CASE REPORT PAROXYSMAL ATRIAL FIBRILLATION IN A RACEHORSE R. J. ROSEAND P. E. DAVIS Department of Veterinary Clinical Studies, University of Sydney, New South Wales, 2006 SUMMARY: A 4-year-old thoroughbred stallion with a history of loss of racing form was studied over a period of approximately 7 months. At the initial examination he showed positive T waves in 1 chest lead and wandering of the pacemaker. This was followed by an episode of paroxysmal atrial fibrillation which disappeared spontaneously and was replaced by significant T wave changes in all the chest leads. During a period when these changes persisted, there was progressive lengthening of the P wave and the P-R interval. Because the last ECG showed evidence of intra-atrial block, first degree A-V block and T wave changes, the owner was advised that a fluctuating myocarditis was affecting the horse’s performance and it was retired to stud. This appears to be the first report of paroxysmal atrial fibrillation in Australia, and it demonstrates the value of regular follow-up examinations in horses with initial electrocardiographs showing only minor departures from normal. The case also suggests that when sharp reversals of racing form occur, the possibility of paroxysmal atrial fibrillation being the cause should be kept in mind.
Introduction
Atrial fibrillation (AF) is one of the common arrhythmias encountered in the horse (Roos 1924; Donald and Elliott 1948; Detweiler 1955; Steel 1963a; Holmes et a1 1969; Fregin, 1970). It is responsible for a dramatic decrease in the performance of the racehorse (Amada et a1 1974) and may occur during a race (Amada and Kurita 1975). Most reports of AF have involved older horses and there are few reports of its affecting young racehorses. Else and Holmes (1971), reporting on 45 autopsies of horses with AF, found 36 with gross lesions involving the valves and atria. This would suggest that many cases of atrial fibrillation occur as a sequel to cardiac pathology. Paroxysmal atrial fibrillation (PAF) has been reported infrequently (Detweiler 1952; Brooijmans 1957; Glazier and Kavanagh 1967; Amada and Kurita 1975). When an attack occurs there is an abrupt onset and a variable duration. In a series of 5 cases presented by Amada and Kurita (1979, the affected horses showed abrupt deceleration of speed during a race and finished
a long way behind the winners. Repeated postrace examination showed spontaneous disappearance of the AF with all the horses resuming a normal sinus rhythm within 48 hours. HiSt0l.Y
A 4-year-old thoroughbred stallion was presented on the 19/11/75 with the complaint that it was showing a decreased level of performance during the terminal stages of 1200 and 1400 metre races. As a 2 and 3-year-old, the horse had 14 starts, winning 5 races, with 6 placings. The wins included semi-classic and metropolitan stakes races. From August 1975 until June 1976, he started 18 times for 2 wins and 4 places. Clinical Examination
A full physical examination and rhinolaryngoscopy revealed no abnormalities. A n electrocardiogram (ECG) was recorded and measurement of the QRS intervals in leads I, I1 and I11 gave the horse a heart score (Steel 1963a) of 123 (Figure 1). In lead CL.LA the tracing showed wandering of the pacemaker and positive, peaky T waves.
TABLE 1 Sequential Serum Electrolyte Values -
Observation
Sodium (mmol/l) Potassium (mmolll) Chloride (rnmol/l) Bicarbonate (rnmol/l)
19 November 1976 140 3.8 1 04 27
~~
~~
8 February 1976
25 March 1976
5 May 1976
144 3.9
135 3.2 95 30
145 3.8 104 27
1 00
26
Artstralian Veterinary Journal, Vol. 53, November, 1977
W i s i n g Runs (Williamson 1975)
139-143 3.7-4.0 100-103 26-28 545
Blood was taken for a full blood count and glutamic oxaloacetic transaminase, alkaline phosphatase, lactic dehydrogenase, protein electrophoresis, sodium, potassium, chloride and bicarbonate estimation (metabolic profile). The results of all estimations gave values within the normal range. Because Williamson (1975) has drawn attention to the effects of changes in electrolyte levels on performance, the relevant electrolyte levels at the first and subsequent investigations of this horse are shown in Table 1.
