Arrhythmias can develop as isolated electrical disorders (eg, lone AF or complete heart block) or secondary to other etiologic factors, including (1) structural heart disease; (2) metabolic and endocrine disorders; (3) systemic inflammation; (4) hypotension, hemorrhage, anemia, and ischemia; (5) autonomic influences; (6) toxicosis/envenomations; and (7) drugs.
Electrocardiography (ECG) is the test of choice for confirming the diagnosis of heart rhythm disturbances. A base-apex (rhythm strip) ECG is usually sufficient, but additional surface leads, intracardiac leads, or transesophageal leads are needed to better evaluate the ECG waveforms in some cases. A portable ECG unit is useful in the field for documenting arrhythmias. A continuous 24-hour Holter ECG is indicated to characterize intermittent arrhythmias. An exercising ECG is often indicated to determine if an arrhythmia has potential for impairing performance or might become a safety issue.
The workup of the horse with a nonphysiologic arrhythmia should also include (1) a history including all drugs and supplements administered; (2) a complete echocardiogram; and (3) appropriate laboratory tests.
The examiner must be familiar with physiologic, vagally mediated arrhythmias that include sinus arrhythmia, second degree AVB, and sinoatrial bock. These are normal at rest and immediately after exercise.
Second Degree Atrioventricular Block (AVB)
This rhythm is normal in equine athletes. The HR is in the low normal range and there are usually several conducted P waves before the AVB. Auscultation is characterized by an irregular rhythm with a repetitive pattern. Fourth (atrial) heart sounds that are not followed by first and second heart sounds might be audible in the regular pauses in some horses. Physical activity or increased sympathetic tone should cause the arrhythmia to disappear, although AVB is likely to resume quickly.
Diagnosis and Evaluation
In some cases, an exercising ECG is needed to confirm the physiologic basis of the arrhythmia. When second degree AV block results in more than 2 consecutively blocked P waves, the term “high-grade” is used and the rhythm considered abnormal. If the horse with high-grade second degree AVB cannot be exercised, an atropine response test can be used to determine if a 1 : 1 conduction develops. A continuous 24-hour Holter ECG with simultaneous video recording should be obtained when there is a history of collapse.
Summary: Key Recommendations for High-Grade Second Degree AVB
- Horses with high-grade second degree AVB that disappears with exercise should only be ridden or driven by an informed adult, and the HR and rhythm should be frequently monitored.
- Horses with high-grade second degree AVB during exercise or after atropine administration should be rested and re-evaluated; they are considered less safe to ride or drive than their age-matched peers.
- Horses with symptomatic bradyarrhythmias generally have a poor prognosis and are not safe to ride or drive.
Atrial fibrillation (AF) is the most common arrhythmia affecting performance. In some Standardbred racehorses, it has been identified as a heritable lesion. With acute onset of AF, spontaneous conversion to normal sinus rhythm (NSR) can occur, usually within 24–48 hours. This is referred to as paroxysmal AF. AF in the absence of detectable underlying heart disease is called lone AF. Microstructural lesions or channelopathies that predispose to AF might be present in some of these horses, but cannot be detected using routine diagnostic tests. Structural heart diseases can predispose horses to recurrent or persistent AF.
AF is usually recognized during auscultation and is characterized by an irregularly irregular rhythm that can sound like a combination of premature beats and long pauses. The atrial (fourth) sound is absent. The resting HR is usually normal. Resting tachycardia suggests underlying heart disease, sympathetic nervous system (SNS) stimulation because of stress or pain, or in unusual cases, presence of an accessory atrioventricular conduction pathway. Some horses have AF with a patterned AV conduction sequence that must be distinguished from second degree AVB. Although AF often sounds more regular at higher HRs, the rhythm remains irregular and careful auscultation will reveal this. Horses with AF also should be examined critically for relevant murmurs that might indicate the presence of atrial enlargement and remodeling, creating a substrate for AF.
