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Free radicals may be good for you

Fear of free radicals may be exaggerated, according to scientists from the Swedish medical university Karolinska Institutet. A new study, published in the Journal of Physiology, shows that free radicals act as signal substances that cause the heart …

Gene for cellular receptors could be key for lower heart risk

People with a certain form of a gene that influences blood flow may have a lower risk of having a heart attack and dying from heart disease, according to a new study in today’s rapid access issue of Circulation: Journal of the American Heart Association. The gene controls variations in beta-2 adrenergic receptors, which are on the surface of heart muscle cells and blood vessel cell walls. When activated by adrenaline and noradrenaline, these receptors set in motion a series of events that dilate the blood vessels and increase heart rate.

Mechanical Support Induces Genetic Changes in Failing Hearts

Using new DNA microarray technology, researchers have found significant changes in the expression pattern of hundreds of genes in heart muscle cells after mechanical pumps are used to take over from failing hearts. This finding represents a first step, they say, in a line of research that could help predict how heart failure patients will respond when supported by a left ventricular assist device (LVAD). These devices are employed when the heart’s left ventricle — the chamber of the heart that pumps blood throughout the body — is too weak to pump enough blood to nourish the body’s tissues. They have been used as successful short-term “bridges to heart transplant” and are increasingly being considered as long-term heart failure destination therapy, also known as “bridge to recovery.”

Vitamin C transforms mouse stem cells into heart muscle cells

Vitamin C helped convert mouse embryonic stem cells growing in the laboratory to heart muscle cells, researchers report. This basic-research discovery could lead to future research on ways to treat people suffering from damaged heart muscle. “Although the findings of this study are very preliminary with respect to their impact on human lives, this line of research has enormous implications for the future care of thousands of patients who develop heart failure each year,” says Robert O. Bonow, M.D., president of the American Heart Association.

Mutation Causes Specific Arrhythmia and Sudden Cardiac Death

An international team of researchers has demonstrated a genetic basis for a fatal form of inherited cardiac arrhythmia that usually strikes young, seemingly healthy people. Basing their research on a French family with a form (Type 4) of inherited Long QT Syndrome (LQTS) and experiments in mice, the researchers found the mutation in a specific gene encoding ankyrin-B, a protein within heart muscle cells. Their discovery identifies what appears to be a novel mechanism for cardiac arrhythmia.

Defective Trigger for Muscle Growth, Survival Implicated in Heart Failure

Researchers have determined the molecular machinery that triggers normal cardiac muscle growth and survival, and have linked defects in this complex to an inherited form of human cardiomyopathy, a type of heart failure where an enlarged heart loses its ability to pump blood. Published in the December 27, 2002 issue of the journal Cell, the study also identifies a subset of German cardiomyopathy patients with a specific gene mutation that disrupts the heart muscle’s normal stretch activity. This mutation has apparently been passed down through several generations of Northern Europeans.