## Overview Aortic rupture is a spontaneous tear in the wall of the aorta, the main artery leaving the heart. In most breeds the tear occurs at the aortic root and is rapidly fatal due to cardiac tamponade or massive hemorrhage. In Friesian horses a breed-specific form occurs in the aortic arch near the ligamentum arteriosum and frequently creates an aortopulmonary fistula; some of these horses survive for months to years with progressive signs. No effective treatment exists once rupture has occurred. ## Causes The cause is unknown in most cases. In Friesians, disorganization of collagen fibers in the aortic wall has been documented and is believed to predispose to rupture at the arch. In other breeds, rupture is often associated with older age and strenuous exercise, although many horses show no premonitory signs. ## Diagnosis Most horses are found dead or die within minutes of onset. Survivors (primarily Friesians with aortopulmonary fistulation) may show tachycardia, bounding pulses, jugular pulsation, peripheral edema, coughing, or recurrent colic-like episodes. Echocardiography can identify the fistula or pericardial effusion in living horses. Definitive diagnosis is usually made at necropsy. ## Treatment No treatment reverses the rupture. Supportive care is unrewarding. Humane euthanasia is recommended once the diagnosis is confirmed in a living horse. ## Recovery and Prognosis Prognosis is grave. Acute root ruptures are almost uniformly fatal within minutes. Friesian horses with chronic aortopulmonary fistulas may survive for a variable period but remain at high risk of sudden death. ## Prevention No preventive measures are known. Breeding decisions in Friesians may eventually be informed by ongoing genetic research.
sudden death; collapse; tachycardia; pale mucous membranes; bounding arterial pulses; jugular pulsation; peripheral edema (chronic cases)
## Overview Aortic rupture is a spontaneous tear in the wall of the aorta, the main artery leaving the heart. In most breeds the tear occurs at the aortic root and is rapidly fatal due to cardiac tamponade or massive hemorrhage. In Friesian horses a breed-specific form occurs in the aortic arch near the ligamentum arteriosum and frequently creates an aortopulmonary fistula; some of these horses survive for months to years with progressive signs. No effective treatment exists once rupture has occurred. ## Causes The cause is unknown in most cases. In Friesians, disorganization of collagen fibers in the aortic wall has been documented and is believed to predispose to rupture at the arch. In other breeds, rupture is often associated with older age and strenuous exercise, although many horses show no premonitory signs. ## Diagnosis Most horses are found dead or die within minutes of onset. Survivors (primarily Friesians with aortopulmonary fistulation) may show tachycardia, bounding pulses, jugular pulsation, peripheral edema, coughing, or recurrent colic-like episodes. Echocardiography can identify the fistula or pericardial effusion in living horses. Definitive diagnosis is usually made at necropsy. ## Treatment No treatment reverses the rupture. Supportive care is unrewarding. Humane euthanasia is recommended once the diagnosis is confirmed in a living horse. ## Recovery and Prognosis Prognosis is grave. Acute root ruptures are almost uniformly fatal within minutes. Friesian horses with chronic aortopulmonary fistulas may survive for a variable period but remain at high risk of sudden death. ## Prevention No preventive measures are known. Breeding decisions in Friesians may eventually be informed by ongoing genetic research.
sudden death; collapse; tachycardia; pale mucous membranes; bounding arterial pulses; jugular pulsation; peripheral edema (chronic cases)