C.M. Marr

Consultant Editor

J.M. Reimer

Chapter contents

INTRODUCTION

In horses, the prevalence of cardiovascular disease is low although it can cause poor performance (q.v.) or cardiac failure and is frequently implicated in sudden death. Cardiovascular diseases can be classified on anatomic, pathologic or functional criteria. A functional approach serves the clinician well as it defines clinical manifestations and, often, appropriate management. A functional classification of equine heart disease is listed in Table 8.1.

Volume overload is the most common type of heart failure in the horse and occurs when valvular regurgitation or an intra- or extra-cardiac shunt leads to one or both ventricles receiving excessive quantities of blood. There is activation of the autonomic nervous system and the renin–angiotensin–adrenergic system, progressive ventricular dilatation and, in response, ventricular hypertrophy. Ultimately cardiac dysfunction and irreversible changes within the myocardium ensue.

Pressure overload occurs when there is an anatomic or physiologic obstruction impeding ventricular ejection. In response to increased afterload, the myocardial cells in the affected ventricle increase in diameter as myofibrils are laid down in parallel within them. Myocardial failure occurs as cellular function deteriorates. Lesions resulting in pressure overload such as aortic or pulmonic stenosis are uncommon in horses and this form of heart failure is rare.

Both volume and pressure overload ultimately lead to failure of the affected ventricle. Accumulation of fluid and congestion in the vascular compartments develops “upstream” to the affected ventricle. Left-sided heart failure leads to congestion in the pulmonary circulation, pulmonary edema and respiratory signs ( Box 8.1). Right-sided heart failure leads to fluid accumulation in the systemic circulation, signs of venous distension and ventral edema. There can be effusions in the pleural and peritoneal cavities and, rarely, bowel edema and diarrhea ( Box 8.1). Usually, failure of one ventricle will lead to failure of the other, so that biventricular failure ensues and the clinical presentation includes both left- and right-sided signs ( Box 8.1).

Primary myocardial (pump) failure implies that there is a primary defect in myocardial contractility leading to a reduction in stroke volume. The low cardiac output reduces perfusion and can lead to multiple organ dysfunction (see Box 8.1). This is seen in association with severe cardiomyopathies. Clinical signs produced by low cardiac output will also occur as myocardial failure develops in volume or pressure overload. Where the venous return is severely compromised, e.g. by effusive pericarditis (q.v.), low output heart failure also occurs.

CLINICAL EVALUATION OF THE CARDIOVASCULAR SYSTEM

MYOCARDIAL DISEASE

There are few known causes of primary myocardial disease (cardiomyopathy) in the horse. The ionophore antibiotics (monensin, salinomycin), common additives in cattle and poultry feed, produce myocardial necrosis in the horse. Other proposed etiologies include viral and immune-mediated myocarditis. Nutritional deficiencies are common causes of cardiomyopathy in other species and, in the horse, vitamin E–selenium deficiency produces cardiomyopathy as well as skeletal muscle disease (white muscle disease) (q.v.).

Myocardial dysfunction is often secondary, resulting from extracardiac systemic disease or drug reactions. Significant reductions in myocardial contractility have been noted in horses with lymphosarcoma (q.v.) (without cardiac infiltration), electrolyte disturbances, severe metabolic derangements, endotoxemia and septicemia.

Myocardial disease is characterized by cardiac arrhythmias and/or ventricular dysfunction with ventricular dilatation and reduced myocardial contractility. The presenting signs depend on the severity of myocardial dysfunction and range from varying degrees of exercise intolerance to signs of congestive or low output heart failure in severe cases (see Box 8.1).

The diagnostic procedures that are useful in investigation of myocardial disease are listed in Table 8.3. Echocardiography is used to assess ventricular function while electrocardiography is used to categorize arrhythmias and can reveal S-T segment changes or changes in the duration of complexes. Prolongation of ECG intervals may be associated with primary myocardial disease, however this should alert the clinician to the possibility of electrolyte or metabolic imbalances.

