26 Oct 2016
Common diseases are common, but, as Gayle Hallowell explains, "zebra"-type cardiac conditions do occur – and can be diagnosed using a care-based approach.
Gayle Hallowell
Job Title
Equine cardiology: simple, right?
Cardiology in the horse is simple.
You only need to be able to recognise five pathological conditions – mitral, tricuspid and aortic regurgitation, ventricular septal defect and atrial fibrillation – and be able to differentiate these from variations of “normal”, such as physiological aortic flow murmurs and second-degree atrioventricular blockades.
Easy, right? Well, sort of, because, largely, these statements are true, in that, these conditions are the most common. Deciding their significance regarding safety for ridden work or suitability for purchase, however, is challenging.
Basically, not all horses have read “the book” – some appear to have forgotten Theodore Woodward’s famous medical proverb: “When you hear hoof beats, think of horses, not zebras.” Therefore, this article concentrates on the weird and uncommon, using a case-based approach.
A logical approach using tests performed in more common manifestations of cardiac disease – such as resting and exercising electrocardiography, and echocardiography – often allow a diagnosis to be made, despite the underlying aetiology being unknown. Therapeutic monitoring may be possible too.
Compared with small animals and people, heart failure is uncommon in the horse. It is discussed in the literature that when heart failure occurs, it is usually secondary to mitral regurgitation (or tachydysrhythmias). However, horses with almost any cardiac disease can present in heart failure.
A six-year-old Welsh pony mare presented with loud left pansystolic and right holosystolic murmurs consistent with a ventricular septal defect. The pony was fairly highly strung in ridden work with a five-year-old rider, but the owners had noticed no abnormalities. Heart rate was challenging to obtain, with the “resting” heart rate of 56 beats per minute to 60 beats per minute, assumed increased because of the animal’s nature.
Routine evaluation of this murmur included echocardiography, which revealed left ventricular dimensions one would have expected to find in a Thoroughbred racehorse with reduced fractional shortening. A defect in the ventricular septum was 50% of the diameter of the aorta, and resting heart rate obtained with a Holter monitor revealed, even when relaxed, the pony’s heart rate was never below 52 beats per minute.
Although ventricular septal defects are usually well tolerated, this case reminds us size is everything and, the bigger the defect, the more likely it is to progress.
An 11-year-old Icelandic pony mare presented with lethargy, tachycardia (rate 72 beats per minute to 90 beats per minute), ventral oedema and diarrhoea. Auscultation revealed no obvious cardiac murmurs and a resting ECG revealed sinus tachycardia. Echocardiography revealed normal valvular function, a significantly enlarged left ventricle and reduced fractional shortening, consistent with dilated cardiomyopathy.
The diarrhoea in this case was thought to be secondary to bowel wall oedema, resulting from congestive heart failure.
This horse was managed for heart failure and improved clinically for 7 to 10 days, but cardiac dilatation continued to develop and postmortem examination revealed significant narrowing of the aorta at the level of the aortic root – an area that cannot be imaged echocardiographically because of obscuration by the pleural surface.
Histopathology identified the narrowing was caused by fibrous tissue assumed secondary to aberrant parasite migration. Although the presumptive diagnosis had been wrong, and the management ineffective, it was difficult to consider a more appropriate therapeutic strategy for this horse.
A 10-year-old cob gelding presented with ataxia, lethargy, weight loss and anorexia. It was tachycardic (60 beats per minute) and tachypnoeic (20 breaths per minute), with left-sided systolic and diastolic murmurs.
Echocardiography found moderate mitral and aortic regurgitation, with a normal-sized left ventricle and increased fractional shortening. The myocardium was thickened and heterogeneous, with prominent vasculature and dilated coronary arteries, and an irregular mass around the aorta.
The horse was treated for heart failure and potential myocarditis, but showed minimal improvement. A postmortem revealed the horse had primary cardiac lymphoma1. This is rare in horses, but often seen in large-breed dogs, usually with a concurrent pericardial effusion.
If one listens in the correct place and the horse is not obese, murmurs are found in most of them – about 90%. Most of these, particularly in younger horses, are physiological flow murmurs associated with turbulent flow in the sinus of Valsalva, and most pathological murmurs are associated with degeneration of valves or due to ventricular septal defects. However, exceptions exist.
Infections of cardiac valves are relatively rare in horses, compared with cattle, and are usually associated with the mitral and aortic valves. Horses will often present with pyrexia, anorexia and tachycardia; some 60% will have murmurs and acute phase proteins, and white blood cell counts will be increased.
A two-year-old Thoroughbred in race training presented with poor performance. The horse was tachycardic at rest (48 beats per minute) and pyrexic (38.8°C), but no cardiac murmurs were noted.
