What is the relationship between serotonin and heart valve disease?

Researchers in the United States have found that serotonin affects the mitral valve of the heart and can cause valvular heart disease.

Serotonin affects the mitral valve of the heart, potentially Heart disease Known as degenerative mitral regurgitation, according to a new study led by researchers at Columbia University Surgery in collaboration with the Children’s Heart Valve Center at Children’s Hospital of Philadelphia (CHOP), the University of Pennsylvania, and the Valley Hospital Heart Institute. increase. we.

Serotonin It binds to specific receptors on the cell surface and signals the cell to act accordingly. A protein known as the serotonin transporter (SERT or 5-HTT) moves serotonin into the cell for reuptake and reuse. This process is known as serotonin reuptake.

Degenerative mitral regurgitation (DMR) is one of the most common types of heart valve disease. The mitral valve is located between the left atrium and left ventricle of the heart. When the heart contracts, it closes tightly to prevent blood from flowing back into the left atrium.

This image shows the mitral valve of a mouse heart lacking the serotonin transporter (SERT) gene. Valves were stained with plicosirius red to show collagen. SERT knockout mice had thicker mitral valves compared to normal mice. (Credit: Columbia University Irving Medical Center)

DMR distorts the shape of the mitral valve and prevents it from closing completely. This allows blood to leak in the opposite direction. lung (reflux), which limits the amount of oxygen-rich blood that moves through the heart to the rest of the body.

researchers published in Science Translational Medicinestudied live mouse model using transgenic mice lacking insert Genetic mouse and normal mouse. They are, insert The gene developed thicker mitral valves, and normal mice treated with high-dose SSRIs also developed thickened mitral valves.

Using genetic analysis, we identified a genetic variant that affects SERT activity in the SERT gene region 5-HTTLPR. They found that a ‘long’ mutant of 5-HTTLPR reduced the activity of her SERT in mitral valve cells. This is especially noticeable when he has two copies (one maternal and one paternal). DMR patients with the “long-long” variant required mitral valve surgery more frequently than those with other variants.

Mitral valve cells from DMR patients with the “long-long” variant tended to respond to serotonin by altering mitral valve shape and producing more collagen. Mitral valve cells with the ‘long-long’ variant of were more sensitive to fluoxetine than those with other variants.

This study shows that in patients with DMR who have the “long-long” variant, taking SSRIs reduces SERT activity in the mitral valve. The researchers proposed to test whether a DMR patient might have low SERT activity by genotyping her 5-HTTLPR. This can be easily determined from DNA samples obtained from blood or mouth swabs.

“Evaluating decreased SERT activity in patients with DMR may help identify early those patients who need mitral valve surgery,” said Dr. Giovanni Ferrari of Surgery, Columbia University. Prompt repair of the mitral valve can protect the heart and prevent congestive heart failure.”

Cells from healthy human mitral valves were not adversely affected by normal doses of SSRIs or the “long-long” variant.

“A healthy mitral valve can probably withstand low SERT activity without deformity,” explained Ferrari. “Low SERT is unlikely to cause degeneration of the mitral valve itself. Once the mitral valve begins to degenerate, it may become more susceptible to serotonin and low SERT.”

Additional studies are investigating whether patients with DMR who respond well to SSRIs need to be seen regularly to assess the progression of mitral valve degeneration, and whether patients who are poor responders to SSRIs need to be seen at lower doses of SSRIs. It may help determine whether switching to a non-SSRI antidepressant should be considered instead of increasing. SSRIs.

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