Coronary Biomarker Breakthrough: More hope for hearts

What’s your body’s most important muscle that never takes a lunch break or a mid afternoon snooze? You guessed it…it’s your heart! And a new study identified a gene coding for surface proteins located on arterial plaques, which may ultimately be used to prevent heart attack or stroke. The heart is in fact a muscle, made up of tissue that differs slightly from your biceps or hamstring muscles. Cardiac muscle tissue gracefully contracts in a synchronized manner, in response to an involuntary pathway resulting in an electrical impulse… And the heart beats! It should be in our best interest to exercise and protect our hearts. Cardiac research is of high priority in the medical field, as heart disease is the leading cause of preventable death worldwide.* Atherosclerosis, the hardening and thickening of the arteries (the formation of plaques) is a condition that if controlled, can significantly lower the risk of negative cardiac events. A recently published study in the journal of Cell Metabolism, based on research conducted at Columbia University Medical Center in Manhattan, has pinpointed the molecular process that can lead to harmful arterial plaque rupture. These findings came as a surprise to the university’s researchers because they discovered that not all ruptured plaque led to the same life threatening outcomes. While the majority of ruptured plaques will benignly pass through the vessels, about 2% form clots, block critical vessels resulting in stroke and or heart attack. The research conducted by Dr. Ira Tabas, M.D., Ph.D.’s lab pinpointed a specific gene marker that codes a potentially dangerous stress reaction pathway resulting in cell death. The study focused on the structures located at the core of arterial plaque. The core is comprised of cells that remain practically harmless until they necrose, causing the deterioration of the outer plaque wall, which ultimately bursts causing harmful clots. The gene involved in this stress reaction when turned off, or deleted, was found to quiet this type of cellular stress, thus resulting in the possible reduction of life threatening cardiac events. Dr. Ira Tabas believes that these findings will lead to the development of key tools for preventing, and soothing dangerous atherosclerotic plaques. It is widely accepted in the medical field that the majority of the population shows signs of atherosclerosis by the age of 20; clearly flagging the importance of the results of Dr. Tabas’ research and its huge potential impact on heart disease therapies...

What’s your body’s most important muscle that never takes a lunch break or a mid afternoon snooze? You guessed it…it’s your heart! And a new study identified a gene coding for surface proteins located on arterial plaques, which may ultimately be used to prevent heart attack or stroke.

The heart is in fact a muscle, made up of tissue that differs slightly from your biceps or hamstring muscles. Cardiac muscle tissue gracefully contracts in a synchronized manner, in response to an involuntary pathway resulting in an electrical impulse… And the heart beats! It should be in our best interest to exercise and protect our hearts. Cardiac research is of high priority in the medical field, as heart disease is the leading cause of preventable death worldwide.* Atherosclerosis, the hardening and thickening of the arteries (the formation of plaques) is a condition that if controlled, can significantly lower the risk of negative cardiac events.

A recently published study in the journal of Cell Metabolism, based on research conducted at Columbia University Medical Center in Manhattan, has pinpointed the molecular process that can lead to harmful arterial plaque rupture. These findings came as a surprise to the university’s researchers because they discovered that not all ruptured plaque led to the same life threatening outcomes. While the majority of ruptured plaques will benignly pass through the vessels, about 2% form clots, block critical vessels resulting in stroke and or heart attack.

The research conducted by Dr. Ira Tabas, M.D., Ph.D.’s lab pinpointed a specific gene marker that codes a potentially dangerous stress reaction pathway resulting in cell death. The study focused on the structures located at the core of arterial plaque. The core is comprised of cells that remain practically harmless until they necrose, causing the deterioration of the outer plaque wall, which ultimately bursts causing harmful clots. The gene involved in this stress reaction when turned off, or deleted, was found to quiet this type of cellular stress, thus resulting in the possible reduction of life threatening cardiac events.

Dr. Ira Tabas believes that these findings will lead to the development of key tools for preventing, and soothing dangerous atherosclerotic plaques. It is widely accepted in the medical field that the majority of the population shows signs of atherosclerosis by the age of 20; clearly flagging the importance of the results of Dr. Tabas’ research and its huge potential impact on heart disease therapies.
Current treatment for reducing the amount of plaque stuck to our arteries involves lowering “bad” cholesterol (LDL), and raising “good” cholesterol (HDL). Until recently, researchers believed these treatments might cure heart disease. However, clinical testing has revealed that certain HDL boosting drugs may not be the “holy grail” in preventing plaque rupture; but there is certainly hope for the favorable findings of Dr. Tabas’ research for controlling atherosclerosis.
While we may not see the immediate results of these findings in hospitals and clinics, we must keep in mind all of the recommended strategies to reduce the risk of heart disease.

*World Health Organization
For more information on Dr. Tabas’ study, visit Columbia University’s website.