L3
AVP
Figure 2. 24 March 1976
- Atrial
fibrillation
Diagnosis and Prognosis
At a heart rate of 35 beats per min, positive T waves in lead CL.LA may be an early indication of the onset of myocarditis (Davis and Rose, unpublished data). Because of this, the owner was advised to rest the horse for 2 months and then have it re-examined. Subsequent Investigations
-
Figure 1. 19 November 1975 wandering pacemaker and positive T waves in lead CL.LA. P wave duration - 0.16 secs., P wave Deak interval 0.06 secs., PR interval - 0.36 secs.
-
546
When examined on 8 February 1976 the horse had been in training for 4 weeks. A full Australian Veterinary Journal, Vol. 5 3 , November, 1977
blood count and metabolic profile were again performed with results that were within the normal range. A second ECG was recorded and this was similar to the one obtained on the 19 November 1975. On 24 March 1976 the horse raced over 1200 metres. He performed well for the first 600 metres, then according to the jockey, "he stopped like he was shot" and finished last in a field of 17 horses. During an examination 2 hours after this race, auscultation of the thorax revealed a
Lz
-2,
LZ *
L3
AVR
L1-
-
4--
Figure 4. 9 June 1976 - T wave changes in Leads CV.LA, CR.LA, CF.LA and CL.LA. P wave duration - 0.18 secs.. P wave peak interval - 0.09 secs., P-R interval - 0.40 secs.
*r'
, 4
-
Figure 3. 25 March 1976 - T wave changes in Leads CV.LA. CR.LA, CF.LA, CL.LA and aVR. P wave duration 0.17 secs.. P wave peak interval - 0.07 secs., P-R interval - 0.38 secs.
heart rate of 68 and an irregular cardiac arrhythmia. An ECG taken at this time showed the horse to be in AF (Figure 2). Twelve hours later a further ECG showed a return to normal sinus rhythm but there were positive peaked T waves in leads CV.LA, CR.LA, CF.LA and CL.LA with an amplitude of 0.8-0.9 millivolts (Figure 3). There was also a negative T wave (-0.2 millivolts) in lead aVR. As the heart rate during recording was 40 beats per minute, these T wave changes satisfied the criteria of Steel (1963a) for ventricular myopathy. It was also
TABLE 2 ECG Measurements During the Observation Period Observation
P wave duration (secs) P wave peak interval (secs) P-R interval (secs) Mean QRS (leads I, 11, 111) (secs)
19 November 1975
8 February 1976
0.16 0.06 0.36 0.123
0.16 0.06 0.36 0.123
noted that the P wave duration and P-R interval had increased. The observed changes in P wave duration, P wave peak interval and P-R interval in lead I1 in the series of ECG’s recorded from this horse are shown in Table 2. At this time, electrolyte determinations revealed a hypokalaemic alkalosis (Table 1). The horse was treated by adding 120 grams of a salt mixture consisting of 2 parts sodium chloride and 1 part potassium chloride to the drinking water for the next 10 days. For the next 6 weeks the horse was given only light work and a further blood sample was taken on 5 May 1976. The blood count was normal and the electrolyte levels showed a return to optimal values (Table 1). The training programme was then increased and the horse was given a start in a race over 1200 metres on 18 May 1976. His performance improved and he finished fourth. An ECG taken 3 hours after the race showed changes similar to those in a previous record (Figure 3) but the T wave amplitude in leads CV.LA, CR.LA, CF.LA and CL.LA was now 1.4 to 1.6 millivolts. A summary of changes in the direction and amplitude of the T waves seen in the series of ECG’s recorded is shown in Table 3. He raced again on 9 June 1976 over 1000 metres, after 3 weeks of only light exercise and finished last in a field of 12 horses. An ECG recorded 2 hours after the race (Figure 4) showed changes similar to those seen in the previous
- (Lead 11)
25 March 1976
18 May 1976
9 June 1976
0.17 0.08 0.38 0.123
0.18 0.09 0.40 0.123
0.17 0.07 0.38 0.123
tracing but the P wave duration and the P-R interval had increased to 0.18 and 0.40 seconds respectively. The P wave peak interval was 0.09 seconds. These changes were indicative of intra-atrial block and first degree A-V block (Steel 1963a). Because the ECG’s recorded from this horse between November and June had shown changes indicative of a progressive abnormality affecting both the atria and the ventricles it was suggested to the owner that the prognosis for further racing success was poor. This advice was accepted and the horse has been retired to stud. Discussion
