Heart Damage Treatments Arlington VA

During a heart attack, vessels that supply blood to the heart become blocked, preventing enough oxygen from getting through. The heart muscle dies or is permanently damaged.

Richard Hart, MD
(703) 241-1010
6400 Arlington Blvd
Falls Church, VA
Business
MSG of NOVA
Specialties
Cardiology

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Navid Kazemiashtiani, MD
Arlington, VA
Specialties
Cardiology
Gender
Male
Education
Medical School: Suny At Stony Brook Hlth Sci Ctr, Stony Brook Ny 11794
Graduation Year: 1996

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Todd Gregg Matros, MD
2201 Wilson Blvd Apt 1008
Arlington, VA
Specialties
Cardiology
Gender
Male
Education
Medical School: Tulane Univ Sch Of Med, New Orleans La 70112
Graduation Year: 1998

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Ambrish K Gupta
(703) 998-6666
611 S Carlin Springs Rd Ste 504
Arlington, VA
Specialty
Cardiology, Cardiovascular Disease

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Brian Neal Glick
(703) 671-2490
611 S Carlin Springs Rd
Arlington, VA
Specialty
Cardiology, Cardiovascular Disease

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Zia Moizuddin Ahmad, MD
(314) 729-1430
Arlington, VA
Specialties
Cardiology
Gender
Male
Education
Medical School: Dow Med Coll, Univ Of Karachi, Karachi, Pakistan
Graduation Year: 1982

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Thien Minh Do, MD
(703) 933-7060
611 S Carlin Springs Rd Ste 501
Arlington, VA
Specialties
Cardiology
Gender
Male
Education
Medical School: George Washington Univ Sch Of Med & Hlth Sci, Washington Dc 20037
Graduation Year: 1990

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Raymond R Hoare
(703) 525-8863
3833 N Fairfax Dr
Arlington, VA
Specialty
Cardiology, Cardiovascular Disease

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Ambrish Kumar Gupta, MD
(703) 998-6666
611 S Carlin Spring Rd Pat 504
Arlington, VA
Specialties
Cardiology
Gender
Male
Education
Medical School: Christian Med Coll, Punjab Univ, Ludhiana, Punjab, India
Graduation Year: 1981

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M Rafiq Zaheer, MD
(703) 933-0700
611 S Carlin Springs Rd Ste 201
Arlington, VA
Specialties
Cardiology
Gender
Male
Education
Medical School: Avicenna State Med Inst Of Kabul, Fac Of Med, Kabul, Afghanistan
Graduation Year: 1981

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Heart Damage Treatments

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Doctors have been unable to help injured heart tissue renew itself after a heart attack -- until now.

During a heart attack, vessels that supply blood to the heart become blocked, preventing enough oxygen from getting through. The heart muscle dies or is permanently damaged.

But researchers at Children's Hospital Boston report progress toward someday being ale to regenerate heart tissue after a heart attack or heart failure and even in children who are born with congenital heart defects.

In a study on mice, they showed that neuregulin 1 (NRG1), a growth factor involved in the development of the heart and nervous system, can fuel heart-muscle growth and recovery of cardiac function when injected after a heart attack.

This is a significant development because coronary heart disease, which causes heart attack and angina, is the leading cause of death in America.

After birth, heart-muscle cells stop dividing and proliferating. But experts, led by Dr. Bernhard Kuhn and Kevin Bersell of the cardiology department at Children's, restarted the cell cycle with NRG1, spurring the heart-muscle cells to divide and make copies of themselves.

When the team injected NRG1 into live mice once a day for three months after the animals had heart attacks, heart regeneration increased and the pumping function improved, compared with untreated mice.

In addition, the NRG1-injected mice did not show some common aftereffects of heart failure.

The study, funded by the cardiology department at Children's Hospital Boston, the Charles Hood Foundation and the American Heart Association, found that cell growth does not have to come from stem cells. A report on the research appears in the July 24 issue of Cell.

"Although many efforts have focused on stem cell-based strategies, our work suggests that stem cells aren't required and that stimulating differentiated cardiomyocytes [heart-muscle cells] to proliferate may be a viable alternative," Kuhn, the study's senior investigator, said in a news release from the hospital.

More information

The American Heart Association has tips on maintaining a healthy heart.

SOURCE: Children's Hospital Boston, news release, July 23, 2009

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