Cumulative out-of-pocket expenses for the treatment of chronic heart disease led to significant financial burdens for low-income families, even for those with health insurance, according to preliminary research presented at the American Heart Association’s Quality of Care and Outcomes Research Scientific Sessions 2018, a premier global exchange of the latest advances in quality of care and outcomes research in cardiovascular disease and stroke for researchers, healthcare professionals and policymakers.
The study focused on the effect of out-of-pocket health expenses for treating atherosclerotic cardiovascular disease on low-income families, defined as those with an income below 200 percent of the federal poverty limit. During the study period (2006-2015), that ranged from $20,000 to $24,250 per year for a family of four.
Atherosclerotic cardiovascular disease is a group of conditions caused by atherosclerosis — a build-up of plaque that can harden and narrow the arteries and consequently result in a heart attack, stroke or death. It’s the leading cause of death, a major cause of disability and a major source of healthcare costs. The researchers defined high and catastrophic health expenses as out-of-pocket expenses of more than 20 percent and more than 40 percent of family income, respectively.
In the featured article of the March 2017 issue of “The Journal of Nuclear Medicine,” researchers demonstrate that a new positron emission tomography (PET) radiotracer, gallium-68 (Ga-68)-pentixafor, can quickly and non-invasively identify life-threatening atherosclerotic plaques. The tracer binds to the CXCR4 receptor on inflammatory cells present in atherosclerotic plaques — making it possible to find and treat atherosclerosis early.
Atherosclerosis represents the main cause of heart attack and stroke. According to the Centers for Disease Control and Prevention, every year about 735,000 Americans have a heart attack and 800,000 have a stroke. Stroke kills more than 130,00 Americans a year, and about 610,000 die from cardiovascular disease.
Atherosclerosis develops over decades with the progressive accumulation of lipids, inflammatory cells and connective tissue within the inner layer of arterial walls leading to a local thickening of the vascular wall called atherosclerotic plaque. These plaques can remain asymptomatic for years, but an inflammatory reaction can develop causing the plaques to rupture and stimulate clot formation. If a clot completely blocks an artery, no oxygen can reach the downstream tissue — resulting in the sudden development of heart attack or stroke. The challenge is to identify patients with these dangerous atherosclerotic plaques before a heart attack or stroke occurs.
Researchers at the University of Tübingen, working with colleagues in other parts of Germany and in the United States, have identified an enzyme as a kind of biological gauge regulating inflammation in the human body. Professor Alexander Weber of the Interfaculty Institute of Cell Biology says the enzyme — Bruton’s tyrosine kinase or BTK — is switched on when an inflammation occurs in the body, playing a key role in the inflammation’s subsequent development.
Inflammation is an important for recovery mechanism from many diseases. Yet in disorders like gout, Alzheimer’s, atherosclerosis, heart attack or stroke, inflammation can also have negative effects and reinforce the damage done by the disease. Inflammation is driven — among other processes — by molecular machinery known as the inflammasome. First, immune cells are activated which release certain inflammation-promoting messenger proteins, called cytokines.