Inflammation overload may harm heart

UC DAVIS (US) — New research about inflammation’s role in heart disease underscores the need to consider a broader range of immune-system factors to find accurate biomarkers, especially in relation to age.

A study published in the journal Arteriosclerosis, Thrombosis and Vascular Biology shows that systemic inflammation, the immune system’s defense against disease or injury that can contribute to cancer and diabetes, increases with age in people with heart-disease symptoms, but inflammation specific to vascular disease does not.

“Age is a known risk factor for heart disease, but the underlying disease processes that contribute to that risk are not well understood,” says Lars Berglund, senior study author and senior associate dean for research at the University of California, Davis.

[sources]

“Our study shows that the search for answers should look beyond the inflammation linked particularly with vascular disease and instead evaluate the overall burden of inflammation.”

Lifestyle factors including physical activity, diet, and tobacco use are currently the best predictors of heart disease, but become less reliable with age.

Treatment usually begins when symptoms of blood-vessel conditions, such as atherosclerosis, become apparent, but by then the disease process is well under way.

Finding an accurate immune-system biomarker, or cluster of biomarkers, could lead to earlier diagnosis and interventions that reduce the impact of heart disease, which affects more than 83 million Americans, costs an estimated $444 billion annually, and is the nation’s leading cause of death.

For the study, Berglund included 336 Caucasian and 224 African-American patients of two New York hospitals who were about to undergo diagnostic coronary arteriography, a test given to patients with heart-disease symptoms to detect blood flow to the heart and blockages. Ages ranged from 24 to 72.

Researchers measured blood levels of markers for systemic inflammation—C-reactive protein, fibriniogen, and serum amyloid-A—along with markers of vascular inflammation—lipoprotein-associated phospholipase A2 (Lp-PLA2) and pentraxin-3.

The older a study participant was, the higher their blood levels of systemic inflammation markers. Blood levels of vascular inflammation markers remained stable across ages. The findings didn’t change among patients of different racial backgrounds, genders, or body weights.

The outcome suggests that inflammation factors beyond those that directly affect blood vessels may be responsible for increased heart-disease risk as we age, Berglund says.

“It could be that we accumulate an inflammatory load over a lifetime that eventually does harm to blood vessels. Now that we have an idea of how systemic inflammation compounds over time, we can test that possibility.”

Developing heart-disease treatments that target the immune system is complicated, since the goal is to reverse harmful effects without altering protective qualities.

“We want to treat the cause but not shoot down the disease-fighting mechanisms,” Berglund explains. “We still have work to do before we can define heart disease as more than a lifestyle disease and make major breakthroughs in fighting what has become the plague of our time.”

Researchers from the University of Rochester and the University of Vermont contributed to the research that was funded by grants from the National Heart, Lung and Blood Institute, the UC Davis Clinical and Translational Science Center and the American Heart Association.

More news from UC Davis: http://www.news.ucdavis.edu/