Although paroxysmal A F does not appear to have been reported previously in Australia, it may be more common than is realised as a cause of reversal of form. Details of a case of persistent A F in a thoroughbred gelding were reported by Steel (1963b). The history in this case and in the cases reported by Amada and Kurita (1975) is characterised by an abrupt drop in speed during the race and this probably coincides with the onset of AF. The aetiology of those cases of PAF SO far reported has not been determined. A possible relationship between multiple atrial premature beats and the initiation of AF has been suggested by Amada and Kurita (1975). In man the causes reported include rheumatic heart disease, potassium deficiency, digitalis intoxication and thyrotoxicosis (Braunwald et al 1970). It is also
TABLE 3 Summary of T W a v e Changes (Direction and Amplitiide) Date 19 November 1975 8 February 1976 25 March 1976 18 May 1976
9 June 1976
548
CV.LA
CR.LA
CL.LA
0.8mv
0.8mv
+ 1.6mv +
+ + + 0.9mv + 1.6mv +
1.lmv
I.Ornv
l.lmv
-
+ + 1.4mv +
4
CF.LA
+ + 1.4mv +
0.9mv
I.lmv
aVR
+ + 0.2mv
+ +
Australinn Veterinary Journal, Vol. 53, November, 1977
known that AF may occur without clinical evidence of organic heart disease (Howard 1960). Electrolyte disturbances including hypo-. kalaemia were present at the time of AF, and may have contributed to its onset, in this case. Although there was no recurrence of AF, the 4 chest leads normally recorded developed positive, peaked T waves and there was progressive lengthening of the P wave and the P-R interval. Taken together these changes would indicate the development of ventricular and atrial pathology. Using defined diagnostic criteria Steel (1963a) reported that horses with intraatrial block raced poorly. This observation has been confirmed in other cases seen by the authors. In horses, the labile nature of the T wave is well recognised (Steel 1963a; Holmes and Rezakhani 1975). Using a standardised method of recording the ECG, SteeI (1963a) defined normal T waves for the racehorse. He also stated that the criteria used were only valid when the horse was standing correctly and its heart rate was less than 42 beats per min. The authors have found changes in the T waves as described by Steel (1963a) and Irvine (1975), to be highly significant in the evaluation of poor racing performance. Although Steel (1963a) classified ECG’s showing T wave changes in 1 or 2 leads as being “within normal limits”, it is the experience of the authors that such changes commonly occur prior to the development of electrocardiographic abnormalities with serious performance implications. Lead CL.LA is frequently the first lead to show a positive T wave, in horses that subsequently develop T wave changes in 5 or
more leads. These observations suggest that when T wave changes are found in 1 or 2 leads, the phrase “within normal limits” should be regarded as a warning that the ECG is not perfectly normal and that follow-up examinations of the horse should be undertaken at regular intervals. References Amada, A. and Kurita, H. (1975)-Exp. Rep. Equine Hlth Lab. 12: 89. Amada, A,, Senta, T., Kubo, K., Oh-ishi, S. and Kiryu, K. (1974)-Exp. Rep. Equine Hlth Lab., 11: 51. Braunwald, E., Eddleman, E. E., Resnik, W. H. and Principles of Harrison, T . R. ( I970)-‘%Iarrison’s Internal Medicine”. 6th edn, McGraw-Hill, New York. Brooijmans, A. W. M. ( 1957)-Electrocardiography in horses and cattle, Uitgeverij Cantecleer, Utrecht, p 69. Detweiler, D. K. (1952)-Proc. Am. vet. med. Ass. 89: 119. Am. vet. med. Ass. 126: Detweiler, D. K. (1955)-J. 47. Donald, D.E. and Elliott, F. J. (1948)--Ver. Rec. 60: 473. Else, R. W. and Holmes, J. R. (1971)--Equine vet. J. 3: 56. Fregin, G. F. (1970)-Proc. Am. Ass. Equine Practnr., p 383. Glazier, D. B. and Kavanagh, J. F. (1967)--lrish vet. 1. 21: 107. Holmes, J. R., Darke, P. G. G. and Else, R. W. (1969) -Equine vet. I. 1: 212. Holmes, J. R. and Rezakhani, A. (1975)-Equine vet. J . 7: 55. Howard, E. J. (1960)-Am. Heart J. 5 9 343. Irvine, C. H. G. (1975)-N.Z. vet. J. 23: 262. Roos, J. (1924)-Heart 11: 1. Steel, J. D. ( 1963a)-“Studies on the electrocardiogram of the racehorse”. Australasian Medical Publishing Co. Ltd.. Svdnev. Steel, J. D: (i9636)-Vet. Rec. 75: 1063. Williamson, H. M. (1975)-J1 S. Afr. vet. Ass. 45: 335.
