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Ventricular septal defect and atrial fibrillation in an adult horse: A case report
\:S
Reviewed
VENTRICULARSEPTALDEFECTAND ATRIAL FIBRILLATIONIN AN ADULTHORSE:A case report Thomas L. Seahom, DVM, MS and Cyprianna E. Honnanski, DVM
SUMMARY A D-year-old Tennessee Walking Horse was admitted for evaluation of ventral edema. Examination revealed clini-
cal signs indicative of heart failure. An electrocardiogram confirmed a diagnosis of atrial fibrillation. Echocardiography revealed a large ventricular septal defect in what had been a normal and athletic horse until the recent onset of edema. Postmortem examiuation confirmed the presence of a 7.5 cm ventricular septal defect and cardiac enlargement.
CASE HISTORY A 13-year-old Tennessee Walking Horse was admitted for evaluation of ventral edema of 2 weeks' duratiorL The horse had been used as a field trial horse and had no history of illness prior to the development of edema. The horse had been vaccinated annually against Eastern and Western Encephalomyelytis, tetanus, and influenza. Parasite control included paste dewormers administered at 8-week intervals. The patient was in good body condition but had ventral midline edema extending from the pectoral muscles to the prepuce, The body temperature, respiratmy rate, capillary refill time, and mucous membrane color were within normal limits. The jugular veins were distended from the thoracic inlet to the ramus of the mandible and pulsations were apparent with each contraction of the heart. The heart rate was 72 beats per minute and the heart rhythm was irregularly Authors' address: Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 708036410.
36
Table 1. Measurements from M-mode echocardiography of a horse with a ventricular septal defect and atrial fibrillation. Patient
Normal 10
64 mm
32-52 mm
137 mm 108 mm 21%
80-130 mm 43-79 mm 32-55%
systole
28 mm 29 mm
20-40 mm 32-56 mm
Ventricular septal thickness: diastole systole
25 mm 35 mm
19-43 mm 35-62 mm
Right ventricular diameter Left ventricular diameter: diastole systole Left ventricular shortening fraction Left ventricle wall thickness:
diastole
irregular. A grade 3/5 holosystolic murmur was ausculted over the left heart base and a grade 4/5 pansystolic murmur was ausculted over the right heart base. Blood was collected for a complete blood cell count and serum chemistry panel and all values were within normal limits. Electrocardiography demonstrated fibrillation waves and an irregular R-R interval confu'ming atrial fibrillatiort Two-dimensional, real-time echocardiography revealed cardiac enlargement (Table 1) and a ventricular septal defect (Figure 1). Because of this patient's prognosis for return to normal activity, the horse was euthanatized. Necropsy confirmed the clinical diagnosis and demonstrated a 7.5 cm ventricular septal defect located under the septal leaflet of the tricuspid valve (Figure 2).
DISCUSSION Ventfiodar septal defect is the most common congenital cardiac malformation of the horse,1 The defect is usnallyhigh JOURNAL OF EQUINE VETERINARY SCIENCE
Figure1. Two-dimensional ultrasonogram obtained via a 2.5 MHz sector transducer at the right thoracic 5th intercostal space.Aventricularseptal defect (VSD) isapparent adjacent to the aortic valve. RV=right ventricle; LV=left ventricle; AO=aortic outflow tract.
