Clinical cardiologists well know the fact that up to 40% of patients with documented coronary artery disease (CAD) have normal cholesterol values. The cholesterol and lipid assay, though helpful, is not sensitive enough to detect abnormalities in lipid metabolism at the level of the coronary artery. Since 1995, studies have pointed to an inflammatory component as a cause of CAD. Some agent causes the cells that make up the cell wall of the coronary artery to become inflamed or irritated. Some think bacteria or viruses incite this inflammatory process. Whatever the cause, the body notices the damage and sends specialized blood cells to destroy the foreign substance and then repair the damage. However, this process itself causes further compromise of the coronary artery lumen. The damage culminates in a tear or dissection of the coronary artery wall. This releases the lipids within the wall. The blood cells, when it detects the lipids released into the blood, respond by clotting. This culminates in blockage of the entire lumen resulting in a heart attack.
Yet in 40% of people with this process going on, have “normal” cholesterol values. Dr. Richter in 1997 published in the New England Journal of Medicine a common assay used to measure inflammation—the CRP (C-Reactive Protein)—if measured in tiny increments can detect ongoing coronary artery inflammation even when cholesterol values are normal. CRP in medical terms is called an acute phase reactant: a protein in blood that rises when inflammation or infection is actively going on. CRP has been used by doctors since 1950s to measure progress of antibiotic treatment on an infection. If the CRP is going down, then the antibiotic regimen is working. If the CRP continues to rise, the antibiotic regimen chosen is not working and a change is warranted. CRP is usually measured 1-500 pg/ml.
Dr. Richter used CRP not in the 100s but only in the range of 0-5 pg/ml. This Ultrasensitive CRP was measured in patients with already documented CAD. He noticed that people who have documented CAD and have normal cholesterol values who also have elevated values of Ultrasensitive CRP went on to have future coronary events. Those patients with CAD with normal cholesterol values who have low Ultrasensitive CRP tended not to end up having as many coronary events. He, therefore, recommended patients with documented CAD to be followed with Ultrasensitive CRP especially when they have normal cholesterols. What is not known is if the Ultasensitive CRP is brought down, does this then reduce the chances of the coronary event occurring in the future? This will need to be proven with clinical research.
Dr. Nanavati has been using Ultrasensitive CRP assay on all his patients with CAD since 1999.