BOOK REVIEW VETERINARY HISTOLOGY This book“ provides a text and reference work for those interested in Veterinary Histology. It will be useful for the veterinary student. The style and format are similar to that of medical histology texts and includes introductory chapters on cytology, epithelium, connective and supportive tissues: with later chapters on the organ systems. Each chapter is well illustrated; mostly photomicrographs with support from meaningful electron micrographs and schematic diagrams. Most of the domestic animals dealt with by veterinarians are used to illustrate histological features. The chapters dealing with the histology of the organ systems, apart from providing basic information, are * Textbook of Veterinary Histology. Horst-Dieter Dellrnann and Esther M. Brown. Philadelphia Lea & Febiger 1976. S13p. sA30.75. Copy Supplied by A N 2 Book Co P/L; b.0. Box 459, Brookvale, NSW 2100.
Australian Veterinary Journal, Vol. 53, November, 1977
also useful for their comparative information between species. This is seen especially in the chapters dealing with integument, placentation and reproductive systems. The histology of specialized structures such as hoof, horn, anal glands and placentation is emphasised; a feature lacking in most medical histology books. Perhaps a disappointing feature is the lack of information on the development of structures and organ systems; it is treated superficially especially in the chapters dealing with the respiratory and digestive systems. The book is not recommended for “light reading”, i t generally requires slow digestion and passage of information before one has something solid to remember, but it is a text to have on the shelf for those people occasionally aroused by the animal body at the microscopic level! P. Canfield
549
Introduction
Atrial fibrillation (AF) is one of the common arrhythmias encountered in the horse (Roos 1924; Donald and Elliott 1948; Detweiler 1955; Steel 1963a; Holmes et a1 1969; Fregin, 1970). It is responsible for a dramatic decrease in the performance of the racehorse (Amada et a1 1974) and may occur during a race (Amada and Kurita 1975). Most reports of AF have involved older horses and there are few reports of its affecting young racehorses. Else and Holmes (1971), reporting on 45 autopsies of horses with AF, found 36 with gross lesions involving the valves and atria. This would suggest that many cases of atrial fibrillation occur as a sequel to cardiac pathology. Paroxysmal atrial fibrillation (PAF) has been reported infrequently (Detweiler 1952; Brooijmans 1957; Glazier and Kavanagh 1967; Amada and Kurita 1975). When an attack occurs there is an abrupt onset and a variable duration. In a series of 5 cases presented by Amada and Kurita (1979, the affected horses showed abrupt deceleration of speed during a race and finished
a long way behind the winners. Repeated postrace examination showed spontaneous disappearance of the AF with all the horses resuming a normal sinus rhythm within 48 hours. HiSt0l.Y
A 4-year-old thoroughbred stallion was presented on the 19/11/75 with the complaint that it was showing a decreased level of performance during the terminal stages of 1200 and 1400 metre races. As a 2 and 3-year-old, the horse had 14 starts, winning 5 races, with 6 placings. The wins included semi-classic and metropolitan stakes races. From August 1975 until June 1976, he started 18 times for 2 wins and 4 places. Clinical Examination
A full physical examination and rhinolaryngoscopy revealed no abnormalities. A n electrocardiogram (ECG) was recorded and measurement of the QRS intervals in leads I, I1 and I11 gave the horse a heart score (Steel 1963a) of 123 (Figure 1). In lead CL.LA the tracing showed wandering of the pacemaker and positive, peaky T waves.
