A new study may be the last word in a controversy that's plagued cardiovascular disease research for years: whether a marker of inflammation known as C-reactive protein (CRP) drives heart attacks and strokes. In a survey of more than 128,000 people, researchers have found that genes that raise CRP levels don't make cardiovascular disease more likely. Although the study arrives at the same conclusion as earlier work, its massive size makes it statistically the most powerful test yet of this question and tough to refute, say experts. Produced by the liver, CRP has long been eyed as a suspect in heart disease. In part, that's because of observational studies, which regularly find that higher CRP levels are associated with later heart trouble. CRP is also a vague indicator of many health problems that hike the risk of heart attacks and strokes, including obesity and type 2 diabetes. But these kinds of associations don't mean that CRP is actually causing heart attacks. Indeed, last fall, Danish researchers reported that genes that raise CRP don't appear to cause cardiovascular disease (ScienceNOW, 29 October 2008). Now, a team of three dozen researchers from the United Kingdom, Canada, Germany, and elsewhere have teamed up to examine the question again. They drew on numerous health studies, which have banked DNA from tens of thousands of participants. Like the earlier Danish group, this one, led by epidemiologist Paul Elliott of Imperial College London, began with a simple premise: If high CRP levels cause heart attacks, then genes that raise CRP levels should also raise the risk of heart attacks. The researchers studied three variants that each raised CRP by about 20%. Then they tested whether having at least one of these variants made cardiovascular disease more likely in more than 28,000 people with disease and in 100,000 people without. The result: The genes had no effect on heart disease.

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Sepsis in humans frequently follows the body's attempt to thwart infectious agents such as bacteria, viruses and fungi. In many respects, the development of sepsis represents the harmful consequences of exuberant innate immune responses, resulting in high levels of proinflammatory mediators that are associated with organ failure, primarily in the heart, lungs, liver and kidneys. The early phases of sepsis are often associated with the onset of immunosuppression, which may compromise the body's ability to cope with infectious agents1. After the onset of sepsis, patients often develop 'septic shock', which is associated with a decrease in blood pressure, requiring the administration of vasopressors to maintain adequate blood pressure for organ perfusion. Such support may restore blood pressure, but does not address the cause, and it sometimes fails to adequately improve vascular perfusion of vital organs, including the brain. Very little is understood about the cause of falling cardiac output in septic shock, although cardiac failure of this type, referred to as septic cardiomyopathy, is considered to be reversible and does not seem to involve structural damage of the heart2. Several recent studies have provided insights into how the contractile power of the heart wanes during septic shock2. These studies have identified cardiosuppressive factors that are induced during sepsis and impair contractility of cardiomyocytes, the contractile cells of the heart. At least three types of factors adversely affect cardiomyocytes: bacterial lipopolysaccharide (LPS), the complement activation product C5a and certain cytokines (interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and IL-6). Blockade of these factors or their signaling pathways may be a promising therapeutic approach to treat complications of sepsis.