Abnormalities of the Cardiovascular System in Animals

Auscultation of a cardiac murmur can indicate an underlying structural cardiac disease or a physiological change (eg, elevated cardiac output). A heart murmur is generated by turbulent blood flow that can be auscultated with a stethoscope.

As detailed in the specific cardiac disease sections that follow, the location, timing and duration, pitch and quality, 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 the hemithorax)

• Grade IV: consistent, loud, radiating widely WITHOUT a palpable precordial (chest wall covering the heart) thrill

• Grade V: consistent, widely radiating WITH a palpable precordial thrill (vibration felt in the chest wall over the heart) 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

The intensity of the heart murmur correlates with the severity of disease in dogs and other species specifically with MMVD, as the intensity of the left apical systolic murmur correlates well with the degree of mitral regurgitation (volume of leak at the valve). This does not hold true in the face of systolic dysfunction or for myocardial disease such as DCM in dogs. This principle also cannot be applied to cats.

Inadequate closure (coaptation) of valves leads to regurgitation (backflow of blood), which occurs most commonly as mitral regurgitation, or mitral and tricuspid regurgitation (concurrent tricuspid regurgitation occurs in approximately 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. Myxomatous degeneration is accumulation of gel-like mucopolysaccharides in connective tissue disrupting the extracellular matrix, weakening it. Valvular disease can occur in any species, including horses, cats, cattle, and exotic species.

MMVD is characterized by changes to valvular tissue including deposition of and infiltration with glycosaminoglycans, disorganization and net destruction of collagen and elastin within the extracellular matrix, and lack of an inflammatory component. As blood regurgitates through either set of atrioventricular (AV) valves, a typical holosystolic murmur is heard between the first (S1: closure of atrioventricular valves) and second (S2: closure of semilunar valves) heart sounds. A midsystolic click (extra heart sound heard between S1 and S2), 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, dilation of the left atrium and left ventricle is common. 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 MMVD. MMVD occurs more often, and at a younger age, in Cavalier King Charles Spaniels than in any other dog breed; however, there is NOT a major difference in the time frame of progression to onset of congestive heart failure (CHF) in this breed compared with other dog breeds. The disease affects roughly 10% of dogs 5–8 years old, 20–25% of those 9–12 years old, and 30–35% of dogs > 13 years old (additional information regarding MMVD and cardiac disease in cats and dogs can be found via the Cardiac Education Group website and ACVIM MMVD consensus statement).

Aortic regurgitation occurs most often in older horses because of calcification or noninflammatory degeneration of the aortic valve. It may also develop, particularly in large-breed dogs, secondary to aortic endocarditis (infection of the valve leaflets). The left ventricle and atrium can become dilated because of aortic regurgitation, and the degree of dilation 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 Shepherd Dogs). If a valve opens inadequately, greater pressure must be generated to maintain the normal volume of blood flowing across it. The ventricular muscle responsible for pumping blood through the stenotic valve concentrically hypertrophies (thickens) in proportion to the degree of tightness of the stenosis.

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.

Medications (beta-blockers) or interventional procedures (eg, balloon valvuloplasty) may be recommended in cases of severe subaortic or pulmonary valve stenosis. Additional interventions for severe pulmonary valve stenosis may include placement of an intracardiac stent or conduit.

Impaired force of contraction is termed reduced systolic function (pump failure) or systolic dysfunction, and it occurs most commonly with DCM. DCM occurs primarily in large- or giant-breed dogs (Dobermans, Great Danes, Irish Wolfhounds, etc), as a feature of Boxer cardiomyopathy, in cats that are taurine-deficient or are in the end stages of other types of cardiomyopathy, and with longstanding mitral regurgitation.

The DCM phenotype can also occur in association with nutritional deficiencies (eg, taurine, L-carnitine) or nontraditional (eg, boutique, exotic ingredients, grain-free) diets, tachycardia-induced cardiomyopathy, doxorubicin-induced cardiomyopathy, and myocarditis. 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 without an identified underlying etiology, this is usually termed idiopathic DCM.

Impaired ventricular relaxation is termed reduced or impaired diastolic function, and it occurs most commonly when the cardiac muscle suffers oxygen debt and the consequent lack of energy to fuel relaxation. Diastolic dysfunction is observed 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.

HCM is most common in cats. Probably > 85% of cats with heart disease have HCM. 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 (additional information regarding the classification, diagnosis, and management of cardiomyopathies in cats can be found in the ACVIM Consensus Statement).