TABLE 1 Sequential Serum Electrolyte Values -
Observation
Sodium (mmol/l) Potassium (mmolll) Chloride (rnmol/l) Bicarbonate (rnmol/l)
19 November 1976 140 3.8 1 04 27
~~
~~
8 February 1976
25 March 1976
5 May 1976
144 3.9
135 3.2 95 30
145 3.8 104 27
1 00
26
Artstralian Veterinary Journal, Vol. 53, November, 1977
W i s i n g Runs (Williamson 1975)
139-143 3.7-4.0 100-103 26-28 545
Blood was taken for a full blood count and glutamic oxaloacetic transaminase, alkaline phosphatase, lactic dehydrogenase, protein electrophoresis, sodium, potassium, chloride and bicarbonate estimation (metabolic profile). The results of all estimations gave values within the normal range. Because Williamson (1975) has drawn attention to the effects of changes in electrolyte levels on performance, the relevant electrolyte levels at the first and subsequent investigations of this horse are shown in Table 1.
L3
AVP
Figure 2. 24 March 1976
- Atrial
fibrillation
Diagnosis and Prognosis
At a heart rate of 35 beats per min, positive T waves in lead CL.LA may be an early indication of the onset of myocarditis (Davis and Rose, unpublished data). Because of this, the owner was advised to rest the horse for 2 months and then have it re-examined. Subsequent Investigations
-
Figure 1. 19 November 1975 wandering pacemaker and positive T waves in lead CL.LA. P wave duration - 0.16 secs., P wave Deak interval 0.06 secs., PR interval - 0.36 secs.
-
546
When examined on 8 February 1976 the horse had been in training for 4 weeks. A full Australian Veterinary Journal, Vol. 5 3 , November, 1977
blood count and metabolic profile were again performed with results that were within the normal range. A second ECG was recorded and this was similar to the one obtained on the 19 November 1975. On 24 March 1976 the horse raced over 1200 metres. He performed well for the first 600 metres, then according to the jockey, "he stopped like he was shot" and finished last in a field of 17 horses. During an examination 2 hours after this race, auscultation of the thorax revealed a
Lz
-2,
LZ *
L3
AVR
L1-
-
4--
Figure 4. 9 June 1976 - T wave changes in Leads CV.LA, CR.LA, CF.LA and CL.LA. P wave duration - 0.18 secs.. P wave peak interval - 0.09 secs., P-R interval - 0.40 secs.
*r'
, 4
-
Figure 3. 25 March 1976 - T wave changes in Leads CV.LA. CR.LA, CF.LA, CL.LA and aVR. P wave duration 0.17 secs.. P wave peak interval - 0.07 secs., P-R interval - 0.38 secs.
