Try our beta test site
IMPORTANT: Listing of a study on this site does not reflect endorsement by the National Institutes of Health. Talk with a trusted healthcare professional before volunteering for a study. Read more...

Calcium Current in Human Heart Cells

This study is currently recruiting participants. (see Contacts and Locations)
Verified August 2016 by Emory University
Information provided by (Responsible Party):
Michael Davis, Emory University Identifier:
First received: October 24, 2005
Last updated: August 3, 2016
Last verified: August 2016
The study team will use small pieces of human hearts which are removed as part of a required surgical procedure to study how calcium ions pass through the membrane of heart cells in order to tell the heart cell how much force to contract with when the heart beats. Investigators will also study the proteins and RNA of these pieces to determine how the newborn heart cells control their force of contraction differently from adult heart cells. Investigators hypothesize that infant hearts have different regulation of calcium entry than adult hearts.

Congenital Heart Disease
Tetralogy of Fallot

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Prospective
Official Title: Calcium Current in Human Atrial Myocytes

Resource links provided by NLM:

Further study details as provided by Emory University:

Primary Outcome Measures:
  • Calcium Current Measures [ Time Frame: Duration of Study (Up to 13 Years) ]
    Calcium currents including transients and modulation of calcium handling by activation of different pathways in isolated cells from waste tissue obtained at the time of surgical repair for CHD will be measured for the duration of the study.

Biospecimen Retention:   Samples Without DNA
tissue obtained from surgical waste tissue

Estimated Enrollment: 600
Study Start Date: April 2005
Estimated Study Completion Date: July 2017
Estimated Primary Completion Date: July 2017 (Final data collection date for primary outcome measure)
Detailed Description:

Extrapolating pharmacological and surgical therapies from adult (AD) studies to infant (INF) patients is problematic because the knowledge of cellular electrophysiology and molecular biology of human INF heart cells is limited. The investigators have studied developmental differences in rabbit ventricular cells and now extend these studies to atrial and ventricular cells isolated from AD, young adult (YAD) or INF patients.

The study aims are as follows:

  1. Developmental differences in transient outward current of atrial cells. Investigators will extend their studies to isolated cells and tissue from YADs (age 14-20). In addition, several other accessory beta-subunits have been found in cardiac myocytes and may interact with Kv channels and regulate the function of these channels. The study team will determine relative amounts of these putative regulators of human atrial Ito to determine which correlate with developmental changes in Ito kinetics.
  2. Developmental differences in amplitude and regulation of calcium current in atrial cells. Investigators hypothesize that INF atrial cells have tonic inhibition of adenylyl cyclase (and thus of ICa) mediated by inhibitory G proteins, possibly related to constitutive activity of the adenosine A1 receptor, and that, compared to AD or YAD cells, have greater sensitivity to inhibitors of phosphatases and phosphodiesterases, and that developmental changes in basal ICa amplitude and beta-sympathetic modulation correlate with inhibitory G protein levels, receptor numbers for M2 and A1 receptors, and constitutive inhibitory activity.
  3. Modulation of atrial cell calcium transients by changes in AP waveform and developmental age. The study team will test the hypothesis that prolongation of the early repolarization phase of the AP increases Ca2+ entry and that YAD cells have faster removal of Ca2+ from cytoplasm than INF cells and will determine if the Na- Ca2+ exchange current (INCX) is greater in INF vs. AD or YAD cells.
  4. Developmental differences in Ca current and transients and contractility in ventricular cells. Investigators propose that INF cells and tissue have lower basal ICa, lower potency for ISO stimulation, higher levels of Gialpha3 and A1 receptors, greater inhibitory potency for adenosine, and tonic inhibition of ICa. We also propose that the YAD cells have lower levels of NCX and lower INCX, higher levels of SERCA and faster removal of Ca2+ from the cytoplasm. Previous animal studies have indicated various developmental changes in cardiac cells. We will specifically study human postnatal developmental changes in Ito, regulation of ICa and intracellular Ca2+ transients.

Ages Eligible for Study:   up to 18 Years   (Child, Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population
Children undergoing surgery for repair of congenital heart disease

Inclusion Criteria:

  • Patients undergoing cardiopulmonary bypass surgery

Exclusion Criteria:

  • Prior cardiac surgery
  • History of atrial fibrillation or other atrial arrhythmias prior to operation
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its identifier: NCT00243776

Contact: Michael E Davis, PhD 404-727-9858
Contact: Janet Fernandez, RN 4047851731

United States, Georgia
Emory University School of Medicine Recruiting
Atlanta, Georgia, United States, 30322
Principal Investigator: Mary B Wagner, PhD         
Sponsors and Collaborators
Emory University
Principal Investigator: Michael E Davis, PhD Emory University
  More Information

Responsible Party: Michael Davis, Associate Professor, Emory University Identifier: NCT00243776     History of Changes
Other Study ID Numbers: IRB00005500
NIH R01HL077485
Study First Received: October 24, 2005
Last Updated: August 3, 2016

Additional relevant MeSH terms:
Heart Diseases
Heart Defects, Congenital
Tetralogy of Fallot
Cardiovascular Diseases
Cardiovascular Abnormalities
Congenital Abnormalities processed this record on April 21, 2017