in the septumjust below the aortic valve and opens under the septal leaflet of the llicuspid valve on the fight When a VSD is present, the Usualftow pattem is fromthe leftventricle to the right ventricle, resulting in pulmonary overperfusion and volume overload of both ventricles. 2 Prolonged overdistension is associated with progressive slippage between muscle fibers and loss of register between myofibrils. These changes result in profound depression of contractility in the late stages of volume overloading.3 Decompensation ultimately occurs when contmcllity is depressed to a level that cannot be compensated for by further increments in preload or by cardiac hypertrophy. Auscultation of animals with VSD often reveals a grade Ill or louderholosystolic murinuraudible onboth sides ofthe thorax, but usually louder over the right a ~ r i o r thorax.2 Diagnosis of VSD may be supported by auscultation, ultmsonography, cardiac catheterization, and contrast radiography. Animals with large-diameter defects are often unthrifty, may die prematurely, or are euthanatized at an early age.4 Animals with small defects may remain clinically normal for life.4 Atrial fibrillation is a cardiac dysrhythmia characterized by a lack of coordinated atrial electrical activity. It is caused by an abnormality of impulse conduction that results from random reentram activation of the atria.5Normally electrical impulses withinthe heartproceedfromthecardiac pacemaker (SA node), through the internodal pathway, to the AV node. Following a delay period associated with AV node conduclion, impulses spread throughthe ventricles via the AVbundle and Purkinje fibers.6 Theoretically, atrial fibrillation may occur in two ways. 6 Single or multiple irritable ectopic foci within the atrial myocardium may send impulses in multiple directions through the atria causing high frequeucyincoordihated contractions. Areas of myocardial necrosis can serve as such ectopic foci. The second theoly concerning the occurrenceof atrial fibrillation is termed reentrant activatioxt In the Volume 13, Number 1, 1993
Figure 2. Pathology specimen showing the 7.5 ventricular septal defect (arrows) below the septal leaflet of the tricuspid valve. The apex of the heart is to the lelt. normal state, atrial myocardial cells remain refractory to returning impulses. However, in the pathologic state, if the atrial cells repolarize before the impulse returns, they may again depolarize thus continuing the impulse abnormally (i.e. reenay). This reenay phenomenonmay occur if a) the length of the pathway that the impulse travels is increased; b) the velocity of conductionthrough the atria is decreased; or c) the refractory period of the atrial muscle cells have become shortened. Increased length of pathway and decreased conduction velocity are seen with atrial dilation and myocardial ischemia, respectively. Inthe horse, highvagal tone facilitates a relatively short refractoly period and inhomogeneity of myocardial cells.7 Because of the relatively large atria of the normal horse, fibiillationmaybesustained afteritbeginseven if the initiating factor is removed.a Although not determined in this patient, compensatory changes in preload, afterload, and myocardial contractih'ty most likely allowed this patient to live a normal life but exercise demands necessitated cardiac enlargement. In theory, the heart at some point, reached a critical size that, in combination with ischemia and vagal tone, facilitated the development of reentram impulses resulting in atrial fibrillation.9Atrial fibrillation was most likely not the cause of heart failure in patient, but may have been a contributing factor in the development and progression of clinical signs. Treatment was not attempted in the patient of this report because correctionof the primmy problem (ventricular septal defect) was not considered possible and return to athletic performance was considered unlikely. Quire'dinesulfate (1 g/ 45.45 kg administered every 2 hours until conversion to sinus rhythmor a total of 60 g) has been effectivein treating horses with atrial fibrillation of slloIt duration and which do not have underlying heart disease.9Horses with poor myocardial contractility as illustrated by a reduced shortening fraction have additionally be treated with digoxin (1 mg/454.5 kg I.V. or 5 mg/454.5 kg PO) prior to quinidine sulfate admires"tmtiorL9
37
REFERENCES 1. Leipold HW, Saperstein G, Woollen NE: Congenital defects in foals. In Smith BP (ed), Large Animal Internal Medicine, Philadelphia:CV Mosby Co., p170,1990. 2. Button C: Congenital disorders of cardiac blood flow. In Robinson NE (ed), Current Therapy in Equine Medicine, Philadelphia:WB Saunders Co., pp167-168,1987. 3. Knight DH: Pathophyalology of heart failure. In Ettinger SJ (ed), Textboodof VeterinaryInternaIMedicine, Philadelphia:WB Saundars Co., pp899-922,1989. 4. Pipers FS, Reef V, Wilson J: Echocardiographic detection of ventricular septal defects in large animels. JAmer Vet Med Assoc 187(8):810-816,1985.
