Aortic rupture is not a condition that is unique to Friesian horses. Horses of all breeds may suffer from this alarming and fatal condition. In all other breeds of horses, aortic rupture is most often seen in older horses engaged in strenuous physical activity at the time of rupture. In other breeds, the classic location for the aorta to rupture is at the connection between the aorta and the heart, also known as the aortic root. However, in Friesian horses, the thoracic aorta never ruptures at its root, and researchers find this very peculiar. Instead, the aorta always ruptures in the area of the aortic arch, very near the scar of the ductus arteriosus.
The ductus arteriosus is a blood vessel that is only functional during fetal life when the unborn foal is still in the womb. After birth, the ductus arteriosus, which serves the function of connecting the fetal aorta with the fetal pulmonary artery, actually closes itself. The only proof of the ductus arteriosus after birth is actually a small scar that can be used as a point of orientation while looking at the heart. The fact that all Friesian horses rupture at this exact location suggests this is a breed-specific condition. In no other horse or animal species is aortic rupture known to occur at this location.
Postmortem examination of the aortic wall of Friesians diagnosed with aortic rupture revealed significant disorganization of collagen fibers. These findings suggest a connective tissue disorder affecting elastin or collagen in the aortic media is the potential underlying cause of aortic rupture in Friesian horses. It is noteworthy that in humans with aortic disease, there are several known related connective tissue abnormalities, one of them being increased collagen cross-linking. It is conceivable that an underlying genetic defect of the connective tissue in the aortic media predisposes Friesian horses to aortic rupture, dissection, and aorto-pulmonary fistulation at this specific location. The Friesian horse is also the only known animal species in which aorto-pulmonary fistulation is regularly encountered. While more research is needed, these unusual findings in Friesian horses support the theory that a general collagen-based systemic disorder might be responsible for several, if not all, connective tissue-related disorders in Friesian horses.
THREE TYPES OF AORTIC RUPTURE Aortic rupture occurs as a result from a spontaneous break in the wall of the aorta, the main artery that carries blood from the heart’s left ventricle (the main pumping chamber) to all other arteries except the pulmonary artery. While the location remains the same in Friesian horses (near the scar of the ductus arteriosus), the way in which the rupture occurs can vary, creating different scenarios.
ACUTE AORTIC RUPTURE (IMMEDIATE) When Friesian horses die of acute aortic rupture, the rupture occurs outside the pericardial sac. This is the equivalent of a large hole in a high-pressure firehose. Blood fills the thoracic cavity within seconds. There are no clinical signs prior to acute aortic rupture in Friesian horses. These horses die suddenly and are most often found dead in their stall or the pasture, or they may collapse during exercise or physical exertion with no warning.
SUB-ACUTE AORTIC RUPTURE (DAYS – WEEKS) Sub-acute aortic rupture occurs when a tear in the aorta causes blood to leak from the heart into the pericardial sac, which due to enormous pressure, squeezes the heart. Due to the pressure, the heart must pump harder to supply enough blood-rich oxygen to the rest of the body. Sometimes, the tear leaks blood into the pulmonary artery, which causes the formation of a fistula, an abnormal connection between two body parts. The pulmonary fistula causes a significant amount of pressure in the lungs and leads to pulmonary edema. Depending on how large the initial tear is, the horse may live for days or weeks, but eventually, the tear will enlarge and lead to an abrupt and rapid decline of the horse and cardiac failure. In Friesian horses with sub-acute aortic rupture, there are often various clinical signs, including but not limited to:
Colic-like symptoms
Nose bleeds
Sudden onset of heavy cough
Sudden poor performance
Increased or “bounding” pulse at rest
Intermittent lameness
Swollen joints
Alternating leg resting
Intermittent edema (especially between the front legs and chest, along the abdomen)
CHRONIC AORTIC RUPTURE (WEEKS – MONTHS) Chronic aortic rupture occurs when a tear in the aorta is stabilized by the surrounding tissue, applying compression to the leaking area almost like a pressure bandage. This scenario does not progress as rapidly as acute or sub-acute aortic rupture, but it will eventually become fatal. Over a period of weeks or months, the tissue surrounding the leaking aorta cannot withstand the enormous amount of blood pressure, and over time blood expands into separate chamber-like spaces in the tissue in an attempt to hold more of the blood. Inevitably at some point, the pressure is too great, and the chamber wall will fail, spilling blood into the pulmonary artery and rapidly accelerating into an acute and fatal cardiac failure. Such as with sub-acute aortic rupture, the initial size of the leak determines how long the situation remains viable.
Symptoms of chronic aortic rupture may be present for weeks or months prior to cardiac failure. If the owner is aware of what to look for and has the horse examined by a veterinarian, a small aorto-pulmonary fistula may be appreciated via cardiac ultrasound. The signs of chronic aortic rupture are similar to sub-acute aortic rupture and include but are not limited to:
Poor performance
Change in disposition (quieter)
Heavy cough
Intermittent edema (especially between the front legs and chest, along the abdomen)
Continuous high pulse at rest (56 – 120 beats per minute)
Fluctuating fever
Pale mucous membranes
Nose bleeds
Colic-like symptoms
‘Bounding” pulse at rest
Intermittent lameness
Swollen joints
Alternating leg resting.
THE IMPORTANCE OF A NECROPSY A necropsy is not something most horse owners contemplate until they are faced with the death of their horse. Particularly in cases where the death is sudden, a grief-stricken owner may not be in the right frame of mind to consider if a necropsy is warranted. The unfortunate thing, however, is that sudden deaths, especially sudden deaths where the cause is not obvious, are the most important cases in which to have a necropsy performed.
In the event of an unexplained, sudden death of a Friesian, where aortic rupture is a possibility, it is critical for owners to advise their veterinarian of the possibility of aortic rupture. This is because most cardiac incision protocols for necropsies damage the region of interest in the heart where aortic rupture can be confirmed. Care must be taken not to apply the classic cardiac necropsy incisions so that a correct diagnosis can be made.
As a Friesian owner, we’d encourage you to think about just how important a necropsy can be. Without the crucial data gained from a necropsy, research into aortic rupture in Friesian horses is incredibly difficult. Cases of confirmed aortic rupture in Friesians via necropsy and corresponding blood DNA samples are extremely valuable for research purposes. If you suspect your horse may be suffering from aortic rupture, please contact the Fenway Foundation for Friesian Horses.
For more information or support regarding aortic rupture, please join our Facebook Support Group, Equine Aortic Rupture
References:
Delesalle, C. Aortic Rupture in Friesian Horses. Phryso.
Ploeg, Margreet. “Challenging Friesian horse diseases: aortic rupture and megaesophagus.” (2015).
Ploeg M, Saey V, de Bruijn CM, Gröne A, Chiers K, van Loon G, Ducatelle R, van Weeren PR, Back W, Delesalle C. Aortic rupture and aorto-pulmonary fistulation in the Friesian horse: characterisation of the clinical and gross post mortem findings in 24 cases. Equine Vet J. 2013 Jan;45(1):101-6. doi: 10.1111/j.2042-3306.2012.00580.x. Epub 2012 May 20. PMID: 22607232.
Ploeg M, Saey V, de Bruijn CM, et al. 2012. Aortic rupture in friesian horses: 3 scenarios
revealed. Phryso.