Diagnosis and Evaluation
The diagnosis is confirmed with an ECG, which is characterized by an irregularly irregular R-R interval with normal QRS morphology, the absence of P waves and the presence of “f” waves. Concurrent PVCs might be found. Atrial flutter represents a slow macro-reentry variation on AF. Flutter waves resemble saw-toothed P waves without an isoelectric shelf and have a regular atrial rate of about 170–275/min, while fibrillation waves are less organized and faster (275–500/min on intracardiac electrograms). AV conduction in atrial flutter is usually variable, resulting in a ventricular rate response that can be irregular or regular during periods of increased sympathetic tone. Patterns of 3 : 1, 2 : 1, or 1 : 1 atrial-to-ventricular conduction can be observed.
A complete echocardiogram should be performed to identify any underlying structural heart disease, valvular regurgitation, and cardiac (atrial) enlargement as described above. A slight increase in LA size can result from AF, even in the absence of MR. Additionally, an ECG exercise test should always be performed when a horse is used for performance and cardioversion is not an option or could not be attained.
The suspected duration of AF should be determined when possible because it affects the prognosis for successful conversion and the likelihood of recurrence. AF induces time-dependent electrical and structural remodeling within the atria, factors known to promote its persistence.[30, 35-37] These changes might also decrease the chance of successful cardioversion and increase the risk of recurrent or persistent AF, even after successful treatment. Additionally, atrial disease might be associated with recurrent premature atrial complexes (PACs) that can act as triggers for recurrent AF after successful treatment. A sudden change in performance and results of previous veterinary examinations provide the best estimate for the onset of the AF. When this information is lacking, it should be assumed that AF is long-standing. Significant LA enlargement reduces the likelihood of successful cardioversion and increases the risk for recurrence. Horses with AF secondary to CHF or with PHT have a grave prognosis and should be retired.
Evidence of LVD, typically a decreased shortening fraction, might indicate underlying myocardial disease in the horse with AF. However, assessment of LV function is hampered during AF because of ventricular dyssynchrony, tachycardia-induced LV dysfunction and preload and HR dependence of many of the echocardiographic indices used to assess LV function. If horses fail to return to their previous level of performance after AF has been successfully corrected, then persistent LVD should be suspected.
The level of intended activity influences clinical decision making as sustained AF is likely to limit rigorous athletic work and occasionally impairs performance at mid to low levels of activity. Other horses with persistent AF are able to perform successfully when used for less intense athletic work. However, cardioversion of AF is recommended when the average maximal HR during exercise at an intensity that is at or slightly exceeding the horse's normal activities is greater than 220/min. Although uncommon, collapse during exercise has been reported with AF. Additionally, ventricular ectopy during exercise or during SNS stimulation indicates a possible risk for SCD, particularly when short R-R intervals or R-on-T phenomenon are observed. AF associated with exercise-induced VA resulting in SCD has been documented in at least one horse. For this reason, treatment for AF is also recommended when concurrent VA are observed. These usually resolve after cardioversion.
Management strategies for AF include no treatment, pharmacologic cardioversion, and transvenous electrical cardioversion (TVEC). Details have been described elsewhere.[38-49] Horses with CHF and AF should be treated for CHF and are not candidates for cardioversion.
Cardioversion is generally not performed for the first 24–48 hours of a documented, recent onset of AF because spontaneous cardioversion might occur. However, after spontaneous cardioversion, an evaluation is still indicated, including measurement of serum K+, and Mg++, fractional excretion of K+ (in racehorses), echocardiography, continuous 24-hour ECG, and optimally an exercising ECG test to identify atrial triggers or other arrhythmias. These tests are also appropriate in a horse with NSR if paroxysmal AF is suspected from the clinical history. However, if AF persists beyond 48 hours, prompt treatment of AF is recommended to deter progressive atrial remodeling.
Cardioversion to NSR
Cardioversion is desirable in all horses performing rigorous athletic work. Successful treatment allows a return to the previous level of performance, assuming an absence of clinically relevant underlying cardiac disease. Cardioversion of AF should only be performed in a controlled setting with continuous (ECG) monitoring, regardless of the treatment method. There are no prospective, randomized studies directly comparing the efficacy of quinidine to TVEC. Success rates of 65–90% have been reported for both. Young racehorses with lone AF probably have a better prognosis for successful cardioversion, independent of treatment modality. Horses with advanced valvular heart disease and moderate to severe atrial enlargement are poorer candidates for cardioversion and long-term maintenance of NSR.
