Abstract 2180: Relationship of Left Ventricular Systolic Function to Persistence or Development of Electrocardiographic Left Ventricular Hypertrophy in Hypertensive Patients: Implications for the Development of New Heart Failure
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 heart failure (HF) compared with regression or continued absence of LVH. We postulated that this relationship might be in part mediated via worse LV systolic function in patients with new and persistent LVH.
Methods: Baseline and year-3 ECG LVH and LV midwall shortening (MWS) were examined in 725 patients in the LIFE echocardiographic substudy. MWS was measured and considered abnormal if <14.2%; stress-corrected MWS (scMWS) was considered abnormal if 2440 mm-msec.
Results: Between baseline and 3 years follow-up, there was continued absence (n=260) or regression (n=167) of LVH in 427 patients and persistence (n=259) or development (n=39) of ECG LVH in 298 patients. Although there was no difference in baseline prevalence of abnormal MWS (23.4 vs 26.5%, p=0.389) or abnormal scMWS (24.6 vs 26.4%, p=0.663) between groups, after 3 years follow-up persistence or development of new LVH was associated with significantly lower mean MWS and scMWS and with higher prevalence and odds of abnormal MWS and scMWS than continued absence or regression of LVH (Table⇓). After controlling for differences in age, gender, race, treatment group, baseline and change from baseline to year-3 of heart rate, Sokolow-Lyon voltage, systolic and diastolic pressure and baseline severity of LVH by Cornell product, persistent or new ECG LVH remained associated with a >2-fold increased risk of abnormal MWS or scMWS at year 3.
Conclusions: Persistence or development of new ECG LVH during antihypertensive therapy is associated with an increased risk of LV systolic dysfunction after 3 years of follow-up. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with changing risk of developing HF. <