Ignite Creation Date:
2025-12-24 @ 11:14 PM
Ignite Modification Date:
2025-12-25 @ 8:49 PM
Study NCT ID:
NCT00005369
Status:
COMPLETED
Last Update Posted:
2016-02-18
First Post:
2000-05-25
Is NOT Gene Therapy:
False
Has Adverse Events:
False
Brief Title:
Coronary Artery Disease Mechanisms in High Risk Families--Racial Difference
Sponsor:
National Heart, Lung, and Blood Institute (NHLBI)
Organization:
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2002-04
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
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.
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.
The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
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.
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?:
Secondary ID Infos
| Secondary ID | Type | Domain | Link | View |
|---|---|---|---|---|
| R01HL049762 | NIH | None | https://reporter.nih.gov/quic… | View |