Cardiovascular Diseases Clinical Trial
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.
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.
The study completion date listed in this record was obtained from the "End Date" entered in
the Protocol Registration and Results System (PRS) record.
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