Abnormalities of the Cardiovascular System

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 constitutes >75% of all heart disease in dogs. 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 myxomatous degeneration (infiltration with glycosaminoglycans). Mitral regurgitation 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 time frame of progression to onset of CHF.

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. Pulmonic 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 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 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. Medications (β-blockers) or interventional procedures (balloon valvuloplasty) may be recommended in cases of severe subaortic or pulmonic stenosis, respectively.

Impaired force of contraction is termed reduced systolic function (pump failure), which occurs most commonly with DCM—primary DCM in large-breed dogs, 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. 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 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), or with pericardial disease when either the thickened pericardium or fluid contained within the pericardial sac interferes 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 cardiomyopathy, in which the heart fills poorly because the walls are stiffer than normal, 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. 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), sick sinus syndrome (seen mainly in aged Miniature Schnauzers), persistent atrial standstill (seen in Labrador Retrievers and English Springer Spaniels), 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 contractions (also called ventricular premature beats or depolarizations) 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 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 with arrhythmogenic right ventricular cardiomyopathy (previously termed Boxer 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.

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. See also Congenital and Inherited Anomalies of the Cardiovascular System.

Tetralogy of Fallot (see 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 (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 (see 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.