heart rate of 68 and an irregular cardiac arrhythmia. An ECG taken at this time showed the horse to be in AF (Figure 2). Twelve hours later a further ECG showed a return to normal sinus rhythm but there were positive peaked T waves in leads CV.LA, CR.LA, CF.LA and CL.LA with an amplitude of 0.8-0.9 millivolts (Figure 3). There was also a negative T wave (-0.2 millivolts) in lead aVR. As the heart rate during recording was 40 beats per minute, these T wave changes satisfied the criteria of Steel (1963a) for ventricular myopathy. It was also
TABLE 2 ECG Measurements During the Observation Period Observation
P wave duration (secs) P wave peak interval (secs) P-R interval (secs) Mean QRS (leads I, 11, 111) (secs)
19 November 1975
8 February 1976
0.16 0.06 0.36 0.123
0.16 0.06 0.36 0.123
noted that the P wave duration and P-R interval had increased. The observed changes in P wave duration, P wave peak interval and P-R interval in lead I1 in the series of ECG’s recorded from this horse are shown in Table 2. At this time, electrolyte determinations revealed a hypokalaemic alkalosis (Table 1). The horse was treated by adding 120 grams of a salt mixture consisting of 2 parts sodium chloride and 1 part potassium chloride to the drinking water for the next 10 days. For the next 6 weeks the horse was given only light work and a further blood sample was taken on 5 May 1976. The blood count was normal and the electrolyte levels showed a return to optimal values (Table 1). The training programme was then increased and the horse was given a start in a race over 1200 metres on 18 May 1976. His performance improved and he finished fourth. An ECG taken 3 hours after the race showed changes similar to those in a previous record (Figure 3) but the T wave amplitude in leads CV.LA, CR.LA, CF.LA and CL.LA was now 1.4 to 1.6 millivolts. A summary of changes in the direction and amplitude of the T waves seen in the series of ECG’s recorded is shown in Table 3. He raced again on 9 June 1976 over 1000 metres, after 3 weeks of only light exercise and finished last in a field of 12 horses. An ECG recorded 2 hours after the race (Figure 4) showed changes similar to those seen in the previous
- (Lead 11)
25 March 1976
18 May 1976
9 June 1976
0.17 0.08 0.38 0.123
0.18 0.09 0.40 0.123
0.17 0.07 0.38 0.123
tracing but the P wave duration and the P-R interval had increased to 0.18 and 0.40 seconds respectively. The P wave peak interval was 0.09 seconds. These changes were indicative of intra-atrial block and first degree A-V block (Steel 1963a). Because the ECG’s recorded from this horse between November and June had shown changes indicative of a progressive abnormality affecting both the atria and the ventricles it was suggested to the owner that the prognosis for further racing success was poor. This advice was accepted and the horse has been retired to stud. Discussion
Although paroxysmal A F does not appear to have been reported previously in Australia, it may be more common than is realised as a cause of reversal of form. Details of a case of persistent A F in a thoroughbred gelding were reported by Steel (1963b). The history in this case and in the cases reported by Amada and Kurita (1975) is characterised by an abrupt drop in speed during the race and this probably coincides with the onset of AF. The aetiology of those cases of PAF SO far reported has not been determined. A possible relationship between multiple atrial premature beats and the initiation of AF has been suggested by Amada and Kurita (1975). In man the causes reported include rheumatic heart disease, potassium deficiency, digitalis intoxication and thyrotoxicosis (Braunwald et al 1970). It is also
TABLE 3 Summary of T W a v e Changes (Direction and Amplitiide) Date 19 November 1975 8 February 1976 25 March 1976 18 May 1976
9 June 1976
548
CV.LA
CR.LA
CL.LA
0.8mv
0.8mv
+ 1.6mv +
+ + + 0.9mv + 1.6mv +
1.lmv
I.Ornv
l.lmv
-
+ + 1.4mv +
4
CF.LA
+ + 1.4mv +
0.9mv
I.lmv
aVR
+ + 0.2mv
+ +
Australinn Veterinary Journal, Vol. 53, November, 1977