LIBRARY ( EQUINE REPRODUCTION (1993); Edited by Angus O. McKinnon and James L. Voss; Published by Lea & Febiger; 1137 pages; 8 1/2" X 11"; U.S. $99.50. This might well be the equine reproduction book to end all equine reproduction books. The list of 95 authors is a virtual "Who's Who" in equine reproduction. The editors said about this giant volume, "The practice of veterinary medicine is progressing rapidly toward species specialization; within this, discipline specialization now occurs. However, the nature of our service necessitates talented general practitioners, and for the foreseeable future, they will remain the backbone of the profession. At the same time, education of the client has improved through greater access to information, and many clients have become more demanding and critical of veterinary services. This has placed many of us in unenviable situations. How do we remain cognizant of all the latest and pertinent research findings? Publication of most current research, at best, is scattered widely through many research and veterinary oducationaljournals. Researchers without a veterinary educational background have contributed greatly to recent discoveries and have published reports, albeit unwittingly, in journals beyond our usual access. How many practicing veterinarians routinelyscrutinize journals such as Biology of Reproduction, Animal Science, or even Reproduction and Fertility, apart from special supplements? Similarly, how many basic and applied equine researchers read the Proceedings of the American Association of Equine Practitioners or articles in popular equine magazines and have a real understanding of the relative importance of problems of the equine industry?"
38
5. McGuirk SM, Shaftoe S, Lunn DP: Diseases of the cardiovascular system. In Smith BP (ed), Large Animal Internal Medicine, Philadelphia:CV Mosby Co., pp485-488,1990. 6. Guyton AC: Rhythmic excitation ofthe heart. In Textbook of Medical Physiology 5th ed, Philadalphia:WB Saunders Co., pp177-189,1976. 7. Marr CM: An echocardiographic study of atrial fibrillation in horses before and after treatment with quinidine sulfate. Proceedings 9th Amer Col Vet Int Med, pp367-369,1991. 8. Bertone JJ: Atrial fibrillation in horses. Compend Contin Educ Pract Vet 9(7):763-771,1 987. 9. Reef VB, Levitan CW, Spencer PA: Factors affecting prognosis and conversion in equine atrial fibrillation. J Vet Internal Med 2:1-6,1988. 10. Bonagure JD, Herring DS, Welker F: Echocardiography. In Bonagura JD (ed), Vet C/in of N Arner: Equine Pract, Philedelphia:WB Saunders Co., pp311-333,1985.
From this the editors make the case for a need of a text which combines recent informationwithin the discipline of equine reproduction into a format useful for practicing equine veterinarians. This editor agrees with them that "Veterinarians in mixed practice, veterinary students, basic and applied scientists, and graduate students may benefit from the breadth and specificity of the informationpresented hem in 118 well referenced chapters." The two major parts of the book are The Mare and The Stallion. Them is also a short pan The Neonate, and a fourth part of Appendices. The part on the neonate is really too small to be considered complete. The 40 pages am divided into two parts: Cam of the mare and foal in the neonatal period, and Diseases of foals during the neonatal period; a total of 14 chapters. As a book of this title should be, nearly half of the neonate section is about mare cam, and much more informationis included in part 1 of the book about The Mare--- chapters on parturition, dystocia, lactation, congenital defects in foals, retained placenta, uterine involution and. Important chapters for every equine practitioners who does any broodmaro work am the chapters onAssessment of fetal well-being, postnatal cam of the foal, and identification of the mare and foal at high risk for perinatal problems. The major sections in the mare part of the book am: anatomy; physiology/endocrinology; breeding management; diseases of the reproductive tract; reproductive surgery of the mare; pregnancy, parturition and the puerperal period. With the same organization, the part on the stallion is divided into sections: anatomy, physiology,and endocrinology; breeding management; diseases of the stallion's reproductive tract; and reproductive surgery of the stallion. The book is available from Lea & Febiger on 90 day approval from 200 Chester Field Parkway, Malvern, PA 19355-9725; 1-800-638-0673.
