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Published on: April 8, 2013
Lack of reduction of left ventricular mass in treated hypertension: the strong heart study
Giovanni de Simone1, Richard B Devereux, Raffaele Izzo
1Department of Translational Medical Sciences, Federico II University, Napoli, Italy. simogi@unina.it
Insights
Hypertensive left ventricular mass (LVM) often does not decrease with treatment, especially in those with higher body mass index (BMI). Lack of LVM reduction is linked to kidney damage, not just blood pressure control.
Area of Science:
- Cardiology
- Nephrology
- Public Health
Background:
- Hypertensive left ventricular mass (LVM) is typically expected to decrease with antihypertensive therapy.
- Clinical trials suggest LVM reduction is a positive outcome of treatment.
Purpose of the Study:
- To assess the 4-year change in echocardiographic LVM in a free-living hypertensive population.
- To identify factors influencing LVM changes during antihypertensive treatment.
Main Methods:
- Analysis of echocardiographic LVM in 851 hypertensive participants over 4 years.
- Categorization of systolic blood pressure (SBP) and LVM variations.
- Statistical adjustment for baseline characteristics, treatment, and demographic factors.
Main Results:
- Despite treatment, LVM increased over time, more in men than women.
- Higher baseline body mass index (BMI) and urinary albumin/creatinine excretion predicted lack of LVM decrease.
- Lack of LVM reduction was independent of blood pressure control and antihypertensive medication type.
Conclusions:
- Higher BMI is associated with less reduction in hypertensive left ventricular hypertrophy (LVH).
- Failure to reduce LVM is linked to renal damage, irrespective of blood pressure control or treatment type.
Background:
Hypertensive left ventricular mass (LVM) is expected to decrease during antihypertensive therapy, based on results of clinical trials.
Methods And Results:
We assessed 4-year change of echocardiographic LVM in 851 hypertensive free-living participants of the Strong Heart Study (57% women, 81% treated). Variations of 5% or more of the initial systolic blood pressure (SBP) and LVM were categorized for analysis. At baseline, 23% of men and 36% of women exhibited LV hypertrophy (LVH, P<0.0001). At the follow-up, 3% of men and 10% of women had regression of LVH (P<0.0001 between genders); 14% of men and 15% of women, free of baseline LVH, developed LVH. There was an increase in LVM over time, more in men than in women (P<0.001). Participants whose LVM did not decrease had similar baseline SBP and diastolic BP, but higher body mass index (BMI), waist/hip ratio, heart rate (all P<0.008), and urinary albumin/creatinine excretion (P<0.001) than those whose LVM decreased. After adjusting for field center, initial LVM index, target BP, and kinship degree, lack of decrease in LVM was predicted by higher baseline BMI and urinary albumin/creatinine excretion, independently of classes of antihypertensive medications, and significant effects of older age, male gender, and percentage increase in BP over time. Similar findings were obtained in the subpopulation (n=526) with normal BP at follow-up.
Conclusions:
In a free-living population, higher BMI is associated with less reduction of hypertensive LVH; lack of reduction of LVM is independent of BP control and of types of antihypertensive treatment, but is associated with renal damage.
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