Pericardial disease is most common in older, large-breed dogs with tumors bleeding into the pericardial sac (eg, hemangiosarcoma or chemodectoma). Additional etiologies for pericardial effusion include effusion-constrictive pericardial disease associated with idiopathic pericarditis or other types of neoplasia, such as lymphoma.

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 extracardiac 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, weakness, syncope, or exacerbation of CHF. The most common arrhythmias include the following:

• atrial fibrillation: common in horses and giant-breed dogs, and in any size dog with advanced cardiac disease and severe atrial enlargement

• ventricular premature depolarizations: most common in Boxers and Doberman Pinschers (ie, dogs that develop ARVC or DCM)

• sinus nodal dysfunction/sick sinus syndrome: mainly in aged Miniature Schnauzers, Pugs, and West Highland White Terriers

• persistent atrial standstill: occurs in Labrador Retrievers and English Springer Spaniels

• third-degree AV block: primarily 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, complexes, or depolarizations) arise from regions of electrical instability in the ventricles. This commonly results from chronic stretch of the fibers, fibrosis or fibrofatty infiltration, oxygen debt (ischemia or hypoxia), or drug effects. A single premature beat does not typically cause clinical signs and can be relatively benign; however, premature beats may evolve into short paroxysms (bursts) or long runs at a heart rate > 160 bpm (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 ARVC and warrants immediate treatment with antiarrhythmics.

With either sick sinus syndrome (ie, transient arrest of discharge of the sinoatrial node alternating with periods of tachycardia) or complete (third-degree) 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, weakness, syncope, or sudden death. A pacemaker is indicated in all dogs with persistent high-grade AV block or persistent atrial standstill (complete absence of electrical and mechanical activity in the atria) and in dogs with clinical signs of sick sinus syndrome.

Interference with 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; however, 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. Additional information can be found in the current ACVIM consensus statement on diagnosis and management of systemic hypertension in dogs and cats.

Abnormal communications between the left and right sides of the circulation are termed cardiovascular shunts. These take the following forms (from most to least prevalent):

• patent ductus arteriosus (between the aorta and pulmonary trunk)

• ventricular septal defect (between the left and right ventricles)

• 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 and development of congestive heart failure.

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 (right ventricular concentric hypertrophy occurs secondary to pressure overload). 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 (erythrocytosis).

Tetralogy of Fallot is the most common form of cyanotic heart disease in animals with a right-to-left shunt, although any large atrial or ventricular septal defect can result in right-to-left shunting (referred to as Eisenmenger physiology) secondary to pulmonary hypertension from chronic pulmonary overcirculation and reactive vasoconstriction. Right-to-left shunting with patent ductus arteriosus also occurs 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 occurs 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, combine to impede flow through the lungs. Severe, persistent pulmonary hypertension may result in right ventricular hypertrophy, increased right-sided filling pressure, and eventual development of right-sided CHF (cor pulmonale).

The disease progresses at a varying rate in dogs but usually lasts < 2 years in cats. Both species can develop syncope or cor pulmonale from pulmonary hypertension or 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, and strict cage rest is necessary in the month after adulticide therapy to reduce chances of pulmonary embolism. Pretreatment with doxycycline and a macrocyclic lactone to kill Wolbachia organisms (intracellular bacteria with a symbiotic relationship to heartworms) before adulticide treatment may also mitigate the pulmonary pathology resulting from worm death.

Heartworms (Dirofilaria immitis) have a complex life cycle. The American Heartworm Society guidelines for treatment of heartworm disease should be strictly followed because each step intentionally targets different aspects of the life cycle.

• Keene BW, Atkins CE, Bonagura JD, et al. ACVIM consensus guidelines for the diagnosis and treatment of myxomatous mitral valve disease in dogs. J Vet Intern Med. 2019;33:1127-1140.

• Luis Fuentes V,  Abbott J,  Chetboul V, et al. J Vet Intern Med. ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats. 2020;34:1062-1077.

• Reinero C, Visser LV, Kellihan HB, et al.ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs.  J Vet Intern Med.  2020;34:549-573.

• Acierno MJ, Brown S, Coleman AE, et al. ACVIM consensus statement: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats.  J Vet Intern Med. 2018;32:1803-1822.

• Wess G, Domenech O, Dukes-McEwan J, Häggström J, Gordon S. European Society of Veterinary Cardiology screening guidelines for dilated cardiomyopathy in Doberman Pinschers. J Vet Cardiol. 2017;19(5):405-415.

• Wess G. Screening for dilated cardiomyopathy in dogs. J Vet Cardiol. 2022;40:51-68.

• Cardiac Education Group.

• American Heartworm Society.

• Also see pet owner content regarding disorders of the cardiovascular system in dogs, cats, and horses.