Abstract
BACKGROUND: In patients with end stage renal disease (ESRD), left ventricular (LV) hypertrophy with impaired LV function, which is called uremic cardiomyopathy (UC) is often observed. The UC historically has been considered a contraindication for kidney transplantation (KTx). Currently, moderate LV dysfunction does not exclude the possibility of KTx. The amelioration of uremia after KTx improved cardiac function in patients with LV dysfunction. There is a little information on the function of the left atrium (LA) after the KTx procedure. There are no studies evaluating (LA) changes in patients with UC after KTx and determining the possibility of inhibiting the occurrence of LA unfavourable changes (remodelling) and even a possible LA recovery process (reverse remodelling) as a result of a successful KTx. The aim of the study was to assess the LA reverse remodelling in patients with ESRD undergoing KTx. METHODS: The study group consisted of 42 patients, aged 43.3 ± 12.6 followed for 36 months after a deceased donor KTx. The patients were studied at five time points: 1, 3, 6, 12 and 36 months after KTx. In all patients transthoracic echocardiography was performed in order to assess the following LA planimetric parameters: LA(max), LA(min), LA(waveP). LA(shortmax), LA(shortmin), LA(shortwaveP), LA(longmax), LA(longmin), LA(longwaveP), LA(circmax) and LA(areamax), volumentric parameters: LA volume (LAV), LA volume index (LAVI), and hemodynamic indices: LA ejection fraction (LA(EF)), LA active emptying fraction (LA(AE)), LA passive emptying fraction (LA(PE)), LA index of expansion (LA(IE)) and LA fractional shortening (LA(FS)). RESULTS: The LAVI values were 34.63 ± 10.34 ml/m(2), 32.24 ± 9.59 ml/m(2) (p < 0,001), 31.36 ± 9.20 ml/m(2) (p < 0,001), 28.29 ± 8.32 ml/m(2) (p < 0,001) and 27.57 ± 8.40 ml/m(2) (p < 0,001), after: 1, 3, 6, 12 and 36 months after KTx, respectively. The reduction of the LA size was accompanied by gradual LA contractility improvement, which was manifested as an increase of the LA hemodynamic indices such as LA(EF), LA(AE), LA(IE), LA(FS) and a decrease of LA(PE). CONCLUSIONS: LA remodelling secondary to atrial uraemic cardiomyopathy is an example of complex cardiomyopathy with elements characteristic of both congestive and infiltrative cardiomyopathy. Early LAVI reduction post KTx mostly depends on changed haemodynamic conditions, whereas the main reason for further decrease of LAVI values is related to resolution of uraemic toxaemia.