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Saturday, October 12, 2002The media’s reporting of this particular study wasn’t much better. The Washington Post quoted the study’s lead researcher as saying, “The genetic combination plays a role in one-quarter of the cases of congestive heart failure diagnosed each year among blacks,” but the combination didn’t even count for one-quarter of congestive heart failure among the blacks in the study - it only accounted for 15 out of 78 cases, or almost one-fifth of cases. The study looked at the expression of genes that code for two cell receptors that regulate the action of norepinephrine. One gene was for the alpha2c adrenergic receptor found at the ends of nerve cells. This receptor inhibits the release of norepinephrine from the nerve ending. A defect or deletion in the gene means that the nerve cells release more norepinephrine. The other gene was for a receptor found on the surfaces of heart muscle cells, the beta1 adrenergic receptor. This receptor enhances the heart cell’s response to norepinephrine. The particular defect in the gene involved in the study creates a receptor that is hyperfunctional, causing the heart cells to hyper-respond to norepinephrine. Norepinephrine is one of those chemicals that the body produces in its “flight or fight” response. It increases the heart rate, makes muscles contract more forcefully and enhances the general state of alertness. The theory is that a person having both defective genes would have a doubly hyperactive heart. Now, heart failure can be caused by a number of diseases. The most common cause is damage from coronary artery disease. Other causes include viral infections, autoimmune disorders, alcoholism, hypertension, and the great umbrella category of idiopathic, which is a fancy way of saying “we have no idea.” In this particular study, the vast majority of the black patients (83%) had idiopathic heart failure. The majority of white patients (54%) had heart failure caused by coronary artery disease. Not surprisingly, more of the black patients than white patients had at least one of the gene mutations, since in the majority of cases they had no known cause for their heart failure, making it more likely to be caused by some malfunctioning of their cells. The double mutation occurred in only 2% of blacks and whites without congestive heart failure, but it occured in 19% of blacks with heart failure and only 4% of whites with heart failure. It hardly argues for a racial difference in genetic causes of heart failure, however. If the study had only included patients with idiopathic heart failure, regardless of race, the incidences of the mutations may have been the same. The results are interesting, though, in their implication for the treatment of heart failure, especially idiopathic heart failure. A lot of our treatment is already focused on decreasing the effects of norepinphrine on the cardiac cells, but this gives us a basis for predicting how some people might respond better to those treatments than others. If someone has the mutation for the nerve cell receptor, then they might respond better to drugs that inhibit nerve cell release of norepinphrine. Another patient with the muscle cell receptor mutation might respond better to beta-blockers, and someone with both might do best with both medications. It’s exciting to think that someday soon we’ll be able to design our therapy to complement our patient’s unique body chemistry. This is the true import of the study, not what it says about race. posted by Sydney on 10/12/2002 11:35:00 AM 0 comments 0 Comments: |
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