Link Between Chronic Inflammation And Atherosclerosis Studied
Main Category: Arthritis / RheumatologyAlso Included In: Lupus; Cardiovascular / Cardiology; Smoking / Quit Smoking
Article Date: 29 May 2007 - 16:00 PST
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Rheumatoid arthritis, lupus, and other inflammatory rheumatic diseases are associated with a high rate of death from heart disease. One explanation is a greater susceptibility to atherosclerosis. Although atherosclerosis is linked to inflammation in healthy individuals as well, the mechanism of inflammation and the reason for accelerated atherosclerosis in patients with inflammatory rheumatic disease remain unclear. Does atherosclerosis result from systemic inflammation, a hallmark of these rheumatic diseases, or from local inflammation of vessels?
To shed light on the link between chronic inflammation and atherosclerosis, a team of researchers in Norway and the United States, affiliated with the Cleveland Clinic Foundation and Brigham and Women's Hospital in Boston, focused on the aortas of recent recipients of coronary artery bypass graft (CABG) surgery, comparing biopsy specimens from patients with inflammatory rheumatic disease to those from patients without it. Their study, presented in the June 2007 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), affirms inflammatory rheumatic disease and smoking as independent predictors of vessel wall inflammation. The vascular inflammation might be a factor that promotes atherosclerosis and the formation of aneurysms.
Aortic samples were obtained during CABG surgery, performed at two cardiac centers in Norway, from 66 patients with inflammatory rheumatic disease and 51 control patients. The inflammatory rheumatic disease group included patients with rheumatoid arthritis, psoriatic arthritis, lupus, ankylosing spondylitis, polymyalgia and other diseases. Age, body mass index, family history of heart disease, and other traditional cardiovascular risk factors were similar in both groups. All specimens were evaluated, by light microscope, for evidence of chronic inflammatory cell infiltration in the aortic wall. This was achieved by counting and measuring the mononuclear cell infiltrates (MCI) in the aorta, with particular attention to the adventitia, the deepest layer of vascular tissue. Using statistical analysis, the relationship between these inflammatory infiltrates and established lifestyle risk factors for heart disease was also assessed.
In the adventitia, MCIs occurred more frequently in patients with inflammatory rheumatic disease -- 47 percent of this group, compared with 20 percent of the control group. Along with greater prevalence, these inflammatory cells were larger in size. In the middle layer of the vessel wall (the media), MCIs were detected only in patients with inflammatory rheumatic disease. What's more, MCIs were observed in 6 of 7 patients with a history of aortic aneurysm. In addition to inflammatory rheumatic disease, current smoking was independently associated with more pronounced chronic inflammatory infiltration in the inner adventitia.
"The opportunities for detecting aortic inflammation are limited," acknowledges the study's spokesperson, Ivana Hollan, M.D. "Our method of tissue examination allows the condition to be diagnosed in patients undergoing CABG surgery without increasing the preoperative risk."
Despite the limitations of its small sample size, this groundbreaking study of aortic inflammation in patients with inflammatory rheumatic disease indicates the need for further investigation into an inflammatory process that may increase vulnerability to dying from a heart attack or aneurysm.
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Article: "Inflammatory Rheumatic Disease and Smoking Predict Aortic Inflammation: A Controlled Study of Biopsy Specimens Obtained at Coronary Artery Surgery," Ivana Hollan, Helge Scott, Kjell Saatvedt, Richard Prayson, Knut Mikkelsen, Hans C. Nossent, Ingjerd Lien Kvelstad, Matthew H. Liang, and 'wystein T. Forre, Arthritis & Rheumatism, June 2007; (DOI: 10.1002/art.22690).
Contact: Amy Molnar
John Wiley & Sons, Inc.
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Atherosclerosis From Mechanical Injury
posted by Gregory Marlow on 26 May 2010 at 10:46 amHave you ever considered that atherosclerosis could be the result of mechanical injury? In our modern industrial society we don't do enough physical work to maintain our muscles. The wasting of skeletal muscles is very apparent, but what happens to the smooth arterial muscles? It seems reasonable to assume that they waste away in a similar fashion. At some point they will no longer provide the tension required for driving the heart's ventricular output through the circulatory system.
The body seeks a new source for arterial tension. It retains sodium to increase the arterial volume until it finds tension in the other arterial layers. These layers weren't designed to provide the arterial reflex contraction. They don't have the correct volume versus tension profile that healthy smooth arterial muscles provide. To compensate, the systolic pressure has to be higher.
The higher pressure tears at arterial layers causing longitudinal fissures and inflammation. This subsequently results in the longitudinal (streaky) fat deposits characteristic of atherosclerosis. Athletes don't get atherosclerosis, because while they exercise their skeletal muscles, they also exercise their arterial muscles with a larger blood volume and higher pressure per heartbeat than that at rest.
The recommendation to reduce sodium intake to lower blood pressure reduces arterial volume so that the higher pressure the body seeks cannot be achieved. But one would think that lowering arterial volume would also restrict blood flow. In individuals with healthy smooth arterial muscles one would then expect to see an increase in blood pressure. I do see this in my own athletic body.
Because the majority of our industrial population may have atrophied smooth arterial muscles, I think we have confused normal observed arterial action with healthy arterial action when it comes to sodium levels. Experiments need to be done to verify my assumption that smooth arterial muscles atrophy when underused. Then the recommendation to lower sodium consumption to decrease blood pressure needs to be reexamined.
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