Abstract 1833: Relationship of Left Atrial Enlargement to Persistence or Development of Electrocardiographic Left Ventricular Hypertrophy in Hypertensive Patients: Implications for the Development of New Atrial Fibrillation
Background: We have previously demonstrated that persistence or development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria are associated with an increased risk of developing atrial fibrillation (AF) compared with regression or continued absence of LVH. We postulated that this relationship might be in part mediated via greater left atrial enlargement (LAE) in patients with new and persistent LVH.
Methods: Baseline and year-3 ECG LVH and LA systolic diameter (LASD) were examined in 663 patients in the LIFE echocardiographic substudy in sinus rhythm with no history of AF. LASD was measured and considered enlarged if >3.8 cm in women or >4.2 in men. Cornell product LVH was considered abnormal if >2440 mm-msec.
Results: After 3 years of follow-up, there was continued absence of LVH in 238 patients (35.9%), regression of LVH in 156 (23.5%), development of new LVH in 33 (5%) and persistence of ECG LVH in 236 patients (35.6%). Compared with continued absence of LVH, there were step-wise increases in mean LASD, prevalence and odds of LAE across groups defined by the presence or absence of LVH at baseline and year-3 (Table⇓). After controlling for differences in age, gender, baseline systolic pressure, body mass index and baseline severity of LVH by Cornell product and Sokolow-Lyon voltage, patients with persistent or new LVH had a 2 to 3 fold greater risk of LAE at year 3. In patients with regression of LVH between baseline and year 3, the risk of LAE was similar to those with continued absence of LVH.
Conclusions: Persistence or development of new ECG LVH during antihypertensive therapy are associated with an increased risk of LAE after 3 years of follow-up, whereas regression of LVH is not associated with an increased risk of LAE. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with changing risk of developing AF.