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(Circulation. 2007;116:700-705.)
© 2007 American Heart Association, Inc.

Arrhythmia/Electrophysiology

Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death

The LIFE Study

Kristian Wachtell, MD, PhD; Peter M. Okin, MD; Michael H. Olsen, MD, PhD; Björn Dahlöf, MD, PhD; Richard B. Devereux, MD; Hans Ibsen, MD; Sverre E. Kjeldsen, MD, PhD; Lars H. Lindholm, MD; Markku S. Nieminen, MD; Kristian Thygesen, MD

From the Department of Internal Medicine, Glostrup University Hospital, Glostrup, Denmark (K.W., M.H.O., H.I.); Greenberg Division of Cardiology, Weill Medical College of Cornell University, New York, NY (K.W., P.M.O., R.B.D.); Department of Internal Medicine, Sahlgrenska University Hospital-Östra, Gothenburg, Sweden (B.D.); Department of Internal Medicine, Ullevål University Hospital, Oslo, Norway (S.E..K.); Department Preventive Medicine, Umeå University Hospital, Umeå, Sweden (L.H.L.); Department of Cardiology, Helsinki University Hospital, Helsinki, Finland (M.S.N.); and Department of Internal Medicine, Århus University Hospital, Århus, Denmark (K.T.).

Correspondence to Kristian Wachtell, MD, PhD, Department of Cardiology B2142, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100, Copenhagen, Denmark. E-mail kristian{at}wachtell.net

Received September 24, 2006; accepted May 18, 2007.

Background— Sudden cardiac death (SCD) occurs more often in patients with ECG left ventricular (LV) hypertrophy. However, whether LV hypertrophy regression is associated with a reduced risk of SCD remains unclear.

Methods and Results— The Losartan Intervention for End Point Reduction in Hypertension (LIFE) study included 9193 patients 55 to 80 years of age with essential hypertension and ECG LV hypertrophy by gender-adjusted Cornell product (CP) (RaVL+SV₃ [+6 mm in women]) · QRS duration>2440 mm · ms) and/or Sokolow-Lyon voltage (SLV) (SV₁+RV_5/6>38 mm). During follow-up (mean, 4.8 years), 190 patients (2%) experienced SCD. In time-dependent Cox analyses, absence of in-treatment LV hypertrophy was associated with a decreased risk of SCD: every 1-SD-lower in-treatment CP (1050 mm · ms) was associated with a 28% lower risk of SCD (hazard ratio [HR], 0.72; 95% CI, 0.66 to 0.79) and 1-SD-lower SLV (10.5 mm) with a 26% lower risk (HR, 0.74; 95% CI, 0.65 to 0.84). After adjustment for time-varying systolic and diastolic blood pressures, treatment allocation, age, gender, baseline Framingham risk score, ECG strain, heart rate, urine albumin/creatinine ratio, smoking, diabetes, congestive heart failure, coronary heart disease, atrial fibrillation, and occurrence of myocardial infarction, atrial fibrillation, heart failure, and noncardiovascular death, both in-treatment CP and SLV remained predictive of SCD: each 1-SD-lower CP was associated with a 19% lower risk of SCD (HR, 0.81; 95% CI, 0.73 to 0.90) and 1-SD-lower SLV with an 18% lower risk (HR, 0.82; 95% CI, 0.70 to 0.98). Absence of in-treatment LV hypertrophy by both SLV and CP was associated with a 30% lower risk of SCD (HR, 0.70; 95% CI, 0.54 to 0.92).

Conclusions— Absence of in-treatment ECG LV hypertrophy is associated with reduced risk of SCD independently of treatment modality, blood pressure reduction, prevalent coronary heart disease, and other cardiovascular risk factors in hypertensive patients with LV hypertrophy.

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