(PHILADELPHIA) -- The following summaries are based on presentations by Thomas Jefferson University researchers at the American College of Cardiology’s (ACC) 56th Annual Scientific Sessions in New Orleans.
Outpatient Medication Usage Not Associated with Anemia in Patients Admitted with Decompensated Heart Failure.
(Embargoed for release 9 am, Tuesday, March 27; Abstract #1028-68)
Although anemia is a common problem in heart failure patients, the medications the patients take to control their heart failure are not the cause of the anemia, according to researchers at Jefferson Medical College. Nor do they make the anemia any better or worse.
In a retrospective study of 759 patients with severe heart failure who were admitted to Thomas Jefferson University Hospital in Philadelphia between 2004 and 2005, the researchers determined that “in contrast to recent studies,” there is no significant relationship between outpatient heart failure medications and anemia.
Patients in the study were taking many varieties of prescription medications to control their heart failure condition. They included ACE-inhibitor/angiotensin receptor blockers, beta blockers, aldosterone antagonists or loop diuretics. By analyzing a number of measures, including hemoglobin concentration (the component of red blood cells that carry oxygen) which determines the severity of the anemia, the researchers found no significant difference between these medications and their affect on a patient’s anemia.
They conclude that despite the fact that many patients who suffer from severe heart failure also have anemia, the medications the patients take to control their anemia have no effect on the patient’s heart failure.
Members of the team who conducted this study at Thomas Jefferson University in Philadelphia, Pa., are:
Saum Shamimi-Noori, M.D.,
Emmanuel D. Chryssos, M.D., Stephanie Cho, Abhijit Dasgupta, Ph.D,
Suzanne Adams, R.N., MPH; Jocelyn Andrel, Paul Mather, M.D.,
Sharon Rubin, M.D. and David Whellan, M.D.
Beta Blocker Dose Adjustment upon Hospitalization for Acute Decompensated Heart Failure.
(Embargoed for release 9 am, Tuesday, March 27; Abstract #1028-66)
When a patient with chronic heart failure is admitted to the hospital, it is likely that she or he is already on a beta blocker therapy. Yet the role of these medications in the patient’s length of stay (LOS) as well as a treatment for her or his condition remains unclear.
To clarify the situation, researchers at Jefferson Medical College conducted a retrospective study of patients who were admitted to Thomas Jefferson University Hospital with severe heart failure (ADHF) in 2004 and 2005 and who were on outpatient beta blocker therapy.
They found:
- Blood pressure was a significant predictor of beta blocker dose reduction or cessation.
- Patients whose beta blocker dose was reduced or stopped had a significantly increased LOS.
- Patients who were admitted to the Family Medicine service were more likely to have their beta blocker stopped or decreased than those who were admitted to the Cardiology service.
In conducting the research, the daily outpatient dosage was compared to the inpatient dose on the first day of admission and analyzed for numerous associations including dosage changes admitting specialty and LOS.
Of 464 patients, 84 percent were continued on a beta blocker during the first day of their hospitalization. Most--96 percent--were continued on their outpatient dosage. In those cases where the beta blocker remained the same, 41 percent had dose decrease, 50 percent continued their outpatient dose and nine percent had their dose increased.
The researchers suggest that physicians who are caring for hospitalized chronic heart failure patients who are already on a beta blocker regimen when hospitalized, should weigh the benefits of reducing or stopping the beta blocker. Those patients whose initial inpatient beta blocker dose was reduced or stopped had a significantly increased LOS suggesting that it may be detrimental to decrease outpatient beta blocker dosage upon hospitalization for ADHF.
Members of the team who conducted this study at Thomas Jefferson University in Philadelphia, Pa., are:
Saum Shamimi-Noori, M.D.,
David Whellan, M.D.,
Abhijit Dasgupta, Ph.D,
Suzanne Adams, CRN,
Paul Mather, M.D.,
Sharon Rubin, M.D.,
Jocelyn Andrel and
Arthur Feldman, M.D., Ph.D.
Extracellular Matrix Protein, Fibulin-2, Enhances Acute Wound Healing After Experimental Myocardial Infarction in Mice
(Embargoed for release 10 am, Tuesday, March 27; Abstract #1025-75)
After surviving a heart attack, a big issue for a patient is the healing of the wound. Researchers at Thomas Jefferson University and Alfred I. DuPont Hospital for Children have found something that may help; they’ve identified a protein that contributes to the wound healing process after a heart attack.
The researchers will present the study at the American College of Cardiology’s 56th Annual Scientific Session in New Orleans on March 27 at 10 am (abstract 1025-75).
They used mice to examine the role of Fibulin-2, an extracellular matrix protein, to better understand its role in wound repair. Fibulin-2 is naturally occurring in embryonic development as well as in tissue remodeling after various injuries.
Extracellular matrix, which embraces and connects cells within the tissue, may provide structural integrity during tissue remodeling after injury, but little is known about its functional aspects.
By comparing the results of heart attacks in mice that did not have the Fibulin-2 protein with normal mice at both 24 and 72 hours after the heart attack, the researchers found that acute wound healing was significantly delayed in the mice lacking Fibulin-2. After 72 hours, they found that the damaged (infarct) area was much larger in the mice lacking Fibulin-2.
The researchers found that the wound healing process was much slower in the mice lacking Fibulin-2 after a heart attack due to delayed scar tissue formation in the damaged area. The study demonstrated that Fibulin-2 facilitates heart wound healing probably with the help of (TGF)-?, a growth factor that promotes wound healing.
The researchers are also currently looking into the role of Fibulin-2 as a factor in the development of chronic heart failure.
Members of the team who conducted this study at Thomas Jefferson University in Philadelphia, Pa., and Alfred I DuPont Hospital for Children in Wilmington, Del., are:
Takeshi Tsuda, M.D.;
Erhe Gao, M.D., Ph.D.;
Francois X. Sicot, Ph.D.;
Hailong Dong, M.D., Ph.D.;
Dessislava Markova, Ph.D.,
Xinliang Ma, M.D., Ph.D. and
Mon-Li Chu, Ph.D.