Okin, Peter M3; Wachtell, Kristian4; Gerdts, Eva3; Dahlöf, Björn3; Devereux, Richard B3
1 Graduate School of Health and Medical Sciences, Faculty of Health and Medical Sciences, Københavns Universitet2 Department of Clinical Medicine, Department of Clinical Medicine, Faculty of Health and Medical Sciences, Københavns Universitet3 unknown4 Graduate School of Health and Medical Sciences, Faculty of Health and Medical Sciences, Københavns Universitet
implications for the development of new heart failure
BACKGROUND: Persistence or development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria is associated with an increased risk of developing heart failure compared with regression or continued absence of LVH. We postulated that this association might be in part mediated via worse left ventricular systolic function in patients with new or persistent ECG LVH. METHODS: Baseline and year-3 ECG LVH and left ventricular midwall shortening (MWS) were examined in 725 hypertensive patients in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. Sex-specific criteria were used for abnormal MWS (<14% in men and <16% in women) and abnormal stress-corrected MWS (scMWS; <87% in men and <90% in women). Cornell product LVH greater than 2440 mm ms defined ECG LVH. RESULTS: Between baseline and year-3 follow-up, there was continued absence or regression of ECG LVH in 427 patients and persistence or development of new LVH in 298 patients. At baseline, although there were no significant differences in the mean values of MWS and scMWS, patients with persistence or development of ECG LVH at year 3 had significantly higher baseline prevalences of abnormal MWS (41.9 vs. 30.2%, P = 0.001) and abnormal scMWS (27.4 vs. 20.5%, P = 0.034). At year-3 follow-up, persistence or development of new LVH was associated with significantly lower mean MWS (16.5 ± 2.3 vs. 17.2 ± 1.9%, P < 0.001) and scMWS (104.2 ± 13.1 vs. 106.5 ± 10.9%, P = 0.005), and with higher prevalence and odds of abnormal MWS [23.8 vs. 10.8%, P < 0.001, odds ratio (OR) 2.50, 95% confidence interval (CI) 1.66-3.75, P < 0.001] and abnormal scMWS (11.0 vs. 5.8%, P = 0.011, OR 2.02, 95% CI 1.16-3.51, P = 0.013). After controlling for differences in age, sex, 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 two-fold increased odds of abnormal MWS (OR 2.20, 95% CI 1.39-3.47, P = 0.001) or scMWS (OR 1.90, 95% CI 1.03-3.50, P = 0.040) at year 3. CONCLUSION: Persistence or development of new ECG LVH during antihypertensive therapy is associated with an increased risk of left ventricular systolic dysfunction after 3 years' follow-up. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with the changing risk of developing heart failure. CLINICAL TRIALS REGISTRATION: http://clinicaltrials.gov/ct/show/NCT00338260?order=1.
Journal of Hypertension, 2014, Vol 32, Issue 12, p. 2472-8