NATIONAL HARBOR, MD. – Testing to identify mutations in the gene that codes for the muscle protein titin is now a reasonable step in routine clinical practice for selected people with either early-onset atrial fibrillation (AFib) or a family history of atrial fibrillation, or other cardiac disorders that have been strongly linked with titin-gene mutations, Patrick T. Ellinor, MD, said at the annual International AF Symposium.

Every third death worldwide is due to cardiovascular disease. What happens on the cellular level, however, is still barely understood. Bayer researchers are collaborating with scientists from the renowned Broad Institute of MIT and Harvard to find out what goes on during this process. In the long term, this research could open new avenues of exploration that will lead to new medications.

Mutations in TTN, a gene associated with several forms of heart disease and heart failure, may also play key roles in early form of a common heart arrhythmia.

Atrial fibrillation (Afib), a heart condition that causes a rapid, irregular heartbeat that increases a person’s risk of stroke and heart failure, is fairly common among older adults. A nationwide research team, led by scientists at the Broad Institute of MIT and Harvard and Massachusetts General Hospital, has found a strong relationship between early-onset Afib and mutations that break TTN, a gene that helps maintain the structure of heart muscle.

Massachusetts General Hospital cardiologists led a population-based genome-wide association analysis (GWAS) of individuals with HF that yielded multiple genetic mechanisms for established risk factors. Moreover, phenotypic refinement of the analysis allowed the team to discover novel genetic signals that correlate with distinct subtypes of HF.

Massachusetts General Hospital’s Dr. Patrick Ellinor will lead the work at the Broad’s precision cardiology lab.BROAD INSTITUTE It’s the leading...

In this video for MGH’s Advances in Motion series, Dr. Ellinor discusses his team’s recent work leveraging genome-wide association studies to identify over 100 different genetic determinants of atrial fibrillation, and his hope of using those variants to develop new drugs to treat atrial fibrillation in the years to come.

Patients with atrial fibrillation (AF), a condition causing a rapid, irregular heart rate that can increase the risk of stroke, could use some new treatment options. Despite how common the condition is, the current treatment options don’t always work.

Macrophages have a previously unrecognized role in helping the mammalian heart beat in rhythm. Researchers have discovered that macrophages aggregate around central cardiac cells that regulate electrical impulses within the mouse heart, helping the cells conduct electricity. Mice that were genetically engineered to lack macrophages have irregular heartbeats, hinting that these immune cells may also play a role in heart disease.