J. Sottiaux, DECVIM-CA (Cardiology)
With the exception of one case of reversible left ventricular dilatation in a kitten, there is little information on the consequences of severe anaemia on the intact heart in cats. This study was designed to evaluate the impact of anaemia on the diastolic and systolic function of the right ventricle (RV) and left ventricle ( LV ) and to determine the patterns of cardiac remodeling associated with this condition.
10 cats with moderate to severe anaemia (haemoglobin < 7 gr/dl; hematocrit < 21% ) and signs of cardiac involvement ranging from heart murmur to overt heart failure were included in this study. Normality for distribution of all parameters was checked using the Kolmogorov-Smirnov test. Each parameter was compared with the reference values obtained from healthy patients in our hospital using the Mann-Wittney rank-sum test.
All patients were euthyroid. The systolic blood pressures were within normal range (110-145 mm Hg). 7 patients had a high LV output (>245 ml/kg/mn). High LV output resulted from stroke volume augmentation (4.4 +/-1.2 ml versus 2.7+/-0.6 ml. p: 0.001). LV systolic hyperfunction was indicated by the increased fractional shortening (52+/-11% versus 40+/-7%. p: 0.009) which resulted from a hyperkinetic state. Hyperkinetic state was demonstrated by the increased systolic thickness of the septum ( 0.64+/-0.11 cm versus 0.51+/-0.09 cm. P: 0.01) and of the LV free wall (0.82+/-0.11 cm versus 0.59+/- 0.07 cm.p: 0.001 ). The significant prolongation of the pulmonary flow acceleration time ( 59+/-19 ms versus 44+/- 6 ms. P<0.001 ) suggested a depressed RV systolic function. There was no significant change in the LV diastolic and systolic diameter. Cardiac remodeling consisted of significantly increased LV free wall thickness ( 0.54+/- 0.08 cm versus 0.40+/-0.06 cm. p: 0.003 ) with free wall hypertrophy ( > 0.55 cm ) in 4 patients. Follow-up of the patients with LV wall hypertrophy showed decreasing wall thickness, increasing LV diastolic and systolic diameter, and prolongation of the LV pre-ejection period with the correction of anaemia.
The adaptive response of the intact heart to severe anaemia consist of reversible LV hypertrophy and systolic hyperfunction with a decreased peak systolic wall stress. The RV appears to be more vulnerable to the hypoxia generated by severe anaemia.