known that AF may occur without clinical evidence of organic heart disease (Howard 1960). Electrolyte disturbances including hypo-. kalaemia were present at the time of AF, and may have contributed to its onset, in this case. Although there was no recurrence of AF, the 4 chest leads normally recorded developed positive, peaked T waves and there was progressive lengthening of the P wave and the P-R interval. Taken together these changes would indicate the development of ventricular and atrial pathology. Using defined diagnostic criteria Steel (1963a) reported that horses with intraatrial block raced poorly. This observation has been confirmed in other cases seen by the authors. In horses, the labile nature of the T wave is well recognised (Steel 1963a; Holmes and Rezakhani 1975). Using a standardised method of recording the ECG, SteeI (1963a) defined normal T waves for the racehorse. He also stated that the criteria used were only valid when the horse was standing correctly and its heart rate was less than 42 beats per min. The authors have found changes in the T waves as described by Steel (1963a) and Irvine (1975), to be highly significant in the evaluation of poor racing performance. Although Steel (1963a) classified ECG’s showing T wave changes in 1 or 2 leads as being “within normal limits”, it is the experience of the authors that such changes commonly occur prior to the development of electrocardiographic abnormalities with serious performance implications. Lead CL.LA is frequently the first lead to show a positive T wave, in horses that subsequently develop T wave changes in 5 or
more leads. These observations suggest that when T wave changes are found in 1 or 2 leads, the phrase “within normal limits” should be regarded as a warning that the ECG is not perfectly normal and that follow-up examinations of the horse should be undertaken at regular intervals. References Amada, A. and Kurita, H. (1975)-Exp. Rep. Equine Hlth Lab. 12: 89. Amada, A,, Senta, T., Kubo, K., Oh-ishi, S. and Kiryu, K. (1974)-Exp. Rep. Equine Hlth Lab., 11: 51. Braunwald, E., Eddleman, E. E., Resnik, W. H. and Principles of Harrison, T . R. ( I970)-‘%Iarrison’s Internal Medicine”. 6th edn, McGraw-Hill, New York. Brooijmans, A. W. M. ( 1957)-Electrocardiography in horses and cattle, Uitgeverij Cantecleer, Utrecht, p 69. Detweiler, D. K. (1952)-Proc. Am. vet. med. Ass. 89: 119. Am. vet. med. Ass. 126: Detweiler, D. K. (1955)-J. 47. Donald, D.E. and Elliott, F. J. (1948)--Ver. Rec. 60: 473. Else, R. W. and Holmes, J. R. (1971)--Equine vet. J. 3: 56. Fregin, G. F. (1970)-Proc. Am. Ass. Equine Practnr., p 383. Glazier, D. B. and Kavanagh, J. F. (1967)--lrish vet. 1. 21: 107. Holmes, J. R., Darke, P. G. G. and Else, R. W. (1969) -Equine vet. I. 1: 212. Holmes, J. R. and Rezakhani, A. (1975)-Equine vet. J . 7: 55. Howard, E. J. (1960)-Am. Heart J. 5 9 343. Irvine, C. H. G. (1975)-N.Z. vet. J. 23: 262. Roos, J. (1924)-Heart 11: 1. Steel, J. D. ( 1963a)-“Studies on the electrocardiogram of the racehorse”. Australasian Medical Publishing Co. Ltd.. Svdnev. Steel, J. D: (i9636)-Vet. Rec. 75: 1063. Williamson, H. M. (1975)-J1 S. Afr. vet. Ass. 45: 335.
BOOK REVIEW VETERINARY HISTOLOGY This book“ provides a text and reference work for those interested in Veterinary Histology. It will be useful for the veterinary student. The style and format are similar to that of medical histology texts and includes introductory chapters on cytology, epithelium, connective and supportive tissues: with later chapters on the organ systems. Each chapter is well illustrated; mostly photomicrographs with support from meaningful electron micrographs and schematic diagrams. Most of the domestic animals dealt with by veterinarians are used to illustrate histological features. The chapters dealing with the histology of the organ systems, apart from providing basic information, are * Textbook of Veterinary Histology. Horst-Dieter Dellrnann and Esther M. Brown. Philadelphia Lea & Febiger 1976. S13p. sA30.75. Copy Supplied by A N 2 Book Co P/L; b.0. Box 459, Brookvale, NSW 2100.
Australian Veterinary Journal, Vol. 53, November, 1977
also useful for their comparative information between species. This is seen especially in the chapters dealing with integument, placentation and reproductive systems. The histology of specialized structures such as hoof, horn, anal glands and placentation is emphasised; a feature lacking in most medical histology books. Perhaps a disappointing feature is the lack of information on the development of structures and organ systems; it is treated superficially especially in the chapters dealing with the respiratory and digestive systems. The book is not recommended for “light reading”, i t generally requires slow digestion and passage of information before one has something solid to remember, but it is a text to have on the shelf for those people occasionally aroused by the animal body at the microscopic level! P. Canfield
549