Quinidine sulfate is the mainstay of pharmacologic cardioversion of AF. Indications for quinidine treatment include lone AF, AF with mild LA enlargement, and comorbidities in which general anesthesia or TVEC are not options. Relative or absolute contraindications to quinidine cardioversion include rapid ventricular response to AF and complex ventricular ectopy owing to the proarrhythmic effect of quinidine and risk of polymorphic VT. Quinidine also carries the risk for adverse drug effects that necessitates close monitoring, and sometimes discontinuation of treatment or coadministration of other drugs (such as digoxin) to control the ventricular response rate. The reader is directed elsewhere for details.[34, 38, 43, 44]
TVEC involves a timed shock delivery on the R-wave. The procedure should be performed by experienced operators using specialized equipment. TVEC can be used to treat lone AF, AF with mild LA enlargement, and horses either intolerant of or unresponsive to quinidine treatment or horses in which quinidine is contraindicated (see above). The risks of TVEC include general anesthesia[50, 51] or rarely, development of a fatal arrhythmia. The immediate recurrence of AF (IRAF) within the first 24 hours after cardioversion, although infrequent, is more likely than with quinidine cardioversion. Pretreatment with antiarrhythmic drugs before TVEC or administration of an antiarrhythmic drug during and after anesthesia might minimize the likelihood of IRAF.[45, 53] In the long term, recurrence rates after TVEC and quinidine cardioversion are believed to be similar. The reader is referred elsewhere for a more detailed description of the procedure.[39-42, 45, 54]
Recurrent atrial arrhythmias can be observed in some horses following successful cardioversion and these are best identified using a continuous 24-hour ECG. However, the optimal timing of this examination, the influence of premature atrial complexes on long-term prognosis, and the best approach to management of recurrent atrial ectopy are unknown. A complete echocardiogram after cardioversion can evaluate LV and LA mechanical function and reassess heart size and valvular function. LV function should return to normal within 3 days. Recovery of LA contractile function can occur within a few days or might take several weeks when AF has been long-lasting.[53, 55, 56] Persistent LA contractile dysfunction can be caused by AF-induced atrial remodeling or underlying primary cardiomyopathy and might portend recurrent AF.
Most recommendations to minimize the risk of AF recurrence are based on human studies or experimental animal models. Chronic antiarrhythmic drug treatment potentially effective against atrial arrhythmias in human patients includes propafenone, sotalol, flecainide, amiodarone, and phenytoin. While these could be beneficial to horses with frequent atrial ectopy after cardioversion, clinical studies of efficacy and safety are needed. Drugs known to predispose to ectopic impulse formation should be avoided, including furosemide, supplements containing sodium bicarbonate, and thyroid hormones. Potassium chloride supplementation is indicated in most horses administered furosemide before racing or in those with low fractional urinary excretion of potassium.
The type of AF, AF duration, and concurrent cardiac abnormalities help determine the time out of training following cardioversion. Ideally, rest is enforced until atrial electrical and contractile function has normalized or nearly so. Horses with paroxysmal AF and short-duration, lone AF can return to training within 1 week unless LA stunning or postconversion arrhythmias are detected. Horses with long-standing AF might need a month or longer of rest.
Recurrence of AF
The recurrence rate of AF is lowest (about 15%) with lone AF of recent onset (≤1 month).[34, 39] Recurrence rate of AF is higher in horses with underlying cardiac disease, especially chronic valvular regurgitation with atrial enlargement. Horses with a high number of PACs or runs of atrial tachycardia are more likely to experience recurrent AF, and these ECG findings should be considered a poor prognostic indicator. Persistent LA mechanical dysfunction is thought to indicate irreversible atrial remodeling and might also represent a poor prognostic sign.
Summary: Key Recommendations for AF
- Select the most appropriate method of cardioversion based on the risk factors for pharmacologic cardioversion or TVEC.
