THE ESSENTIAL
- Symptoms of mitral insufficiency are fatigue, shortness of breath, difficulty breathing, cough with reddish sputum and palpitations.
- Currently, there is no treatment for mitral valve degeneration. If it becomes serious, it is possible to perform an operation to repair or replace it.
- The mitral valve is located between the left atrium and the left ventricle of the heart. When healthy, it closes tightly when the heart contracts to prevent blood from flowing back into the left atrium.
Mitral regurgitation, also called degenerative mitral regurgitation (DMR), is one of the most common forms of heart valve disease. It is characterized by a deformation of the heart valve which prevents it from closing completely. This results in a backflow of blood, disrupting blood circulation.
Researchers from Columbia University, in partnership with teams from the Children’s Hospital of Philadelphia, the University of Pennsylvania and the Valley Hospital Heart Institute, have discovered a link between serotonin and this cardiac pathology.
Mitral insufficiency: serotonin can aggravate the disease
For this study, the medical files of more than 9,000 patients who had heart surgery due to mitral insufficiency were analyzed. In addition, the researchers studied 100 mitral valve biopsies.
“By studying data from these patients, we found that taking a Selective Serotonin Reuptake Inhibitor (SSRI, antidepressants that increase serotonin levels) was associated with severe mitral regurgitation that needed to be treated with surgery at a younger age than for patients not taking SSRIs”, explains Professor Giovanni Ferrari of Columbia University, author of the study.
The researchers also studied transgenic mice lacking the gene SERT (gene that affects the activity of serotonin transporter) and therefore having high levels of serotonin. They also observed rodents receiving large doses of antidepressants.
They discovered that animals without genes SERT developed thicker mitral valves. The same was true for those treated with SSRIs.
In addition, they succeeded in identifying the region of the gene SERT which had an impact on the activity of the protein capable of managing serotonin. “Long” 5-HTTLPR Mutation Reduces SERT Protein Activity in Mitral Valve Cells”, they write. The effect is even greater if the patient has two copies (maternal and paternal). “Patients with RMD who had the ‘long-long’ type frequently required mitral valve surgery”they specify in their study published in the journal Science Translational Medicine.
Mitral valve cells from patients with RMD with the “long-long” variant were more likely to respond to serotonin by producing more collagen, changing the shape of the mitral valve. Moreover, those with the “long-long” variant of 5-HTTLPR were more sensitive to fluoxetine (SSRI treatment) than cells with other mutations.
Additional tests for patients with the offending mutation?
For the researchers, it would be interesting to carry out a genetic test for patients suffering from degenerative mitral regurgitation. “Assessing patients with RMD for low SERT activity may help identify patients who may need mitral valve surgery sooner”, the Pr Giovanni Ferrari estimates. “Fixing a badly leaking mitral valve quickly would protect the heart and could prevent congestive heart failure.”he explains.
Furthermore, his team did not find any negative effect with SSRIs or the “long-long” mutation on healthy human mitral valves. “A healthy mitral valve can presumably withstand low SERT activity without becoming deformed. It is unlikely that low SERT on its own can cause mitral valve degeneration. SSRIs are generally safe for most patients”, he adds. On the other hand, “once the mitral valve begins to degenerate, it may be more responsive to serotonin and low SERT”he warns.
Additional studies will be carried out to determine whether patients with mitral insufficiency should be monitored more regularly or whether it is preferable to consider other types of psychotropic treatments.