Measurement of serum concentrations of cardiac troponins and CK-MB and HBDH (cardiac isoenzymes of creatinine kinase [CK] and lactate dehydrogenase [LDH], respectively) can be helpful as increases indicate active or recent myocardial damage. However, normal results have been found in horses with significant myocardial necrosis and in chronic myocardial disease. In addition, concurrent damage to other organ systems must be taken into consideration because CK-MB and HBDH are not cardiac-specific in the horse.

Feed analysis for ionophore antibiotics, assessment of acute and convalescent viral titers (e.g. influenza, herpesvirus [q.v.]) or virus isolation is appropriate for determining the etiology of myocarditis in individual cases. Myocardial biopsy has not been attempted successfully in the horse.

Appropriate therapy depends on the presence and significance of any arrhythmias, and the degree of myocardial dysfunction. Certainly, any electrolyte or metabolic imbalances, or systemic disease should be corrected or excluded as a cause of myocardial disease (q.v. arrhythmias for further details of management of those horses with clinically significant arrhythmias).

Therapy for myocardial dysfunction includes rest, diuretics (furosemide) and, if the horse is showing signs of heart failure, positive inotropic agents such as digoxin or, in emergency situations, dobutamine. Digoxin is contraindicated in ionophore poisoning. Activated charcoal or mineral oil may be beneficial in horses that are known to have ingested ionophore very recently.

The prognosis for myocardial disease varies, and is based on the severity of the myocardial insult, the extent of irreversible changes and the degree of ventricular dilatation. Although horses with arrhythmias are often tentatively diagnosed as suffering from “myocarditis” or “myocardial disease”, these horses can have very localized inflammation of the conducting tissue alone. Horses with a pathologic arrhythmia as the only abnormality have a better prognosis than those with accompanying myocardial dysfunction and ventricular dilatation. Thus, echocardiographic assessment of ventricular function is the most accurate means of formulating a prognosis.

Horses with recent onset of myocardial dysfunction, including those with ionophore poisoning, may recover completely and return to their previous level of performance. However, if the damage is extensive, irreversible myocardial fibrosis will ensue. These horses may survive the cardiac disease, but their athletic capability can be markedly reduced. In other cases, cardiac dilatation progresses over weeks to years and the animal eventually dies of congestive heart failure.

CARDIAC ARRHYTHMIAS

Cardiac arrhythmias are common in horses, both at rest and during exercise. They are often physiologic in nature, produced by normal neurohumoral mechanisms as a means of regulating the heart rate and modifying blood pressure. However, arrhythmias can also be pathologic, signifying myocardial disease. The equine clinician is frequently required to determine the significance of arrhythmias. A methodical approach allows precise characterization of the rhythm disturbance and its origin and thus provides the basis for assessment of the importance of the arrhythmia.

Diagnosis of arrhythmias

Careful cardiac auscultation will enable the detection of most cardiac arrhythmias in the horse and in some instances a tentative diagnosis can be made from auscultation alone. However, an ECG is required to diagnose definitively the type of arrhythmia present, and should always be performed if a pathologic arrhythmia is suspected (see Table 8.3). The base-apex lead is used routinely in the horse for assessment of the heart rate and rhythm because movement artifacts are minimized and waveforms are easily visualized.

For the base-apex lead placement is as follows:

1. The negative (“right arm”) electrode is sited dorsal to the right scapula, or in the right jugular groove, two thirds of the way down the neck.

2. The positive (“left arm”) electrode is sited over the cardiac apex (just above the point of the elbow in the sixth intercostal space on the left side).

3. The ground (“right leg”) electrode is sited anywhere on the body, remote from the heart.

Multiple leads can be necessary for the accurate diagnosis of some complex arrhythmias and the standard limb leads used in other species are adequate in the horse. PR, QRS and QT interval determinations are most commonly calculated from lead II ( Table 8.5).

Table 8.5

Normal interval durations in the equine ECG (lead II)

Interval	Duration
P-R	0.22–0.56 s
QRS	0.08–0.17 s
Q-T	0.32–0.64 s

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