Drug May Cut Aneurysm Risk for Heart Defect Patients
The drug doxycycline delays dangerous aneurysm rupture in mice genetically engineered to have many of the clinical features of humans with Marfan syndrome, says a U.S. study.
In Marfan syndrome, a genetic flaw causes the walls of the heart's major arteries to weaken.
Thoracic aneurysms are the main cardiovascular complication in Marfan syndrome patients. This study found that doxycycline -- a non-specific matrix metalloproteinases (MMP) inhibitor -- blocked the proteins that break down the aorta and significantly delayed aneurysm rupture, tears and bleeding.
The researchers also found that doxycycline reduced elastin degradation and expression of two MMPs -- MMP-2 and MMP-9 -- believed to play an important role in aneurysms.
The Marfan syndrome mice who received doxycycline in their drinking water lived nearly twice as long as mice who did not receive doxycycline.
The study was to have been presented Saturday in Baltimore at the annual meeting of the Society for Vascular Surgery.
In the past, beta blockers have been used to lower blood pressure and slow the heart rate in an attempt to delay the aorta's enlargement, study author Dr. B. Timothy Baxter, a professor in the department of surgery at the University of Nebraska Medical Center in Omaha, said in a prepared statement.
However, beta blockers provide only modest benefit to patients and the side effects caused by drugs have a negative impact on a patient's quality of life.
"In patients with Marfan syndrome, the need for surgical intervention is determined by following the aortic enlargement with ultrasound or CT scans done at six- to 12-month intervals, until a specific threshold of growth is reached when surgery is recommended. This approach of watchful waiting is unsettling and stressful for patients," Baxter said.
He said more research is needed to determine whether treatment with doxycycline can delay or prevent the need for surgery in Marfan syndrome patients
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