- Perform a continuous 24-hour ECG and ideally evaluate LA function after cardioversion.
- Return to training within 1 week with paroxysmal AF or short-duration lone AF if normal after cardioversion; rest horses with long-standing AF for 4–6 weeks.
- Avoid the use of furosemide, supplements containing sodium bicarbonate, and thyroid hormones after cardioversion.
- Supplement oral potassium chloride to horses administered furosemide before racing or demonstrating low fractional excretion of potassium.
- Because safety is a concern with persistent AF, the horse should be cardioverted or retired when the exercising HR during sustained maximal exercise exceeds 220 beats/min or if concurrent VA are detected during exercise or with SNS stimulation.
- Horses with persistent AF should only be ridden or driven by an informed adult and limited to an exercise level considered relatively safe based on an exercising ECG. The use of a HR monitor might be useful to track heart rate during exercise and modify the rigor of the work performed.
Premature Atrial Complexes
PACs are usually detected during auscultation as premature beats interrupting an otherwise regular rhythm. At times, PACs are difficult to differentiate from marked sinus arrhythmia. PACs are an uncommon cause for poor performance. The greatest concern about PACs relates to their potential to incite atrial flutter and AF.
The ECG is needed for definitive diagnosis, and continuous ECG monitoring enables the clinician to more completely characterize the atrial ectopy. PACs are characterized by ectopic, premature atrial activation (P), usually with changes in normal P-wave morphology. PACs can be conducted with a variable P-R interval or blocked at the AV node. PACs are easily missed when buried in the ST segment or T wave, especially at higher HR. The conducted QRS is generally normal in morphology, but ventricular conduction can be aberrant resulting in wider, taller or bizarre QRS complexes with secondary ST segment and T wave changes.
Summary: Key Recommendations for PACs
- A continuous 24-hour ECG is recommended to assess frequent PACs.
- Horses with occasional PACs that are overdriven during exercise and those with occasional PACs during exercise are considered as safe to ride or drive as their age-matched peers.
- Underlying causes should be sought.
- The risk for AF should be appreciated.
Premature Ventricular Complexes and Ventricular Tachycardia
PVCs are also usually detected during auscultation and are characterized by premature beats interrupting an otherwise regular rhythm, usually followed by a compensatory pause. VT is an abnormal rhythm caused by 3 or more repetitive or linked PVCs. Auscultation of VT is characterized by a rapid, usually regular rhythm, with variable intensity and often booming heart sounds (“bruit de cannon”). Because of intermittent aortic valve opening, the rhythm can sound irregular on auscultation and an intermittent pulse deficit could be present. Abnormal jugular pulses (cannon waves) are frequently observed.
An ECG is needed for definitive diagnosis. PVCs are characterized by premature ventricular activation without an associated P wave. The QRS complex is typically wide and bizarre and followed by a large T wave of opposite polarity. Impulses arising from high in the ventricle (near the bundle of His) can be difficult to distinguish from a junctional (nodal) rhythm.
Defining the safety risks to the horse and to the rider or driver is paramount in cases of ventricular ectopy. The complexity of a ventricular arrhythmia (see below) is presumed to relate to the risk of hypotension and sudden cardiac death (SCD) because of ventricular fibrillation (VF). However, risk stratification for VA is imperfect. In the absence of clear evidence, the panel believes recommendations should be biased toward safety, as opposed to maintaining athletic activity. A history of collapse raises great concern in a horse with PVCs. Similarly ventricular ectopy in association with important structural heart disease (and cardiomegaly) poses another long-term safety concern (as discussed above, exercise ECGs are generally recommended for those horses). Detection of systemic hypotension during a documented run of VT is another indication of a serious arrhythmia. But in the absence of clinical signs or of serious structural heart disease, the risk of ventricular ectopy is usually defined by electrocardiographic characteristics, accepting the limitations of this analysis. This assessment includes the morphology, timing, and rate of the ectopic activity.