JOURNAL OF EQUINE VETERINARY SCIENCE
Reviewed
VENTRICULARSEPTALDEFECTAND ATRIAL FIBRILLATIONIN AN ADULTHORSE:A case report Thomas L. Seahom, DVM, MS and Cyprianna E. Honnanski, DVM
SUMMARY A D-year-old Tennessee Walking Horse was admitted for evaluation of ventral edema. Examination revealed clini-
cal signs indicative of heart failure. An electrocardiogram confirmed a diagnosis of atrial fibrillation. Echocardiography revealed a large ventricular septal defect in what had been a normal and athletic horse until the recent onset of edema. Postmortem examiuation confirmed the presence of a 7.5 cm ventricular septal defect and cardiac enlargement.
CASE HISTORY A 13-year-old Tennessee Walking Horse was admitted for evaluation of ventral edema of 2 weeks' duratiorL The horse had been used as a field trial horse and had no history of illness prior to the development of edema. The horse had been vaccinated annually against Eastern and Western Encephalomyelytis, tetanus, and influenza. Parasite control included paste dewormers administered at 8-week intervals. The patient was in good body condition but had ventral midline edema extending from the pectoral muscles to the prepuce, The body temperature, respiratmy rate, capillary refill time, and mucous membrane color were within normal limits. The jugular veins were distended from the thoracic inlet to the ramus of the mandible and pulsations were apparent with each contraction of the heart. The heart rate was 72 beats per minute and the heart rhythm was irregularly Authors' address: Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 708036410.
36
Table 1. Measurements from M-mode echocardiography of a horse with a ventricular septal defect and atrial fibrillation. Patient
Normal 10
64 mm
32-52 mm
137 mm 108 mm 21%
80-130 mm 43-79 mm 32-55%
systole
28 mm 29 mm
20-40 mm 32-56 mm
Ventricular septal thickness: diastole systole
25 mm 35 mm
19-43 mm 35-62 mm
Right ventricular diameter Left ventricular diameter: diastole systole Left ventricular shortening fraction Left ventricle wall thickness:
diastole
irregular. A grade 3/5 holosystolic murmur was ausculted over the left heart base and a grade 4/5 pansystolic murmur was ausculted over the right heart base. Blood was collected for a complete blood cell count and serum chemistry panel and all values were within normal limits. Electrocardiography demonstrated fibrillation waves and an irregular R-R interval confu'ming atrial fibrillatiort Two-dimensional, real-time echocardiography revealed cardiac enlargement (Table 1) and a ventricular septal defect (Figure 1). Because of this patient's prognosis for return to normal activity, the horse was euthanatized. Necropsy confirmed the clinical diagnosis and demonstrated a 7.5 cm ventricular septal defect located under the septal leaflet of the tricuspid valve (Figure 2).
DISCUSSION Ventfiodar septal defect is the most common congenital cardiac malformation of the horse,1 The defect is usnallyhigh JOURNAL OF EQUINE VETERINARY SCIENCE
Figure1. Two-dimensional ultrasonogram obtained via a 2.5 MHz sector transducer at the right thoracic 5th intercostal space.Aventricularseptal defect (VSD) isapparent adjacent to the aortic valve. RV=right ventricle; LV=left ventricle; AO=aortic outflow tract.
