Cardiologists at William Beaumont Hospital (Royal Oak, Michigan) have reported making an important breakthrough in understanding why and how heart attacks occur, identifying multiple blocked arteries as a key to understanding these dynamics. The Beaumont Hospital study followed 253 heart-attack patients and found that one in three had multiple arteries that contained unstable plaques. Previously, heart attack was thought to be a local occurrence, confined to one unstable artery, but in the Beaumont study, patients with multiple unstable arteries were more likely to develop another heart attack and had a greater likelihood of requiring repeat angioplasty or heart bypass surgery in the following year. Study findings support growing evidence implicating widespread inflammation in the coronary blood vessels as an important trigger leading to unstable arteries, according to the researchers.
"This study tells us that in heart attack patients with multiple unstable arteries, it may not be enough to treat only the area where the heart attack occurred," said Beaumont cardiologist James Goldstein, MD. "Other areas that are inflamed and at risk for rupture must also be treated to help prevent future problems." Goldstein said the next step in the group's research effort will be to determine whether treatments designed to heal unstable plaques, including anti-inflammatory medications and cholesterol-lowering drugs, can help prevent future heart attacks in the patients. It needs to be established if combinations of medications and the placement of multiple stents via angioplasty can prevent further arterial narrowing and subsequent heart attacks.
Researchers ID new enzyme cardiac marker
An enzyme carried in the blood in tandem with low-density lipoprotein (LDL), the carrier molecule containing the so-called "bad" cholesterol, may play a direct role in heart attacks, according to a report in the Oct. 18 issue of the New England Journal of Medicine. In a study by investigators at Glasgow University (Glasgow, Scotland), it was found that the enzyme Lp-PLA2 (lipoprotein-associated phospholipase A2) may serve as an important new marker, independent of LDL, to predict the risk of heart attack. And the study also suggests the potential importance of Lp-PLA2 as a novel target for preventing heart attack, with that potential therapy based on a strategy different than reducing cholesterol.
The cascade of cellular and biochemical events in which Lp-PLA2participates is long and complex. Lp-PLA2 in the bloodstream is usually bound to LDL, though blood levels of Lp-PLA2 may vary among individuals with equivalent LDL levels. Once Lp-PLA2 has entered the walls of certain arteries, including the coronary arteries which nourish the heart, its association with LDL continues, sometimes with pathological results. As LDL undergoes a change called oxidation, Lp-PLA2 breaks down the fats in LDL, producing substances that attract inflammatory cells. These cells engulf LDL and contribute to the formation of atherosclerotic plaques, with the growth and rupture of these plaques leading to blood clotting and blockage of the coronary arteries.
Given this sequence, the study demonstrated that blood levels of the enzyme do correlate with heart attacks and other adverse events related to atherosclerosis, based on blood samples collected during the West of Scotland Coronary Prevention Study, an earlier, landmark investigation in the cardiovascular field. The Lp-PLA2 study examined the cases of 580 men who had suffered either heart attacks or procedures performed to prevent heart attacks, namely angioplasty or coronary artery bypass surgery. These cases were compared with those of 1,160 other men who had not suffered adverse events. Examining five ranges of Lp-PLA2 levels, the study found a strong correlation between Lp-PLA2 and adverse events, the risk of an adverse event was about two times greater in the highest range than in the lowest range. The risk associated with Lp-PLA2 was observed whether the men studied went on to take pravastatin, a member of the statins class of cholesterol-lowering drugs, or placebo – further evidence that lowering Lp-PLA2 levels may offer benefit independently of lowering cholesterol.
Chris Packard, PhD, professor of pathological biochemistry at Glasgow, said, "Lp-PLA2 emerges from this study as a new focus for efforts to better identify and manage patients at risk of heart attack, still a leading killer in industrialized societies despite the benefit of cholesterol-lowering therapy." He noted that there is no one-to-one correlation between above-normal cholesterol and heart attack. "So it is important that we examine other potential factors, like Lp-PLA2, if we are to continue to reduce the toll of heart disease."
Other research concentrating on Lp-PLA2 is under way. Contributing to the study in the NEJM were scientists at SmithKline Beecham (Philadelphia, Pennsylvania) and diaDexus (Santa Clara, California), with the assay used in the study developed by diaDexus.
Night shift a cardiac risk sign?
A new study by a group of Italian researchers concludes that rotating shift work – including all-night shifts – is damaging to the heart. The greater risk night shift work causes may result from the heart's need to rest at night, the researchers suggest, with that desire turned on and off by the body's natural body rhythms. "Shift work is associated with an increased rate of [heart] disease and accidents," according to lead author Raffaello Furlan, MD, of the University of Milan (Milan, Italy).
The study followed 22 healthy males working a rotating schedule of three different shift periods – 6 a.m.-2 p.m.; 2 p.m.-10 p.m. and 10 p.m.-6 a.m. – monitoring their hearts at regular intervals. The investigators found that the shift changes did not alter the overall built-in clock that controls nervous system changes during waking and sleeping; for instance, the normal morning increase of nervous system activity was present regardless of work schedule.
"This resistance of the body's internal clock to change with varied work schedules indicates that people don't adapt as easily as we think to shift work, and could explain why shift workers are at higher risk" of heart disease, Furlan explained in a statement issued by the American Heart Association (Dallas, Texas), which published the study results in the Oct. 17 issue of its journal Circulation.
The conclusion of the authors: The conflicting messages that the heart is receiving – the person's desire to be up and doing physical work despite the body's built-in clock, which causes it to rest – may be a key factor in higher rates of heart disease among shift workers. Besides increased cardiovascular risk, the stress on the heart may be the cause of increased accidents by this group. "The reduced values of the [nervous system] during night work might be related to the presence of sleepiness or diminished alertness, which in turn could facilitate errors and accidents," the researchers conclude.
Greater risk for women after CABG
Two studies presented during the mid-October meeting of the American Society of Anesthesiologists in San Francisco, California, indicated that women with heart disease are at higher risk of mental decline and stroke after undergoing coronary artery bypass surgery.
One study conducted by Dr. Fun-Sun Yao at the Weill Cornell Medical Center (New York) found that women have lower brain oxygen levels while undergoing bypass surgery than men, and that that may explain why women are more likely to experience memory problems after such surgery.
In the second study, Dr. Charles Hogue and colleagues at the Washington University School of Medicine (St. Louis, Missouri) found that 50% of women who had a post-bypass stroke had previously had a stroke, and that such women had a 40 times higher risk of having a stroke – Hogue called it an "astronomically" higher risk – than the general population.