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Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study
Institution:1. Department of Medicine, Cardiology Division, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States;2. Department of Medicine, Cardiology Division, Medical University of South Carolina, Charleston, South Carolina, United States;3. Department of Cardiology, University Medical Center Groningen, the Netherlands;4. Program of Applied Translational Research, Yale University, New Haven, Connecticut, United States;1. Division of Infectious Diseases; the;2. Division of Cardiology, Department of Medicine;3. Duke Clinical Research Institute, Duke University Medical Center,;4. Duke Global Health Institute, Durham, North Carolina;1. Division of Cardiology, Mitsui Memorial Hospital, Tokyo, Japan;2. Division of General Medicine, Mitsui Memorial Hospital, Tokyo, Japan;3. Division of Internal Medicine, Mitsui Memorial Hospital, Tokyo, Japan
Abstract:Background and aimsClusters of metabolic abnormalities resembling phenotypes of metabolic syndrome predicted outcome in the LIFE study, independently of single risk markers, including obesity, diabetes and baseline ECG left ventricular hypertrophy (LVH). We examined whether clusters of two or more metabolic abnormalities (MetAb, including obesity, high plasma glucose without diabetes, low HDL-cholesterol) in addition to hypertension were associated to levels of ECG LVH reduction comparable to that obtained in hypertensive subjects without or with only one additional metabolic abnormality (no-MetAb).Methods and resultsWe studied 5558 non-diabetic participants without MetAb (2920 women) and 1235 with MetAb (751 women) from the LIFE-study cohort. MetAb was defined by reported LIFE criteria, using partition values from the ATPIII recommendations. Time-trends of Cornell voltage–duration product (CP) over 5 years was assessed using a quadratic polynomial contrast, adjusting for age, sex, prevalent cardiovascular disease and treatment arm (losartan or atenolol). At baseline, despite similar blood pressures, CP was greater in the presence than in the absence of MetAb (p < 0.0001). During follow-up, despite similar reduction of blood pressure, CP decreased less in patients with than in those without MetAb, even after adjustment for the respective baseline values (both p < 0.002). Losartan was more effective than atenolol in reducing CP independently of MetAb.ConclusionsClusters of metabolic abnormalities resembling phenotypes of metabolic syndrome are related to greater initial ECG LVH in hypertensive patients with value of blood pressure similar to individuals without metabolic abnormalities, and are associated with less reduction of ECG LVH during antihypertensive therapy, potentially contributing to the reported adverse prognosis of metabolic syndrome.
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