Influence of regression of left ventricular hypertrophy on left atrial size and function in patients with moderate hypertension

Objectives. The aim of the study was to evaluate the effect of regression of left ventricular (LV) hypertrophy on left atrial(LA) size and function in patients treated with telmisartan, an angiotensin II receptor blocker. Methods. Patients populationincluded 80 patients with mild–moderate LV hypertrophy treated with telmisartan. Patients were followed over a period of12 months from the start of telmisartan treatment. LA size was measured during systole from the parasternal long-axis viewfrom M-mode. Atrial function was assessed by Doppler-echocardiography and the following parameters were measured:transmitral peak A velocity, atrial filling fraction, atrial ejection force (AEF), peak E velocity, deceleration time andisovolumic relaxation time, LA maximal and minimal volume, and LV cardiac mass index (LVMI). Results. All patients hadan increased LVMI and decrease during follow-up. LA dimensions were greater at baseline and reduced after 1 year oftreatment. LA volume indexes maximal volume, minimal volume and P volume were reduced compared with baseline value(maximal volume from 35¡5 to 32¡5, pv0.05; minimal volumes from 14¡2 to 10¡4, pv0.05). AEF, a parameter ofatrial systolic function, increased from 12¡3 to 15¡2.4 (pv0.01). The reduction of LA volumes correlate with reductionof LVMI (LA maximal volume and LVMI r50.45; pv0.01; LA minimal volume and LVMI r50.34; pv0.05). A positivecorrelation was also found between LV mass index and P volume (r50.41; pv0.01), LV mass index and LA activeemptying volume (r50.39; pv0.01), and LV mass index and LA total emptying volume (r50.38; pv0.05). Conclusions.The present study suggests that regression of LV hypertrophy due to telmisartan is associated with reduction of LA volumesthat expresses variation of LV end-diastolic pressure. The reduction of LV end-diastolic pressure is associated with anincrease in diastolic filling and with a significant reduction of active and passive emptying contribution of left atrium to LVstroke volume.