Journal of Veterinary Emergency and Critical Care 24(6) 2014, pp 759–763 doi: 10.1111/vec.12251
Case Report
Sudden death of a horse with supraventricular tachycardia following oral administration of flecainide acetate Katarzyna A. Dembek, DVM, MS, DACVIM; Samuel D.A. Hurcombe, BVMS, MS, DACVIM, DACVECC; Karsten E. Schober, DVM, PhD, DECVIM and Ramiro E. Toribio, DVM, MS, PhD, DACVIM
Abstract
Objective – To describe a case of supraventricular tachycardia and sudden death in a horse following administration of flecainide acetate. Case Summary – An 8-year-old Hanoverian warmblood gelding was treated for chronic, naturally occurring, supraventricular tachycardia with digoxin, procainamide hydrochloride, quinidine sulfate, and flecainide acetate. After oral administration of flecainide, polymorphic ventricular tachycardia (torsades de pointes) and ventricular fibrillation developed, leading to cardiovascular collapse and death. New or Unique Information Provided – Atrial fibrillation is the most commonly diagnosed dysrhythmia associated with poor performance in horses, while atrial tachycardia is rarely documented. Here, we describe a case of sudden death in a horse with atrial tachycardia following the oral administration of flecainide acetate, after the lack of response to other antiarrhythmic drugs. Information provided in this case report is new and will make clinicians aware of the potential complications of flecainide alone or in combination with other drugs, in horses with cardiac dysrhythmias. (J Vet Emerg Crit Care 2014; 24(6): 759–763) doi: 10.1111/vec.12251 Keywords: arrhythmias, atrial fibrillation, atrial tachycardia, equine, flecainide
Abbreviations
AF AT AV ECG SVT
atrial fibrillation atrial tachycardia atrioventricular electrocardiography supraventricular tachycardia
Introduction Cardiac dysrhythmias are common in horses and can be associated with cardiac (eg, myocarditis, endocarditis, degenerative valve disease, atrial enlargement) and noncardiac (eg, septicemia, endotoxemia, metabolic acidosis, electrolyte disturbances, overexertion, autonomic From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210. Address correspondence and reprint requests to Dr. Ramiro E. Toribio, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon L. Tharp Street, Columbus, OH 43210, USA. Email: [email protected] Submitted March 10, 2013; Accepted September 30, 2014. C Veterinary Emergency and Critical Care Society 2014
imbalance, administration of drugs such as quinidine and digoxin) diseases or conditions.1,2 Atrial fibrillation (AF) is the most common dysrhythmia in horses, with an estimated prevalence of 0.66% among Standardbred and 0.23% among Thoroughbred horses;2–6 however, other types of dysrhythmias may also be observed. Atrial tachycardia (AT) is a rapid supraventricular rhythm originating from an ectopic atrial focus distinct from the sinoatrial node.1,7 AT can be caused by myocardial disease or may be indicative of atrial pathology from atrioventricular (AV) valvular disease or congenital heart disease,1,7 but is rarely diagnosed in horses. When AT is persistent (>7 d present), structural heart disease is presumed.1,7,8 Treatment for AT is well documented in dogs9 and people,10,11 but limited information exists in horses. In small animals, pharmacological therapy for AT includes the use of Vaughan-Williams class I (sodium channel blockers), class II (-blockers), class III (potassium channel blockers), and class IV (calciumchannel blockers) antiarrhythmic drugs, administered alone, combined, or in conjunction with digoxin.9,12 Class I agents can be further divided according to their effects on the refractory period and the rate of 759
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repolarization. Class Ia drugs prolong the effective refractory period and delay repolarization (quinidine, procainamide), class Ib drugs shorten the refractory period (lidocaine), and class Ic agents have no effect on the refractory period (flecainide). Class I and III agents are commonly used for cardioversion of supraventricular tachycardias (SVTs), while class II and IV drugs are used predominantly for slowing the ventricular response rate by decreasing AV nodal conduction.11 In people, calcium and potassium channel blockers are most commonly used to treat AT.11 In horses, class I drugs such as quinidine and flecainide have been used to treat AF;4,5,13–15 however, limited information exists on their use to treat AT. This report describes a case of sudden death in a horse with persistent AT following the oral administration of flecainide acetate.
