A new LIFE Study data analysis indicates use of losartan to reduce left ventricular hypertrophy is much less effective and less beneficial in patients with diabetes and hypertension than in non-diabetic peers, according to an article in the March 28 issue of Circulation.

"Diabetics have less regression of the condition -- called left ventricular hypertrophy (LVH) -- than nondiabetics after treatment aimed at lowering blood pressure. And even when LVH does regress, these patients don't get the same degree of benefit, in terms of reductions in death, heart attack or stroke, than patients without diabetes," said lead author Peter Okin, MD, Professor of Medicine in the Greenberg Division of Cardiology at Weill Cornell Medical College.

The findings suggest treatment for left ventricular hypertrophy is not a "one size fits all" proposition.

The current study builds on groundbreaking work conducted earlier by the same research group, whose paper published in 2004 in the Journal of the American Medical Association (JAMA) found that reducing left ventricular hypertrophy with losartan improved patient outcomes. That data came from the Losartan Intervention for Endpoint [LIFE] Reduction in Hypertension Study.

"At the time, we noticed an intriguing observation: That diabetics in the LIFE population had less regression of hypertrophy than nondiabetics," Okin said.

In the current analysis, the researchers compared five-year outcomes for 9,193 hypertensive patients (1,195 of them diabetic) treated with losartan or atenolol. Patients with diabetes had less regression of left ventricular hypertrophy than peers without diabetes, as well as higher rates of cardiovascular death, death from any cause, and non-fatal myocardial infarction or stroke.

Nondiabetic patients who achieved significant reduction in left ventricular hypertrophy via antihypertensive drug therapy had a 17-to-35 percent reduction in death or serious cardiovascular events. In contrast, diabetic patients received no such benefit -- even when their ventricular hypertrophy showed signs of improvement.

"The findings may help explain the increased vulnerability of hypertensive diabetic patients," Okin said.

He added, "Perhaps diabetics have simply developed a much more difficult form of left ventricular hypertrophy over a longer period of time, so they have more damage to make up for. Or, it may be that they experience a greater fibrosis of the heart muscle -- a type of tissue growth that's more resistant to blood-pressure-lowering therapy."

Whatever the reasons, these early findings point to a need for treatments tailored to diabetic patients, according to the experts.

"For example, there are new treatment modalities that might work better to reverse fibrotic changes in heart muscle," Okin said. "Or diabetics may need more aggressive antihypertensive therapy than nondiabetic patients to achieve the same effect. This work should serve as a springboard to investigate those possibilities."