in the septumjust below the aortic valve and opens under the septal leaflet of the llicuspid valve on the fight When a VSD is present, the Usualftow pattem is fromthe leftventricle to the right ventricle, resulting in pulmonary overperfusion and volume overload of both ventricles. 2 Prolonged overdistension is associated with progressive slippage between muscle fibers and loss of register between myofibrils. These changes result in profound depression of contractility in the late stages of volume overloading.3 Decompensation ultimately occurs when contmcllity is depressed to a level that cannot be compensated for by further increments in preload or by cardiac hypertrophy. Auscultation of animals with VSD often reveals a grade Ill or louderholosystolic murinuraudible onboth sides ofthe thorax, but usually louder over the right a ~ r i o r thorax.2 Diagnosis of VSD may be supported by auscultation, ultmsonography, cardiac catheterization, and contrast radiography. Animals with large-diameter defects are often unthrifty, may die prematurely, or are euthanatized at an early age.4 Animals with small defects may remain clinically normal for life.4 Atrial fibrillation is a cardiac dysrhythmia characterized by a lack of coordinated atrial electrical activity. It is caused by an abnormality of impulse conduction that results from random reentram activation of the atria.5Normally electrical impulses withinthe heartproceedfromthecardiac pacemaker (SA node), through the internodal pathway, to the AV node. Following a delay period associated with AV node conduclion, impulses spread throughthe ventricles via the AVbundle and Purkinje fibers.6 Theoretically, atrial fibrillation may occur in two ways. 6 Single or multiple irritable ectopic foci within the atrial myocardium may send impulses in multiple directions through the atria causing high frequeucyincoordihated contractions. Areas of myocardial necrosis can serve as such ectopic foci. The second theoly concerning the occurrenceof atrial fibrillation is termed reentrant activatioxt In the Volume 13, Number 1, 1993
Figure 2. Pathology specimen showing the 7.5 ventricular septal defect (arrows) below the septal leaflet of the tricuspid valve. The apex of the heart is to the lelt. normal state, atrial myocardial cells remain refractory to returning impulses. However, in the pathologic state, if the atrial cells repolarize before the impulse returns, they may again depolarize thus continuing the impulse abnormally (i.e. reenay). This reenay phenomenonmay occur if a) the length of the pathway that the impulse travels is increased; b) the velocity of conductionthrough the atria is decreased; or c) the refractory period of the atrial muscle cells have become shortened. Increased length of pathway and decreased conduction velocity are seen with atrial dilation and myocardial ischemia, respectively. Inthe horse, highvagal tone facilitates a relatively short refractoly period and inhomogeneity of myocardial cells.7 Because of the relatively large atria of the normal horse, fibiillationmaybesustained afteritbeginseven if the initiating factor is removed.a Although not determined in this patient, compensatory changes in preload, afterload, and myocardial contractih'ty most likely allowed this patient to live a normal life but exercise demands necessitated cardiac enlargement. In theory, the heart at some point, reached a critical size that, in combination with ischemia and vagal tone, facilitated the development of reentram impulses resulting in atrial fibrillation.9Atrial fibrillation was most likely not the cause of heart failure in patient, but may have been a contributing factor in the development and progression of clinical signs. Treatment was not attempted in the patient of this report because correctionof the primmy problem (ventricular septal defect) was not considered possible and return to athletic performance was considered unlikely. Quire'dinesulfate (1 g/ 45.45 kg administered every 2 hours until conversion to sinus rhythmor a total of 60 g) has been effectivein treating horses with atrial fibrillation of slloIt duration and which do not have underlying heart disease.9Horses with poor myocardial contractility as illustrated by a reduced shortening fraction have additionally be treated with digoxin (1 mg/454.5 kg I.V. or 5 mg/454.5 kg PO) prior to quinidine sulfate admires"tmtiorL9
37
REFERENCES 1. Leipold HW, Saperstein G, Woollen NE: Congenital defects in foals. In Smith BP (ed), Large Animal Internal Medicine, Philadelphia:CV Mosby Co., p170,1990. 2. Button C: Congenital disorders of cardiac blood flow. In Robinson NE (ed), Current Therapy in Equine Medicine, Philadelphia:WB Saunders Co., pp167-168,1987. 3. Knight DH: Pathophyalology of heart failure. In Ettinger SJ (ed), Textboodof VeterinaryInternaIMedicine, Philadelphia:WB Saundars Co., pp899-922,1989. 4. Pipers FS, Reef V, Wilson J: Echocardiographic detection of ventricular septal defects in large animels. JAmer Vet Med Assoc 187(8):810-816,1985.
