NewYork-Presbyterian/Weill Cornell-Led Team Finds Less Regression of Heart Muscle in Diabetics, and Less Impact on Outcomes When Regression Does Occur
Mar 17, 2006
Standard blood-pressure-lowering treatment to reduce dangerously enlarged hearts is much less effective and less beneficial in diabetic vs. nondiabetic patients, a team led by NewYork-Presbyterian Hospital/Weill Cornell Medical Center researchers reports in this month's 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," says lead researcher Dr. Peter Okin, Professor of Medicine in the Greenberg Division of Cardiology at Weill Cornell Medical College, and Director of Clinical Affairs at NewYork-Presbyterian/Weill Cornell, New York City.
The findings suggest LVH treatment is not a "one size fits all" proposition.
"We may need to be treating diabetics with LVH differently understanding that we may not be getting the same 'bang for the buck' with blood-pressure-lowering therapies that we are seeing in nondiabetics," Dr. Okin explains.
LVH, an unhealthy thickening of cardiac muscle, typically arises as the heart's response to chronic high blood pressure. The condition is often present in patients with advanced heart disease or congestive heart failure.
This latest study builds on groundbreaking work conducted earlier by Dr. Okin's group, whose paper published in 2004 in the Journal of the American Medical Association (JAMA) found that reducing LVH with the antihypertensive drug 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," Dr. Okin said.
That's especially important, he said, because diabetic patients with LVH typically fare much worse than nondiabetics with higher rates of heart attack, stroke and death.
In this latest study, Dr. Okin along with colleagues in Scandinavia and elsewhere turned again to the LIFE data. They compared five-year outcomes for 9,193 hypertensive patients (1,195 of them diabetic) treated with losartan or another drug, atenolol.
The result: "Patients with diabetes had less regression of their LVH than nondiabetics as well as higher rates of cardiovascular death, death from any cause, and non-fatal heart attack or stroke," Dr. Okin said.
Nondiabetic patients who achieved significant LVH reduction via antihypertensive drug therapy were rewarded with a 17-to-35 percent reduction in death or serious cardiovascular events, the researchers found.
In contrast, diabetic patients received no such benefit even when their LVH showed signs of improvement.
"The findings may help explain the increased vulnerability of hypertensive diabetic patients," Dr. Okin says.
The reasons for this "treatment gap" between patients with diabetes and those without the blood sugar disease remain unclear.
"Perhaps diabetics have simply developed a much more difficult form of LVH over a longer period of time, so they have more damage to make up for," Dr. Okin speculates. "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, the experts say.
"For example, there are new treatment modalities that might work better to reverse fibrotic changes in heart muscle," Dr. Okin says. "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."
The study was funded, in part, by a grant from Merck & Co., the makers of losartan.
Co-authors include Dr. Richard B. Devereux of Weill Cornell Medical College; Dr. Eva Gerdts of the University of Bergen, Norway; Dr. Steven M. Snapinn of Amgen, Inc., Thousand Oaks, Calif; Dr. Katherine E. Harris of Merck & Co., West Point, Pa.; Dr. Sverker Jern and Dr. Bjorn Dahlof of Sahlgrenska University Hospital/Ostra, in Goteborg, Sweden; Dr. Sverre E. Kjeldsen of Ulleval University Hospital, Oslo, Norway; Dr. Stevo Julius of the University of Michigan Medical Center, Ann Arbor; Dr. Jonathan Edelman of Merck & Co., Whitehouse Station, N.J.; and Dr. Lars H. Lindholm of Umea University, Umea, Sweden.