PVCs can be characterized by QRS complex morphology, including uniform or multiform appearance; number (singles, couplets, or VT); average frequency (per hour or per 24 hours); distributional pattern (eg, haphazard, bigeminy, interpolated); coupling interval relative to the previous QRS complex (fixed versus variable; short coupling versus late-diastolic); and prematurity or timing relative to the previous QRS-T (as with ‘R-on-T’ complexes). Runs of VT are further classified by their rate (absolute rate/min and rate relative to the sinus node); duration of VT (nonsustained versus sustained), and morphology (uniform versus polymorphic, including torsades de pointes). As a general rule, the following are features of complex or potentially “malignant” VA: multiform or polymorphic QRS morphology; short coupling intervals (especially R-on-T timing); sustained VT; rapid ventricular rate (exceeding 120 beats/min); and repetitive ectopic activity (couplets, VT). Polymorphic VT can be observed with diffuse myocardial disease or with drug toxicity (quinidine toxicosis) and induces both hemodynamic and electrical instability. Conversely, the well-tolerated accelerated idioventricular rhythm (AIVR) tends to be monomorphic, start with a relatively long coupling interval, and become established at relatively slow ventricular rates (50–80/min at rest).
Occasional monomorphic PVCs overdriven with exercise or only detected in the immediate postexercise period are not usually a cause for poor performance. A wide range of VA occur during and immediately after intense exercise in normally performing horses.[57-60] The importance of these arrhythmias and the risk of SCD requires further investigation. PVCs can also occur during exercise and are a cause for concern. Their relationship with poor performance is also uncertain and requires further investigation.
Assessment of the overall clinical picture is important because VA can be associated with medical or surgical disorders and often resolve with correction of the underlying problem. A clinical laboratory profile, including plasma or serum cardiac troponin I (cTnI) concentration should be obtained from affected horses. While an echocardiogram might be valuable in any horse with VA, this test is specifically recommended for horses with VT or complex VA; when VA is recurrent or persistent; or when VA is identified in the clinical settings of poor performance, collapse, a clinically relevant cardiac murmur, or a moderately to severely increased cTnI. The echocardiogram should include imaging for abnormal myocardial echo texture, thickness, or scar, and exclusion of dissecting aortic aneurysm or aorto-cardiac fistula. LVD might be secondary to tachycardia-induced cardiomyopathy or ventricular dyssynchrony. In horses with sustained VT, the echocardiogram should be repeated once the horse has returned to NSR. A continuous 24-hour ECG should also be obtained to more completely evaluate the VA as they are often intermittent. Further workup of a horse with PVCs or AIVR, in the absence of underlying systemic disease, should include an exercising ECG. Horses with VT or complex VA should not be exercise tested.
Summary: Key Recommendations for PVCs and VT
- Underlying causes should be sought and managed if possible.
- Horses with occasional PVCs at rest or during exercise or with sustained AIVR that is overdriven by exercise can be ridden or driven with caution by an informed adult. Owing to ongoing concerns about underlying myocardial or electrical disease and increased risks of exercise associated collapse and SCD, these horses should not be used by a child or as a lesson horse.
- Horses with sustained monomorphic VT should be rested and treated. NSR should be present for at least 4 weeks before re-evaluation is performed. A continuous 24-hour ECG is indicated before returning the horse to work. If normal, an exercising ECG should be performed, followed by another exercising ECG once the horse has returned to full work. Horses affected by a single episode generally have a favorable prognosis, but on occasion monomorphic VT can recur.
- Horses with symptomatic or complex VA should be rested and treated. Follow-up examinations are similar as for horses with sustained monomorphic VT although the safety of these horses remains uncertain. These horses should only be ridden or driven by an informed adult.
- Rigorous athletic work is not recommended for horses that showed VA in the setting of moderate or severe structural heart disease, including echocardiographic lesions suspected to indicate myocardial fibrosis or scar, and moderate to severe AR. These horses should only be ridden or driven by an informed adult because of the risk of possible recurrence of VT. These horses are not safe for use by a child or as a lesson horse.
- For horses with a history of VT that remain in work follow-up 24-hour and exercising ECGs should be performed at least annually.