EQUINE | African Horse Sickness
EQUINE | African Horse Sickness
once they reached the clinical end-point and a postmortem was performed . Virus in myocardial tissue was confirmed as African horse sickness virus types 3 , 5 , 9 by type specific real time qPCR .
Results
All horses developed clinical signs of AHS , and signs included hypothermia ; tachycardia ; tachypnoea ; supraorbital fossa oedema ; and petechial haemorrhages . Infected horses showed severely impaired left ventricular systolic function characterised by myocardial dyskinesis ; decreased ejection fraction and fractional shortening . cTnI was elevated in all cases , suggesting myocardial injury . Post mortem changes were consistent with the mixed form of AHS in all cases , and included pulmonary oedema , subcutaneous and intramuscular oedema , hydrothorax , hydropericardium , myocardial haemorrhages and ascites .
Conclusions and significance
We concluded that AHS is associated with severely impaired left ventricular function secondary to myocardial injury . This implies an alternative ( or additional ) cardiogenic mechanism for the pulmonary ( and interstitial ) oedema seen in clinical cases and provides a framework for therapeutic intervention using cardiac specific drugs . Diuretics , angiotensinconverting enzyme ( ACE ) inhibitors and positive ionotropic drugs are the mainstay of treatment for cardiac diseases resulting in heart failure , and are the logical choice for horses with AHS demonstrating myocardial dysfunction and clinical evidence of heart failure . Diuretics are used to reduce water and sodium retention by the kidneys , thereby reducing intravascular volume , ventricular filling pressures ( preload ) and wall stress . Furosemide is a loop diuretic that prevents reabsorption of sodium and chloride from the thick ascending loop of Henle , and is considered to the most widely used diuretic in the treatment of heart failure .
The pharmacokinetics and dosing of furosemide has been extensively studied in the horse , and it has been demonstrated that an intravenous dose of 0.5 – 1mg / kg is sufficient to induce diuresis 19 . Systemic availability of furosemide when administered orally is poor however , and an equivalent dose of 1 mg / kg PO does not induce diuresis in horses 20 .
Furosemide has been used for many years by veterinarians in Southern Africa to treat pulmonary oedema in horses with AHS with variable anecdotal success . However , prolonged use of furosemide in these cases without concomitant use of ACE inhibitors is counterproductive . As blood volume decreases following a dose of furosemide , the renin‐angiotensinaldosterone system ( RAAS ) is activated ; and counteracts the previous dose of furosemide by increasing blood volume until the next dose of furosemide is given . ACE inhibitors work by preventing the conversion of angiotensin I to angiotensin II , thereby reducing the activity of the RAAS . In addition , ACE inhibitors lower arteriolar resistance and increase venous capacity by attenuating the potent vasoconstrictor effects of angiotensin II . This reduces afterload by decreasing systemic vascular resistance , thus increasing forward stroke volume . ACE also breaks down bradykinin , a vasodilator substance .
Therefore , ACE inhibitors , by blocking the breakdown of bradykinin , increase bradykinin levels , which can contribute to the vasodilator action of ACE inhibitors . The benefits of ACE inhibitors for the treatment of heart failure have been well established in humans and dogs
21,22
, however there is little information in horses . The pharmacokinetics of ACE inhibitors have undergone preliminary investigation , and it has been found that systemic bioavailability after oral administration is poor . In a comparative pharmacodynamics study , is has been established that benazapril was most effective at inhibiting serum ACE inhibition 23 ; and at a dose of
50 • Equine Health Update •