News tips from the 2005, 54th Annual Scientific Sessions of the American College of Cardiology
MODERN IMPLANTABLE HEART DEVICES SAFE FOR USE IN MRI SCANS
(Embargoed for release at 9 a.m. ET, Tuesday, March 8; Poster presentation #1116-58, Hall E1, Orange County Convention Center.)
Johns Hopkins scientists have found that modern, implanted heart devices – such as pacemakers and defibrillators – are safe for use in magnetic resonance imaging (MRI) machines, a diagnostic and imaging tool long ruled potentially unsafe and off-limits for more than 2 million Americans who currently have them in their bodies. The Hopkins team has also developed new guidelines for their use, making MRI scans more available to people who might benefit from early detection of cancer and other diseases, when treatments are most likely to succeed, and for guiding devices during minimally invasive surgery.
During a four-month period, the Hopkins team tested 18 different pacemakers and 15 implantable defibrillators previously found safe in animal experiments. In a study of 33 patients undergoing 38 separate scans, the researchers adjusted the device's pacing program and lowered MRI sequence energy levels to see if the scan affected the settings or caused any other kind of problem, such as heating of the electrical leads and surrounding tissue. All patients and devices were closely monitored during the scans, some of which lasted up to 1.5 hours, and repeat measurements were made on average 24 days after the MRI to measure any long-term complications. No ill effects were observed. The only complaint cited was claustrophobia, which is commonly associated with the close confines of the MRI scanner.
The researchers' new guidelines caution that only modern devices, predominantly models from the last seven years, are safe in MRIs and call for low-energy-level scans, avoiding scan settings higher than 2 watts per kilogram, which might lead to overheating. The protocol also advises close monitoring by a cardiologist and a radiologist, and using MRIs only when clinically necessary and when alternative diagnostic tests are not recommended.
Evaluation of a safety protocol for clinically indicated magnetic resonance imaging of patients with permanent pacemakers and implantable defibrillators at 1.5 Tesla. Saman Nazarian, Ariel Roguin, Menekhem Zviman, Albert Lardo, Timm Dickfield, Ronald Berger, David Bluemke, and Henry Halperin.
DISRUPTED FAT CELL SIGNALING IN OBESE MICE LINKED TO INCREASED CELL DEATH IN ENLARGED HEARTS
(Embargoed for release at 4:15 p.m. ET, Tuesday, March 8; Abstract presentation #860-4, Room 230-B, Orange County Convention Center.)
Disrupted fat cell signaling in obese mice has been linked to increased cell death, or apoptosis, in enlarged hearts. According to the Johns Hopkins researchers who led the study, the research is needed to understand how obesity contributes to enlarged hearts (hypertrophy), subsequent heart failure and increased risk of death.
"The work also suggests a biological route for potential therapies that could block or reverse obesity's harmful effects on the heart," says lead investigator and cardiologist Lili Barouch, M.D., an assistant professor at The Johns Hopkins University School of Medicine and its Heart Institute.
The researchers studied heart muscle enlargement and cell death in more than 20 male and female mice, some normal and others inbred for obesity due to changes in the amount and function of the hormone leptin. Some mice were leptin deficient, while others had nonworking leptin receptors. Made by fat cells, leptin regulates appetite and energy balance. Normally, greater quantities of leptin are released from fat cells when an animal is "full," as a signal to stop eating, but the signal is blocked in obesity. Comparison of heart tissue samples from obese mice and normal mice showed that when leptin signaling was disrupted, the hearts became enlarged and apoptosis increased by more than 10 times what occurs in normal tissue. When leptin levels and function were restored, apoptosis activity returned to nearly normal levels.
Cardiac myocyte apoptosis is associated with left ventricular hypertrophy in murine models of obesity. Lili Barouch, Daquing Gao, Lei Chen, Shakil Khan, Shubha Raju, Koenraad Vandegaer, Christopher O'Donnell, Dan Berkowitz, Chiming Wei, and Joshua Hare.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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