Case Report An 8-year-old Hanoverian warmblood gelding was presented for evaluation of a dysrhythmia ausculted by the referring veterinarian during a routine prepurchase examination. The horse was used as a jumper and had no history of exercise intolerance. On initial physical examination, the gelding was asymptomatic, in good body condition (body condition score 6/9),16 with a body weight of 670 kg and a heart rate on auscultation of approximately 60/min, with an irregularly irregular rhythm, a respiratory rate of 28/min, and a rectal temperature of 38°C. Electrocardiography (ECG) using a standard base-apex lead performed within 1 hour of admission revealed fast AT (atrial rate between 195 and 250/min) with high-grade second-degree AV block with 2:1 to 11:1 AV-nodal conduction and a ventricular rate that averaged around 40/min (Figure 1A). Ectopic P waves were easily identifiable and resembled atypical P waves (P’), whereas the QRS complexes appeared normal (narrow and negative). The presumptive diagnosis was fast AT with intermittent AV conduction. Echocardiographic evaluation revealed mild left atrial and left ventricular enlargement, right atrial enlargement, and mild tricuspid and aortic regurgitation. There was no evidence of valvular heart disease, and the pericardium was considered normal. Left ventricular fractional shortening was decreased at 21% (reference, >25%).17–19 Cardiac rate and rhythm during the echocardiographic study as documented on the monitor of the echocardiograph were similar to that recorded with the base-apex single-lead ECG (Figure 1). Routine hematological and biochemical analyses revealed no abnormalities, and serum cardiac troponin Ia concentration was
Case Report
Sudden death of a horse with supraventricular tachycardia following oral administration of flecainide acetate Katarzyna A. Dembek, DVM, MS, DACVIM; Samuel D.A. Hurcombe, BVMS, MS, DACVIM, DACVECC; Karsten E. Schober, DVM, PhD, DECVIM and Ramiro E. Toribio, DVM, MS, PhD, DACVIM
Abstract
Objective – To describe a case of supraventricular tachycardia and sudden death in a horse following administration of flecainide acetate. Case Summary – An 8-year-old Hanoverian warmblood gelding was treated for chronic, naturally occurring, supraventricular tachycardia with digoxin, procainamide hydrochloride, quinidine sulfate, and flecainide acetate. After oral administration of flecainide, polymorphic ventricular tachycardia (torsades de pointes) and ventricular fibrillation developed, leading to cardiovascular collapse and death. New or Unique Information Provided – Atrial fibrillation is the most commonly diagnosed dysrhythmia associated with poor performance in horses, while atrial tachycardia is rarely documented. Here, we describe a case of sudden death in a horse with atrial tachycardia following the oral administration of flecainide acetate, after the lack of response to other antiarrhythmic drugs. Information provided in this case report is new and will make clinicians aware of the potential complications of flecainide alone or in combination with other drugs, in horses with cardiac dysrhythmias. (J Vet Emerg Crit Care 2014; 24(6): 759–763) doi: 10.1111/vec.12251 Keywords: arrhythmias, atrial fibrillation, atrial tachycardia, equine, flecainide
Abbreviations
AF AT AV ECG SVT
atrial fibrillation atrial tachycardia atrioventricular electrocardiography supraventricular tachycardia
Introduction Cardiac dysrhythmias are common in horses and can be associated with cardiac (eg, myocarditis, endocarditis, degenerative valve disease, atrial enlargement) and noncardiac (eg, septicemia, endotoxemia, metabolic acidosis, electrolyte disturbances, overexertion, autonomic From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210. Address correspondence and reprint requests to Dr. Ramiro E. Toribio, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon L. Tharp Street, Columbus, OH 43210, USA. Email: [email protected] Submitted March 10, 2013; Accepted September 30, 2014. C Veterinary Emergency and Critical Care Society 2014
imbalance, administration of drugs such as quinidine and digoxin) diseases or conditions.1,2 Atrial fibrillation (AF) is the most common dysrhythmia in horses, with an estimated prevalence of 0.66% among Standardbred and 0.23% among Thoroughbred horses;2–6 however, other types of dysrhythmias may also be observed. Atrial tachycardia (AT) is a rapid supraventricular rhythm originating from an ectopic atrial focus distinct from the sinoatrial node.1,7 AT can be caused by myocardial disease or may be indicative of atrial pathology from atrioventricular (AV) valvular disease or congenital heart disease,1,7 but is rarely diagnosed in horses. When AT is persistent (>7 d present), structural heart disease is presumed.1,7,8 Treatment for AT is well documented in dogs9 and people,10,11 but limited information exists in horses. In small animals, pharmacological therapy for AT includes the use of Vaughan-Williams class I (sodium channel blockers), class II (-blockers), class III (potassium channel blockers), and class IV (calciumchannel blockers) antiarrhythmic drugs, administered alone, combined, or in conjunction with digoxin.9,12 Class I agents can be further divided according to their effects on the refractory period and the rate of 759
K. A. Dembek et al.
repolarization. Class Ia drugs prolong the effective refractory period and delay repolarization (quinidine, procainamide), class Ib drugs shorten the refractory period (lidocaine), and class Ic agents have no effect on the refractory period (flecainide). Class I and III agents are commonly used for cardioversion of supraventricular tachycardias (SVTs), while class II and IV drugs are used predominantly for slowing the ventricular response rate by decreasing AV nodal conduction.11 In people, calcium and potassium channel blockers are most commonly used to treat AT.11 In horses, class I drugs such as quinidine and flecainide have been used to treat AF;4,5,13–15 however, limited information exists on their use to treat AT. This report describes a case of sudden death in a horse with persistent AT following the oral administration of flecainide acetate.
Case Report An 8-year-old Hanoverian warmblood gelding was presented for evaluation of a dysrhythmia ausculted by the referring veterinarian during a routine prepurchase examination. The horse was used as a jumper and had no history of exercise intolerance. On initial physical examination, the gelding was asymptomatic, in good body condition (body condition score 6/9),16 with a body weight of 670 kg and a heart rate on auscultation of approximately 60/min, with an irregularly irregular rhythm, a respiratory rate of 28/min, and a rectal temperature of 38°C. Electrocardiography (ECG) using a standard base-apex lead performed within 1 hour of admission revealed fast AT (atrial rate between 195 and 250/min) with high-grade second-degree AV block with 2:1 to 11:1 AV-nodal conduction and a ventricular rate that averaged around 40/min (Figure 1A). Ectopic P waves were easily identifiable and resembled atypical P waves (P’), whereas the QRS complexes appeared normal (narrow and negative). The presumptive diagnosis was fast AT with intermittent AV conduction. Echocardiographic evaluation revealed mild left atrial and left ventricular enlargement, right atrial enlargement, and mild tricuspid and aortic regurgitation. There was no evidence of valvular heart disease, and the pericardium was considered normal. Left ventricular fractional shortening was decreased at 21% (reference, >25%).17–19 Cardiac rate and rhythm during the echocardiographic study as documented on the monitor of the echocardiograph were similar to that recorded with the base-apex single-lead ECG (Figure 1). Routine hematological and biochemical analyses revealed no abnormalities, and serum cardiac troponin Ia concentration was