Haematology revealed a leukocytosis due to an absolute neutrophilia and increased fibrinogen and serum amyloid A concentrations, and echocardiography revealed tricuspid valve vegetation consistent with endocarditis (Figure 1).
The literature suggests, with appropriate treatment, these horses can return to previous athletic function2, so appropriate treatment was implemented. Initially, the horse improved clinically and the vegetation reduced in size.
However, the horse then re-presented with further respiratory signs and obtundation, and, eventually, was euthanised due to the development of epilepticus. Postmortem revealed military abscessation throughout the lungs and brain.
Development of loud murmurs, especially if sudden, may be associated with sudden changes in valve structure. Chordae tendineae rupture in the mitral valve is reported in the literature and how it manifests depends on the defect created.
An eight-year-old Thoroughbred-cross mare presented with a loud left-sided pansystolic murmur that was not present four weeks earlier. Resting heart rate was normal, and echocardiography revealed severe mitral regurgitation because of a small chord rupture (Figure 2). Tears can also occur in the aortic valve.
An 18-year-old Arab gelding, previously diagnosed with aortic regurgitation, was found at re-examination to have a murmur louder, and of a different character, when compared with a visit six months previously.
Echocardiography revealed a tear in the left coronary cusp, leading to a significantly larger aortic regurgitant jet compared to the previous visit. Left ventricular dimensions had also become significantly larger. However, over the following three years, the tear remained the same size and the ventricular dimensions have not significantly increased.
It is frequently stated ponies don’t get valve disease, or don’t get it as often as horses. It is less common, but aortic regurgitation is seen in ponies. A three-year-old, minimally handled Welsh pony gelding presented for evaluation of polyuria/polydipsia. On auscultation, it had a loud right-sided pansystolic murmur and quieter left-sided holosystolic murmur.
A ventricular septal defect (VSD), I hear you say? Echocardiography did not identify this, but found disease of the tricuspid valve, which – in this breed and age of pony – was assumed to be tricuspid valve dysplasia (Figure 3) and secondary severe tricuspid regurgitation with right-sided enlargement. Therefore, one has to be aware assumptions can be incorrect.
Another assumption often made is, if animals have no clinical signs associated with congenital cardiac disease as adults, they, therefore, have restrictive disease. This often applies, but cannot always be relied on, as outlined in the case in the aforementioned heart failure section.
This case is another that breaks the usual assumptions. A five-year-old Welsh pony presented with left-sided and right-sided systolic murmurs and tachycardia. Echocardiography revealed a VSD and an overriding aorta (Figure 4) consistent with a tetralogy of Fallot, which was confirmed at postmortem. Again, this case highlights the need to evaluate cardiac disease in these animals.
Conditions resulting in marked tachycardia often present mimicking abdominal pain. Several conditions can fit this criterion, although many are associated with ventricular tachycardia. Some animals will have ventricular tachycardia secondary to structural cardiac disease.
A yearling Thoroughbred gelding presented three days following castration with signs of abdominal pain. It had a resting heart rate of 100 beats per minute, with no audible cardiac murmurs and normal gastrointestinal borborygmi, and was passing faeces. Echocardiography found no significant abnormalities, while electrocardiography revealed ventricular tachycardia.
The horse was treated with antidysrhythmics and sinus rhythm was restored briefly. However, the horse reverted back to a rhythm of ventricular tachycardia within two hours, which quickly developed into ventricular fibrillation.
Postmortem revealed marked fibrosis of the interventricular septum of unknown cause. Therefore, the author believes, in the case of colic – where heart rate does not match the rest of the clinical parameters – an ECG should be performed.
A 14-year-old Thoroughbred-cross presented for signs of abdominal pain. Heart rate about 100 beats per minute, while a continuous left-sided murmur was audible. Echocardiography revealed an aortic root rupture. This horse was euthanised, but one description exists of a case (Bowen, personal communication) where an aortic root rupture – which bled into the pericardial space – was resealed using echocardiography.
A 15-year-old pony presented as an out-of-hours emergency, having been recovered from a ditch, with a hock wound and septic tarsocrural joint. At presentation, the pony had an increased heart rate, which was still present following surgery. Resting electrocardiography revealed a ventricular tachycardia that did not convert to sinus rhythm with lidocaine. Echocardiography revealed no abnormalities, but further therapy did result in conversion to sinus rhythm.
Follow-up examinations have confirmed the pony has remained in sinus rhythm, so it is hard to know whether trauma and electrolyte derangements led to the underlying cardiac condition or if the pony collapsed with ventricular tachycardia.
Common diseases are common, but it is always best to remember rarer manifestations of common diseases – as well as separate disease entities – do occur. Sometimes, “looking like a duck and sounding like a duck doesn’t always make you a duck”.
The approach to these cases needs to be logical. In some cases, knowledge of conditions in other species may help, especially when it comes to progression and prognosis.
