Chapter 4 Cardiac disease and pathology
The function of the cardiovascular system depends on both contraction and relaxation in a regular and controlled manner. Due to the integrated nature of the heart, the vasculature, lungs and kidneys, disease of any of these can potentially lead to changes in the other. In the horse, endocardial disease is the predominant form of cardiac disease and myocardial remodelling most commonly occurs as sequel to valvular insufficiencies. Cardiac enlargement and remodelling are however important and contribute to the syndrome of cardiac failure due to excessive chamber enlargement. However, most studies investigating cardiac remodelling relate to human patients with either hypertension or myocardial ischaemia and therefore it may not be appropriate to extrapolate these data to the horse. The purpose of this chapter is to review the mediators of cardiac pathology that are important for the progression of cardiac disease in the horse and relate these to pathological changes in the equine heart.
Most pathological techniques to examine the heart are designed to examine each chamber in isolation, usually opening the chamber along its border with the intraventricular septum and displaying its internal surface for examination and determination of weight.1 While this technique does have several advantages it does not enable the clinician to visualize the heart in the manner to which it has been examined by echocardiography. Therefore, a more clinically orientated approach to gross pathological examination of the heart is recommended.2 This approach is lesion orientated and therefore should commence by examining the side of the heart which is most affected by disease.
The pericardium should be examined for evidence of pathology, and the pericardial fluid volume should be determined and a sample obtained for cytological and/or bacteriological examination. The left side of the heart is examined by placing metal rods (blunt ended and at least 30 cm in length) through a small hole made in the left atrium and advanced through the mitral valve and rested at the cardiac apex; it is advisable not to place the rod through one of the pulmonary veins as this will not create the correct anatomical view. A second metal rod should be placed through the aortic valve and placed at an angle so that it reaches the same point on the cardiac apex. A large flat knife, such as a 12-inch disposable dissection knife, should then be used to cut alongside these metal guides to create a sagittal section and open the ventricle to mimic a left parasternal view of the left ventricle and left ventricular outflow tract (Fig. 4.1). The right ventricle should be examined in a similar manner by placing a metal rod down through the pulmonary artery and another through the right atrium into the right ventricular apex through the tricuspid valve. Care should be taken to avoid the moderator band within the ventricular lumen (trabeculae septomarginalis). This will mimic the cranially angled right parasternal view of the right ventricle and right ventricular outflow tract.
Figure 4.1 Post mortem appearance of equine heart following preparation to mimic imaging planes obtained by echocardiography showing left ventricle (A: right parasternal long axis view of the left ventricle) and right ventricle (B: right ventricular inflow-outflow view) demonstrating left ventricle (LV), left atrium (LA), left ventricular outflow tract (and aorta – LVOT) with arrow pointing towards aortic outflow, intraventricular septum (IVS), right ventricle (RV), right atrium (RA), tricuspid valve (TV), right ventricular outflow tract (RVOT) leading to pulmonary artery (depicted by arrow), aorta (Ao) and coronary artery (arrow head).
The heart should subsequently be examined for evidence of congenital, myocardial, endocardial and valvular pathology. Dimensions can be obtained and ventricular mass can be established; however, changes in myocardial mass can be difficult to interpret since myocardial mass will change in response to eccentric hypertrophy in the trained animal as well as in response to pathological chamber enlargement. In order to take into account changes in body weight it is usual to express changes in left ventricular mass in relation to either body weight or right ventricular mass. There is better correlation between left ventricular mass and right ventricular mass in the normal horse (r2 = 0.71) than between left ventricular mass and body weight (r2 = 0.19) in the normal horse (n = 37; I. M. Bowen, unpublished observations) and the ratio of right ventricle (free wall):left ventricle (including intraventricular septum) in the normal animal is 1:2.81 ± 0.4 (reference range 1:1.98–3.63; n = 37). These figures are based on the weight of myocardial tissue after removal of the atria, pericardium and fat. In interpreting these data it is important to recognize that volume loading, induced by valvular pathology in the horse, creates chamber dilation, rather than thickening of the ventricular wall and in the same study there was no difference in left ventricular mass from horses with mild and moderate aortic insufficiency (n = 17), expressed either as ventricular mass, right ventricle:left ventricle or left ventricle:body weight. Therefore, cardiac dimensions may be a more reliable method of documenting changes in cardiac size than ventricular weights.
Primary myocardial disease occurs rarely in the horse; dilated cardiomyopathies are occasionally reported and are described in Chapter 19. Myocardial fibrosis has been associated with ventricular tachycardia, presumably due to disruption of the cardiac conduction system of the ventricle, but can also be detected as an incidental finding.3 The gross appearance of these changes are of discolouration within the myocardium, but are rarely specific to a particular disease process (Fig. 4.2).
Figure 4.2 Gross post mortem appearance of intraventricular septum showing nonspecific pathology of the myocardium in a 12-month-old colt that presented with lethargy and depression and was found to have multifocal ventricular tachycardia that was resistant to therapy. Histological examination showed a mixed pattern of inflammation, necrosis and fibrosis. No specific aetiology was identified.
Picture courtesy of Dr Gayle Hallowell.
In most cases a local ischemic event was assumed to be the primary disease process whereas a primary inflammatory aetiology has also been implicated.4 However, as fibrosis is an end-stage process the primary disease process can be difficult to confirm. In a group of horses microemboli from parasitic lesions were suspected based on statistical associations.3 In human patients and animal models, fibrosis is associated with myocardial remodelling and this process is described below in more detail. Myocarditis is often a clinical diagnosis based on the presence of ventricular dysrhythmias with no apparent underlying cause, although viral and bacterial causes, including Streptococcus equi var equi, have been implicated;1 however, in many cases the primary initiating cause is unknown. ( ET)
Other primary myocardial pathologies are rare, although do occur sporadically (Fig. 4.3) and usually present clinically with cardiac dysrhythmias or signs of low cardiac output (see Chapter 19). ( CN)
Figure 4.3 Gross post mortem appearance of the left ventricle showing expansive subepicardial haemorrhagic mass in the right ventricular free wall and interventricular septum (arrows) from a 3-year-old Arab mare that was presented with signs of congestive heart failure. Histological examination confirmed the diagnosis of an intramyocardial haemorrhage, with fibrosis and a lymphocytic-plasmacytic infiltrate, although no cause was identified.