A recent study provides new insights regarding the use of trientine (TETA), a copper chelator traditionally used to treat copper overload conditions such as Wilson’s disease, in the treatment of heart disease.
It reports that low dose TETA therapy restores copper levels and improves heart function while high doses are detrimental.
Heart disease remains the leading cause of death throughout the world.
Myocardial ischemia occurs when the heart muscle (myocardium) does not receive enough oxygen to function normally.
Cardiac hypertrophy is an abnormal enlargement of the heart in response to pathophysiological events.
Both ischemia and hypertrophy are accompanied by structural and functional changes in the heart that include loss of copper.
Studies in animal models have shown that copper replenishment reverses the structural and functional alterations that occur in the ischemic or hypertrophic heart.
In addition, patients treated with TETA exhibit normal cardiac copper levels and improved heart function.
The beneficial increase in cardiac copper levels is paradoxical because TETA is a copper chelator and removes copper from cells/tissues.
Ascertaining the mechanism by which TETA increases cardiac copper levels would improve therapy for patients with cardiac ischemia or hypertrophy.
In the current study, the team examined the effects of TETA treatment in an animal model of cardiac hypertrophy. Lower doses of TETA delivered copper selectively to the hypertrophic heart.
The functional lower dose did not alter copper levels in other organs or the normal heart. In contrast, higher doses further reduced copper content in the hypertrophic heart.
Both low and high doses reduced copper concentrations in the blood.
Since most patients with ischemic or hypertrophic heart suffer from an elevated copper level in the blood and reduced copper content in the heart, this simple and safe treatment with low dose TETA is an approach of ‘kill two birds with one stone’.
This would help to develop alternative approaches to treat patients with ischemic heart disease.
The study was led by Dr. Y. James Kang, a professor at Sichuan University West China Hospital in Chengdu, China and the Memphis Institute of Regenerative Medicine at University of Tennessee.
The study is published in Experimental Biology and Medicine.
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Source: Experimental Biology and Medicine.
