hS-CRP, IS IT DEPENDENT ON RACE?

There is an article circulating in the internet, purportedly written by a retired cardiac surgeon, saying that coronary artery disease ( CAD ) is not the result of raised cholesterol levels, but from inflammation. That statement is partly true, but it certainly is not as simple as that. Inflammation causing CAD is what I thought I will discuss here, since I am asked to explain what the retired cardiac surgeon meant.
Since the 60s, large population studies have shown conclusively, that raised cholesterol levels was associated with an increased incidence of CAD. As a portion of the blood ( serum ) cholesterol comes from food, it made alot of sense that we should educate our patients to take less cholesterol rich food, in an attempt to lower or blood cholesterol and so our risk of heart disease. Blood cholesterol, in the medical eyes, is just one amongst many risk factors for CAD. The rest being cigarette smoking, hypertension, diabetes mellitus, obesity. The minor risk factors are gout, sedentary lifestyle, stress, etc, etc. No body is saying that cholesterol is the only risk factor for heart disease. The pharmaceutical industry, sensing an opportunity, had gone ahead to find drugs that will lower cholesterol effectively ( and they have with the "statins" ). With their high powered marketing, send out the message that cholesterol is all important and that we must reduce our cholesterol till it reaches ground zero ( or as low as possible ). They obviously have much to gain, if all of us do that. What is often not said , is the significant risk associated with too low a serum cholesterol level for that individual. Afterall, God did give us serum cholesterol for a purpose. Anyway, I am digressing.
So it became that serum cholesterol was almost made synonymous with the presence or absence of CAD. That is wrong. Afterall, almost 50% of people with heart attacks have a normal or below normal serum cholesterol level.
In the 80s, researchers began looking into this issue of inflammation as a cause of CAD. They looked at bacterial and virus infections as a cause of inflammation causing CAD, and came out blank, except for some association of dental infections and CAD. Bad oral hygiene can be associated with CAD. They were also trying to associate Rheumatoid Arthritis ( an inflammatory joint disease ) with CAD, and there is some association. Some research workers in USA, especially the group working around the Boston area, found that LDL-cholesterol, was itself a toxic agent in the artery wall, and it excites inflammation. This was easily shown in basic science research. The inflammation, under the microscope was obvious, and easily demonstrated. What we did not have in the 80s was a bedside way of identifying who was having inflammation and who was not.
Since the 80s, there was a blood test available for us to monitor our patients suffering for inflammatory joint disease call the C-Reactive Protein ( CRP ). When the C-Reactive Protein level was elevated, it meant that the joint condition ( be it SLE or Rheumatoid Athritis ), was flaring up and a relapse was coming. This allowed us to increase the steroid doses to lessen the inflammation and control the joint inflammation. So C-Reactive protein became a blood maker for inflammation. But CAD is not joint disease, although inflamed joint can trigger CAD.
The workers around the Boston area ( led by a researcher call Dr Paul Ridker ) is credited with measuring micro levels of CRP, in patients with CAD, without joint inflammation, and associated it with CAD. Infact his work was mainly to associate miro-CRP or what highly selective or highly sensitive CRP ( hS-CRP ), with heart disease and postulated that hS-CRP was another risk factor for heart disease.
Needles to say, waiting by the side are the pharmas, who have a drug to lower hS-CRP, and so lower heart disease. ( Remember my earlier article in this blog about the close relationship between physicians and pharmas ). So convenient. This was studied in a large clinical trial sponsored by Astra Zeneca, called the " JUPITER study ". On the basis of this study, they convince the FDA ( who I think did not need much convincing, with Pharmas behind prompting ), to add their indication that Rosuvastatin, the AZ drug that lowers serum cholesterol and hS-CRP, is indicated to lower hS-CRP.
What prompted this blog is a study, published in the September 28th issue of Circulation CVS Genetics, by a group of workers across the pond, namely University College, London UK, who showed that hS-CRP was variable and their baseline values varied according to race and ethnicity. You see, the background is that although the Boston group from this side of the pond believed heavily in hS-CRP, their colleagues on the other side of the pond, UK and Europe, do not quite share their enthusiasm. Yes, hS-CRP may have some association with CAD but not quite the same importance as stated by the Boston boys. It is just another risk factor, like cigarette smoking, not anymore important.
So the controversy goes on.
In our own experience, we see clinical kit out commercially, and every Tom, Dick and Harry is measuring hS-CRP, with varying degrees of accuracy. The results are so variable, that I could not rely on them for decision making. So in a way, I am on the side of the pond that says that hS-CRP is another risk factor and not the "critical " risk factor that some would like to make it out to be. It is so variable.
Maybe, it again raises the whole bigger issue of too close a relationship between physician and pharmas. Certainly, the conclusions of the " JUPITER study " was questioned and some differ strongly. Well, we are small fry, so will just conclude that hS-CRP makes inflammation and many things else, and is just another risk factor for CAD. By the way, all statins lower hS-CRP, to varying degrees.
And the controversies continues.