LIBRARY ( EQUINE REPRODUCTION (1993); Edited by Angus O. McKinnon and James L. Voss; Published by Lea & Febiger; 1137 pages; 8 1/2" X 11"; U.S. $99.50. This might well be the equine reproduction book to end all equine reproduction books. The list of 95 authors is a virtual "Who's Who" in equine reproduction. The editors said about this giant volume, "The practice of veterinary medicine is progressing rapidly toward species specialization; within this, discipline specialization now occurs. However, the nature of our service necessitates talented general practitioners, and for the foreseeable future, they will remain the backbone of the profession. At the same time, education of the client has improved through greater access to information, and many clients have become more demanding and critical of veterinary services. This has placed many of us in unenviable situations. How do we remain cognizant of all the latest and pertinent research findings? Publication of most current research, at best, is scattered widely through many research and veterinary oducationaljournals. Researchers without a veterinary educational background have contributed greatly to recent discoveries and have published reports, albeit unwittingly, in journals beyond our usual access. How many practicing veterinarians routinelyscrutinize journals such as Biology of Reproduction, Animal Science, or even Reproduction and Fertility, apart from special supplements? Similarly, how many basic and applied equine researchers read the Proceedings of the American Association of Equine Practitioners or articles in popular equine magazines and have a real understanding of the relative importance of problems of the equine industry?"
38
5. McGuirk SM, Shaftoe S, Lunn DP: Diseases of the cardiovascular system. In Smith BP (ed), Large Animal Internal Medicine, Philadelphia:CV Mosby Co., pp485-488,1990. 6. Guyton AC: Rhythmic excitation ofthe heart. In Textbook of Medical Physiology 5th ed, Philadalphia:WB Saunders Co., pp177-189,1976. 7. Marr CM: An echocardiographic study of atrial fibrillation in horses before and after treatment with quinidine sulfate. Proceedings 9th Amer Col Vet Int Med, pp367-369,1991. 8. Bertone JJ: Atrial fibrillation in horses. Compend Contin Educ Pract Vet 9(7):763-771,1 987. 9. Reef VB, Levitan CW, Spencer PA: Factors affecting prognosis and conversion in equine atrial fibrillation. J Vet Internal Med 2:1-6,1988. 10. Bonagure JD, Herring DS, Welker F: Echocardiography. In Bonagura JD (ed), Vet C/in of N Arner: Equine Pract, Philedelphia:WB Saunders Co., pp311-333,1985.
From this the editors make the case for a need of a text which combines recent informationwithin the discipline of equine reproduction into a format useful for practicing equine veterinarians. This editor agrees with them that "Veterinarians in mixed practice, veterinary students, basic and applied scientists, and graduate students may benefit from the breadth and specificity of the informationpresented hem in 118 well referenced chapters." The two major parts of the book are The Mare and The Stallion. Them is also a short pan The Neonate, and a fourth part of Appendices. The part on the neonate is really too small to be considered complete. The 40 pages am divided into two parts: Cam of the mare and foal in the neonatal period, and Diseases of foals during the neonatal period; a total of 14 chapters. As a book of this title should be, nearly half of the neonate section is about mare cam, and much more informationis included in part 1 of the book about The Mare--- chapters on parturition, dystocia, lactation, congenital defects in foals, retained placenta, uterine involution and. Important chapters for every equine practitioners who does any broodmaro work am the chapters onAssessment of fetal well-being, postnatal cam of the foal, and identification of the mare and foal at high risk for perinatal problems. The major sections in the mare part of the book am: anatomy; physiology/endocrinology; breeding management; diseases of the reproductive tract; reproductive surgery of the mare; pregnancy, parturition and the puerperal period. With the same organization, the part on the stallion is divided into sections: anatomy, physiology,and endocrinology; breeding management; diseases of the stallion's reproductive tract; and reproductive surgery of the stallion. The book is available from Lea & Febiger on 90 day approval from 200 Chester Field Parkway, Malvern, PA 19355-9725; 1-800-638-0673.
JOURNAL OF EQUINE VETERINARY SCIENCE