Regression of LVH in Patients with Hypertension


Am Fam Physician. 2005 Mar 1;71(5):972.

Clinical Question: Should antihypertensive therapy be targeted at regression or prevention of left ventricular hypertrophy (LVH)?

Setting: Outpatient (any)

Study Design: Cohort (retrospective)

Synopsis: In this study, investigators wished to assess the possible association between reduction of LVH as determined by electrocardiography (ECG) during antihypertensive treatment and a reduction in rates of morbidity and/or mortality. They examined data from the previously published Losartan Intervention For Endpoint (LIFE) reduction in hypertension study, which randomized patients with hypertension and ECG-determined LVH to treatment with losartan or atenolol. Follow-up assessments, including at least one annual ECG, continued for four years or more.

After controlling for treatment group assignment, baseline cardiovascular risk scores, baseline and in-treatment blood pressure, and severity of baseline ECG-determined LVH, over time the less severe in-treatment ECG-determined LVH was associated with a significantly reduced risk of adverse cardiovascular outcomes, including a reduced risk of cardiovascular death, myocardial infarction, or death.

Another study evaluating LVH that was determined by echocardiogram reported similarly that lower left ventricular mass during antihypertensive treatment was associated with a reduced risk of adverse outcomes (Devereux RB, et al. Prognostic significance of left ventricular mass change during treatment of hypertension. JAMA 2004;292:2350–6). The authors of both papers suggested that antihypertensive therapy should be targeted at regression or prevention of ECG- or echocardiogram-determined LVH.

This method of study design, however, was inadequate to make a firm recommendation on the value of measuring LVH regression, and may instead simply measure the value of patient compliance. In other words, patients from both treatment groups who were most compliant with their antihypertensive medication regimens were more likely to show a reduction in LVH than those who were not. Likewise, those same patients were more likely to follow other physician advice about smoking, diet, exercise, and so forth, and, therefore, would be more likely to have a reduced risk of adverse cardiovascular events.

As noted in an editorial in this same issue, the only study design that was clearly able to conclude that antihypertensive therapy should be directed by the effect of treatment on a reduction of LVH, instead of by meeting target blood pressure goals, is a direct comparison of outcomes of patients randomly assigned to one treatment group or the other.

Bottom Line: During antihypertensive therapy, less severe LVH is associated with a reduced risk of cardiovascular morbidity and mortality. This risk reduction is independent of blood pressure treatment modality and actual blood pressure reduction. The current study design is inadequate for evaluating treatment guided by LVH reduction compared with the current method of goal-directed blood pressure lowering. Further studies are needed before clinical practice should be changed. (Level of Evidence: 2b)

Study Reference:

Okin PM, et al. Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events. JAMA. November 17, 2004;292:2343–9.

Used with permission from Slawson D. Regression of LVH with hypertension predicts reduced CVD risk. Accessed online December 28, 2004, at: http://www.InfoPOEMs.com.



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