Coronary Artery Disease Mechanisms in High Risk Families--Racial Difference

This study has been completed.
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00005369
First received: May 25, 2000
Last updated: June 23, 2005
Last verified: April 2002
  Purpose

To examine whether differences existed between asymptomatic white and African Americans known to be at high risk for premature coronary artery disease (CAD) in risk factor distributions, prevalence of occult coronary disease, and mechanisms of coronary disease expression.


Condition
Cardiovascular Diseases
Coronary Disease
Heart Diseases

Study Type: Observational

Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: September 1992
Estimated Study Completion Date: August 1996
Detailed Description:

BACKGROUND:

The investigators hypothesized that increased platelet activation and coronary artery vasoconstriction exist in African Americans, due to greater vascular endothelial dysfunction, heightened adrenergic drive, and greater vascular reactivity, resulting in excess sudden death and the occurrence of myocardial infarction in people with less severe angiographic coronary disease.

The study was one of eight grants awarded as part of the Request for Applications "Mechanisms Underlying Coronary Heart Disease in Blacks". The initiative was released in October 1991 and awarded in September 1992.

DESIGN NARRATIVE:

Previous studies had demonstrated high prevalences of coronary disease risk factors and occult coronary disease in this sibling population. Subjects were recruited to come for a one day screening, with measurement of coronary disease risk factors (blood pressure, smoking, lipid profile, apolipoproteins B and A1, lipoprotein(a), blood glucose, insulin, and fibrinogen), and a maximal treadmill test with tomographic thallium imaging to identify occult coronary disease. Platelet function was assessed by spontaneous in-vitro aggregation, activated IIa/IIIb receptor density, and serum thromboxane B2 concentration. Factors contributing to sudden cardiac death were assessed by an echocardiogram for left ventricular mass, electrocardiogram (ECG) for QRS late potentials, and 24 hour ECG monitoring for ventricular arrhythmias, episodes of silent ischemia, and heart rate variability (to assess adrenergic drive). Vascular reactivity was characterized by heart rate and blood pressure changes during Stroop color card and cold pressor testing. Siblings with an abnormal exercise ECG and/or thallium scan were offered coronary arteriography to assess the severity of angiographic coronary disease and the vasomotor responses to isometric handgrip and intracoronary acetylcholine, an endothelium-dependent vasodilator. In coronary arteries with minimal angiographic disease, changes in coronary vascular resistance during handgrip and acetylcholine were also measured with a doppler flow velocity catheter and the proximal arteries were imaged with intravascular ultrasound.

  Eligibility

Genders Eligible for Study:   Male
Accepts Healthy Volunteers:   No
Criteria

No eligibility criteria

  Contacts and Locations
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No Contacts or Locations Provided
  More Information

Publications:
ClinicalTrials.gov Identifier: NCT00005369     History of Changes
Other Study ID Numbers: 4260
Study First Received: May 25, 2000
Last Updated: June 23, 2005
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Cardiovascular Diseases
Heart Diseases
Coronary Artery Disease
Coronary Disease
Myocardial Ischemia
Arteriosclerosis
Arterial Occlusive Diseases
Vascular Diseases

ClinicalTrials.gov processed this record on September 22, 2014