2.2.8 Myocardial failure
2.2.8 Myocardial failure

The term myocardial failure implies that there is a reduction in contractility of the myocytes. However, this should not be confused with CHF. Myocardial disease, in which there is a primary problem with contractility, is relatively uncommon. In many cases, CHF is attributable to regurgitant valvular disease and myocardial function is normal. In only a few cases of chronic valvular disease associated with volume overload and tachycardia is contractility reduced.

With the exception of monensin toxicity (see section 6.7.2), there are few reports concerning mechanisms of myocardial failure in the horse. It must be assumed that myocardial failure involves the same cellular processes in horses as in other species, even if the aetiological agent is different. Numerous cellular mechanisms have been implicated. These include abnormal energy metabolism defective calcium release and resorption by the sarcoplasmic reticulum, abnorcross-bridge formation and release by contractile proteins, slippage between sarcomeres, down-regulation of beta receptors and exhaustion of synaptic noradrenaline. At the ventricular level, changes such as tachycardia, arrhythhypoxia, fibrosis, and myocyte loss may affect systolic and diastolic funcThese changes may be due to primary cardiac disease, or occur secondary to systemic disease or electrolyte disturbances.