is seen in most cardiac diseases as they progress to heart failure. The ventricular myocardium also relaxes poorly in hypertrophic cardiomyopathy (ie, when the muscle is too thick, stiff, and noncompliant), or with pericardial disease when either the thickened pericardium or fluid contained within the pericardial sac interferes with diastolic function. Hypertrophic cardiomyopathy is most common in cats. Probably >85% of cats with heart disease have hypertrophic cardiomyopathy. A small number of cats will have so-called restrictive cardiomyopathy, in which the heart fills poorly because the walls are stiffer than normal, nonspecific cardiomyopathy (formerly known as unclassified cardiomyopathy), or valvular disease. Pericardial disease is most common in older, large-breed dogs with tumors bleeding into the pericardial sac (eg, hemangiosarcoma or chemodectoma).
Any cardiac rhythm falling outside the normal sinus rhythm is termed an arrhythmia. Arrhythmias develop secondary to underlying structural heart disease, abnormalities of electrical pathways, or secondary to extra-cardiac causes. 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 CHF. The most common arrhythmias are atrial fibrillation (seen commonly in horses and giant-breed dogs, or in any size dog with advanced cardiac disease and severe left atrial enlargement), ventricular premature depolarizations (seen most commonly in Boxers and Doberman Pinschers [ie, dogs that develop arrhythmogenic right ventricular cardiomyopathy or DCM), sick sinus syndrome (seen mainly in aged Miniature Schnauzers, Pugs, and West Highland White Terriers), persistent atrial standstill (seen in Labrador Retrievers and English Springer Spaniels), and third-degree AV block (seen in older dogs with AV nodal fibrosis).
In atrial fibrillation, depolarization of the atria is not coordinated, stimulation of the AV node is frequent but random, and the heart rate is typically rapid and irregular (irregularly irregular rhythm with absence of P waves on ECG). Ventricular premature contractions (also called ventricular premature beats or depolarizations) arise from regions of electrical instability in the ventricles. This commonly results from chronic stretch of the fibers, fibrosis or fibrofatty infiltration, as well as from oxygen debt (ischemia or hypoxia) or drug effects. A single premature beat does not typically cause clinical signs and can be relatively benign, but premature beats may evolve into short paroxysms (bursts) or long runs (ventricular tachycardia) that lead to hemodynamic impairment and syncope, or even to a complete loss of coordination of ventricular activity (ventricular fibrillation) and sudden death. Ventricular tachycardia commonly occurs in Doberman Pinschers with DCM and in Boxers or Bulldogs with arrhythmogenic right ventricular cardiomyopathy and warrants immediate treatment with antiarrhythmics.
With either sick sinus syndrome (ie, transient arrest of discharge of the SA node alternating with periods of tachycardia) or complete heart block (in which no atrial depolarization enters the ventricles), the ventricular rate is exceptionally slow and may lead to hemodynamic impairment (low cardiac output failure, hypoperfusion, hypoxemia), exercise intolerance, syncope, or sudden death. A pacemaker is indicated in all dogs with persistent high-grade AV block or persistent atrial standstill and in dogs that are symptomatic for sick sinus syndrome.
Interference to blood flow through systemic arterioles (systemic hypertension) 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, such as angiotensin-converting enzyme (ACE) inhibitors and amlodipine, are a mainstay of antihypertensive therapy. The American College of Veterinary Internal Medicine (ACVIM) consensus statement on diagnosis and management of systemic hypertension in dogs and cats has recently been updated.
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 may ultimately lead to myocardial failure. See also 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 with pulmonary valve stenosis, 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 (right-to-left shunt) and produces a bluish tinge (cyanosis) to the mucous membranes and increased numbers of RBCs (polycythemia). Tetralogy of Fallot is the most common form of a right-to-left shunt, although any large atrial or ventricular septal defect can result in right-to-left shunting (Eisenmenger physiology) secondary to pulmonary hypertension from chronic pulmonary overcirculation. Right-to-left shunting patent ductus arteriosus is also seen infrequently and typically results from persistent pulmonary hypertension from birth. Any cardiac or extracardiac shunt can also originate as a left-to-right shunt and reverse in direction if the pressure within the pulmonary circulation or right heart becomes greater than the pressure in the aorta or left heart.
Heartworm disease is seen predominantly in dogs but also in cats and is transmitted via mosquitoes. In heartworm disease, adult heartworms in the pulmonary vessels, and the pulmonary arterial changes they induce, impede flow through the lungs. Severe, persistent pulmonary hypertension may result in right ventricular hypertrophy, increased right-side filling pressure, and eventual development of right-side CHF (cor pulmonale). The disease progresses at a varying rate in dogs but usually lasts <2 yr in cats. Both species may develop syncope or cor pulmonale from pulmonary hypertension or may develop pulmonary thromboembolism from in situ thrombus formation or adult worm death. Antigenic stimulation from the heartworms may also cause changes in the lungs, resulting in eosinophilic pneumonitis. The death of adult worms secondary to adulticide therapy always results in some degree of pulmonary thromboembolism. Strict cage rest is necessary in the month after adulticide therapy, and pretreatment with doxycycline and ivermectin to kill Wolbachia organisms before adulticide treatment may also mitigate the pulmonary pathology resulting from worm death.
Signs associated with any of the above diseases are due either to inadequate organ perfusion (eg, exercise intolerance, weakness, syncope, azotemia) or to blood damming up in organs in which the venous effluent is emptied inadequately (eg, pulmonary edema, ascites, pitting edema, other 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 low output, or forward heart failure. An animal showing signs caused by buildup of fluid or congestion in poorly drained organs is said to be in congestive heart failure (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 polycythemia may develop.
Animals with heart failure may deteriorate gradually, due most often to worsening pulmonary edema or renal dysfunction (either primary or secondary to chronic diuretic administration); or they may die suddenly, due to arrhythmias, chordae tendinae rupture, or left atrial tear.
Systolic myocardial failure is described as reduced myocardial contractile function, characterized by a reduced force of contraction for 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 degree of myocardial failure on the cellular level, but such animals may remain compensated without clinical signs of heart failure for a prolonged time.
Low output heart failure and CHF are clinical syndromes in which an animal manifests signs referable to a complex interaction between a failing heart and the blood vessels. In low output heart failure, cardiac output is insufficient to perfuse organs with enough oxygenated blood for the organs to function properly either at rest or during periods of exertion. In CHF, blood dams up in or around organs—usually the lungs but occasionally in the systemic organs—and causes the congested organs to function abnormally, become edematous, or both. There are several classifications of heart failure, the most recent and perhaps most practical of which is based on the course of heart disease expressed in four basic stages (A, B1, B2, C, D) described in the ACVIM Consensus Statement on canine chronic valvular heart disease.